THE ULTIMATE REVIEWER in

MICROBIOLOGY &
PARASITOLOGY
for the PHYSICIAN LICENSURE EXAMINATION

To God be the Greatest Glory!

 PRIMER SVEDBERG UNIT
- Non-SI unit for sedimentation rate
MICROORGANISMS - Sedimentation rate is the rate at which particles of a given size
- Minute organisms that are too small to be seen by the unaided and shape travel to the bottom
eye individually - This reflects to the rate at which a molecule sediments under the
centrifugal force of a centrifuge
Why study microbiology? - The Svedberg is technically a measure of time, and is defined as
-13
• Causative agents of infectious diseases exactly 10 s (100 fs)
• Normal flora
• Environmental importance THE ENDOSYMBIONT THEORY
o Decomposers
o Produce oxygen
o Food chain
o Sewage treatment (bioremediation)
• Industrial importance
o Food industry

o Brewing industry
o Pharmaceutical industry
o Genetic engineering

• Research à genetics and metabolism

o Simple cell structure

o Rapid rate of growth

o Inexpensive to culture



Review of Taxonomy

Domain Kingdom Examples

Archaea Archaebacteria Methanogens, Halophiles
Bacteria Eubacteria Streptococcus, E. coli
Eukarya Protista Amoeba, Paramecium
Fungi Mushroom, yeasts
Plantae Mosses, ferns, flowering plants
Animalia Worms, insects, fish, mammals














GENERALITIES

Roadmap
I. Overview
II. Bacteria Structure
III. Bacterial Growth Cycle
IV. Bacterial Oxygen Metabolism • A large anaerobic heterotrophic prokaryote takes in a small aerobic
prokaryote. Evidence strongly suggests that the prokaryote was an
V. Bacterial Genetics
ancestor of modern-day rickettsia, the group of bacteria that cause
VI. Normal Flora
typhus and other diseases.
VII. Bacterial Pathogenesis • Aerobic endosymbiont has evolved into a mitochondrion.
VIII. Laboratory Diagnosis • A portion of the plasma membrane invaginated and is seen in the
process of evolving into a nuclear envelope and associated
I. OVERVIEW endoplasmic reticulum.
• In one path, a primitive eukaryote evolves into a non-photosynthetic
PROKARYOTES VS. EUKARYOTES protist, fungal and animal cells.
Characteristics PROKARYOTES EUKARYOTES • In the other path, a primitive eukaryote takes in a photosynthetic
prokaryote, which will become an endosymbiont and evolve into a
DNA within a nuclear
No YES chloroplast.
membrane

Mitotic division No YES
GROUPS OF PATHOGENIC MICROORGANISMS
DNA associated with
No YES
Histones
Chromosome number One More than one
Membrane-bound
No YES
organelles
Size of Ribosome 70S 80S
(50S + 30S) (60S + 40S)
Cell wall containing
YES No
peptidoglycan

Prokaryotic ribosomes: 50 + 30 = 70 *Viruses technically speaking, are not considered organisms because they are
S stands for Svedberg unit noncellular pathogens that can only reproduce when present within a living
cell. Remember that the cell is the basic unit of life.
 COMPARISON OF MEDICALLY IMPROTANT MICROORGANISMS























VIROIDS SPONGIFORM ENCEPHALOPATHIES
• obligate intracellular but acellular parasites of plants • appearance of the vacuolated neurons with loss of function
• naked RNA and the lack of an immune response or inflammation
• cause several plant diseases but are not implicated in any
human disease HUMAN PRION DISEASES
• Creutzfeldt-Jacob disease (CJD)
TRANSPOSONS à “transposable” elements • Kuru
• mobile genetic elements • Varian CJD
• DNA pieces that move readily from one site to another either • Gerstmann-Straussler-Scheinker (GSS syndrome)
within or between the DNA of bacteria, plasmids, and • Fatal Familial Insomnia (FFI)
bacteriophagesà “jumping genes” • Sporadic Fatal Insomnia
• Replicative transposition
- DNA replication followed by insertion of new copy into ANIMAL PRION DISEASES
another site • Scrapie (sheep and goats)
• Direct transposition • Transmissible mink Encephalopathy
- DNA is excised from the site without replicating and then • Bovine Spongiform Encephalopathy (BSE)à Mad Cow Disease
inserted into the new site • Chronic wasting disease (mule, deer, elk)
• Code for drug-resistant enzymes, toxins, or metabolic enzymes
• Cause mutations in genes into which they insert or alter the Pathogenesis
expression of nearby genes • Impevious to standard viral disinfection procedures
• Very long incubation periods, as long as 30 years
PRIONS
• Noncellular infectious particles that are composed solely of Transmission
protein (i.e., they contain no detectable nucleic acid) • Sporadic
• Naked proteins that have the same amino acid sequence as • Via infected tissue, cuts in skin
certain normal human cell surface but have folded differently • Transplantation of contaminated tissues (cornea)
c
• The cellular form of the protein PrP is encoded by the host’s • Use of contaminated medical devices (brain electrodes)
chromosomal DNA • Ingestion of infected tissues (cannibalism)
c
• PrP is susceptible to protease and soluble in detergent • Via inherited syndrome
res
• Abnormal isoform (PrP ) modify folding of normal prion-like
proteins found in the body (coded by human genes) and has Susceptible Populations
high beta-sheath content • Women and children of the Fore tribe in New Guinea
• implicated as the cause of certain “slow” diseases called • Neurosurgeons and brain surgery patients
transmissible spongiform encephalopathies • Transplant surgeons and transplant patients
• Prion proteins are encoded by a cellular gene.
o normal, alpha-helix configuration à nonpathogenic Spectrum of Disease
o beta-pleated sheet configuration à aggregate into • Progressive, neurodegenerative diseases
filaments à disrupts neuronal function and results in the o Loss of muscle control
symptoms of disease o Shivering
• highly resistant to inactivation by nucleases, proteases, many o Myoclonic jerks and tremors
chemicals and normal autoclaving à inadvertently transmitted o Loss of coordination
by human growth hormone and neurosurgical instruments o Rapidly progressive dementia
• normal human proteins à do NOT elicit an inflammatory o Death
response or an antibody response in humans
Treatment and Prevention
• No treatment available
• Cessation of ritual cannibalism
• Elimination of animal products from livestock feed
• Disinfection of neurosurgical tools and electrodes
o 5% hypochlorite solution of 1.0 M sodium hydroxide or
autoclaved at 15 psi for 1 hour



PATHOGENESIS OF PRION INFECTION

(a) Tertiary structure of the normal (PrPC) protein as determined by NMR spectroscopy. The orange portions represent -helical segments, and the blue portions
are short strands. The yellow dotted line represents the N-terminal portion of the polypeptide, which lacks defined structure. (b) A proposed model of the
abnormal, infectious (PrPSc) prion protein, which consists largely of -sheet. The actual tertiary structure of the prion protein has not been determined. The two
molecules shown in this figure are formed by polypeptide chains that can be identical in amino acid sequence but fold very differently. As a result of the differences
in folding, PrPC remains soluble, whereas PrPSc produces aggregates that kill the cell. (The two molecules shown in this figure are called conformers because they
differ only in conformation.)


II. BACTERIAL STRUCTURE BACTERIAL CELL WALL
• All bacteria have a cell wall composed of peptidoglycan EXCEPT
BACTERIAL SHAPE AND SIZE Mycoplasma
• Three shapes: o Peptidoglycan = sugar backbone (glycan) + peptide side
o Spheres à cocci chains (peptido) cross-linked by transpeptidase
o Rods à bacilli • LYSOZYMES
o Spirals à spirochetes - kill bacteria by cleaving the glycan backbone (ß 1à4 linkage
• Cocci arranged in three patterns: between GlcNAc and MurNac) of peptidoglycan
o Pairs à diplococci • PORIN PROTEINS
o Chains àstreptococci - play a role in facilitating the passage of small, hydrophilic
o Clusters à staphylococci molecules into the cell
• Smallest bacteria: Mycoplasma species - In the outer membrane of gram-negative bacteria, they act
• Largest bacteria: Thiomargarita namibiensis as a channel to allow the entry of essential substances such
• Largest medically important bacteria: Borrelia burgdorferi as sugars, amino acids, vitamins, and metals as well as many
(causative agent Lyme disease) antimicrobial drugs such as Penicillins




















 Component Gram-Positive Cells Gram-Negative Cells MNEMONICS- Bacteria Not Seen in Gram Stain
Peptidoglycan Thicker; multilayer Thinner; single layer These Little Microbes May Unfortunately Lack Real Color
Teichoic acids YES No But Are Everywhere
Lipopolysaccharides No YES Treponema
Periplasmic space No YES Leptospira
Mycobacteria
GRAM-NEGATIVE CELL WALLS Mycoplasma
• Outer membrane of gram-negative bacteria contains Ureaplasma
endotoxin (lipopolysaccharide/LPS) Legionella
• Consists of lipid A (toxic portion; induces TNF and IL-1) Rickettsia
and O antigen Chlamydia
• Listeria monocytogenes: the only gram-positive bacteria that Bartonella
produce endotoxin Anaplasma
Ehrlichia
GRAM STAINING
STEP PROCEDURE REAGENT ESSENTIAL COMPONENTS OF BACTERIA
1 Primary Stain CRYSTAL VIOLET Cell Wall As described previously
2 Mordant IODINE Cytoplasmic Lipoprotein bilayer Site of oxidative and
3 Decolorizing Agent ACETONE membrane without sterols transport enzymes
4 Counterstain SAFRANIN Ribosome RNA and protein in 50S Protein synthesis
and 30S subunits
COLOR CHANGES DURING GRAM STAIN Nucleoid DNA Genetic material
Mesosome Invagination of plasma Participates in cell
membrane division and secretion
Periplasm Space between plasma Contains many hydrolytic
membrane and outer enzymes, including ß-
membrane lactamases

NON-ESSENTIAL COMPONENTS OF BACTERIA
Capsule Polysaccharide Protects against phagocytosis
Pilus or Glycoprotein Attachment, Conjugation
Fimbria
Glycocolyx Polysaccharide Mediates adherence to
surfaces

Flagellum Protein Motility

Spore Keratin-like coat, Resistance to heat, and

dipicolinic acid chemicals

Plasmid DNA Genes for antibiotic resistance

and toxins
BACTERIA NOT SEEN IN GRAM STAIN
Name Reason Alternative Approach
Granule Glycogen, lipids, Site of nutrients in cytoplasm
Mycobacteria Too much lipid in cell wall polyphosphates
ACID-FAST STAIN
so dye cannot penetrate
Spirochetes Too thin to see • Bacterial capsules are composed of polysaccharide, EXCEPT
DARKFIELD in Bacillus anthracis, which has a capsule of polymerized
(Treponema,
MICROSCOPY D-glutamic acid.
Leptospira)
Mycoplasma sp. No cell wall; very small NONE (SEROLOGIES) • SPORE: formed by gram-positive rods, especially Bacillus
Legionella spp. Poor uptake of red and Clostridium spp.
SILVER STAIN
counterstain
Chlamydiae Intracellular; very small;
lack classic peptidoglycan SPORE-FORMING BACTERIA
INCLUSION BODIES • Some bacteria can form spores at the end of the stationary
because of Ü muramic
acid. phase when nutrients are limited.
Rickettsiae Intracellular; very small GIEMSA/ TISSUE • Spores are highly resistant to heat and chemicals
STAIN • Have dipicolinic acid in their core.
• Have no metabolic activity.
SPORULATION IN BACTERIA • Must autoclave to potentially kill spores (as is done to
O
surgical equipment) by steaming at 121 C for 15 minutes.



Bacillus anthracis Anthrax

Bacillus cereus Food poisoning

Clostridium botulinum Botulism
Clostridium difficile Pseudomembranous colitis
Clostridium perfringens Gas Gangrene
Clostridium tetani Tetanus












PLASMIDS IV. BACTERIAL OXYGEN METABOLISM
• extrachromosomal, double-stranded, circular DNA capable of
replicating independently of the bacterial chromosome AEROBIC and ANAEROBIC GROWTH RATE
• can sometimes be integrated into the bacterial chromosome • Oxygen metabolic generates toxic products such as superoxide
• occur in both gram-positive and gram-negative bacteria and hydrogen peroxide
• several different types of plasmids can exist in one cell: • Superoxide dismutase, peroxidase and catalase are needed to
o Transmissible: from cell to cell by conjugation; large, survive in aerobic environments
contain about a dozen genes for synthesis of the sex pilus
and for the enzymes required for transfer
o Nontransmissible: small, do not contain the transfer genes;
frequently present in many (10-60) copies per cell.
• Significance:
o Antibiotic resistance
o Resistance to heavy metals such as mercury and silver
o Resistance to UV light, which is mediated by DNA repair
enzymes
o Pili (fimbriae): mediate adherence to epithelial cells AEROBIC METABOLISM
o Exotoxins, including several enterotoxins Ø OBLIGATE AEROBES
o Bacteriocins: toxic proteins produced by certain bacteria - completely dependent on oxygen for ATP generation
that are lethal for other bacteria Ø MICROAEROPHILES
§ Colicins made by Escherichia coli - use fermentation but can utilize low amounts of oxygen
§ Pyocins made by Pseudomonas aeruginosa because they have superoxide dismutase
o Nitrogen-fixing enzymes in Rhizobium in the root nodules of
legumes ANAEROBIC METABOLISM
o Tumors caused by Agrobacterium in plants Ø FACULTATIVE ANAEROBES
o Several antibiotics produced by Streptomyces - Utilize oxygen if it is present, but can use fermentation in
o Degradative enzymes produced by Pseudomonas capable of its absence
cleaning up environmental hazards such as oil spills and Ø AEROTOLERANT ANAEROBES
toxic chemical waste sitesà oligoribonuclease - Exclusively anaerobic but insensitive to the presence of
(Bioremediation) oxygen
Ø OBLIGATE ANAEROBES
III. BACTERIAL GROWTH CURVE - Cannot grow in the presence of oxygen because they LACK
the three important enzymes: superoxide dismutase,
peroxidase, and catalase

COMPARISON OF BACTERIAL OXYGEN METABOLISM
ENVIRONMENT
GROUP O2 EFFECT
Aerobic Anaerobic
Obligate aerobe Growth NO growth Required
Microaerophile Required but at low
Growth NO growth
levels (<0.02 atm) only
Facultative Not required for
Anaerobe Growth Growth growth but utilized
when available
Aerotolerant Not required and not
Growth Growth
Anaerobe utilized
PHASE 1: LAG PHASE Obligate Toxic
- Cells are depleted of metabolites as the result of unfavourable No growth Growth
Anaerobe
condition; adaptation to new environment

- Nutrients are incorporated; vigorous metabolic activity occurs
CLASSIFICATION OF BACTERIA BASED ON OXYGEN METABOLISM
but cells do not divide
Obligate • Nocardia
- zero growth rate
aerobes • Neisseria

PHASE 2: LOG OR EXPONENTIAL PHASE • Pseudomonas
- rapid cell division occurs • Mycobacterium
- constant growth rate • Bacillus cereus
- ß-Lactam antibiotics act during this phase • Bordetella
- Continues until either one or more nutrients in the medium • Brucella
become exhausted, or toxic metabolites accumulate and inhibit • Legionella
growth Noisy and Nagging Pests Must Breathe Lots of Oxygen
Microaerophiles • Streptococcus
PHASE 3: MAXIMUM STATIONARY PHASE • Spirochetes (Borrelia, Treponema)
- Exhaustion of nutrients or the accumulation of toxic products • Campylobacter
cause growth to cease completely • Helicobacter
- zero growth rate
- spores are formed Facultative • Mycoplasma (non-pneumonia)
Anaerobes • Corynebacterium
PHASE 4: DECLINE OR DEATH PHASE • Bacillus anthracis
- most of the cells die because nutrients have been exhausted • Listeria
- negative growth rate • Staphylococcus

Aerotolerant • Propionibacterium
PHASE GROWTH RATE
Anaerobes • Lactobacillus
Lag Zero
Exponential / Log Constant Obligate • Clostridium
Maximum Stationary Zero Anaerobes • Bacteroides
Decline / Death Negative • Fusobacterium
• Actinomyces
Can’t Breathe Fresh Air
V. BACTERIAL GENETICS • TRANSDUCTION
BACTERIAL GENETICS o Generalized Transduction
• consists of single chromosome of circular DNA located in the - A “packaging” event
nucleoid - Lytic phage infects bacterium, leading to cleavage of
• bacteria are haploid while eukaryotic cells are diploid bacterial DNA
• bacterial DNA is circular; human nuclear DNA is linear - Parts of bacterial chromosomal DNA may become
• Plasmids are extrachromosomal pieces of DNA encoding both packaged in phage capsid.
exotoxins and enzymes - Phage infects another bacterium, transferring these
genes.
DNA TRANSFER WITHIN BACTERIAL CELLS
• PROGRAMMED REARRANGEMENTS
o the movement of genes from inactive (storage) sites into
active sites of transcriptions; e.g. relapsing fever caused by
Borrelia recurrentis
o consists of the movement of a gene from a silent storage
site where the genes is not expressed to an active site
where transcription and translation occur
o there are many silent genes that encode variants of the
antigens, and the insertion of a new gene into the active
site in a sequential, repeated programmed manner is the
source of the consistent antigenic variation
o these movements are not induced by an immune response
but have the effect of allowing the organism to evade it. o Specialized Transduction
- An “excision” event.
• TRANSPOSITION - Lysogenic phage infects bacterium; viral DNA
o Segment of DNA (eg, transposon) that can “jump” (excision incorporates into bacterial chromosome.
and reintegration) from one location to another, can - When phage DNA is excised, flanking bacterial genes
transfer genes from plasmid to chromosome and vice versa. may be excised with it.
o When excision occurs, may include some flanking - DNA is packaged into phage capsid and can infect
chromosomal DNA, which can be incorporated into a another bacterium.
plasmid and transferred to another bacterium - Genes for the following 5 bacterial toxins are encoded
o Example: vanA gene from vancomycin-resistant in a lysogenic phage (ABCD’S):
Enterococcus to S. aureus î Group A strep erythrogenic toxin
î Botulinum toxin
î Cholera toxin
î Diphtheria toxin
î Shiga toxin





DNA TRANSFER BETWEEN CELLS
• CONJUGATION
F+ X F-
- F+ plasmid contains genes required for sex pilus and
conjugation. Bacteria without this plasmid are termed F–.
- Sex pilus on F+ bacterium contacts F− bacterium.
- A single strand of plasmid DNA is transferred across the
conjugal bridge (“mating bridge”).
- No transfer of chromosomal DNA.
• TRANSFORMATION
- Competent bacteria are able to bind and import short
pieces of environmental naked bacterial chromosomal
DNA (from bacterial cell lysis).
- The transfer and expression of newly transferred genes is
called transformation.
- A feature of many bacteria, especially S. pneumoniae, H.
HFR X F- influenzae type B, and Neisseria (SHiN).
- F+ plasmid can become incorporated into bacterial - Any DNA can be used.
chromosomal DNA, termed high frequency - Adding deoxyribonuclease to environment will degrade
recombination (Hfr) cell. naked DNA in medium à no transformation seen.
- Transfer of leading part of plasmid and a few flanking
chromosomal genes
- High-frequency recombination may integrate some of
those bacterial genes.
- The recipient cell remains F– but now may have new
bacterial genes.

Transfer Type of Cells
Process
Procedure Involved
DNA transferred from one
Conjugation Prokaryotic
bacterium to another
DNA transferred by a virus from
Transduction Prokaryotic
one cell to another
Prokaryotic OR
Transformation Purified DNA taken up by a cell
Eukaryotic

MUTATIONS
Result from 3 types of molecular changes:
• Base substitution
• Frameshift mutation
• Transposons or insertion sequences

Mutations can be caused by chemicals, radiation, or viruses

TRANSDUCTION

























GRIFFITH’S EXPERIMENT - TRANSFORMATION











































VI. NORMAL FLORA ENZYMES IN BACTERIAL INVASION
NORMAL FLORA • Collagenase and Hyaluronidase (spreading factor)
• Microorganisms that are the permanent residents of the body - spread through subcutaneous tissue
• Normal flora are low-virulence organisms in their usual • Coagulase
anatomic site - accelerates formation of a fibrin clot coating the organisms
• Colonization Resistance occurs when normal flora occupy with a layer of fibrin
receptor sites preventing pathogens from binding • Immunoglobulin A (IgA) protease
- allows adherence to mucous membranes
Skin Staphylococcus epidermidis • Leukocidin
Nose Staphylococcus aureus - destroys both neutrophilic leukocytes and macrophages
Mouth Viridans streptococcus
Dental plaque Streptococcus mutans BACTERIA WITH IgA PROTEASE
Colon Bacteroides > E.coli SHiNe My Gong
Vagina Lactobacillus vaginalis, E. coli, Streptococcus pneumonia
Streptococcus agalactiae Haemophilus Infuenzae
Neisseria Meningitidis
INFECTION BIOLOGY Neisseria Gonorrhea
PATHOGENESIS
• Pathogens are microbes that can cause disease VIRULENCE FACTORS
• Opportunistic pathogens cause disease only in • Polysaccharide Capsule
immunocompromised people o most important antiphagocytic factor
• Virulence is a measure of a microbe’s ability to cause disease o protect against phagocytosis
o Determined by virulence factors such as capsules, o anticapsular antibodies allow more effective phagocytosis
exotoxins, or endotoxins to occur (opsonization)
• ID50 is the number of organisms required to cause disease in • Cell Wall Proteins
50% of the population o M proteins of S. pyogenes
- antiphagocytic
BACTERIAL INFECTION - shares similar epitopes to human cellular proteins
• Infection has 2 meanings: (molecular mimicry)
o the presence of microbes in the body - possibly underlies the autoimmune response seen in
o the symptoms of disease acute rheumatic fever
• Presence of microbes in the body does not always result in o Protein A of S. aureus
symptom of disease - Binds to IgG and prevents the activation of
o Example: Salmonella carriage in the gallbladder complement

MECHANISMS OF BACTERIAL DISEASE EXOTOXINS
• Invasion of tissue followed by inflammation • Polypeptides secreted by certain bacteria that alter specific cell
• Production of toxins (both exotoxins and endotoxins) functions resulting in the symptoms of disease
• Immunopathogenesis • Have an A-B subunit structure:
o A subunit: active (toxic) subunità less toxic in toxoids
MODES OF TRANSMISSION o B subunit: binding subunit
HUMAN TO HUMAN NON-HUMAN TO HUMAN • All exotoxins are heat labile, EXCEPT Staphylococcal
o Direct (sexual, transvaginal) o Soil enterotoxin and E. coli heat-stable toxin
o Fecal-oral o Water
o Inhalation o Direct animal source Mechanism of Action of Exotoxins
o Transplacental o Vector-borne MOA Exotoxin
o Blood-borne o Animal excreta ADP-ribosylation î Diphtheria toxin
o Fomites î Cholera toxin
î E. coli heat-labile toxin
BACTERIAL ADHERENCE î Pertussis toxin
• Pili mediate attachment of bacteria Superantigen î Toxic Shock Syndrome toxin
• Glycocalyx mediates strong adherence to the surface of î Staphylococcal enterotoxin
human cells î Erythrogenic toxin
• After the bacteria attach, they often form a protective matrix Protease î Tetanus toxin
called a biofilm consisting of various polysaccharides and î Botulinum toxin
proteins. î Lethal factor of Anthrax toxin
o The production of biofilms by bacteria such as î Scalded skin toxin
Pseudomonas is controlled by the process of quorum Lecithinase î Clostridium perfringens alpha toxin
sensing *Superantigens can elicit widespread activation of the complement
• Surface proteins called curli (Salmonella and E. coli) mediate and coagulation cascades
binding to endothelium and to extracellular proteins such as
fibronectin ENDOTOXINS
o thought to play a role in the production of the thrombi • Lipopolysaccharides (LPS) located in the outer membrane of
seen in the disseminated intravascular coagulation (DIC) gram-negative bacteria
associated with sepsis caused by these bacteria • Lipid A is the toxic component of LPS
o Induces the overproduction of cytokines such as TNF
IN VIVO BIOFILM-PRODUCING BACTERIA and IL-1
S. epidermidis Catheter and prosthetic device o Activates complement cascade
infections o Activates coagulation cascade, resulting in DIC or
Viridans streptococci (S. Dental plaques, infective Disseminated Intravascular Coagulation
mutans, S. sanguinis) endocarditis

P. aeruginosa Respiratory tree colonization in

patients with cystic fibrosis,
ventilator-associated pneumonia.
Contact lens–associated keratitis
Nontypeable (unencapsulated) Otitis media
H. influenzae

 EXOTOXINS vs ENDOTOXINS

ENDOTOXINS














































 EXOTOXINS




































GENERALITIES ON BACTERIAL STRUCTURE SEROLOGIC TESTS
All bacteria have cell walls composed Mycoplasma pneumonia • Determine whether antibodies are present in the patient’s
of Peptidoglycan EXCEPT serum
All gram-positive bacteria have NO Listeria monocytogenes • Detect the antigens of the organism in tissues or body fluids
endotoxin EXCEPT • At least a fourfold increase in titer between the acute and
All bacterial capsules are composed Bacillus anthracis convalescent samples
of Polysaccharides EXCEPT • IgM antibody for acute infection
All exotoxins are heat-labile EXCEPT Staphylococcal enterotoxin
& E. coli heat-stable toxin MOLECULAR TESTS
• Nucleic acid amplification tests, nucleic acid probes, and
VII. LABORATORY DIAGNOSIS nucleic acid sequence analysis
Laboratory Diagnosis • Highly specific, quite sensitive and much faster than culture
• Includes bacteriologic, immunologic (serologic), and molecular • Especially useful for those bacteria that are difficult to culture
(nucleic acid-based) tests such as Chlamydia and Mycobacterium species

BACTERIOLOGIC TESTS IMMUNODEFICIENCY DISORDERS
• Staining the patient’s specimen
• Observing the organism in the microscope IMMUNODEFICIENCY
• Culturing on blood agar • State in which the immune system’s ability to fight infectious
• Performing various test to identify the causative organism disease is compromised
• Obtaining a pure culture is essential to accurate diagnosis • Can occur if any of the four major components of the immune
system are compromised:
PROPERTIES OF GROWTH MEDIA o B cells
• SELECTIVE MEDIA o T cells
î Favors the growth of particular organism while preventing o Phagocytes
growth of other organisms o Complement
î eg, Thayer-Martin agar contains antibiotics that allow the
selective growth of Neisseria by inhibiting the growth of IMMUNODEFICIENCY STATES
other sensitive organisms 1. Recurrent infections with pyogenic bacteria indicate a B-cell
• INDICATOR (DIFFERENTIAL) MEDIA deficiency
î Yields a color change in response to the metabolism of 2. Recurrent infections with fungi, viruses or protozoan indicate
certain organisms a T-cell deficiency
î eg, MacConkey agar contains a pH indicator; a lactose
fermenter like E. coli will convert lactose to acidic Types:
metabolites à color change PRIMARY IMMUNODEFICIENCY SECONDARY IMMUNODEFICIENCY
Genetic susceptibility to Acquired susceptibility to
SPECIALIZED MEDIA FOR BACTERIAL GROWTH infections since childhood infection as a result of external
Agar Bacteria Isolated Properties of Agar processes or diseases
Blood Agar Various gram- Determines pattern of EXAMPLES: EXAMPLES:
positive cocci hemolysis
î IgA deficiency î Malnutrition
MacConkey Various enteric Selects against gram-positive
î Bruton’s X-linked î Aging
gram-negative rods bacteria and differentiates
agammaglobulinemia (XLA) î Drugs
Eosin-methylene Various enteric between lactose fermenters
gram-negative rods and non-fermenters
î AIDS
blue (EMB)
Various enteric Distinguishes lactose

Triple sugar Iron
gram-negative rods fermenters from non- PRIMARY IMMUNODEFICIENCIES
(TSI)
fermenters and H2S
producers from B CELL DISORDERS
nonproducers
1. X-LINKED AGAMMAGLOBULINEMIA / BRUTON’S
Bacteria Agar AGAMMAGLOBULINEMIA
Clostridium perfringens Egg yolk Mechanism:
Corynebacterium diphtheriae Tellurite, Löffler medium • Very low levels of all immunoglobulins
Group D Streptococci Bile Esculin - Virtual absence of B cells due to tyrosine kinase
Staphylococci Mannitol salts mutation
N. meningitides, N. gonorrheae Chocolate • Cell-mediated immunity is normal
from sterile sites (Blood, CSF)
N. gonorrhoeae from nonsterile Thayer-Martin Clinical presentation:
sites (oral, GUT discharge) • Male infants at about 6 months of age
Haemophilus influenzae Chocolate + Factors X & V • Recurrent pyogenic bacterial infections
Mycobacterium tuberculosis Löwenstein-Jensen • Recurrent enteroviral infections
• Recurrent giardiasis
Vibrio cholera Thiosulfate Citrate Bile Salts

(TCBS)
Treatment:
Bordetella pertussis Bordet-Gengou,
• Pooled gamma globulin
Regan-Lowe medium

Campylobacter, Helicobacter Skirrows 2. SELECTIVE IgA DEFICIENCY
Borrelia burgdorferi Barbour-Stoenner Kelly (BSK) Mechanism:
Mycoplasma pneumoniae Eaton • Failure of isotype switching
Pseudomonas aeruginosa Cetrimide
Salmonella, Shigella Xylose-Lysine-Deoxycholate Clinical presentation:
(XLD) • Recurrent bacterial sinus and lung infections
Leptospira interrogans Ellinghausen-McCollough-
Johnson-Harris (EMJH)/ Treatment:
Fletcher’s • DO NOT treat with gamma globulin preparations
Legionella Charcoal yeast extract agar - Form antibodies against foreign IgA
buffered with cysteine and iron - Cross-reaction depletes their already low IgA or
may cause anaphylaxis
 3. COMMON VARIABLE IMMUNODEFICIENCY 2. WISKOTT-ALDRICH SYNDROME
- Most common form of severe antibody deficiency Mechanism:
affecting both children and adults • X-linked (affects male infants)
• Inability to mount IgM response
Mechanism: • Mutation in WASP gene for actin filament assembly
• Defect in B-cell maturation to plasma cells
Clinical manifestation:
Clinical presentation: • Recurrent pyogenic infections, eczema, and bleeding
• Diagnosis of exclusion due to thrombocytopenia
• Recurrent pyogenic bacterial infections
Treatment:
Treatment: • Bone marrow transplant
• Pooled gamma globulin
Wiskott-Aldrich Syndrome
T-CELL DISORDERS “How do you TIE a WASP?”

Thrombocytopenia
1. DI GEORGE SYNDROME
Infections
aka Velocardiofacial Syndrome
Eczema

WASP mutation
Mechanism:
• Profound deficit of T cells
- Failure of development of thymus and parathyroid 3. ATAXIA-TELANGIECTASIA
- Due to a defect in 3rd and 4th pharyngeal pouches Mechanism:
• Humoral immunity is normal • Autosomal recessive disease
• Mutations in DNA repair enzymes
Clinical presentation: • IgA deficiency

• Tetany due to hypocalcemia
Clinical presentation:
• Severe viral, fungi, or protozoal infections during
infancy • Ataxia
• Telangiectasia
Treatment: • Recurrent infections by 2 years of age

• Transplant of fetal thymus (14 weeks old or less)
Treatment:

• Supportive management
DiGeorge Syndrome
CATCH-22 PHAGOCYTIC DISORDERS
Cardiac defect (TOF)

Abnormal facies 1. CHONIC GRANULOMATOUS DISEASE

Thymic aplasia Mechanism:
Cleft palate • Lack of NADPH oxidase activity

Hypocalcemiaà Tetany o Failure of oxidative burst

22q11.2 chromosomal deletion • Normal B- and T-cell activity

Clinical presentation:

• Recurrent infections with:
2. CHRONIC MUCOCUTANEOUS CANDIDIASIS
o Catalase-positive bacteria
Mechanism:
o Fungi (A. fumigatus)
• Specific T-cell deficiency for Candida albicans
• Widespread granulomas of unknown etiology
• Other T-cell and B-cell functions are normal
Treatment:
Clinical presentation: • Antibiotic chemoprophylaxis
• Recurrent candidiasis (skin, mucous membranes) in
children 2. CHEDIAK-HIGASHI SYNDROME
Mechanism:
Treatment: • Autosomal recessive disease
• Azole antifungal drugs • Failure of phagolysosomal fusion
• Faulty microtubules impair neutrophil chemotaxis
COMBINED B- AND T- CELL DISORDERS
Clinical presentation:
1. SEVERE COMBINED IMMUNODEFICIENCY (SCID) • Recurrent pyogenic infections caused by Staphylococci
Mechanism: and Streptococci
• X-linked: defect in IL-2 receptors in T-cell
• Autosomal: Adenosine deaminase (ADA) deficiency Treatment:
- In ADA deficiency, Û dATP à toxicity in • Antibiotics
lymphocytes
3. LEUKOCYTE ADHESION DEFICIENCY (LAD)
Clinical presentation: Mechanism
• Recurrent bacterial, viral, fungal, and protozoal • Autosomal recessive disease
infection in early infancy (3 months of age) • Mutations in integrins
• Defective adhesion (LFA-1) proteins on the surface
Treatment: phagocytes

• Enclosure in plastic bubble
Clinical presentation
• Bone marrow transplant
• Severe pyogenic infections in infancy

• Delayed separation of umbilical cord

Treatment

• Antibiotics

• Bone marrow transplant
COMPLEMENT DISORDERS
EARLY
Complement Deficiency
TERMINAL
Complement Deficiency
FRUITS OF PATHOLOGY

C2 Deficiency Mechanism:
• Specific in C5-C9 STRAWBERRY Cervix Trichomoniasis
• Most common
complement defect • Inability to form membrane- Tongue TSS
• Usually asymptomatic but attack complexes Kawasaki
may develop septicemia or Scarlet Fever
SLE Clinical presentation:
• Bacteremia with Neisseria Gallbladder Cholesterolosis
C3 Deficiency
meningitides or Neisseria
• Recurrent pyogenic BERRY Aneurysms Subarachnoid Hemorrhage
gonorrhoea
infectious due to
ADPKD
Staphylococcus aureus Treatment: Coarctation of Aorta
• Vaccination
MULBERRY Molars Congenital Syphilis
SUMMARY OF PRIMARY IMMUNODEFICIENCIES
DEFICIENCY Bacteria Viruses Fungi Protozoa Examples Tumor Tuberous Sclerosis
Bruton’s, XLA,
B- Cells YES YES No YES IgA deficiency Colonies Mycoplasma pneumoniae
DiGeorge
T- Cells No YES YES YES Syndrome
BLUEBERRY Muffin Baby Congenital Rubella
Cytomegalovirus
B- Cells and T-
YES YES YES YES SCID, WAS, AT
Cells GRAPE-LIKE Vesicles Hydatidiform Mole
CGD, LAD,
Phagocytes YES No YES No Chediak-Higashi
Clusters Staphylococcus aureus
YES
Complement No No No C5-C9 deficiency Bunches Sarcoma Botryoides
Neisseria
Odor Pseudomonas aeruginosa
SECONDARY IMMUNODEFICIENCIES
CHERRY RED Epiglottis Epiglottitis
1. MALNUTRITION
Mechanism: Spot in Macula CRAO
• Decreased supply of amino acids Tay-Sachs
• Decreased synthesis of IgG and Complement Niemann-Pick
Pigment Serratia marsescens
Clinical presentation:
• Malnourished child with recurrent pyogenic infections BANANA- Gametocyte P. falciparum
SHAPED
Treatment: Left ventricle Hypertrophic
• Antibiotics cardiomyopathy
• Nutritional support ORANGE -Peel skin Inflammatory Breast CA

2. AIDS -Cast skin Leptospirosis
Mechanism:
• HIV infects and kills CD4+ Helper T-cells Colonies Nocardia asteroides
• Loss of cell-mediated immunity PEAR-SHAPED Organ Prostate Gland

Clinical presentation: Trophozoites Trichomonas vaginalis
• Opportunistic infections caused by bacteria, viruses,
fungi, and protozoa

Treatment:
• Highly-active Antiretroviral Therapy (HAART)



Who will be the three happiest persons when you
pass the Physician Licensure Examination?

1. __________________________________
2. __________________________________

3. __________________________________
__




Believe in yourself and your dreams


will never be out of reach…





 MEDICAL BACTERIOLOGY

GRAM-POSITIVE COCCI
GRAM-STAIN OTHER FEATURES ORGANISM
Catalase-positive ENCAPSULATED BACTERIA
Staphyloccus aureus - capsules serve as an antiphagocytic virulence factor
Coagulase-positive
Catalase-positive - are opsonized, and then cleared by spleen
Gram Positive Cocci Coagulase-negative Staphyloccus epidermidis - Asplenics have Ü opsonizing ability and thus Û risk for severe infections
- Give S. pneumoniae, H. influenzae, N. meningitidis vaccines
in Clusters Novobiocin-sensitive
Catalase-positive
Some Killers Have Pretty Nice, Elegant, Shiny Bodies
Coagulase-negative Staphyloccus saprophyticus
Novobiocin-resistant Streptococcus pneumoniae
Klebsiella pneumoniae
Haemophilus Influenzae type B
GRAM-STAIN OTHER FEATURES ORGANISM
Catalase-negative Pseudomonas aeruginosa
Alpha-hemolytic Streptococcus pneumoniae Neisseria meningitidis
Bile-optochin-sensitive Escherichia coli
Catalase-negative Salmonella typhi
Alpha-hemolytic Viridans streptococci
Group B Strep
Bile-optochin-resistant

Gram Positive Cocci Catalase-negative Streptococcus pyogenes
in Chains Beta-hemolytic (Group A Beta Hemolytic Streptococcus
Bacitracin-sensitive / GABHS)
CATALASE-POSITIVE ORGANISMS
Catalase-negative - Catalase degrades H2O2 into H2O and bubbles of O2 before it can be
Streptococcus agalactiae converted to microbicidal products by the enzyme myeloperoxidase
Beta-hemolytic
(Group B Streptococcus / GBS)
Bacitracin-resistant - People with chronic granulomatous disease (NADPH oxidase deficiency)
Catalase-negative have recurrent infections with certain catalase-positive organisms
Group D Streptoccocci
Gamma-hemolytic
PLACES NBSH
Pseudomonas
GRAM-POSITIVE BACILLI Listeria

GRAM-STAIN O2 UTILIZATION OTHER FEATURES ORGANISM
Aspergillus
Non-motile
Candida
Box-car-shaped Bacillus anthracis
Aerobic Medusa head E. coli
Motile Staphylococci
Bacillus cereus Nocardia
Reheated Fried Rice
Spore-forming Drumstick-, tennis B. cepacia
gram-positive racket-, or lollipop- Clostridium tetani Serratia
rods like H. pylori
Bulging cans Clostridium botulinum
Anaerobic
Lecithinase
Double hemolysis Clostridium perfringens PIGMENT-PRODUCING BACTERIA
Gas-forming
Actinomyces israelii Yellow “sulfur” granules
Pseudomembranes Clostridium difficile
Staphylococcus aureus Yellow pigment
Non-motile
Non-Spore- Corynebacterium Pseudomonas aeruginosa Blue-green pigment
Curved
diphtheria (pyocyanin and pyoverdin)
forming gram- Aerobic Chinese characters
Curved Serratia marcescens Red pigment
positive rods Listeria monocytogenes
Tumbling Motility




 TREATMENT AND
MICROORGANISM RESERVOIR TRANSMISSION METABOLISM VIRULENCE FACTORS TOXINS CLINICAL SYNDROMES DIAGNOSIS NOTES
PREVENTION
Staphylococcus Human nose Direct contact (Hands) Catalase-positive IMMUNOMODULATORS: Exofoliatin: causes PYOGENIC: Methicillin-sensitive GRAM-STAIN: 95% resistance to
aureus (anterior nares) To test, rub a wire Protein A: prevents epidermal separation SKIN and SOFT TISSUE INFECTIONS SA (MSSA) reveals gram-positive penicillins
and skin Fomites loop across a colony complement activation; in Scalded Skin î bullous impetigo, folliculitis, furuncles, î Penicillinase- cocci in grape-like
of gram-positive binds IgG, preventing Syndrome carbuncles, cellulitis, hidradenitis resistant cluster 60% MRSA in the

Contaminated food cocci and mix on a opsonization and suppurativa, mastitis, surgical site penicillins Philippines
slide with H202. If phagocytosis infections
Enterotoxins (heat- (nafcillin, oxacillin, CULTURE:
bubbles appear,
- Beta-hemolytic Community acquired
stable): superantigens ACUTE ENDOCARDITIS and dicloxacillin)
this indicates that
Coagulase: Allows insoluble causing food - Produces a golden methicillin resistant
H202 is being broken î most common cause of acute
fibrin formation around poisoning Methicillin-resistant yellow colonies on Staphylococcus
down into oxygen endocarditis
organism, protecting it SA (MRSA) blood agar aureus (CA-MRSA)
bubbles and water; î native valve (tricuspid valve) in IV
catalase-positive from phagocytosis Toxic shock î contain altered - “Gold color” is due produces a particular
drug abusers
staphylococci are syndrome toxin penicillin-binding to pigment leukocidin called
present. Hemolysins (cytotoxins): PNEUMONIA protein (PRB) STAPHYLOXANTHIN Panton-Valentine
(TSST-1): superantigen
toxic to hematopoietic cells î nosocomial pneumonia, VAP, î due to resistance Leukocidin
leading to toxic shock
Coagulase-positive necrotizing pneumonia gene mecA Polymerase chain (PVL), which is
syndrome
Leukocidin: specific for î complicated by empyema, abscess or î DOC is reaction (PCR): mecA associated with a

Salt-tolerant on WBCs pneumatocele vancomycin gene for MRSA propensity to form
Alpha toxin: causes
Mannitol salt agar î post-viral pneumonia abscesses
marked necrosis of the
(halotorelant) Catalase: detoxifies
skin and hemolysis OSTEOMYELITIS and SEPTIC ARTHRITIS Vancomycin-
hydrogen peroxide resistant SA (VRSA)
î from hematogenous spread or local
Facultative anaerobe introduction at wound site î DOC is linezolid
Penicillinase: secreted form
î Brodie Abscess: sequestered focus of Causes of
of beta-lactamase; disrupts
osteomyelitis arising in the Necrotizing
the beta-lactam portion of
metaphyseal area of a long bone Pneumonia
the penicillin molecule,
thereby inactivating the TOXIGENIC: î S. aureus
antibiotic GASTROENTERITIS î Pseudomonas
î acute onset (4 hrs) of vomiting and î Aspergillus
TISSUE PENETRANCE: diarrhea due to ingestion of preformed î Viral Pneumonia
Hyaluronidase: "Spreading heat-stable enterotoxin
Factor"; breaks down î source: salad made with mayonnaise
proteoglycans in connective (potato or tuna salad)
tissue (hyaluronic acid)

SCALDED SKIN SYNDROME (Ritter

Fibrinolysin Disease)
(Staphylokinase): dissolves î exfoliatin cleaves desmoglein in
fibrin clots desmosomes
î separation of skin at stratum
Lipase: spread in fat- granulosum (vs TENS/Lyell disease:
containing areas of the separation occurs at dermo-epidermal
body junction)

TOXIC SHOCK SYNDROME
Protease: destroys tissue î fever, hypotension, sloughing of
proteins filiform papillaeàstrawberry tongue,
desquamating rash and multi-organ
involvement (>3)
î usually no site of pyogenic
inflammation; blood CS negative
î tampon-using menstruating women or
in patients with nasal packing for
epistaxis
 TREATMENT AND
MICROORGANISM RESERVOIR TRANSMISSION METABOLISM VIRULENCE FACTORS TOXINS CLINICAL SYNDROMES DIAGNOSIS NOTES
PREVENTION
Staphylococcus Humans (normal Autoinfection Catalase-positive Polysaccharide capsule: Most common cause of: Vancomycin (50% GRAM STAIN: NOVOBIOCIN
epidermidis skin flora) Direct contact (hands) adheres to a variety of - prosthetic valve endocarditis methicillin gram-positive cocci in
Coagulase-negative Sensitive
prosthetic devices; forms a - septic arthritis in prosthetic joints resistance) clusters

- ventriculoperitoneal shunt Epidermidis
Facultative anaerobe biofilm
infections Removal of CULTURE: Resistant
Novobiocin-sensitive Highly resistant to prosthetic device White colonies on Saprophyticus
(Novo SERS) antibiotics blood agar, non-
hemolytic
Staphylococcus Humans Catalase-positive UTI IN WOMEN Fluoroquinolones GRAM STAIN:
nd
î S. saprophyticus is the 2 most gram-positive cocci in

saphrophyticus Coagulase-negative
common cause of UTI in sexually TMP-SMX clusters

Facultative anaerobe

active women
[

Nitrite-negative CULTURE:
(unlike E. coli) Whitish, non-

Novobiocin-resistant hemolytic on blood

(Novo SERS) agar
Streptococcus Humans Respiratory droplets Catalase-negative Hyaluronidase: degrades Erythrogenic toxin: PYOGENIC: DOC is Penicillin G GRAM STAIN: Disease of poverty
pyogenes hyaluronic acid (spreading produces scarlet fever IMPETIGO CONTAGIOSA: perioral Gram-positive cocci in
Bacitracin-sensitive factor) blisters with honey-colored crust; Patients with a chains The antigenic
(B-BRAS) Streptolysin O accumulation of neutrophils beyond the history of rheumatic components of the
Group A Beta- Beta-hemolytic
Bacitracin Streptokinase (fibrinolysin) (oxygen-labile): highly stratum corneum; complication includes fever require long- streptococcal cell
Hemolytic Group B Strep *Anti-streptokinase antigenic, causes AB PSAGN term antibiotic

wall:
Lancefield group A
Streptococcus Resistant antibodies decrease efficiency formation; destroys
prophylaxis to - C carbohydrate:
ERYSIPELAS: superficial infection
(GABHS) Group A Strep of streptokinase in managing RBCs and WBCs; and is prevent recurrence Positive PYR test for Lancefield
Sensitive MI
extending into dermal lymphatics
the reason for the
of the disease PYR test measures typing
beta hemolysis CELLULITIS: deeper infection involving hydrolysis of 1-
- M protein (80
DNase (streptodornase): *ASO Titers to subcutaneous/dermal tissues; facilitated pyrrolidonyl-B-
naphthylamide and types): a major
degrades DNA in exudates document antecedent by hyaluronidase (spreading factor)
or necrotic tissue

release of B- virulence factor
PHARYNGITIS PHARYNGITIS: most common bacterial
*Anti-DNAse B to document naphthylamine, which in for the group A
cause of sore throat the presence of p- streptococcus;
antecedent SKIN infection Streptolysin S

(oxygen-stable): not TOXIGENIC: dimethylaminocinnamal inhibits the

C5a peptidase: inactivates antigenic SCARLET FEVER: “second disease”; dehyde forms a red activation of
complement C5a compound complement and
post-pharyngitic; due to erythrogenic
Advantage: takes <1min protects the
Pyogenic exotoxin A: toxin; seen in lysogenized strains; fever,
to determine whether organism from
superantigen similar to strawberry tongue, sandpaper-like the reaction is positive
TSST centrifugal rash, Pastia’s lines, phagocytosis; also
(S. pyogenes or group D
desquamation; Dick test for the weakest point
strep) or negative (all
Exotoxin B: protease susceptibility other Streptococci) in the organism's
that rapidly destroys
defense
STREPTOCOCCAL TOXIC SHOCK
tissue → necrotizing ACUTE RHEUMATIC FEVER
SYNDROME: clinically similar but milder Fournier's gangrene:
fasciitis - Post-pharyngitic
than S. aureus TSS; due to pyogenic form of necrotizing
- Cross-reacting antibodies to M proteins
exotoxin A; recognizable site of pyogenic fasciitis involving the
and antigens of joint, heart, and brain
inflammation; blood cultures are often male genital area and
tissue
positive perineum; often caused
- Diagnosed using the Jones Criteria by mixed organisms but
NECROTIZING FASCIITIS: rapidly
can be caused by GABHS
progressive infection of deep GLOMERULONEPHRITIS
subcutaneous tissues; facilitated by - Post-pharyngitic (commonly M12) OR
exotoxin B post-impetigo
- M protein incites immune-complex
IMMUNOLOGIC: deposition
ACUTE RHEUMATIC FEVER - S/S: Hypertension, periorbital edema,
APSGN hematuria
 TREATMENT AND
MICROORGANISM RESERVOIR TRANSMISSION METABOLISM VIRULENCE FACTORS TOXINS CLINICAL SYNDROMES DIAGNOSIS NOTES
PREVENTION
Streptococcus Vagina Transvaginally Catalase-negative UTI in pregnant women DOC: Penicillin G Gram-positive cocci in Most common cause
agalactiae / chains of neonatal sepsis in
Group B Transplacentally Bacitracin-resistant NEONATAL PNEUMONIA, SEPSIS, AND Penicillin G + the world (the
(B-BRAS) MENINGITIS: Group B Streptococcus is Aminoglycoside for Beta-hemolytic universe, rather) J
streptococcus
the most common cause; predisposing serious infections
Grows using LIM factors include: intrapartum fever >38C, CAMP test–positive: CAUSES OF
broth PROM (>18h), vaginal colonization, and All pregnant women CAMP factor enlarges NEONATAL
complement deficiency should be screened the area of hemolysis MENINGITIS:
Hydrolyzes hippurate for GBS colonization formed by S. aureus î GBS
ENDOMETRITIS → most commonly at 35-37 wks AOG; if î Escherichia coli

polymicrobial; foul-smelling lochia (+), chemo- Lancefield group B î Listeria
prophylaxis with IV monocytogenes
penicillin or
Ampicillin 4h prior
to delivery
Group D Human colon May enter Catalase-negative UTIs due to indwelling urinary catheters Penicillin plus Gram-positive cocci in There is a remarkable
streptococci bloodstream during and urinary tract instrumentation gentamicin chains association between
GIT or GUT surgery Bile and optochin- S. bovis infection
Urethra and female resistant BILIARY TRACT INFECTIONS Vancomycin for Gamma hemolytic and colon cancer
genital tract can be penicillin-resistance colonies
colonized Hydrolyzes esculin in ENDOCARDITIS in patients who
bile esculin agar underwent GIT surgery due to Linezolid for Lancefield group D
(BEA) Enterococcus faecalis vancomycin-
resistant strains Positive PYR test
E. faecalis can grow MARANTIC ENDOCARDITIS in patients
in 6.5% NaCl while S. with abdominal malignancy due to
bovis cannot Streptococcus bovis
Streptococcus Upper respiratory Respiratory droplets Catalase-negative Polysaccharide Capsule: PNEUMONIA: most common cause of Penicillin G Gram-positive Polyvalent (23-type)
pneumoniae / tract retards phagocytosis; major CAP in adults; rust-colored sputum "lancet-shaped" cocci polysaccharide
Pneumococcus Bile and optochin- virulence factor; has 84
Levofloxacin or in pairs or chains vaccine
sensitive OTITIS MEDIA: most common cause in Vancomycin

serotypes; antigenic Alpha-hemolytic
OVRPS (overpass) children combined with Conjugated vaccine:

*Optochin sensitivity IgA protease: for BACTERIAL MENINGITIS: most common Ceftriaxone for Positive Quellung pneumococcal
differentiates Strep colonization cause in adults penicillin resistance reaction: capsular polysaccharide
pneumoniae from
swelling when mixed with a coupled with carrier
Viridans strep (since SINUSITIS small amount of antiserum protein (diphtheria
c-substance: reacts with
both are alpha (serum with antibodies to toxoid)
CRP SEPTIC SHOCK: splenectomy predisposes the capsular antigens)
hemolytic)
to sepsis from encapsulated bacteria and methylene blue


No Lancefield antigen

Viridans Oral flora Enters bloodstream Catalase-negative Glycocalyx enhances DENTAL CARIES: S. mutans Penicillin G +/- Gram-positive cocci in OVeRPaSs
Streptococci during dental
adhesion to damaged aminoglycoside chains
Bile and optochin- SUBACUTE BACTERIAL ENDOCARDITIS OPTOCHIN
procedures heart valves (Gentamicin)
resistant
(SBE): S. sanguis à most common cause Alpha-hemolytic Viridans
OVRPS (overpass) Vancomycin for
Protected from host of subacute and native valve Resistant
Viridans strep live in the endocarditis penicillin-resistance
mouth because they are defenses within

Pneumoniae
vegetations Linezolid for
not afraid of the chin
(op-to-chin resistant) BRAIN ABSCESSES: S. intermedius Sensitive
vancomycin-
resistant strains

 TREATMENT AND
MICROORGANISM RESERVOIR TRANSMISSION METABOLISM VIRULENCE FACTORS TOXINS CLINICAL SYNDROMES DIAGNOSIS NOTES
PREVENTION
Bacillus anthracis Herbivores Contact with infected Aerobic (but since it Protein capsule: polymer of Exotoxin (encoded on CUTANEOUS ANTHRAX: Cutaneous Anthrax: Aerobic, gram-positive Bacillus anthracis is
(zoonotic): animals or inhalation can grow without gamma-D-glutamic acid; plasmin pXO1) - Most common route of entry (95%) DOC is ciprofloxacin box-car shaped rods; the only bacterium
- Sheep of spores from animal oxygen. It is classified antiphagocytic; encoded contains 3 separate - Direct epidermal contact with spores spore-forming; NON- with a capsule
- Goats hair or wool as a facultative on a plasmid called pXO2 proteins, which by causes localized tissue necrosis, Inhalational / MOTILE composed of protein
- Cattle (woolsorter’s disease) anaerobe) themselves are evidenced by a painless round black Gastrointestinal (poly-D-glutamic
nontoxic but lesion with a rim of edema Anthrax: Medusa head acid).
Habitat is soil Human-to-human Virulence depends on together produce the (malignant pustule) Ciprofloxacin or morphology on
transmission has never acquiring 2 plasmids. One systemic effects of - 20% mortality rate Doxycycline with 1 culture: dry “ground Infections result to
been reported. carries the gene for the INHALATIONAL/PULMONARY ANTHRAX: or 2 additional glass” surface and permanent immunity

anthrax:
protein capsule (pXO2); the - Edema factor (EF): antibiotics irregular with (if the patient
- inhaled spores from animals
other carries the gene for its the active A subunit (Woolsorter’s disease) or from (Rifampin, projections along lines survives)
exotoxin (pXO1) of the exotoxin;
weaponized preparations Vancomycin, of inoculation
calmodulin-
(bioterrorism) Penicillin, RAXIBACUMAB:
dependent
- prolonged latent period (2mos) Imipenem, Serology monoclonal antibody
adenylate cyclase
before rapid deterioration Clindamycin, for use in inhalational
- Protective antigen
- massively enlarged mediastinal Clarithromycin) PCR of nasal swab anthrax
(PA): promotes

entry of EF into lymph nodes; pulmonary
hemorrhage (MCC of death); Vaccine: for high-
Cutaneous Anthrax phagocytic cells
meningeal symptoms risk individuals;
- Lethal factor (LF):
- 100% mortality rate without composed of the
zinc metallo- MCC of death is
immediate treatment protective antigen
protease that pulmonary
(PA); Animal
inactivates protein GASTROINTESTINAL ANTHRAX: hemorrhage in:
vaccine is
kinase; stimulates - ingestion of live spores leads to UGI - Anthrax
composed of a live
the macrophage to ulceration, edema, and sepsis - Leptospirosis
strain, attenuated
release TNF-a and - vomiting abdominal pain, bloody (Weil’s syndrome)
by loss of its
IL-1B à death diarrhea protein capsule
- Congenital syphilis
PA + EF = Edema Toxin - rapidly progressive course
PA + LF = Lethal Toxin - mortality approaches 100%

Bacillus cereus Endospores No capsule ENTEROTOXINS EMETIC FORM DIARRHEAL FORM Food Poisoning: Aerobic, gram-positive
Heat-labile: similar to Rice Meat, vegetables Symptomatic spore-forming rod;
Spores on grains such the enterotoxin of Short IP: <6 hrs Long IP: >6 hrs treatment only; MOTILE
as rice survive cholera and the LT (mean, 2h) (mean, 9h) food poisoning
steaming and rapid from E. coli; causes Vomiting, nausea, Diarrhea, nausea, is caused by the Culture specimen from
frying ADP-ribosylation, abdominal cramps abdominal cramps pre-formed suspected food source
increasing cAMP enterotoxin
Shorter duration: Longer duration:
Spores germinate
8-10h (mean, 9) 20-36h (mean, 24)
when rice is kept Heat-stable: Ophthalmitis:
Heat-stable Heat-labile
warm for many hours staphylococcal-like Vancomycin
enterotoxin enterotoxin
(e.g., reheated fried enterotoxin functions Clindamycin
Similar to Resembles
rice) à Chinese fried as superantigen Ciprofloxacin
staphylococcal clostridial
rice syndrome Gentamicin
food poisoning gastroenteritis


Resistant to beta-
OPHTHALMITIS: occur after penetrating
lactam antibiotics
eye injuries of the eye with soil-

contaminated object; complete loss of
light perception within 48 h of injury
 TREATMENT AND
MICROORGANISM RESERVOIR TRANSMISSION METABOLISM VIRULENCE FACTORS TOXINS CLINICAL SYNDROMES DIAGNOSIS NOTES
PREVENTION
Clostridium tetani Habitat is soil Endospores: Spores germinate Motile: Flagella (so H- Tetanus Toxin TETANUS Debridement of Anaerobic, gram- Obligate Anaerobes
introduced through under anaerobic antigen-positive) (Tetanospasmin) - “the acute onset of hypertonia or … primary wound positive, spore-forming Can’t Breathe Fresh Air
wound or traumatic conditions in the painful muscular contractions (usually
rods, often with an Clostridium
break in the skin wound Tetany occurs after the of the muscles of the jaw and neck) Metronidazole endospore at one end
tetanus toxin is taken up and generalized muscle spasms or Penicillin (see Bacteroides
- Skin popping in IV (terminal spore), giving
drug use at the neuromuscular without other apparent medical notes)
them the appearance Fusobacterium
junction (end plate) and cause” --CDC Actinomyces
- Stepping on a nail is transported to the
of a drumstick, tennis
- strong muscle spasm Tetanus toxoid:
central nervous system racket, or lollipop
- lockjaw (trismus) vaccination with
(retrograde transport).
- risus sardonicus formalin-
There the toxin acts on the
TETANUS PROPHYLAXIS inhibitory Renshaw cell - opisthotonos inactivated toxin

interneurons, preventing - respiratory muscle paralysis (toxoid), part of the
VACCINATION HISTORY Metronidazole (400
the release of GABA and DPT vaccine; given
Uncertain or <3 doses >3 doses mg rectally or 500 mg
WOUND glycine, which are in childhood and IV every 6 h for 7 days)
Toxoid Toxoid inhibitory NEONATAL TETANUS is defined by the q10yrs thereafter
TIG (ATS) TIG (ATS) is the preferred
(TeANA) (TeANA) neurotransmitters. This World Health Organization (WHO) as “an
NO (Yes, only inhibition of inhibitory antibiotic. An
illness occurring in a child who has the Antitoxin (ATS): alternative is penicillin
Clean, minor YES NO if last dose NO interneurons allows motor
normal ability to suck and cry in the first 2 human tetanus Requires anaerobic (100,000–200,000
neurons to send a high
given >10y) days of life but who loses this ability immune globulin IU/kg per day),
frequency of impulses to conditions
NO (Yes, only between days 3 and 28 of life and becomes (TIG) at the wound
muscle cells, which results although this drug
Contaminated YES YES if last dose NO in a sustained tetanic rigid and has spasms.” site à Passive theoretically may
given >5y) contraction. exacerbate spasms.
Supportive therapy: (Harrisons)
may require
ventilator
assistance

Clostridium Habitat is soil Endospores (heat Anaerobic Motile: Flagella (so H- Botulinum toxin: FOOD-BORNE BOTULISM: eye symptoms Trivalent Botulinum Anaerobic, gram- TRIAD OF BOTULISM:
botulinum resistant) antigen-positive) - heat-labile (BOV, diplopia, ptosis, mydriasis), bulbar Antitoxin (for food- positive, spore-forming - Symmetric
Alkaline neurotoxin signs (diplopia, dysphonia, dysarthria, borne and wound rods descending flaccid
vegetables such as - inhibits release of dysphagia) anticholinergic effects (dry botulism) paralysis (with
green beans, acetylcholine from mouth, constipation, abdominal pain), Culture: requires prominent bulbar
peppers and peripheral nerves à bilateral descending flaccid paralysis, Human botulism: anaerobic condition involvement)
mushroom: flaccid paralysis respiratory paralysis immunoglobulin (thioglycollate- - Absence of fever
Home-canned (descending (for infant botulism) enriched agar) - Intact sensorium

Zip-lock pattern) INFANT BOTULISM: when baby ingests Elimination of the
storage bags - Eight immunologic spores found in household dust or organism from GIT Patient’s serum BOTOX is a
types of toxins honey; due to absence of competitive injected into mice commercial

Smoked fish (Judicious use of

- Types A, B, and E: bowel microbes; constipation, flaccid gastric lavage and results in death preparation of
Wild, raw honey: most common in paralysis (FLOPPY BABY SYNDROME) exotoxin A; used in
associated with metronidazole or
humans penicillin) wrinkle removal,
infant botulism - not secreted, rather WOUND BOTULISM: similar to food- torticollis

Bulging canned it is released upon borne except absence of GI prodromal Supportive therapy:
goods the death of the symptoms; due to traumatic incubation and
bacterium implantation and germination of spores ventilator
at the wound site assistance
 TREATMENT AND
MICROORGANISM RESERVOIR TRANSMISSION METABOLISM VIRULENCE FACTORS TOXINS CLINICAL SYNDROMES DIAGNOSIS NOTES
PREVENTION
Clostridium Ubiquitous: Endospores Anaerobic NON-motile Alpha toxin: GAS GANGRENE Gas Gangrene: Anaerobic, gram- Looks motile, but not
perfringens Soil lecithinase (splits - Due to alpha toxin - Wound positive, spore-forming motile on blood agar
GI tract of humans Myonecrosis results lecithin into - Gas produced by anaerobic debridement rods à due to avidity for
and mammals from contamination of phosphocoline and metabolism - Radical surgery lecithin in the blood
wound with soil or diglyceride); cleaves - Pain, edema, and cellulitis with (may require Culture: requires membranes
feces cell membranes crepitation amputation) anaerobic conditions
- Hemolysis and jaundice are common - Penicillin
Food poisoning is 11 other tissue - Hyperbaric Double hemolysis on
transmitted by destructive enzymes FOOD POISONING oxygen blood agar
ingestion of - Due to production of enterotoxin
contaminated food which acts as superantigen Food Poisoning: Growth on egg yolk
- Incubation period: 8-16 hours - Supportive agar: non-motile but

- Watery diarrhea with cramps and PREVENTION: with rapidly spreading
little vomiting Proper wound care growth on culture
- Resolves in 24 hours Adequate cooking media

Clostridium difficile Carried in the Fecal-oral: ingestion of Anaerobic Motile: Flagella (so H- Exotoxins A and B PSEUDOMEMBRANOUS ENTEROCOLITIS: Metronidazole Anaerobic, gram- PO vancomycin
colon: endospores antigen-positive) inhibit GTPases à - antibiotic-associated diarrhea ORAL vancomycin positive, spore-forming because it has poor
- 3% of the general apoptosis and death of - antibiotics suppress normal flora, rods intestinal absorption,
population Hands of hospital enterocytes à allowing C. difficile to overgrow Withdraw causative hence, “coats” the
- up to 30% in personnel are pseudomembranes
nd rd
- Clindamycin, 2 and 3 generation antibiotic Exotoxin ins tool lesions with antibiotic
hospitalized important cephalosporins, ampicillin
detected by cytopathic
Toxin A: diarrhea Replace fluids effect (final phase by
patients intermediaries - non-bloody diarrhea associated with Infection can


pseudomembranes (yellow-white Surgery if toxic which viral cells infect precipitate flare-ups
Toxin B: cytotoxic to cells) on cultured cells
colonic epithelial cells plaques) on the colonic mucosa megacolon of ulcerative colitis
- toxic megacolon can occur develops or ELISA

Colonoscopy

Corynebacterium Throat Respiratory droplets Facultative anaerobe Pseudo-membrane forms in Exotoxin (encoded by DIPHTHERIA Antitoxins Aerobic, non-spore- Schick test: injection
diphtheriae from carrier the pharynx, which serves ß-prophage); obtained - Mild sore throat with fever initially forming, non-motile of diphtheria
Catalase-positive as a base from where it from a temperate - Pseudomembrane forms on pharynx Penicillin or gram-positive rods; exotoxin into the
secretes its toxin bacteriophage by (results from death of mucosal erythromycin Club or comma-shaped skin, to determine
lysogenic conversion epithelial cells) rods arranged in V or L
whether a person is
- Myocarditis Vaccine DPT configuration; looks susceptible to
Subunit A: has ADP- î A-V conduction block - DIPHTHERIA: like Chinese characters
infection by
ribosylating activity; î dysrhythmia formalin- diphtheriae
blocks protein - Neural involvement: inactivated Culture:
synthesis by î peripheral nerve palsies exotoxin, as Potassium tellurite:
inactivating EF2 (which î GBS antibodies to the dark black colonies
is involved in translation î palatal paralysis B-subunit are

ADP-ribosylation
of eukaryotic mRNA into î neuropathies Loeffler’s medium:
protective ß-prophage
proteins) after 12 hours of

- pertussis growth, stain with Corynebacterium
- tetanus methylene blue. Diphtheriae
Subunit B: provides
entry into cardiac and

Elongation factor 2
Reddish
neural tissue metachromatic (Babes- Granules
Ernst / Volutin)
Exotoxin is like a granules can be seen
“human antibiotic”

(inhibits eukaryotic Modified Elek Test:

protein synthesis) for detection of
toxigenicity
 TREATMENT AND
MICROORGANISM RESERVOIR TRANSMISSION METABOLISM VIRULENCE FACTORS TOXINS CLINICAL SYNDROMES DIAGNOSIS NOTES
PREVENTION
Listeria Ubiquitous Ingestion of Facultative anaerobe Motile (via flagella): so has The only gram positive EARLY-ONSET NEONATAL LISTERIOSIS Ampicillin Aerobic, non-spore- Facultative
monocytogenes Plants (vegetables) contaminated raw H-antigen à tumbling bacteria that produces (Granulomatosis Infantiseptica) +/- Gentamicin forming gram-positive intracellular organism
milk or cheese from Catalase-positive motility LPS - transplacental transmission rods, arranged in V- or
Colonizes GI and infected cows - characterized by: TMP-SMX L-shape exhibiting Cell-mediated
female GUT Listeriolysin O: allows î late miscarriage (if allergic to penicillin) tumbling motility immunity is
Vaginally (during escape from the î birth complicated by sepsis, protective
birth) phagolysosomes of multiorgan abscesses, and Narrow zone of beta-
macrophages; major disseminated granulomas NOT hemolysis
Tranplacental virulence factor CEPHALOSPORINS: CAUSES OF
infection of fetus from LATE-ONSET NEONATAL LISTERIOSIS None of the Culture: can grow at NEONATAL
bacteremic mother Internalin: interacts with E- - transmitted during childbirth cephalosporins are temperature as low as MENINGITIS:
cadherin on the surface of - manifests as: active against 4-10C so use cold î GBS
cells î meningitis MRSA, LISTERIA, enrichment technique î Escherichia coli
î meningoencephalitis AND ENTEROCOCCI to isolate from mixed î Listeria
Actin Rockets: propel the flora monocytogenes
bacteria through the ADULT LISTERIOSIS
membrane of one human - second most common cause of
cell into another meningitis in people > 50yo
- most common cause of meningitis in
immunocompromised patients (with
lymphoma, on corticosteroids or
receiving organ transplantation)
- septicemia in pregnant women

GRAM-POSITIVE WITH BRANCHING FILAMENTS

Nocardia asteroides Actinomyces israelii

• Aerobe • Anaerobe
• Weakly Acid fast (Fite-Faraco Stain) • Not acid-fast
• Found in soil • Normal oral, reproductive, and GI flora
• Pulmonary infections in immunocompromised (can mimic • Oral/facial abscesses that drain through sinus tracts
TB but with negative PPD) • Often associated with dental caries/extraction
• cutaneous infections after trauma in immunocompetent • Forms yellow “sulfur granules”
• can spread to CNS à brain abscesses (orange colonies) • Can cause PID with IUDs
• Treatment: Sulfonamides (TMP-SMX) • Treatment: Penicillin
Treatment is a SNAP: Sulfonamides—Nocardia; Actinomyces —Penicillin

OTHER CLOSTRIDIA

C. septicum Nontraumatic myonecrosis in immunocompromised patients

C. sordellii Toxic shock syndrome associated with septic abortion
C. tertium Traumatic wound infections

 GRAM-NEGATIVE BACTERIA

GRAM-STAIN OTHER FEATURES ORGANISM
Encapsulated
Gram-Negative Ferments maltose and glucose
Neisseria meningitidis
Diplococci Insignificant capsule
Neisseria gonorrheae
Ferments glucose only

Other Neisseriaceae
• Eikenella corrodens and Kingella kingae cause culture-negative subacute bacterial endocarditis in patients with preexisting heart disease

HACEK Organisms









GRAM-NEGATIVE RODS – RESPIRATORY SYSTEM
GRAM-STAIN OTHER FEATURES ORGANISM
Enriched chocolate agar Haemophilus influenzae
Polyribitol Phosphate capsule type B
Borget-Gengou Agar
Gram-Negative Regan-Lowe medium Bordetella pertussis
Whooping cough
Rods
Poorly gram staining
Silver stain
Legionella pneumophila
Charcoal yeast agar
AIrconditioning

GRAM-NEGATIVE RODS – GIT and GUT
GRAM-STAIN OTHER FEATURES ORGANISM ENTEROBACTERIACEAE
Lactose fermenters
Escherichia coli MESSY SPECK
Green sheen
Lactose fermenters Morganella Serratia
Urease positive Klebsiella pneumoniae Escherichia Proteus
ESBL
Gram-Negative Shigella Enterobacter
Comma-shaped
Rods Microaerophilic Campylobacter jejuni Salmonella Citrobacter
Skirrow’s agar
Yersinia Klebsiella
Comma-shaped
Urease positive Helicobacter jejuni
Microaerophilic Enterobacteriaceae drink COFFEe!
Motile
Oxidase negative Salmonella spp. Capsular antigen (K)
H2S producer O antigen
Non-motile
Oxidase negative Shigella spp.
Flagellar antigen
Non-lactose- H2S non-producer Ferments glucose
fermenting, Gram- Swarming
Enterobacteriaceae
Negative Rods Oxidase negative
Proteus mirabilis
H2S producer
Urease positive
Oxidase positive
H2S non-producer Pseudomonas aeruginosa
Obligate aerobe

ANTIMICROBIAL PROPHYLAXIS
 TREATMENT AND
MICROORGANISM RESERVOIR TRANSMISSION METABOLISM VIRULENCE FACTORS TOXINS CLINICAL SYNDROMES DIAGNOSIS NOTES
PREVENTION
Neisseria Upper respiratory Respiratory droplets Ferments both Capsule: Endotoxin (LPS) MENINGITIS: Penicillin Gram-negative, Neisseria
meningitidis tract MALTOSE and î 13 serotypes based on î most common cause among aged aerobic, encapsulated, MeninGitidis
High carriage rate in GLUCOSE antigenicity of capsule No exotoxins 2-18 yrs Ceftriaxone (or kidney bean-shaped
Ferments both
HUMANS are the CLOSE QUARTERS: polysaccharides î fever, headache, stiff neck, and cefotaxime): DOC for diplococcus
only natural î Military recruits Oxidase-positive î Serotypes A, B, & C are increased level of PMNs in CSF the treatment of Maltose and
hosts. î Dormitories colonies on associated with epidemics meningococcal meningitis Culture specimen on Glucose
î Camps chocolate agar of meningitis (usually type MENINGOCOCCEMIA: and septicemia blood agar that has
B) î dissemination of meningococci into been heated to 80°C
Neisseria
Neonates are very Grows best in high the bloodstream Rifampin/ for 15 minutes (called

Ciprofloxacin: chocolate agar) Gonorrhoeae
susceptible from 6 to CO2 environment Endotoxin (LPS): causes î multiorgan disease
prophylaxis Ferments
24 months, when blood vessel destruction î consumptive coagulopathy Selective media:
protective anti- (hemorrhage) and sepsis î petechial or purpuric rash of close contacts of Glucose only
prevents growth of
meningococcal lgG is (purpura fulminans) infected persons
bacteria using Thayer
low. IgA1 protease: cleaves IgA POLYSACCHARIDE
Martin Agar
WATERHOUSE-FRIDERICHSEN VACCINE: CAPSULE:
î Vancomycin: inhibits
Have unique proteins that SYNDROME: contains capsular (+) in Meningococci
G (+)
can extract iron from î most severe form of polysaccharide of (-) in Gonococci
î Colistin and
transferrin, lactoferrin and meningococcemia strains A, C, Y, and
trimethoprim: inhibit
hemoglobin î high fever, shock, widespread W-135 coupled to a AVAILABLE VACCINE:
G (-) except Neisseria
purpura, disseminated carrier protein (+) in Meningococci
î Nystatin: inhibits
Pili: allow attachment to intravascular coagulation, (diphtheria toxoid) to (-) in Gonococci
fungi
human nasopharyngeal cells thrombocytopenia, and adrenal enhance
and undergo antigenic insufficiency à bilateral immunogenicity Cell wall contains Complement
variation to avoid attack by hemorrhagic destruction of the cytochrome oxidase deficiencies in late-
the immune system adrenal glands The first meningococcal which oxidizes dye acting complement
vaccine for serogroup B tetramethylphenylene components (C5-C9)
was approved in diamine from colorless predispose to illness
October 2014. to deep pink. Used to à cannot form
identify colonies membrane attack
complexes
Neisseria Humans only (no Sexually-transmitted Facultative-anaerobe Pili: Endotoxin: GONOCOCCAL URETHRITIS Ceftriaxone plus Kidney bean-shaped N. gonorrhoeae is
gonorrhoeae immunity to î Adherence to epithelial lipooligosaccharide - urethritis and epididymitis in men Doxycycline (to cover with concave sides the most common
repeated Passage through birth Ferments GLUCOSE cells (LOS) - most common cause of urethritis for Chlamydia facing each other cause of hyperacute
infections) canal only î Antigenic variation
trachomatis – usual co- forming the appearance bacterial
î Antiphagocytic, binds No exotoxins CERVICAL GONORRHEA of doughnut
infection)) conjunctivitis, the
Habitat is the Oxidase-positive bacteria tightly to host cell - in women, which can progress to Gram-negative most severe form of
human genital protecting it from pelvic inflammatory disease (PID) diplococci
Erythromycin conjunctivitis.
tract Grows best in high phagocytosis î Complications of PID
ointment or Silver
CO2 environment A. Sterility Culture:
nitrate to prevent Most common site of
IgA1 protease B. Ectopic pregnancy Specimen on chocolate asymptomatic
ophthalmia
C. Chronic Pelvic Pain agar
neonatorum. Silver gonococcal infection
Outer membrane protein D. Dyspareunia
nitrate is no longer used in women:
porins: promote E. Peritonitis Selective media: Thayer
invasion into epithelial cells F. Perihepatitis (Fitz-Hugh-
because it can cause
Martin Agar ENDOCERVIX
chemical conjunctivitis.
Curtis Syndrome) à violin-

Opa proteins: promote string adhesions Cell wall contains
Complement
adherence and invasion into cytochrome oxidase
deficiencies in late-
epithelial cells; expression GONOCOCCAL ARTHRITIS which oxidizes dye
acting complement
results in opaque colonies - the most common cause of septic tetramethylphenylene
components (C5-C9)
arthritis in sexually active diamine from colorless
Have unique proteins that predispose to illness
individuals to deep pink; used to
can extract iron from à cannot form
identify colonies
transferrin, lactoferrin and OPHTHALMIA NEONATORUM membrane attack
PCR in bacterial DNA in
hemoglobin - purulent conjunctivitis in newborns clinical specimens complexes
 TREATMENT AND
MICROORGANISM RESERVOIR TRANSMISSION METABOLISM VIRULENCE FACTORS TOXINS CLINICAL SYNDROMES DIAGNOSIS NOTES
PREVENTION
Moraxella Part of the normal OTITIS MEDIA in children Azithromycin or Resistant to penicilins
(Branhamella flora clarithromycin
catarrhalis) SINUSITIS
BRONCHITIS Amoxicillin with
PNEUMONIA clavulanate

COPD EXACERBATION Oral second or third
generation
cephalosporin

TMP-SMX
Haemophilus Man only Transmitted via Haemophilus Capsule ENCAPSULATED H. INFLUENZAE: Amoxicillin Gram stain: small Haemophilus
influenzae (obligate human respiratory route influenzae requires î 6 types, a-f MENINGITIS: +/− clavulanate for gram-negative influenzae is
parasite) two factors for î Type b is most virulent î Most serious manifestation of mucosal infections (coccobacillary) rods formerly called
growth (both found î composed of Hib infection (otitis media, Pfeiffer's bacillus.

The non-typable in blood): polyribitol ribose î Haemophilus influenzae type B is conjunctivitis, Culture specimen on
H. influenzae X factor: Hematin the one of the primary causes of bronchitis) blood agar that has
phosphate o
(NTHi) strains V factor: NAD+ meningitis in infants from 3 to 36 been heated to 80 C
colonize the months of age Ceftriaxone for for 15 minutes (now Affects children
Attachment pili
nasopharynx in Satellite growth î antecedent upper respiratory meningitis called chocolate agar). from 6 months to 1

up to 80% of tract infections are common This high temperature year due to decline
around S. aureus lgA1 protease
individuals î Complications: sensorineural Rifampin lyses the red blood in maternal IgG and
colonies
hearing loss (6%), mental prophylaxis for close cells releasing both immature immune
retardation, seizure, deafness, contacts hematin (called X system
and death factor) and NAD+

ACUTE EPIGLOTTITIS: Hib vaccine: H. (called V factor). Like

î Most common cause influenzae the Neisseria, H.
î Cherry-red epiglottis polysaccharide influenzae grows best
î Fever, sore throat, dysphagia, capsule of type b when the chocolate
drooling, and difficulty breathing strain (Hib) is agar is placed in a high
î Thumb sign on X-ray conjugated to CO2 environment at
o

diphtheria toxoid 37 C
PNEUMONIA:
given between 2 and
î insidious onset and a history of
18 months of age Fluorescently labeled
fever, cough, and purulent
antibodies (ELISA and
sputum production
Passive latex particle
CELLULITIS: Immunization: agglunation)
î Most commonly involves the mother is immunized
buccal and periorbital regions; th
during 8 month of Positive Quellung
usually associated with fever pregnancy to test: due to its

SEPTIC ARTHRITIS in infants increase passive capsule, similar to

antibody transfer in Streptococcus
SEPSIS especially in patients without breast milk pneumoniae
functioning spleen

NON-ENCAPSULATED H.
INFLUENZAE:
OTITIS MEDIA
SINUSITIS
CONJUNCTIVITIS
COPD EXACERBATIONS

 TREATMENT AND
MICROORGANISM RESERVOIR TRANSMISSION METABOLISM VIRULENCE FACTORS TOXINS CLINICAL SYNDROMES DIAGNOSIS NOTES
PREVENTION
Bordetella pertussis Habitat is upper Transmitted via Capsule Pertussis toxin: WHOOPING COUGH Erythromycin Small gram-negative
respiratory tract respiratory droplets î causes ADP - “Tuspirina” (most effective when rods
Beta-lactamase ribosylation - paroxysmal pattern of hacking given in catarrhal
î activates G proteins coughs, accompanied by stage) Culture:
Filamentous hemagglutinin that increases production of copious amounts of Bordet-Gengou agar
(FHA): cAMP resulting in: mucus, that end with an Vaccine: DaPT î potato extract
î pili rod that extends from - á sensitivity to inspiratory “whoop” (Given routinely at
the surface of B. pertussis, histamine ages 2, 4, 6, 15 mos Regan-Lowe charcoal
enabling the bacteria to - á insulin release Incubation Period and between 4-6yo.) medium
bind to ciliated epithelial - á number of î 7-10 days î charcoal, blood, and
cells of the bronchi lymphocytes in
Pertussis vaccination antibiotic
Catarrhal phase
î mediates attachment blood during pregnancy is
î 1-2 weeks
î rhinorrhea, malaise, fever, safe Rapid serologic tests:
Extra-cytoplasmic
sneezing, anorexia (ELISA)
adenylate cyclase:
î patient is highly contagious Treat household î Collect specimen
î “weakens”
î Antibiotics most effective contacts with from posterior
neutrophils
erythromycin. pharynx on a calcium
lymphocytes and Paroxysmal phase
monocytes alginate swab since
î 2-4 weeks B. pertussis will not
î inhibits î Whoop (burst of non-productive
phagocytosis grow on cotton

coughs)
Filamentous î Increased number of lymphocytes Direct fluorescein-
hemagglutinin: in blood smear labeled antibodies
î allows binding to î Antibiotics ineffective during this applied to
ciliated epithelial stage nasopharyngeal

cells Convalescent stage specimens for rapid

î 3-4 weeks (or longer) diagnosis
Tracheal cytotoxin:
î Diminished paroxysmal cough
î kills ciliated
î Development of secondary PCR detection of
epithelial cells
complications (pneumonia, bacterial DNA in
î paralyze cilia
seizure, encephalopathy) respiratory secretions
î causes whooping
Legionella Ubiquitous in man No person-to-person Growth depends on Facultative intracellular Cytotoxins: kill PONTIAC FEVER Azithromycin Aerobic, motile, and Legionnaires disease
pneumophila and natural water transmission the presence of L- parasite hamster ovary cells î mild flu-like illness Levofloxacin nutritionally fastidious (LD) was recognized in
environments cysteine and iron î inhibits macrophage î headache, fever, muscle aches and Doxycycline pleomorphic poorly 1976 after an
î air conditioning PREDISPOSING in special media phagolysosome fusion Endotoxin is sole fatigue gram-negative rods; outbreak of

systems FACTORS: (charcoal yeast î cell-mediated immunity is virulence factor î self-limiting: recovery in a week is visualized with silver pneumonia at an
î cooling towers î Old age important common American Legion
extract agar) PREVENTION: stain
î Smoking convention in

Cu-Zn superoxide dismutase î Reducing cigarette

Freshwater î High alcohol intake and catalase-peroxidase ATYPICAL PNEUMONIA and alcohol Serology (IFA and ELISA) Philadelphia.
Optimal growth
amoebae appear î Immunosuppression î protects bacteria from Accompanied by consumption
temperature is 28- Urinary antigen can be
to be the natural macrophage superoxide î confusion î Eliminating aerosols
40°C; organisms are detected by
reservoir for the and hydroperoxide î nonbloody diarrhea from water sources Legionella is non-
dormant below 20°C radioimmunoassay with encapsulated
organisms. oxidative burst î hyponatremia î High temperatures
and are killed at high sensitivity and

î proteinuria and facultative
temperatures above Pili and flagella specify and will remain intracellular parasite.
60°C. î hematuria hyperchlorination in
î promote attachment and positive for months
hospital water
invasion after infection. Urine
supply

antigen test only
Secretion of protein toxins
detects L. pneumophilia
î like RNAase, serogroup 1, but this
phospholipase A and accounts for 90% of
phospholipase C cases.
 TREATMENT AND
MICROORGANISM RESERVOIR TRANSMISSION METABOLISM VIRULENCE FACTORS TOXINS CLINICAL SYNDROMES DIAGNOSIS NOTES
PREVENTION
Escherichia coli Habitat is human Ascending infection to Indole-positive Fimbriae (pili): attachment/ Endotoxins NEONATAL MENINGITIS UTI: Ampicillin or Facultative Gram- LACTOSE
colon the urethra (UTI) colonization factor; causes î Lipid A portion of
Sulfonamides negative rods FERMENTERS
UTI
Lactose-fermenting cystitis and pyelonephritis lipopolysaccharide Grow on MacConKEES
Colonizes the During birth (neonatal colonies on EMB or (LPS) NOSOCOMIAL SEPSIS Meningitis and Sepsis: Beta-hemolytic
Citrobacter
vagina and meningitis) MacConkey’s agar Adhesins î Causes septic shock
3rd generation
NOSOCOMIAL PNEUMONIA Klebsiella
urethra cephalosporins Typing by O and H
Fecal-oral (diarrhea) Green metallic Capsule (K-antigen): causes Enterotoxins DIARRHEA antigens Escherichia coli
sheen on EMB agar pneumonia (Exotoxins) î ETEC Aminoglycosides Enterobacter
Colonization of LT (heat-labile): - releases LT and ST toxins Serratia
catheters in TSI (Triple Sugar Flagella (H-antigen) î increases cAMP - traveler’s diarrhea (watery) Fluoro-quinolones EMB: purple/black
hospitalized patients Iron) agar shows acid (same as cholera
MacConkey: pink/purple
Green metallic sheen Siderophore: obtains iron î EPEC
slant and acid butt toxin)
on EMB Aspiration - Watery diarrhea of long duration Rehydration is MOST COMMON
with gas but no H2S from human transferrin or

ST (heat-stable) - Mostly in infants, often in effective in traveler’s CAUSES OF NEONATAL

lactoferrin diarrhea
î Increases cGMP developing countries MENINGITIS


Shiga-like toxin (SLT - Flattens villi à prevents î Group B strep
absorption
/ verotoxin) î Escherichia coli
PREVENTION:
î inhibits protein î EIEC î Limit urinary î Listeria
synthesis by - Bloody diarrhea catheterization monocytogenes
inactivating the 60S - with pus in the stool and fever î Switch IV lines
subunit of
promptly HEMOLYTIC-UREMIC
eukaryotic cells (E. î EHEC/STEC î Drink boiled water SYNDROME
coli O157:H7, STEC, - E. coli strain O157:H7 à MC î Renal Failure
EHEC) serotype î Microangiopathic
- Transmitted via undercooked hemolytic Anemia
HT and LT cause meat î Thrombocytopenia
watery diarrhea - secretes shiga-like toxin
SLT causes bloody (verotoxin) à causes Three Most Common
diarrhea (HUS) hemorrhagic colitis and Causes of Diarrhea in
hemolytic uremic syndrome the World:
- Does not ferment sorbitol î Campylobacter
- no fever, no pus in stool jejuni
î ETEC
î Rotavirus
Shigella species Habitat: human Fecal-oral route No H2S production Invades submucosa of Shiga toxin: BACILLARY DYSENTERY Fluoroquinolones Gram-negative non- IgA is best for
colon only 4Fs: Food, Fingers, intestinal tract (distal ileum î inactivates the 60S î Incubation period: 1-4 days (Ciprofloxacin) motile rods immunity
Feces, Flies Non-lactose and colon), but not the ribosome, î Fever and abdominal cramps à - in severe cases
SHIGELLA SPECIES GROUP fermenter lamina propria à local inhibiting protein diarrhea (initially watery then Have O antigens Shigella is more toxic
inflammation with synthesis and killing bloody) Azithromycin and invasive than
S. dysenteriae
Produce no gas from ulceration à bleeding intestinal epithelial î Diarrhea frequently resolves in 2 or TMP-SMX Cultured in XLD (xylose Salmonella
Type 1 Shiga bacillus Most severe form of
the fermentation of cells 3 days lysine deoxycholate)
bacillary dysentery
A glucose Shigella has a low infective î protein synthesis Fluid and electrolyte medium 4Fs of Shigella
MCC of epidemic
dose (200 bacilli) à highly inhibitor of replacement Transmission:
dysentery
infectious EUKARYOTES Stool culture: because Food
Type 2 Schmitz bacillus
** vs Salmonella with an Shigella is never a part Fingers
Flexner’s bacillus;
5 8 of the normal intestinal Feces
B S. flexneri Hiss and Rusell’s infective dose of 10 -10
flora Flies
bacillus
Newcastle Invasion of M cells is key
C S. boydii
Manchester bacillus to pathogenicity.
MCC of bacillary
D S. sonnei Duval’s bacillus
dysentery
 TREATMENT AND
MICROORGANISM RESERVOIR TRANSMISSION METABOLISM VIRULENCE FACTORS TOXINS CLINICAL SYNDROMES DIAGNOSIS NOTES
PREVENTION
Salmonella species S. typhi is found S. typhi is transmitted Produces H2S Motile (H-antigen) ENTERO- S. enteritidis/ î Invasion of the epithelial and Ceftriaxone Facultative Gram- A. Facultative
only in humans via fecal-oral route negative rods intracellular parasite:

COLITIS S. typhimurium subepithelial tissue of small Ciprofloxacin

(colon) Non-lactose Capsule (called the Vi and large intestines
1. Lives within
TMP-SMX
fermenter antigen): protects from î Infectious dose is HIGH WIDAL TEST: detects macrophages in lymph

S. enteritidis is intracellular killing î Gastrectomy or use of Azithromycin antibodies in patient’s nodes

found in enteric antacids lowers infectious serum 2. Can live in gall
tract of humans Siderophores dose significantly In the Philippines, bladder for years
and animals e.g., î Incubation period: 12-48hr first line drugs for Cultured in XLD (xylose (carriers secrete S.
chickens and î Nausea/vomiting à typhoid: lysine deoxycholate) typhi in stool)
domestic livestock abdominal pain and îAmoxicillin medium

nonbloody diarrhea îChloramphenicol B. Persons who are
COURSE OF TYPHOID FEVER TYPHOID S. typhi î Due to Vi capsular antigen îTMP-SMX Culture: blood, stool or asplenic or have non-
Week Presentation Culture Source FEVER î Organisms enter, multiply in urine may contain S. functioning spleens
Stepwise fever, anorexia, malaise, relative Blood Peyer’s patches, and then *Salmonella typhi (sickle cell anemia) are
1
bradycardia, and bacteremia Bone marrow spread to RES gastroenteritis: there at increased risk of
Urine î Predilection for invasion of is little benefit from NEVER part of the infection by this
Abdominal pain, bloating, constipation,
2 Rose spots the gallbladder à chronic antibiotic treatment; intestinal flora organism
rose spots, hepatosplenomegaly, jaundice
Bone marrow carrier state it may prolong carrier
Stool î Incubation period: 5-21days state
3 Bleeding ileitis, pneumonia
Bone marrow SEPTICEMIA S. choleraesuis î Bacteremia results in the PREVENTION:
4 Recovery or death Bone marrow seeding of many organs
î Public health
Bile, Stool, bone with osteomyelitis,
POST Chronic carrier state measures: sewage
marrow pneumonia, meningitis as disposal,

the MC sequelae
Gold standard for the diagnosis of typhoid fever: BONE MARROW CULTURE chorination,
î Commonly seen in patients
“The mainstay of laboratory diagnosis for typhoid fever is blood culture, although the handwashing, food
with sickle cell anemia or safety
gold standard is bone marrow culture” (American Society for Microbiology)
cancer
“Isolation of Salmonella Typhi from bone marrow is the current gold standard method î Vaccines for S. typhi
for confirming a case of typhoid fever” (WHO) î Fever but with little or no
- Oral: live
enterocolitis à focal attenuated S.
symptoms associated with typhi
affected organ (frequently
- IM: Vi Capsular
bone, lung, or meninges)
polysaccharide
Vibrio species V. cholerae: V. cholerae: Oxidase-positive Motile (H-antigen) Choleragen V. CHOLERAE: Cholera: Comma-shaped gram- Pandemics caused by
human colon only Fecal-oral route à Shooting star / fast (enterotoxin): CHOLERA: î Fluid and electrolyte negative rods with a Vibrio cholerae O1
Ferments sugar darting motility like LT of E. coli, acts î severe diarrhea with rice water replacement single polar flagellum biotype El tor
V. parahemoly- V. parahemolyticus: (except lactose) by ADP ribosylation; stools (no pus in stools) î Tetracycline or (cholera El Tor)
ticus and V. Contaminated raw á cAMP, à secretion î Washer woman’s hands sign à Dark field microscopy

Azithromycin
vulnificus: seafood Non-lactose of electrolytes from wirnkled skin due to loss of skin of stool reveals motile
shortens duration Death by dehydration:

saltwater fermenter the intestinal turgor due to dehydration organism that are children affected in

V. vulnificus: epithelium à î Complications: cardiac and renal V. parahemolyticus immobilized with endemic areas 1991:

Trauma to skin, V. secretory diarrhea failure, non-gap acidosis, and V. vulnificus antiserum Latin America
Mucinase: digest mucous
especially in shellfish parahaemolyticus: hypokalemia infection: epidemic
layer so V. cholerae can
handlers, or by halophilic
î Minocycline plus Grows as flat yellow 1993: Epidemic in
V. cholerae: Comma- attach to cells V. PARAHEMOLYTICUS&VULNIFICUS:
ingestion of raw Fluoroquinolone or colonies on selective Bangladesh and India
shaped gram-negative, GASTROENTERITIS
shellfish Cefotaxime media: Thiosulfate-
motile rods with a Fimbriae: helps with î Generally self-limited with an
ADP ribosylation citrate-bile-salts- Only improvements in
single polar flagellum attachment to cells explosive onset of watery diarrhea
Choleragen activates Short term immunity sucrose (TCBS) agar sanitation can lead to
and nausea, vomiting, abdominal
Non-invasive!!! Gs: turns the “ON” on using cholera vaccine effective control of
Pertussis toxin cramps, headache, low-grade fever
à may cause herd the disease
inactivates Gi: turns WOUND INFECTIONS
Has HIGH infectious dose immunity
the “OFF” off î Associated with exposure to
contaminated water

 TREATMENT AND
MICROORGANISM RESERVOIR TRANSMISSION METABOLISM VIRULENCE FACTORS TOXINS CLINICAL SYNDROMES DIAGNOSIS NOTES
PREVENTION
Campylobacter Zoonotic: wild and Uncooked meat Microaerophilic Motile (H-antigen) Enterotoxin: similar to GASTROENTERITIS Symptomatic Microscopic exam of Three Most Common
jejuni domestic animal (especially poultry) cholera toxin and the î Most common cause of bacterial treatment only stool reveals motile, Causes of Diarrhea in
and poultry; Oxidase-positive Invasive: invades the LT of E. coli gastroenteritis curved/comma- or S- the World:
undercooked Unpasteurized milk mucosa of the colon but î Usually caused by ingestion of Erythromycin shaped gram-negative î Campylobacter
chicken Catalase-positive does not penetrate, Cytotoxins: destroy undercooked chicken - for severe disease rods with a single polar jejuni
Fecal-oral therefore, sepsis rarely mucosal cells î Watery, foul-smelling diarrhea flagellum î ETEC
occurs à produces followed by bloody stools Fluoroquinolone
î Rotavirus
histologic damage to the accompanied by fever and severe Selective media with
o
mucosal surfaces of the abdominal pain antibiotic at 42 C:
jejunum î May mimic ulcerative colitis î Skirrow’s agar

Curved, comma- or S- Disease Associations: î Campy’s agar
shaped, gram-negative GUILLAIN-BARRE SYNDROME
rod with a single polar î Antigenic cross-reactivity between Optimum temperature
o
flagellum oligosaccharides in bacterial is 42 C – to inhibit the
capsule and glycosphingolipids on growth of other fecal
surface of neural tissues species


REACTIVE ARTHRITIS (REITER’S
SYNDROME)
î Triad of:
- Urethritis (can’t pee)
- Uveitis (can’t see)
- Arthritis (can’t climb a tree)
Helicobacter pylori Habitat Is the Transmission is by Microaerophilic Urease: produces No toxin PEPTIC ULCER DISEASE Triple Therapy: Curved gram-negative Urease (+) Bacteria:
human stomach ingestion ammonia; makes the î most common cause of duodenal î Omeprazole rods with a tuft of polar PCHUNKSS
Oxidase-positive environment alkaline à ulcers and chronic gastritis î Clarithromycin flagella (lophotrichous)
î Proteus
helps H. pylori survive in î second leading cause of gastric î Amoxicillin or
Catalase-positive acidic mucosa ulcer Metronidazole EGD with biopsy î Cryptococcus

showing H. Pylori î H. pylori
Urease-positive Damages the goblet cells of Disease Associations: Quadruple Therapy:

î Ureaplasma
gastric mucosa î GASTRIC CARCINOMA î Tetracycline Urease breath test,
“Triple Positive” î Nocardia
î MALT LYMPHOMA î Omeprazole H. pylori stool antigen:
Lophotrichous flagella î Klebsiella
î Metronidazole to document cure
î Bismuth î S. epidermidis
subsalicylate î S. saprophyticus
Klebsiella Habitat Is the Aspiration or Urease-positive Capsule NECROTIZING PNEUMONIA Culture-guided Facultative gram- 5A’s of KlebsiellA:
pneumoniae upper respiratory inhalation î Friedlander’s Pneumonia treatment negative rods with Aspiration pneumonia
and GIT Indole-negative î Most common cause in alcoholics large polysaccharide Abscess in lungs and
Ascending spread of **vs E. coli which is î Usually nosocomial Cephalosporins +/- capsule liver
fecal flora indole-positive** î Thick, bloody sputum (currant Aminoglycosides
Alcoholics
jelly sputum) Extended spectrum
beta-lactamase (ESBL) Di-A-betics
URINARY TRACT INFECTIONS activity in drug- “Curr-A-nt jelly”
resistant strains sputum
SEPSIS
î Second to E. coli as the common
Very mucoid colonies cause of sepsis
 TREATMENT AND
MICROORGANISM RESERVOIR TRANSMISSION METABOLISM VIRULENCE FACTORS TOXINS CLINICAL SYNDROMES DIAGNOSIS NOTES
PREVENTION
Proteus mirabilis Urease-positive: Motile No toxins COMPLICATED UTI: Ampicilin Facultative gram- WEIL-FELIX
hydrolyzes urea into î UTI associated with nephrolithiasis TMP-SMX negative rod REACTION: a test that
NH3 and CO2 Fimbriae: for adherence î Urease hydrolyzes urea in the urine Surgery: for large stones uses antibodies

to form ammonia à á pH à Culture: Swarming against certain strains

Indole-negative Lipopolysaccharide alkaline urine à struvite stone pattern colonies on BAP of Proteus to diagnose


formation (staghorn calculi; rickettsial disease
Non-lactose Urease production
composed of magnesium- (as certain rickettsiae
fermenter
ammonium-phosphate) share similar antigens)

Gram-negative rod with
peritrichous flagella
SEPSIS
Pseudomonas Habitat is Transmission is via Non-lactose Motile (polar flagella) Endotoxin SKIN AND SOFT TISSUE INFECTIONS Combination of active Gram-negative rods, It is the most common
aeruginosa environmental water aerosols, fermenter î Burn wound infections antibiotics required obligate aerobe pathogen isolated
water sources aspiration, and fecal Elastase: causes vascular Exotoxin A î Hot tub folliculitis: spa pools, whirl pools, because of resistance from patients who
e.g., in hospital contamination Oxidase-positive necrosis and local tissue î similar to or inadequately chlorinated swimming to multiple antibiotics Culture: have been
respirators and destruction diphtheria toxin pools and hot tubs î Antipseudomonal î Grown on Cetrimide hospitalized longer
humidifiers Medical devices î inhibits protein î Skin graft loss due to infection penicillins agar than 1 week, and it is
Hands of healthcare Proteases: destroy synthesis by î Green nail syndrome (ticarcillin, î greenish, metallic a frequent cause of

Inhabits the skin, workers antibody and blocking EF2 BONE AND CARTILAGE INFECTIONS piperacillin) colonies on blood nosocomial infections.
upper respiratory complement î causes tissue î Puncture wound osteomyelitis î Penicillin + Beta- agar
tract, and colon of (major pathogen for necrosis î Pubic osteomyelitis in IV drug users lactamase inhibitor î with sweet, fruity Nosocomial
about 10% of nosocomial infections Pyocyanin: damages the î Type III secretion ticarcillin- grape-like odor organisms similar
Ecthyma gangrenosum people because of its cilia and mucosal cells; system facilitates EAR INFECTIONS clavulanate, î produces pigments: to Pseudomonas:
ubiquitous presence generates reactive exotoxin transfer î Most common cause of: piperacillin- - Pyocyanin (blue) î Acinetobacter
Soil, Water, Plants, in the hospital oxygen species - Otitis externa tazobactam - Pyoverdin (green, baumannii
Animals, Intestinal environment) - Malignant otitis externa in diabetics rd
î 3 gen fluorescent î Elizabethkingia
Flora, Skin Verdoglobin: from - Chronic suppurative otitis media cephalosporins:
meningo-septicum
hemoglobin breakdown PNEUMONIA ceftazidime î Burkholderia
th
î Ventilator-associated pneumonia î 4 gen cepacia
Hemolysins: lyses RBC î Necrotizing pneumonia (fleur-de-lis cephalosporins:
pattern) cefepime
PSEUDOMONAS
Collagenase î High-risk CAP: î Monobactam:
aztreonam
Pneumonia, pyocyanin
- Immunocompromised
Fibrinolysin î Carbapenems: Sepsis
- Broad-spectrum antibiotics
- Steroid therapy imipenem, Ecthyma gangrenosum
Phopholipase C: - Structural lung lesions meropenem, UTIs
degrades cell membranes • Bronchiectasis doripenem, Diabetes, drug use
Green nail syndrome ertapenem
• Cystic fibrosis Osteomyelitis (eg,
DNAse î Fluoroquinolones: puncture wounds)
GASTROINTESTINAL INFECTIONS ciprofloxacin
î Typhlitis (necrotizing enterocolitis) Mucoid
Antiphagocytic polysaccharide
î Shanghai fever (mild form of typhoid) Examples of suitable
mucopolysaccharide capsule
î Peritonitis in peritoneal dialysis patients combinations:
capsule: may contribute Otitis externa
to chronic pneumonia in URINARY TRACT INFECTONS î Ceftazidime +
(swimmer’s ear)
cystic fibrosis patients rd
î 3 MCC of nosocomial UTIs Amikacin
î Piperacillin +
Nosocomial infections
due to biofilm formation
(catheters,
SEPSIS Amikacin
î Ecthyma gangrenosum (hemorrhagic î Azlocillin + equipment)
lesions) Ciprofloxacin Exotoxin A
î Febrile neutropenia Skin infections (hot
- Leukemia or lymphoma post chemo- Rifampicin is added for tub folliculitis)
or radiation therapy refractory cases
- Severe burns
 TREATMENT AND
MICROORGANISM RESERVOIR TRANSMISSION METABOLISM VIRULENCE FACTORS TOXINS CLINICAL SYNDROMES DIAGNOSIS NOTES
PREVENTION
Bacteroides fragilis Predominant Spreads to blood or Capsular polysaccharide: Lipid A does not elicit Infections commonly due to Metronidazole – DOC Anaerobic, gram- Obligate Anaerobes
anaerobe of the peritoneum during antiphagocytic and a strong host combinations of bacteria in for anaerobic infections negative rods Can’t Breathe Fresh Air
human colon bowel trauma, anticomplement inflammatory synergistic pathogenicity Clindamycin Clostridium

perforation, or response (attenuated) Chloramphenicol
Carbapenems
Bacteroides
surgery Succinate: inhibits PMN à LPS with low ABDOMINAL ABSCESS
phagocytosis endotoxic activity
nd
2 gen FQ Fusobacterium
PERITONITIS Actinomyces
Attachment factors: pili Enterotoxins: causes Surgical drainage of
diarrhea PERICARDITIS abscess Most Common
Bacteria in Colon
ENDOCARDITIS Chloramphenicol is
static, but cidal to the Bacteroides fragilis

following: E. coli
CEREBRAL ABSCESS
î Chloramphenicol is ideal because it No Bf Since Highschool Enterococcus
is lipophilic N. meningitidis
B. fragilis
S. pneumoniae
H. influenzae

Yersinia Zoonotic: can be Ingestion of Non-lactose Virulence factors are Enterotoxin: MESENTERIC LYMPHADENITIS Antibiotics do not Stool or blood cultures Survives refrigeration
enterocolitica found in pigs contaminated food or fermenter temperature sensitive; î similar to the heat- î in children alter the course of the may be positive
o
water expressed at 37 C stable toxin (ST) of î pseudo-appendicitis diarrhea. However, Closely related to
E. coli patients with positive Examination of the Yersinia pestis
Unpasteurized milk V and W antigens î á cGMP levels ACUTE ENTEROCOLITIS blood culture should terminal ileum with
î with fever, diarrhea (MC be treated with colonoscopy will reveal
Motile manifestation) and abdominal pain antibiotics mucosal ulceration

 TREATMENT AND
MICROORGANISM RESERVOIR TRANSMISSION METABOLISM VIRULENCE FACTORS TOXINS CLINICAL SYNDROMES DIAGNOSIS NOTES
PREVENTION
Brucella spp. Direct contact with Obligate aerobe Non-motile BRUCELLOSIS: Pasteurization of milk Aerobic gram-negative Facultative intracellular
contaminated livestock or î Undulating fever (fever peaks in the coccobacilli parasite
Brucellae are that Treat with combination of

Brucella meltitensis Goats aborted placentas Tropism for erythritol, a evening, and returns to normal by
possess a unique ability sugar found in animal morning) doxyxycline Culture blood, bone
(highest pathogenicity)

Ingestion of infected/ to invade both
placentas î Weakness and one other drug: marrow (best yield), liver,

contaminated/ phagocytic and î Loss of appetite - gentamicin
Brucella abortus Cattle or lymph nodes
unpasteurized dairy nonphagocytic cells and - streptomycin

to survive in the
products Includes ABORTIONS in animals - rifampin Serologic tests
Brucella suis Pigs intracellular

environment by finding
Aerozolization in All cattle are immunized Skin test: Indicates
Brucella canis Dogs ways to avoid the
laboratory or possibly due immune system. with a living attenuated exposure only
to bioterrorism strain of Brucella abortus
Francisella Rabbits and Bite of tick (e.g. Obligate aerobe Capsule antiphagocytic TULAREMIA Streptomycin (DOC) Culture (but very Facultative intracellular
tularensis squirrels Dermacentor), deerfly Ulceroglandular: at the site of tick bite Gentamicin dangerous due to its high parasite
or infected animals Requires cysteine Non-motile or direct contact with contaminated rabbit, infectivity, requires

Ticks can serve as a an ulcer develops, with swelling of focal Doxycycline addition of cysteine to

reservoir Direct contact with The ability of F tularensis to lymph nodes blood agar media
infected animal tissue impair phagocyte function and Attenuated vaccine: only
(usually rabbit) survive in infected cells is central Pneumonia: inhalation, or through the for high-risk individuals Skin test
to its virulence. This intracellular
blood
life cycle has been shown to be Measure rise in IgG
Inhaled aerosolized
related to the tightly regulated antibody titer (IgM is not
organisms Oculoglandular: direct inoculation into
expression of a series of genes. very good)
eyes
Ingestion of contaminated
meat or water Typhoidal: ingestion results in
gastrointestinal symptoms (abdominal
Easily transmitted to lab pain) and fever
personnel
Yersinia pestis Wild rodents Flea bite Facultative anaerobe Fraction 1 (F1): this capsular Pesticin: kills other BUBONIC PLAGUE Streptomycin or Gram-negative rods MOST VIRULENT
antigen is antiphagocytic bacteria (including E. coli) î Regional lymph nodes (usually groin) Gentamicin with bipolar staining:
Virulence factors are
BACTERIA!!!
City rats Contact with infected swell, and become red, hot and tender the ends of these rod-
animal tissue temperature sensitive: V and W proteins Intracellular murine (called a bubo) shaped bacteria take up
o Doxycycline Facultative intracellular
Squirrels and prairie only expressed at 37 C toxin: lethal to mice î high fever stain more than the center
parasite
dogs in the US Inhaled aerosolized (temperature inside î conjunctivitis (closed safety pin
Non-motile Killed vaccine is
organisms: human to macrophages)
effective only for a few appearance) Yersinia can accept
human transmission o
Requires calcium at 37 C. SEPTICEMIC PLAGUE months (attenuated plasmids in E. coli, and
Virulence is plasmid-
occurs during epidemics î bacteria survive in macrophages, and vaccine is more effective Blood culture shares many antigens
mediated If insufficient calcium, Y. pestis
spread to blood and organs but also has more side with enteric bacteria
alters its metabolism and protein
î death occurs in 75% in untreated effects) Culture bubo aspirate
production. This trait assists with
Subcutaneous
its intracellular state
PNEUMONIC PLAGUE Serology hemorrhage result in a
The bacteria elaborate a î during epidemics, pneumonia occurs, as blackish skin
lipopolysaccharide bacteria are spread from person to Rapid diagnostic test: discoloration, giving the
person by aerosolized respiratory antibody against F1 name “Black Death”
endotoxin, coagulase, and a secretion (capsular antigen)

fibrinolysin, which are the î 100% fatal if untreated
principal factors in the
pathogenesis of plague.

Pasteurella Part of the normal Bite from dog or cat Facultative anaerobe Capsule WOUND INFECTIONS (following dog Penicillin G Short encapsulated NOT a facultative
flora of domestic and or cat bites): may progress to infection of Doxycycline gram-negative rod that intracellular organism
multocida wild animals Non-motile nearby bones and joints Third generation exhibits bipolar staining
cephalosporin Human bite infection:
Buttery colonies with Eikenella corrodens
musty odor due to
indole production
 TREATMENT AND
MICROORGANISM RESERVOIR TRANSMISSION METABOLISM VIRULENCE FACTORS TOXINS CLINICAL SYNDROMES DIAGNOSIS NOTES
PREVENTION
Mycobacterium Habitat is human Transmission is via Produces catalase Mycolic Acid: large fatty acid No exotoxin nor TYPES OF LESIONS: (see next page) Aerobic, acid-fast, thin, Purified Protein
lungs inhalation of and niacin endotoxin EXUDATIVE LESIONS non-motile rods Derivative (PPD) Test
tuberculosis DIAGNOSTICS
respiratory droplet Mycoside: a mycolic acid î pus from acute inflammatory - Ziehl-Neelsen (or 1. Measure zone of
bound to a carbohydrate RAPID CULTURE: induration:
nuclei produced by response Kinyoun)
Facultative coughing forming a glycolipid Bactec radiometric
Positive reaction:
High lipid content: 40% intracellular growth: GRANULOMATOUS LESIONS culture: a liquid broth in a
Slow-growing on > 5mm (immune-
of total cell dry weight is M. tuberculosis can Cord factor î central area of Langhan’s type bottle, with radioactive
Lowenstein-Jensen compromised host)
lipid survive and multiply palmitate as a carbon
î a mycoside formed by union giant cells surrounded by a zone of source. Mycobacteria medium > 10 mm (have
in macrophages of 2 mycolic acids with a epithelioid ells grow and use the carbon, chronic disease or risk
disaccharide (trehalose) î tubercle is a granuloma surrounded allowing early detection factors for exposure to
Mycolic acids are also
î only found in virulent strain TB)
by fibrous tissue that has (in 1-2 weeks) even found in Nocardia (which
î most important virulence before colonies can be also is acid fast) >15mm (all others)
undergone central caseation
factor seen.

î inhibits neutrophil PPD skin test 2. A positive reaction
PHASES OF INFECTION
migration and damages Chest X-ray (“seroconversion”)
PRIMARY COMPLEX indicates:
mitochondria PCR and DNA probes
î usually in middle or lower lobes - current infection /
î may be responsible for
release of tumor necrosis î subpleural granuloma (Ghon’s Mycobacterium Tb Direct active disease
factor à cachexia focus) + associated lymph node = Test (MTDT): amplifies - past exposure but
Ghon’s complex ribosomal RNA in does not mean active
Sulfatides respiratory secretions, disease
î radiologically detectable - BCG vaccination
î mycoside that resemble cord allowing rapid
calcification (Ranke’s complex) identification of M.
factor with sulfates attached

to the disaccharide REACTIVATION TUBERCULOSIS tuberculosis 3. Negative Test

î exported repetitive indicates:
î usually in apices (Simon’s focus)
QuantiFERON-TB - - no infection
protein î CXR: cicatrical changes, subpleural measures interferon - anergy à
î inhibit phagosome- blebs, cavitation, fibrosis, nodules gamma levels produced in immunocompromised,
lysosome fusion o Secondary colonization with whole blood in response malnutrition, steroids,
A. fumigatus (fungus ball) to addition of specific sarcoidosis
Wax D î Can lead to pneumothorax tuberculosis antigens;
î acts as an adjuvant relative specificity for 4.PPD skin test is type IV
î activates the protective Mycobacterium hypersensitivity mediated
SPECTRUM OF DISEASE
cellular immune system tuberculosis; not positive
î Pulmonary tuberculosis in patient in previous BCG Isoniazid for 9 months
Tuberculin surface protein: î Miliary tuberculosis vaccination for patients who show
î Elicits delayed î Scrofula
seroconversion but no
hypersensitivity î Erythema nodosum Luciferase Reporter clinical symptoms
î Tuberculous meningitis Mycobacteriophage
Iron siderophore î Spondylitis (Pott’s disease) (LRP) Assays - can
(mycobactin) î Gastrointestinal tuberculosis detect M. tuberculosis and Bacillus Calmette-
(ileocecal) characterize Guérin vaccine is also
î Renal tuberculosis mycobacterial drug used as intravesical
î Abdominopelvic tuberculosis susceptibility patterns chemotherapy in
within 24 to 48 h in patients with bladder
positive cultures
cancer
(Luciferase is an enzyme
obtained from fireflies)

 MYCOBACTERIUM TUBERCULOSIS

Diagnostic Algorithm

Screening of Pediatric Drug-Susceptible Household Contacts of TB
 APPROPRIATE SPECIMENS
Pulmonary TB Sputum AFB x 2
TB lymphadenitis Excisional Biopsy
TB Effusion Pleural fluid studies (AFB, Q/Q)
Genitourinary TB Urine AFB
Spinal TB (Pott’s) Tissue Biopsy
Abdominal TB Barium studies for intestinal disease
Abdominal CT for extraintestinal
Peritoneal fluid studies (AFB, Q/Q)
TB Meningitis CSF studies (AFB, Q/Q)
TB Pericarditis Pericardial fluid studies (AFB, Q/Q)

TB DISEASE REGISTRATION GROUPS

MECHANISM OF ACTION OF ANTI-TB DRUGS
Drug Mechanism of Action Mechanisms of Resistance
Rifampicin (RIF) Inhibit DNA-dependent RNA polymerase Mutations in DNA-dependent RNA polymerase
Isoniazid (INH) Inhibit mycolic acid synthesis Mutations of catalase-peroxidase reduce intracellular
transformation to active form
Pyrazinamide (PZA) Interferes with NAD and affects the ETS
Ethambutol (EMB) Inhibit arabinosyl transferase which blocks arabinogalactan synthesis
Streptomycin Interferes with the 30s subunit of ribosomes Mutations of genes encoding the 30s subunit

RECOMMENDED TREATMENT REGIMEN FOR ADULTS AND CHILDREN

MYCOBACTERIUM AVIUM INTRACELLULARE COMPEX (MAI, MAC)
Cause pulmonary disease in immunocompromised hosts (AIDS patients with CD4 <50)
DOC: Azithromycin
 VIRULENCE FACTORS / SPECTRUM OF DISEASE / TREATMENT AND
MICROORGANISM RESERVOIR TRANSMISSION METABOLISM DIAGNOSIS NOTES
TOXINS / PATHOGENESIS CLINICAL SYNDROMES PREVENTION
Mycobacterium Humans Prolonged exposure to Catalase-positive Non-motile LEPROSY / HANSEN DISEASE Tuberculoid Leprosy: Aerobic, acid-fast rods
nasal secretions of î most common cause of crippling of the hand Rifampin

leprae Grows best at low

Armadillos patients with Facultative intracellular î Damage in the following nerves is associated Dapsone CANNOT be cultured in vitro. Can
temperature
lepromatous form growth with characteristic impairments in leprosy: only be cultured in certain
Phenolase-positive: - Ulnar and median: clawed hand Lepromatous Leprosy: animals:
converts DOPA into a - Posterior tibial: plantar insensitivity and Rifampin - Mouse footpad
pigmented product clawed toes Dapsone - Armadillo
(used for diagnosis) - Common peroneal: foot drop Clofazimine - Monkeys
î Radial cutaneous, facial, and greater
Feature Tuberculoid Leprosy Lepromatous Leprosy
auricular nerves (may also be involved) Skin or nerve biopsy will reveal
limited diffusely over the skin acid-fast bacilli (lepromatous) or
Presentation few hypoesthetic, Leonine facies granulomas (tuberculoid)
hairless skin plaques Erythema nodosum leprosum ERYTHEMA NODOSUM LEPROSUM
î Seen in lepromatous form Lepromin skin test - Although not
Number of Lesions One or few Many lesions î Tender red nodules or humps on both shins useful for diagnosis, it allows
Tissue Destruction Little Marked î Signals acute flare-ups of disease positioning of patients on the
î Treated with Thalidomide immunologic spectrum
Number of acid-fast
Few Many - Category X drug
bacilli
- Associated with phocomelia if given
Likelihood of
Low High during pregnancy
transmitting leprosy

Cell-mediated
Present Reduced or absent
response to M. Leprae
Immune response Th1-type Th2-type
Lepromin Test Positive Negative
Rifampicin + Rifampicin + Dapsone +
Treatment
Dapsone Clofazimine

Mycoplasma Habitat is human Respiratory droplets Aerobic Protein P1 adhesin ATYPICAL PNEUMONIA (WALKING Macrolides NOT SEEN ON GRAM STAIN Mycoplasma has
pneumoniae respiratory tract î Toll-like receptor 2 protein PNEUMONIA) (erythromycin, î No cell wall limited biosynthetic
Requires STEROL for î adheres to epithelial cells of î Mycoplasma pneumoniae is the most azithromycin, î Only bacteria with cholesterol capabilities.
tiniest free-living membrane formation the respiratory tract common cause of atypical pneumonia clarithromycin) in cell membrane
organisms capable of î causes inhibition of ciliary î insidious onset, headache, dry, They can be grown in
self-replication motion (ciliostasis) and nonproductive hacking cough, patchy or Tetracyclines High titer of cold agglutinins cell-free media.
necrosis diffuse interstitial infiltrate (doxycycline) (IgM), which can agglutinate or lyse
î Chest X-ray will show patchy infiltrates that RBCs
Hydrogen Peroxide look worse than clinical findings
Quinolones
î contributes to the damage CULTURE:
(ciprofloxacin,
to the respiratory tract cells TRACHEOBRONCHITIS levofloxacin) î Eaton’s agent
î takes 2-3 weeks
Motile (glides) EXTRAPULMONARY MANIFESTATIONS î Requires cholesterol and nucleic
î Stevens-Johnson Syndrome (most common PENICILLIN AND acids
Community-acquired infectious cause is M. pneumoniae) CEPHALOSPORINS î Add penicillin to inhibit growth
respiratory disease toxin î Erythema multiforme î do NOT work as of contaminating bacteria
(CARDS) î Hemolysis mycoplasma does not î Dome-shaped colonies with
î An exotoxin î Raynaud’s have a cell wall “fried egg” appearance or
î Major role in damage to the î Guillain-Barre syndrome “mulberry” appearance (in the
respiratory epithelium case of Mycoplasma pneumoniae)

î ADP-ribosylating and Children with sickle cell disease and functional
Complement fixation test
vacuolating cytotoxin asplenia may be at greater risk for severe

similar to pertussis toxin. respiratory tract disease PCR/Nucleic acid probes
 VIRULENCE FACTORS / SPECTRUM OF DISEASE / TREATMENT AND
MICROORGANISM RESERVOIR TRANSMISSION METABOLISM DIAGNOSIS NOTES
TOXINS / PATHOGENESIS CLINICAL SYNDROMES PREVENTION
Treponema Habitat is the Sexual Microaerophilic Motile PRIMARY SYPHILIS Benzathine Penicillin G Coiled spirochete / thick rigid FALSE-POSITIVE VDRL
pallidum pallidum human genital î Within hours, enters lymphatics and spirals RESULTS
tract Transplacental Highly sensitive to multiplies Erythromycin Viruses (EBV,
elevated î Local non-tender / painless chancre Not seen on Gram stain Hepatitis)
temperatures - Versus painful chancroid of H. ducreyi î Too thin Drugs (Marijuana)
Doxycycline


SECONDARY SYPHILIS Rheumatic fever,
î maculopapular rash on palms and soles Jarisch-Herxheimer Cannot be cultured in vitro: Rheumatoid arthritis
î Condylomata lata: painless, wart-like lesion î lacks tricarboxylic acid (Kreb’s)
reaction: acute Lupus, Leprosy
which occurs in warm, moist places (vulva or cycle
worsening of symptoms


scrotum) after Penicillin is started;

î Occurs after 1-3 months DARKFIELD MICROSCOPY: most
due to lysis of
Pathogenic treponemes î Fever, headache, malaise, anorexia, important (definitive) diagnostic
treponemes
are associated with the lymphadenopathy test for primary syphilis The antigens in non-

following diseases:
treponemal tests
LATENT SYPHILIS
NON-TREPONEMAL TESTS: contain measured
T. pallidum pallidum: î 25% may relapse back to the secondary amounts of
VDRL, RPR
Venereal syphilis stage cardiolipin,
î Screening test for syphilis
T. pallidum pertenue: TERTIARY SYPHILIS î Correlates with disease activity cholesterol, and
Yaws î many years after inoculation î Used to monitor treatment purified lecithin in

T. pallidum endemicum: î granulomas (gummas) of skin and bone quantities sufficient to
Endemic syphilis (bejel) î Cardiovascular syphilis (aortitis) TREPONEMAL TESTS: yield a standardized
- Obliterative invasion of small blood FTA-ABS, TPHA amount of reactivity.
T. carateum: Pinta vessels and vasa vasorum, causing Historically, the
î Confirmatory test
endarteritis î DO NOT repeat even after cardiolipin was
î Neurosyphilis treatment extracted from beef
- Tabes dorsalis î Remain positive throughout life heart or liver with
o Argyll-Robertson pupil (prostitute despite treatment added lecithin and
pupil; can accommodate but do not cholesterol to enhance
react) VDRL: Venereal Disease Research
reaction with syphilitic
- Dementia paralytica Laboratory; RPR: Rapid Plasma Reagin; “reagin” antibodies.

Fluorescent Treponemal Antibody Reagin is a mixture of
CONGENITAL SYPHILIS ABSorption (FTA-ABS); Treponema Pallidum IgM and IgG antibodies
î Snuffles/saddle nose Haemagglutination Assay (TPHA) reactive with the
î Mulberry molar cardiolipin–cholesterol–
î Hutchinson triad (Hutchinson teeth, lecithin complex.
sensorineural hearing loss, interstitial Take Note!!!
keratitis)
î Saber shins FTA-ABS
- Most specific
î Rhagades
- Earliest positive
î Higoumenakis sign (unilateral enlargement
of the sternoclavicular portion of the clavicle - Remains positive longest

à detachment)
î Clutton’s joints (synovitis)
î Pulmonary hemorrhage (MCC of death)

BORRELIA RECURRENTIS
Relapsing Fever
î rapid antigenic changes due to programmed rearrangements of bacteria DNA encoding surface proteins
î transmitted by human body louse (Pediculus humanus)
î Diagnosed by microscopy
î DOC: Tetracycline or Erythromycin
 VIRULENCE FACTORS / SPECTRUM OF DISEASE / TREATMENT AND
MICROORGANISM RESERVOIR TRANSMISSION METABOLISM DIAGNOSIS NOTES
TOXINS / PATHOGENESIS CLINICAL SYNDROMES PREVENTION
Borrelia Animal Bite from deer ticks Microaerophilic LYME DISEASE Early Localized or Weakly staining, gram-negative Thiomargarita
Reservoirs: (Ixodes ticks) Disseminated Lyme spirochetes namibiensis is the

burgdorferi Stage 1: Early localized stage

î White-footed - Together with î Erythema chronicum migrans (ECM) Disease: largest bacteria ever
Largest medically mouse Babesia microti Doxycycline (DOC) Stains well with aniline dyes discovered (not
important bacterium î White-tailed Stage 2: Early disseminated stage Amoxicilin (Giemsa or Wright stain) medically important).

deer Ixodes scapularis: î Multiple smaller ECM Cefuroxime
BAKE a Key LYME Pie
East & Midwest î Neurologic: aseptic meningitis, cranial nerve Cultured on Barbour-Stoenner-
palsies (Bell’s palsy), and peripheral
Bell’s Palsy
Late Manifestations: Kelly (BSK) medium
Ixodes pacificus: neuropathy Arthritis
IV Penicillin
Kardiac Block
West coast î Cardiac: transient AV block or myocarditis Ceftriaxone (for Elevated levels of antibodies
î Brief attacks of arthritis of large joints neurologic disease) against Borellia burgdorferi can be Erythema chronicum
(knee) detected by: migrans

î ELISA
Stage 3: Late stage
î Western immunoblotting
î Autoimmune migratory polyarthritis (onion PREVENTION:
î Insectides
skin lesion)
î Insect repellents
î Acrodermatitis chronica atrophicans
î Protective clothing
î Encephalopathy

Leptospira Zoonotic (dogs, Direct contact with Obligate aerobe Leptospires penetrate intact Incubation Period: 2-20 days Mild Leptospirosis: Thin-coiled spirochetes The traditional system
interrogans cats, livestock, and infected urine or (the other spirochetes mucous membranes or skin î Doxycycline divided the genus into
wild animals) animal tissue: are microaerophiles) through small cuts or ACUTE LEPTOSPIREMIC PHASE: Spiral shaped, with hooks on both 2 species: the
î Ampicillin
Organism penetrate abrasions î organisms in blood and CSF ends (“ice tongs”) à Shepherd’s pathogenic Leptospira
î Amoxicillin
broken skin (i.e. on â î causes high spiking temperature, chills, crook appearance interrogans and the

feet) and mucous Multiply rapidly and damage intense headache nonpathogenic
endothelium of small blood Severe Leptospirosis:
(The resting site membranes î rapid multiplication of leptospires in Darkfield Microscopy: insensitive; Leptospira biflexa.
for leptospires in (swallowing urine- vessels (VASCULITIS) muscles with high oxygen tension à severe î Penicillin G not recommended
the natural host is contaminated water) muscle aches (calf tenderness) î Ampicillin
the lumen of the Organisms found in: î damaged and leaky conjunctival vessels à î Ceftriaxone Microscopic agglutination Test:
Two axial flagella wrap nephron tubules.) History of wading in blood and CSF (early in the conjunctival suffusion (painful and itchy î Cefotaxime î LeptoMAT
rd
around and run along flood water (in 3 disease) and in the but with minimal tearing) î the gold standard / criterion
the length of the world setting) urine (later stages) Jarisch-Herxheimer standard for serologic
organism under the IMMUNE LEPTOSPIRURIC PHASE: reaction may develop identification of leptospires
outer membrane History of exposure to Immune complex-mediated î correlates with emergence of IgM within hours after starting
(periplasmic flagella) animals (butcher) meningitis and î involves recurrence of the above symptoms therapy CULTURE:
glomerulonephritis î aseptic meningitis î Grown on Ellinghausen-
- CSF pleocytosis with or without McCullough-Johnson-Harris
meningeal symptoms PREVENTION: (EMJH) medium or Fletcher’s
- Coincides with appearance of antibody î Doxycycline for medium
titer postexposure î only becomes positive after 2
î Pulmonary involvement chemoprophylaxis weeks of incubation
- Snowflake lesions on CXR î Rat control î First week: culture blood or CSF
î Hepatic necrosis î Vaccination of domestic (on lab media, or by inoculation
î Glomerulonephritis (due to immune livestock and pets into animals
complex deposition î Second week to months: culture
urine
WEIL’S SYNDROME:
î most severe form of leptospirosis Antibody based ELISA to detect
î triad: Bleeding, Jaundice, Uremia Leptospira antigens in the urine
î orange cast skin (severe jaundice)
î MCC of death: respiratory failure due to Polymerase Chain Reaction (PCR)
massive pulmonary hemorrhage to detect bacterial DNA in serum,
CSF and urine
 VIRULENCE FACTORS / SPECTRUM OF DISEASE / TREATMENT AND
MICROORGANISM RESERVOIR TRANSMISSION METABOLISM DIAGNOSIS NOTES
TOXINS / PATHOGENESIS CLINICAL SYNDROMES PREVENTION
Chlamydia Habitat is the Sexual Energy parasites Obligate intracellular TRACHOMA GENITAL AND EYE Gram-negative TRACHOMA
trachomatis human genital that use host ATP bacteria î C. trachomatis types A-C INFECTIONS: lacks classic peptidoglycan layer TYPES A, B, C
tract and eyes During passage î leading infectious cause of blindness Doxycycline (use only due to reduced muramic acid Africa
A-C: trachoma through birth canal Resistant to lysozyme (since î Chronic keratoconjunctivitis for adults) (rendering Beta-lactam antibiotics Blindness
D-K: genital, neonatal (C. trachomatis is their cell wall lacks muramic î scarring of the inside of the eyelid, resulting ineffective)
Chronic infection
L1-L3: LGV strictly human Hand-to eye contact acid) in redirection of the eyelashes onto the Erythromycin (especially
pathogen) corneal surface à corneal scarring and for infants and pregnant Cytoplasmic inclusions in
Prevents phago–lysosome blindness woman) Giemsa: (Halberstaedter-
FORMS: fusion î Scraping from the surface of the conjunctiva Prowazek inclusions)
ELEMENTARY BODY RETICULATE (INITIAL) BODY
will show round to oval intracytoplasmic Azithromycin
Non-motile inclusion bodies within conjunctival
Can classically be grown in chick
Inactive Metabolically active

Extracellular Intracellular No pili epithelial cells (Halberstaedter-Prowazek For STD, add yolk sacs: More commonly
Enters the cells by endocytosis Seen microscopically inclusions) CEFTRIAXONE for chlamydia is cultured in certain cell
No exotoxins possible concomitant lines (McCoy cells for example)
Infectious Replicates the binary fission
GENITAL TRACT INFECTIONS gonorrhea - To enhance the sensitivity of
Elementary body: Enfectious, Enters the cell via Endocytosis
PATHOGENESIS: î C. trachomatis types D-K
McCoy cells to C. trachomatis
Reticulate body: Replicates in cell by fission, Reorganizes into
î balance that is often î Most common cause of STDs Note: Systemic treatment growth, cycloheximide was
elementary bodies. reached between host and î Men: Nongonococcal urethritis, epididymitis is required for any added to culture medium for
parasite, resulting in and prostatitis chlamydial eye infection. cultivating infected cells.
prolonged persistence of î Women: Urethritis, cervicitis and pelvic This is especially true for
infection inflammatory disease (PID) infants, who can develop PCR
î Infection persists in the î Associated with Reiter’s syndrome: triad chlamydial pneumonia
presence of high antibody of conjunctivitis, urethritis, and arthritis following chlamydial Nucleic acid amplification test
titer î Birth complications: neonatal pneumonia, conjunctivitis. (NAAT)
neonatal conjunctivitis

NEONATAL PNEUMONA

î C. trachomatis types D-K
î Late-onset (2-4 weeks)
î Striking tachypnea, characteristic
paroxysmal cough (staccato cough),
absence of fever, and eosinophilia

LYMPHOGRANULOMA VENEREUM
î C. trachomatis types L1-L3
î Papule or vesicular which ulcerates leads to
Elementary body (EB): dense spherule that infects cells
Initial (reticulate) body: After EB enters cell, it transforms into an initial
suppurative inguinal lymphadenitis
body; larger, osmotically fragile; can produce via binary fission; (buboes)
requires ATP from the host. The initial body transform back into EB, î (+) Frei test: intradermal injection of antigen
which leaves the cell to infect the other cells.

Chlamydophila Humans (spread Respiratory route Life cycle similar to ATYPICAL PNEUMONIA Doxycycline Examine blood for elevated titers TWAR: Taiwan Acute
pneumoniae from human to Chlamydia î Viral-like atypical pneumonia (similar to a of antibodies with complement Respiratory agent
(strain TWAR) human) trachomatis Mycoplasma pneumonia) in young adults Erythromycin fixation and immunofluorescence

tests
Associated with atherosclerosis, meningo- Intracytoplasmic inclusion bodies
encephalitis, arthritis, myocarditis, Guillain- that DO NOT STAIN with iodine
Barre syndrome
Chlamydophila Parrots, parakeets, Humans are infected PSITTACOSIS (BIRD FANCIER’S DISEASE) Azithromycin
psittaci macaws, cockatiels by inhaling Chlamydia- î Sudden onset pneumonia with malaises,
laden dust from fever, anorexia, sore throat, photophobia,
feathers or dried-out and severe headache
feces.
 RICKETTSIAE

î Classical detection using Weil-Felix Reaction (cross-reaction with antigens of OX strains of Proteus mirabilis)
î Drug of choice for all rickettsial infections is DOXYCYCLINE.

DISEASE CAUSE VECTOR INCUBATION ONSET RASH ESCHAR MORTALITY
Rocky mountain Macular with centripetal
Rickettsia rickettsii Tick 7 Abrupt NO 10-25%
spotted fever spread
Mites
Rickettsial pox Rickettsia akari
(chiggers)
9 - 14 Abrupt Generalized papulovesicular YES Low

Rickettsia Macular with centrifugal

Epidemic typhus Body louse 8 Abrupt NO 20
prowazekii spread
Endemic typus Rickettsia typhi Rat flea 7-14 Gradual Maculopapular NO Low
Orientia Mites Maculopapular with
Scrub typhus 10-12 Abrupt NO 1-15%
tsutsugamushi (chiggers) centrifugal spread
Q fever Coxiella burnetti None 4-90 Chronic None NO 65%
Erhlichia
Ehrlichiosis Ticks 7-21 Abrupt Maculopapular or petechial NO 2-3%
chaffeensis

Only one without vector: Q fever Q fever is Queer because:
Only one with chronic onset: Q fever 1. No rash
Only one without rash: Q fever 2. No vector
Has highest mortality: Q fever 3. Negative Weil-Felix reaction
4. Not obligate intracellular
Only one with gradual onset: Endemic typus
5. Does not have Rickettsia in its genus name
Only one with eschar: Rickettsial pox


Palm and Sole Rash
Rocky mountain sPotted Fever You drive CARS using your palms and soles
Rash starts in wRIst
Coxsackievirus type A
Spreads centriPetally
Rocky mountain spotted fever

TyPHUs Syphilis

Rash starts in Trunk
Spreads centriPHUgally


MISCELLANEOUS BACTERIA

MICROORGANISM MORPHOLOGY DISEASE CLINICAL FINDINGS OTHERS
Bartonella henselae Gram-negative rod Cat-scratch Disease Cat-scratch fever in Normal oral flora of cats
immunocompetent hosts Transmitted via cat bite or
Bacillary angiomatosis in scratch
immunocompromised
Ehrlichia chaffeensis obligate intracellular gram- Ehrlichiosis
negative bacterium
Forms morulae in cytoplasm of
monocytes
Gardnerella vaginalis Facultative gram-variable rod Bacterial vaginosis Malodorous fishy vaginal Associated with sexual
discharge activity, but not sexually
(+) Amine Whiff test (mixing transmitted
discharge with 10% KOH
enhances fishy odor) Treatment:
(+) Clue cells Metronidazole
Haemophilus ducreyi Small gram-negative rod Chancroid Painful genital ulcer
Culture on chocolate agar with
Heme (Factor X)
Yersinia enterocolitica Gram-negative rod Mesenteric adenitis Pseudoappendicitis Reservoir: domestic
animals
Transmitted via oro-fecal
route
Klebsiella granulomatosis Encapsulated, pleomorphic gram- Granuloma inguinale Small painless papule ulcerates Treatment:
negative bacillus (Donovanosis) to form beefy red ulcer with Azithromycin
Bipolar densities (Donovan velvety surface
bodies) look like closed safety Pseudobuboe formation
pins
















 ANTIMICROBIALS

ANTIMYCOBACTERIAL DRUGS

ANTIFUNGALS

 MEDICAL MYCOLOGY

FUNGI FUNGAL PATHOGENESIS
î eukaryotic organisms (true nucleus, 80s ribosomes, mitochondria) • Two types of host response: granulomatous or pyogenic response
î Differences targeted by antifungals include: • Some can be detected by using skin tests for delayed
1. Fungal cells have cell walls (CW). hypersensitivity reaction
a. Fungal cell walls protect cells from osmotic shock, determine • Reduced cell immunity predisposes to disseminated disease
cell shapes, and have components that are antigenic.
b. Fungal cell walls are composed primarily of complex OVERVIEW OF FUNGAL DISEASES
carbohydrates such as chitin with glucans and mannose- A. FUNGAL ALLERGIES
proteins. • sick building syndrome
c. The CW glucan (not found in humans) is the antifungal target • farmer’s lung
of the echinocandins like caspofungin. • silo worker’s disease
2. Ergosterol is the dominant fungal membrane sterol rather than • allergic bronchopulmonary aspergillosis (Aspergillus fumigatus)
cholesterol, which is an important difference targeted by B. MYCOTOXICOSES
imidazoles, triazoles, and polyenes antifungals. • may result from ingestion of fungal-contaminated foods
î Fungi include organisms called molds, mushrooms, and yeasts. • e.g., St. Anthony’s fire from ergot-contaminated bread or aflatoxin
• HYPHAE are filamentous (tubelike) cells of molds (also known as [a carcinogen] -contaminated peanuts
the filamentous fungi) and mushrooms. Hyphae grow at the tips • ingestion of psychotropic (Psilocybe) or toxic (Amanita) mushrooms.
(apical growth). C. FUNGAL INFECTIONS (MYCOSES)
- Septae or septations are cross walls of hyphae and occur in • Mycoses range from superficial to overwhelming systemic infections
the hyphae of the great majority of the disease-causing fungi. that are rapidly fatal in the compromised host.
They are referred to as septate. • Mycoses are increasing in prevalence as a result of increased use of
- Nonseptate or aseptate hyphae lack regularly occurring cross antibiotics, corticosteroids, and cytotoxic drugs.
walls. These cells are multinucleate and are also called
coenocytic. They often are quite variable in width with broad- LABORATORY DIAGNOSIS OF FUNGI
branching angles - Microscopic examination: rapid methods
- Hyphae may be dematiaceous (dark colored) or hyaline 1. Potassium hydroxide in a wet mount (KOH mount) of skin scrapings
(colorless). breaks down the human cells, enhancing the visibility of the
- Fluffy surface masses of hyphae and their ‘‘hidden’’ growth unaffected fungus
into tissue or lab medium are called mycelia. 2. A nigrosin or India ink wet mount of cerebrospinal fluid (CSF)
• YEASTS are single-celled fungi, generally round to oval shaped. highlights the capsule of Cryptococcus neoformans but is very
They reproduce by budding (blastoconidia). insensitive (misses 50% of cases).
• PSEUDOHYPHAE (hyphae with sausagelike constrictions at 3. A Giemsa or Wright’s stain of thick blood or bone marrow smear may
septations) are formed by some yeasts when they elongate but detect the intracellular Histoplasma capsulatum.
remain attached to each other. 4. Calcofluor white stain ‘‘lights up’’ fungal elements in exudates, small
- Candida albicans is notable for developing into skin scales, or frozen sections under a fluorescent microscope, giving
pseudohyphae and true hyphae when it invades tissues. the fungus a fluorescent blue-white appearance on a black
• THERMALLY DIMORPHIC FUNGI are fungi capable of converting background.
from a yeast or yeast-like form to filamentous form and vice versa. - Histologic staining: special fungal stains for fixed tissues are necessary
- Environmental conditions such as temperature and nutrient because fungi are not distinguished by color with hematoxylin and eosin
availability trigger changes. (H&E) stain.
- Exist in the yeast or a yeastlike form in a human and as the 1. Gomori methenamine-silver stain: fungi are dark gray to black
filamentous form in the environment. (Yeast in the heat; 2. Periodic acid-Schiff (PAS) reaction: fungi are hot pink to red.
mold in the cold) 3. Gridley fungus stain: fungi are purplish rose with a yellow background
- include the major pathogens: 4. Calcofluor white stain: as above
o Sporothrix 5. Immunofluorescent stains are available for some fungal pathogens
o Blastomyces - DNA probes are now available for early detection of some systemic
o Histoplasma pathogens.
o Coccidioides - Cultures for fungi must be specially ordered. They use special media (e.g.,
o Paracoccidioides Sabouraud’s dextrose medium), enriched media (e.g., blood agar) with
• FUNGAL SPORES are formed either asexually or by a sexual process - Fungal antigen detection uses known antibodies to identify circulating
involving nuclear fusion and then meiosis. Fungal morphology fungal antigens in a patient’s serum, CSF, or urine. Antibodies are available
including spores may be used in identification. for Histoplasma and Cryptococcus.
- Conidia are asexual spores of filamentous fungi (molds) or - Serologic testing
mushrooms
- Blastoconidia are the new yeast ‘‘buds’’ ANTIFUNGAL THERAPY
- Arthroconidia are conidia formed by laying down joints in
hyphae followed by fragmentation of the hyphal strand
î Fungi require preformed organic carbon compounds (heterotrophic
nutrition) derived from their environment.
• SAPROBES / SAPROPHYTES live on dead organic material. Some
are opportunistic, causing disease if traumatically implanted into
tissue.
• COMMENSAL COLONIZERS generally live in harmony on humans,
deriving their nutrition from compounds on body surfaces. Some
are opportunists because under certain conditions (e.g., reduced

immune responsiveness) they may invade tissue or vasculature and DRUGS MECHANISM OF ACTION
cause disease. Polyenes Binds to ergosterol in fungal cell membranes,
• PATHOGENS infect the healthy but cause more severe disease in - Amphotericin B forming leaky pores
the compromised hosts. The damage to living cells provides Azoles Inhibit fungal P450-dependent enzymes (lanosterol
nutrition. Most of these are also environmental saprobes. - Ketoconazole 14-a-demethylase) blocking ergosterol synthesis;
- Fluconazole resistance can occur with long-term use
COMPARISON: FUNGI VERSUS BACTERIA - Itraconazole
Feature Fungi Bacteria - Posaconazole
Nucleus Eukaryotic Prokaryotic - Voriconazole
Mitochondria and ER Present Absent Terbinafine Inhibits epoxidation of squalene
Cell membrane sterols Absent Echinocandins Inhibit β-glucan synthase decreasing fungal cell
Present - Caspofungin wall synthesis
(except in Mycoplasma)
Cell wall content Chitin Peptidoglycan - Micafungin
Spores Reproduction Survival - Anidulafungin
Dimorphism Yes No Flucytosine Blocks nucleic acid synthesis by Inhibiting DNA and
Metabolism Aerobic Aerobic or anaeroic RNA polymerases
Griseofulvin interferes with microtubule function in
dermatophytes and may also inhibit the synthesis
and polymerization of nucleic acids
 NAME RESERVOIR / TRANSMISSION MORPHOLOGY PATHOGENESIS / CLINICAL SYNDROME DIAGNOSIS TREATMENT NOTES ANATOMIC LOCATION
DERMATOPHYTES Depending on the particular - Chronic infections often located in the warm, 10% KOH: branched /septate hyphae Topical imidazole Secretes the enzyme CUTANEOUS
Trichophyton species humid areas of the body keratinase, which digests
- Infection of skin, hair, and - Inflamed circular border containing Wood’s lamp: certain species of Oral griseofuivin is used for keratin (infect only
nails Soil (geophilic) papules and vesicles surround a clear Microsporum will fluoresce under tinea unguium and tinea superficial keratinized
Animals (zoophilic) area of normal skin ultraviolet light (green fluorescence) capitis structure)
Microsporum Human (anthropophilic)
- Hypersensitivity causes dermatophytid
- Infection of skin and hair A fungal culture using Sabouraud’s Oral terbinafine For atypical presentations
- Not the cause of tinea Infections due to zoophilic or
reactions (inflammatory reaction to of tinea corporis, further
dermatophytosis to a cutaneous site DISTANT from
agar: hyphae and conidia
unguium geophilic dermatophytes may Keep skin dry evaluation for HIV
the primary infection)
produce a more intense PCR infection and/or an

Epidermophyton inflammatory response than immunocompromised
DERMATOPHYTOSES
- Infection of skin and nails those caused by Fungal DNA identification state should be
Tinea corporis (body): “ringworm”
- Not the cause of tinea anthropophilic microbes considered.
Tinea cruris (groin): “jock itch”
capitis
Tinea pedis (feet): “athlete’s foot”
Transmission: direct contact, Tinea capitis (scalp)
dogs, and cats Tinea unguium (nail): Onychomycosis
Tinea manum
Tinea barbae (facial hair)
Malassezia furfur Naturally found on the skin A basidiomycete TINEA/PITYRIASIS VERSICOLOR KOH prep: reveals short, curved, Dandruff shampoo SUPERFICIAL (SKIN)
surfaces of many animals, î usually characterized by hypopigmented or unbranched hyphae with spherical (containing selenium sulfide)
including humans. Lipophilic, skin hyperpigmented macules and patches on yeast cells (look like “spaghetti and
Isolated in 18% of infants and inhabitant the chest and the back meatballs”) Topical imidazole
90-100% of adults. î In patients with a predisposition, tinea
Predominantly produce versicolor may chronically recur Fluorescence under Wood’s lamp
May be spread from person to yeast-like conidia î fungal infection is localized to the stratum
person, fomites corneum Malassezia is extremely difficult to
Infectious particles: î High temperature, humidity favour propagate in laboratory culture and is
short hyphae, yeast-like occurrence culturable only in media enriched
cells (conidia) î Degradation of lipids leads to production of with C12- to C14-sized fatty acids.
acids and eventual destruction of
melanocytes
Sporothrix schenkii Found on rose thorns Dimorphic SPOROTRICHOSIS KOH exam of aspirates, pus, biopsy Cutaneous form: SpROSEthrix SUBCUTANEOUS
î Gardener’s / Rose-hander’s disease materials (typically unrewarding) Potassium iodide ROSE-hander’s disease
An ascomycete î causes local pustule or ulcer with nodules Oral itraconazole ROSEtte/daisy-like
(Ophiostoma stenoceras) along draining lymphatics (ascending Tissue smears (often negative, cluster of conidia
lymphangitis) sensitivity enhanced by GMS, PAS, Systemic form:
Soil, plant saprophyte î Occur as: FAB) Amphotericin B
- Cutaneous (lymphocutaneous) - Round-oval, cigar-shaped yeast
- Disseminated/systemic (bones, joints) cells
Infectious particles: î Follows a puncture wound (thorn prick, - Asteroid bodies (H&E)
hyphae, conidia splinter)
î frequently an occupational disease Others: direct IF, serology

Culture:
- On SDA (at room temperature):
fine, septate hyphae and
rosette/daisy-like clusters of
conidia on thin conidiophores
- On BHIA (at 37ºC): round to oval
yeast cells
 NAME RESERVOIR / TRANSMISSION MORPHOLOGY PATHOGENESIS / CLINICAL SYNDROME DIAGNOSIS TREATMENT NOTES ANATOMIC LOCATION
Coccidioides immitis Desert areas of the Dimorphic: - Arthospores form spherules filled with Biopsy of affected tissue: lung Drugs-of-Choice: Common oppurtunisitc SYSTEMIC
southwestern United States - Mycelial (mold) forms biopsy, skin biopsy, etc. Amphotericin B infection in AIDS patients
endospores of coccidiodes
and northern Mexico
o
with spores at 25 C Itraconazole from the southwest The most common
- Granulomata in bones and CNS
(soil) Silver stain or KOH prep United States mode of infection of
- Dissemination in those who have defective
Transmission: Respiratory - Spherule (not yeast) If meningitis occurs, systemic fungi is thru
CMI
via inhalation of
o
forms at 37 C (tissues) Culture on Sabouraud’s agar Fluconazole inhalation.


arthrospores VALLEY FEVER
Serology
î Very common in Filipinos living in Latin Systemic mycoses are
caused by dimorphic
America and Southwestern USA
Skin test fungi: cold (20°C) =
î Asymptomatic (in most persons)
mold; heat (37°C) =
î Influenza-like illness
yeast. Only exception is
î Lung infiltrates, adenopathy, or effusions

î Erythema nodosum (desert bumps) Coccidioides, which is

Spherule (much larger than RBC)

filled with endospores of î Arthralgias (desert rheumatism) a spherule (not yeast)
Coccidioides î Meningitis in tissue. (USMLE)

Histoplasma capsulatum Endemic in Mississippi and Dimorphic: - Inhaled microconidia develop into budding Lung biopsy Drugs-of-Choice: Can survive SYSTEMIC
Ohio River Valleys - Mycelial forms with Amphotericin B intracellularly within
yeast inside macrophages

o
spores at 25 C Silver stain specimen Itraconazole macrophages
o - Spreads to liver and spleen
Grows in soil contaminated - Yeast forms at 37 C
- Dissemination in those who have defective Culture on Sabouraud’s agar will
with bird droppings If meningitis occurs,
CMI o
reveal hyphae at 25 C and yeast at
(Starling) or bat guano Two types of asexual Fluconazole
o
37 C
spores:
Trabeculate HISTOPLASMOSIS
Transmission: Respiratory
macroconidia: typical î Asymptomatic (in most persons) Serology
via inhalation of airborne
thick walls and fingerlike î Chronic Pneumonia: lesions calcify, which


microconidia projections; Important in can be seen on chest X-ray (closely mimics Skin test (test for exposure only)

lab identification PTB)
Macrophage filled with î Disseminated: can occur in almost any
Histoplasma Microconidia: smaller, Urine antigen test
thin, smooth-walled organ, especially in lung, spleen, or liver

spores; if inhaled, î Erythema nodosum
transmit the infection î Tongue ulcerations in AIDS patients

Blastomyces Eastern and Central US Dimorphic: BLASTOMYCOSIS Biopsy of affected tissue: lung biopsy, Drug-of-Choice: Rarest systemic fungal SYSTEMIC
dermatitidis - Mycelial forms with î Chronic pneumonia skin biopsy, etc. Itraconazole infection.
Transmission: Respiratory
o
spores at 25 C î Ulcerated granulomas
via inhalation of conidia
o
- Yeast forms at 37 C î Verrucous skin lesions can simulate SCC Silver stain specimen For severe infections,
î Lytic bone lesions Amphotericin B
Round yeast with î Prostatitis Culture on Sabouraud’s agar
broad-based bud
Blastomyces Serology
Buds
Broadly Skin test (test for exposure only)

Sputum specimens processed with
10% potassium hydroxide, cytology
Broad-based budding
of Blastomyces
smears, or a fungal stain

Enzyme immunoassay (EIA)
techniques on sputum, tissue, or
bronchoscopic specimens

 NAME RESERVOIR / TRANSMISSION MORPHOLOGY PATHOGENESIS / CLINICAL SYNDROME DIAGNOSIS TREATMENT NOTES ANATOMIC LOCATION
Paracoccidioides Restricted to Central and Dimorphic: PARACOCCIDIOIDOMYCOSIS Biopsy of affected tissue; this shows Drug-of-Choice: SYSTEMIC
brasiliensis South America - Mycelial forms with î also known as the characteristic wheel-shaped Itraconazole

o
spores at 25 C - "Brazilian Blastomycosis," yeasts
Transmission: Respiratory
o
- Yeast forms at 37 C - "South American Blastomycosis"
- "Lutz-Splendore-de Almeida Disease" Culture shows the agent.
via inhalation of conidia
Thick yeast of with - "Paracoccidioidal Granuloma"
multiple buds in î chronic pneumonia Serology is also used in endemic
wheel configuration î painful ulcers on mouth and nose areas.
“captain’s / mariner’s î typical patient is male 30-50 years old
wheel” formation î rarely causes disease in fertile-age women,
probably due to a protective effect of

estradiol

Budding yeast of
Paracoccidioides with
“captain’s wheel” formation
Candida albicans Normal flora of the skin, URT, Dimorphic: NORMAL HOST: Form germ tubes in serum and Oropharyngeal and CUTANEOUS or
GIT, and FGUT - pseudohyphae and î Oral thrush chlamydo-spores in culture esophageal: Nystatin swish SYSTEMIC (normal host,
O
budding yeasts at 20 C î Vulvovaginitis à thick, white, curdlike, and swallow or opportunistic)
O
- germ tubes at 37 C “cottage cheese” discharge
î Skin infections à satellite lesions Skin infections: Clotrimazole
May appear as oval î Diaper rash
yeast with a single î Intertrigo Disseminated candidiasis:
bud or as î onychomycosis Amphotericin-B

pseudohyphae
IMMUNOCOMPROMISED HOST: Chemoprophylaxis:
î Pseudomembranous esophagitis Fluconazole
î Subcutaneous nodules
î Right-sided endocarditis
î Disseminated candidiasis: acquired by very
sick hospitalized patients, resulting in multi-
organ system failure
î Chronic mucocutaneous candidiasis
Cryptococcus Grows abundantly in soil Oval yeast with CRYPTOCOCCOSIS India ink (clear halo) and Amphotericin B + Opportunistic Mycoses SYSTEMIC
neoformans containing bird (especially narrow-based bud î asymptomatic lung infection mucicarmine (red inner capsule) Flucytosine followed by Predisposing Factors
surrounded by a wide î cryptococcal meningitis Fluconazole for cryptococcal - broad spectrum
pigeon) droppings
polysaccharide î cryptococcal encephalitis Cryptococcal Antigen Latex meningitis antibiotic use

o “soap bubble” lesions in brain - steroid use
capsule seen in India Agglutination System (CALAS) of
î MCC of meningoencephalitis in HIV - hematologic
ink preparation the CSF detects polysaccharide
- transplant recipients
capsular antigen and is more specific. Chemoprophylaxis:

Fluconazole - systemic
Transmission: Respiratory Yeast form only (Not
chemotherapy
dimorphic) Fungal culture
via inhalation of airborne - AIDS
yeast cells

 NAME RESERVOIR / TRANSMISSION MORPHOLOGY PATHOGENESIS / CLINICAL SYNDROME DIAGNOSIS TREATMENT NOTES ANATOMIC LOCATION
Aspergillius fumigatus Ubiquitous: widely distributed Exists only as molds Aspergillus may cause a broad spectrum of disease in Allergic brochopulmonary Allergic bronchopulmonary Rarely found in OPPORTUNISTIC
in nature (not dimorphic) the human host, ranging from hypersensitivity aspergillosis: aspergillosis: treat with individuals who are
Aspergillius flavus reactions to direct angioinvasion
Aspergillius niger - High level of IgE (IgE level > 1000 corticosteroids immunocompetent
Transmission: Respiratory Septate hyphae that ALLERGIC BRONCHOPULMONARY IU/dL)
ASPERGILLOSIS
via inhalation of airborne form V-shaped - Sputum culture Aspergilloma: removal via The FDA has approved an
î IgE-mediated
conidia (dichotomous) - Wheezing patient and chest X-ray thoracic surgery intravenous formulation
î Asthma-type reaction with shortness of with fleeting infiltrates of the triazole antifungal
branches (acute
O breath, high fever, and expectoration of - Increased level of eosinophils Invasive aspergillosis: treat posaconazole (Noxafil),
angles, 45 ) brownish bronchial plugs - Skin test: immediate with voriconazole, possibly which is indicated for the

hypersensitivity reaction
Aspergillus: Acute Angles
ASPERGILLOMA caspofungin (very high prophylaxis of invasive
î Fungus ball Aspergillus and Candida
mortality)
î associated with hemoptysis Aspergilloma: diagnose with chest X- infections in severely

î Monod sign: air around aspergilloma ray or CT scan immunocompromised

adults who are at high
INVASIVE ASPERGILLOSIS
Invasive aspergillosis: sputum risk of developing these
î necrotizing pneumonia
examination and culture infections.
î may disseminate to other organs in
immune-compromised patients
Aflatoxins contaminate
î (+) air crescent sign on radiography
peanuts, grains, and rice
AFLATOXIN CONSUMPTION
î produced by Aspergillus flavus
î can cause liver damage and liver cancer

INFECTIONS: wounds, burns, cornea, external
ear, sinuses
Rhizopus Saprophytic molds Broad, non-septated, MUCORMYCOSIS Biopsy Amphotericin B The disease is rapidly OPPORTUNISTIC
Rhizomucor branching hyphae (right î Causes disease mostly in ketoacidotic Black nasal discharge fatal
o
Mucor angles, 90 ) diabetic and/or neutropenic patients (eg, Surgery
leukemia)
î fungi proliferate in blood vessel walls,
penetrate cribriform plate, and enter
brain
î Rhino-orbito-cerebral infection, frontal
lobe abscess; cavernous sinus thrombosis
î Headache, facial pain, black necrotic
eschar on face; may have cranial nerve
involvement
Pneumocystis jirovecii Unicellular fungi found in the Indeterminate organism PNEUMOCYSTIS JIROVECII PNEUMONIA Diagnosis by staining BAL washings Treatment/prophylaxis: The taxonomic classification of the Pneumocystis
respiratory tracts of many
î Occurs when CD4 <200 î Toluidine blue TMP-SMX (DOC) genus was debated for some time. It was initially
mammals and humans Disc-shaped yeast mistaken for a trypanosome and then later for a
Pneumocystis carinii î Most common AIDS-defining illness î Methenanime silver stain
(former name) Major surface î Cysts in the alveoli induce an inflammatory For sulfa allergy: protozoan. In the 1980s, biochemical analysis of the
Transmission: Respiratory glycoprotein undergoes response consisting plasma cells à frothy Elevated LDH >220 U/L in patients Pentamidine nucleic acid composition of Pneumocystis rRNA and
via inhalation of cysts Dapsone (prophylaxis only) mitochondrial DNA identified the organism as a
programmed exudate that blocks oxygen exchange with PCP
rearrangements î Diffuse interstitial pneumonia with Atovaquone unicellular fungus rather than a protozoan.
Quantitative PCR for pneumocystis Subsequent genomic sequence analysis of multiple

bilateral ground glass infiltrates

î 100% mortality if untreated may become useful in distinguishing Start prophylaxis when CD4+ genes including elongation factor 3, a component
Morphologic stages:
between colonization and active count drops to < 200 of fungi protein synthesis not found in protozoa,
Trophozoite (trophic 3
form): often exists in infection. cells/mm in HIV patients. further supported this notion.
clusters
Sporozoite (precystic
form)
Cyst: contains several

intracystic bodies (spores)
 VIROLOGY

VIRAL STRUCTURE VIRAL GENOME
• Range in size from 20 – 300 nm • ALL viruses are haploid EXCEPT retroviruses
• All viruses have a protein coat (capsid) • Contain either DNA or RNA, but not both
o Composed of repeating capsomers (building blocks of capsid) • Genomes can either be single-stranded or double-stranded
o In some viruses, covered with lipoprotein envelope • Genomes of RNA viruses can either positive-polarity or
o Two types of capsid: icosahedral and helical negative polarity
• Nucleic acid genome + capsid = nucleocapsid • Some RNA viruses have segmented genome

SEGMENTED GENOME
Bunyaviruses
Orthomyxoviruses (influenza)
Arenaviruses

Reoviruses


RNA VIRUSES
VIRAL SYMMETRY • Two types of RNA viruses: positive-stranded or negative-
• Symmetry: spherical (icosahedral) or helical stranded
• All helical viruses are enveloped • POSITIVE-STRANDED RNA VIRUSES
• Icosahedral viruses can be enveloped or naked o RNA is just like a messenger RNA (mRNA)
o All DNA viruses are icosahedral except Poxvirus o When a positive-stranded RNA virus enters a host cell, its
• Only RNA viruses have helical symmetry RNA can immediately translated by the host’s ribosomes
o Most assume a spherical shape except rhabdoviruses, into protein

which have a bullet-shaped capsid.
o Most RNA viruses have helical symmetry except:
§ Flaviviruses
§ Caliciviruses

§ Reoviruses RNA viruses with • NEGATIVE-STRANDED RNA VIRUSES

§ Picornavirus icosahedral symmetry o When negative-stranded RNA viruses enter the cell, they
§ Togaviruses are not able to begin translation immediately
§ Hepevirus o Must transcribe negative strand to positive (–) à (+)
o Virion brings its own RNA-dependent polymerase, which
VIRAL PROTEINS will carry out the transcription of the negative-strand into
• Surface proteins: attachment to host cell receptors positive.
• DNA or RNA polymerases
• Matrix protein: interaction between nucleocapsid and
envelope
• Antigenic (serotypic) variants: evasion of host defenses

NEGATIVE-STRAND RNA VIRUSES

VIRAL ENVELOPE
Always Bring Polymerase Or Fail Replication
• Lipid membrane derived from the host cells
Arenaviruses
o Acquired as the virus exits from the cell in a process called
budding Bunyaviruses
o All enveloped viruses acquire their envelope from plasma Paramyxoviruses (Measles, Mumps, RSV, Parainfluenza)
membrane EXCEPT Herpes virus (from nuclear Orthomyxoviruses (Influenza A&B)
membrane) Filoviruses (Ebola)
• Enveloped viruses are less stable and more easily inactivated Rhabdoviruses (Rabies)


NAKED VIRUSES: Viruses that do not have membranes • RETROVIRUSES are unique because of their ability to
Give PAPP smears and CPR to a naked hippie (hepevirus).
incorporate into the host genome.
Naked DNA Virus Naked RNA Virus • REOVIRIDAE (including ROTAVIRUS) are the only RNA viruses
Papillomavirus Calicivirus with a double-stranded RNA genome

Adenovirus Picornavirus
DNA VIRUSES
Parvovirus Reovirus • Unlike RNA, DNA cannot be translated directly into proteins.
Polyomavirus Hepevirus • It must be transcribed into mRNA with subsequent translation
of mRNA into structural proteins and enzymes

NAKED VIRAL GENOME INFECTIVITY
• Purified nucleic acids of most dsDNA (EXCEPT poxviruses and
HBV) and (+) strand genome ssRNA viruses are infectious

• Most DNA viruses have both a negative strand and a positive
• Naked nucleic acids of (-) strand ssRNA and dsRNA viruses are
strand except PARVOVIRUSES, which have single-stranded
not infectious
DNA genome
o Require polymerases contained in the complete virion
• All double-stranded DNA have icosahedral symmetry except

POXVIRUS in which DNA has complex structural proteins
PRIONS
looking much like a box.
• Infectious particles composed entirely of proteins which cause
• Negative strand refers to the DNA strand that is read; used as
transmissible spongiform encephalopathies
a template for transcription into mRNA,
o Nonpathogenic as alpha-helix
• Positive strand is ignored.
o Pathogenic as beta-pleated sheet
• Highly resistant to inactivation
• Do not elicit an inflammatory response or an antibody response




VIRAL GENETICS LABORATORY DIAGNOSIS
• Mutations can produce antigenic, drug-resistant, or

PRESUMPTIVE IDENTIFICATION
attenuated variants
• Cytopathic effect
• Recombination: exchange of genes between 2 chromosomes
• Hemadsorption: attachment of RBCs to surface of infected cells
by crossing over within regions of significant base sequence
• Interference: interference with CPE by another virus
homology
• Decrease in acid production by infected, dying cells (using
• Genetic reassortment: when viruses with segmented genomes
phenol red)
exchange genetic material; causes epidemics

o Example: influenza viruses
DEFINITIVE DIAGNOSIS
• Complementation: one virus produces a protein that can be
• Complement fixation
used by another virus
• Hemagglutination inhibition
o Example: Hepatitis D and Hepatitis B
• Neutralization
• Phenotype mixing: two different viruses infect the same cell
• Fluorescent antibody assay

• Radioimmunoassay
VIRAL GROWTH CURVE
• Enzyme-linked immunosorbent assay (ELISA)


SEROLOGIC TESTS
• Seroconversion: finding antibody in one who previously had
none
• Presence of IgM: can be used to diagnose current infection
• Presence of IgG: cannot be used to diagnose current infection;
antibody may be due to an infection in the past

DETECTION OF VIRAL ANTIGENS
• Presence of viral proteins, commonly used in diagnosis
• Example: p24 of HIV and HbSAg
• Presence of viral DNA or RNA is the gold standard in viral
diagnosis


VIRAL VACCINES
Phase 0 Entry A single virus infects a cell

LIVE-ATTENUATED VACCINES
Phase 1 Decline Virus decreases in number but
• Induce humoral and cell-mediated immunity but may revert to
continue to function
virulence on rare occasions
Phase 2 Eclipse Period No virus is detectable inside the cell • Dangerous to give to immunocompromised patients or their
close contacts
Phase 3 Rise Period Dramatic increase in amount of
• Examples: (MISS CRY)
detectable viruses
o MMR (the only live-attenuated vaccine that can be given
Phase 4 Latent Amount of detectable viruses reaches a to HIV-positive patients who do not show signs of
plateau immunodeficiency)
Phase 5 Cytopathic Marked derangement of cell function o Influenza (intranasal)
Effect leading to lysis and cell death o Smallpox
Remarkable amplification in number of o Sabin’s polio vaccine
viral particles o Chicken pox
o Rotavirus

o Yellow fever
OUTCOMES OF VIRAL INFECTION

Cytopathic effect Visual or functional change in infected cells KILLED VACCINES
Hallmark of viral infection of cell • Induce only humoral immunity but are stable
Malignant Oncogenic viruses induce transformation and • Examples: (RIP Always; SalK=Killed)
transformation unrestrained growth o Rabies
o Influenza (injected)
Commensal Infected cells appear normal, but are
o Salk’s Polio vaccine
symbiosis producing large numbers of progeny viruses
o Hepatitis A

VIRULENCE FACTORS RECOMBINANT VACCINES
Cytokines decoys Bind cytokines and block their ability to • Examples:
interact with receptors on their intended o Hepatitis B (recombinant HBsAg)
targets o HPV (Types 6, 11, 16, 18)

Virokines Reduce the expression of antigen presenting
RECEPTORS USED BY VIRUSES
cells and inactive complement

Antigenic variants of surface proteins Virus Receptors
CMV Integrins (heparan sulfate)
PERSISTENT VITAL INFECTIONS
EBV CD21
Carrier state Produce virus for long periods of time
Can serve as a source of infection to others HIV CD4, CXCR4, CCR5
Parvovirus B19 P antigen on RBCs
Latent infections Not producing virus at the present but can
be reactivated at a subsequent time Rabies Nicotinic AChR
Slow virus infections Long incubation period, often measured in Rhinovirus ICAM-1
years






CHARACTERISTICS OF VIRUSES ANTIVIRAL DRUGS
DNA or RNA? DNA viruses are HHAPPPPy The rest are RNA.
Hepadna
Herpes
Adeno
Pox
Parvo
Papilloma
Polyoma
Enveloped or Naked DNA Virus Naked RNA Virus
Naked? Papillomavirus Calicivirus
Adenovirus Picornavirus
Parvovirus Reovirus
Polyomavirus Hepevirus
Symmetry All DNA viruses are icosahedral Most RNA viruses have helical symmetry
except Poxvirus à complex except the following which are icosahedral:
§ Flavi
§ Calici
§ Reo (Rota)
§ Picorna
§ Toga
§ Hepe
If RNA, segmented SEGMENTED GENOME
or non-segmented Bunyaviruses
(one-piece)? Orthomyxoviruses (influenza)
Arenaviruses
Reoviruses (Rotavirus)
Double stranded or All DNA viruses have double- All RNA viruses have single-stranded RNA
Single-stranded? stranded DNA EXCEPT: Reovirus (Rotavirus) à dsRNA
EXCEPT: Parvovirus à ssDNA
If ssRNA, positive NEGATIVE-STRAND RNA VIRUSES
sense or negative Always Bring Polymerase Or Fail Replication
sense? Arenaviruses
Bunyaviruses
Paramyxoviruses (Measles, Mumps, RSV, Parainfluenza)
Orthomyxoviruses (Influenza A&B)
Filoviruses (Ebola)
Rhabdoviruses (Rabies)
Site of replication All DNA viruses replicate in the All RNA viruses have replicate in the cytoplasm
nucleus EXCEPT: INFLUENZA VIRUS
EXCEPT: POXVIRUS à cytoplasm RETROVIRUSES
 DNA VIRUSES RNA VIRUSES

HHAPPPPy DNA Viruses: Hepadna, Herpes, Adeno, Pox, Parvo, Papilloma, Polyoma

All DNA viruses have double stranded DNA EXCEPT: PARVOVIRUS (single-stranded) All RNA viruses have single stranded RNA EXCEPT: REOVIRUS (ROTAVIRUS) (dsRNA)
All DNA viruses have linear DNA EXCEPT: PAPILLOMAVIRUS (circular, supercoiled) All RNA viruses have replicate in the cytoplasm EXCEPT: INFLUENZA VIRUS
POLYOMAVIRUS (circular, supercoiled) RETROVIRUSES
HEPADNAVIRUS (circular, incomplete)
All DNA viruses are icosahedral EXCEPT: POXVIRUS (complex)
All DNA viruses replicate in the nucleus EXCEPT: POXVIRUS (cytoplasm; carries own DNA-dependent RNA
polymerase)





































































































































CLINICAL FEATURES OF DNA NAKED VIRUSES













IMPORTANT FEATURES OF COMMON HERPESVIRUS INFECTIONS

 VIRUS MORPHOLOGY TRANSMISSION PATHOGENESIS / SPECTRUM OF DISEASE DIAGNOSIS TREATMENT / PREVENTION NOTES
NAKED DNA VIRUSES
PARVOVIRIDAE: The smallest DNA virus; the only DNA virus that is single-stranded.
Parvovirus B-19 Naked icosahedral Respiratory Droplets ERYTHEMA INFECTIOSUM (FIFTH DISEASE) Illness is self-limited RBC destruction in fetus
î affects children between the ages of 4 to 12 leads to hydrops fetalis and
Single-stranded linear DNA Transplacental î bright red cheek rash (“Slapped cheek”) with fever, coryza, and sore I.V. immunoglobulin can be used death, in adults leads to
virus (negative stranded) throat with aplastic crisis pure RBC aplasia and
rheumatoid arthritis–like
APLASTIC CRISIS:
One serotype symptoms
î Transient but severe aplastic anemia in children with sickle cell anemia,

thalassemia, or spherocytosis

î occurs when the Parvovirus stops the production of red blood cells in the
bone marrow

FETAL INFECTIONS
î First trimester: Fetal death
î Second trimester: Hydrops Fetalis

ARTHRITIS
î Immune-complex arthritis of small joints

CHRONIC B-19 INFECTION

î pancytopenia in immunodeficient patients

ADENOVIRIDAE
Adenovirus Naked icosahedral Aerosol droplet URT: Pharyngitis, conjunctivitis, coryza Histopathology: Illness is self-limited
Double-stranded linear DNA LRT: bronchitis, atypical pneumonia Cowdry type B intranuclear
41 serotypes Fecal-oral GIT: acute gastroenteritis basophilic inclusion bodies
Only virus with fiber GUT: acute hemorrhagic cystitis
Direct contact
PAPOVAVIRIDAE: The second smallest DNA virus
Human Naked icosahedral Direct contact - Infect squamous cells and induce formation of cytoplasmic vacuole Genital warts: Podophyllin Koilocytes: small, round,
Double-stranded circular (koilocytes) deeply basophilic nuclei
Papillomavirus
DNA Sexually - Genes E6 and E7: encode proteins that inactivate tumor suppressor Skin warts: Liquid nitrogen surrounded by a clear
At least 100 types genes. E6 inhibits p53; E7 inhibits Rb halo and pale-staining
- Genes E1 and E2: promote viral DNA replication Plantar warts: Salicylic acid cytoplasm

HPV 1, 2, 4, 7 Skin and plantar warts, verruca vulgaris PREVENTION:
HPV 6 and 11 Genital warts (condyloma acuminata) Vaccine for HPV 6, 11, 16, and
Respiratory tract papillomas 18 for females 9-26 years old
Most common viral STD
HPV 16, 18, 31, 33 Carcinoma of the cervix, vulva, penis, anus

JC Polyoma Virus Naked icosahedral - Only causes disease in immunocompromised hosts JC: Junky Cerebrum
(John Cunningham virus) Double-stranded circular - Causes progressive multifocal leukoencephalopathy in patients
DNA with AIDS
î Demyelinating disease that affects the oligodendrocytes
characterized by deficits in speech, coordination, and memory

BK Polyoma Virus Naked icosahedral - causes disease in immunocompromised hosts BKV blood test or a urine test BK: Bladder, Kidney
Double-stranded circular - causes hemorrhagic cystitis and nephropathy in patients with solid for decoy cells
DNA organ (kidney) and bone marrow transplants Biopsy of the kidneys
PCR techniques

 VIRUS MORPHOLOGY TRANSMISSION PATHOGENESIS / SPECTRUM OF DISEASE DIAGNOSIS TREATMENT / PREVENTION NOTES
ENVELOPED DNA VIRUSES
HERPESVIRIDAE
Herpes Simplex Enveloped icosahedral HSV 1: saliva or - Vesicle filled with virus particles and cell debris Tzanck smear: Drug-of-choice: HSV-1 is the most
Double-stranded linear DNA direct HSV-1 (HHV-1) HSV-2 (HHV-2) multinucleated giant cells Acyclovir common cause of sporadic,
Viruses (HSV)
Gingivostomatitis Genital herpes - Shortens duration of the fatal encephalitis in the
HSV 2: sexual or Herpes labialis (lips) Neonatal herpes (TORCH) Large, pink to purple Cowdry lesions USA
transvaginal Keratoconjunctivitis Aseptic meningitis Type A eosinophilic - Reduces the extent of

shedding of the virus

TEMPORAL LOBE:
Temporal lobe encephalitis intranuclear inclusions
- No effect on the latent state principal target area of the
Herpetic whitlow (fingers) virus
Herpes gladiatorum (trunk)
Site of Latency CSF-PCR for herpes
Trigeminal ganglia Lumbosacral ganglia encephalitis

Varicella-Zoster Virus Enveloped icosahedral Airborne-droplet - Infects the URT, then spreads via the blood to the skin HP: multinucleated giant cells Mild: NO TREATMENT USES OF ASPIRIN IN
Double-stranded linear DNA - Becomes latent in the dorsal root ganglia, which may reactivate as with intranuclear inclusions
(VZV) / HHV-3 PEDIATRIC DISEASES:
Direct contact with zoster Moderate to Severe:
the lesions
- Kawasaki

Large, pink to purple Cowdry Acyclovir
VARICELLA / CHICKEN POX - Shortens duration of the
- ARF
Type A eosinophilic
î Incubation period: 14-21 days lesions - JRA
intranuclear inclusions
î Period of communicability: 48 hours before vesicle formation and 4-5 - Most effective if given within
days after until all vesicles are crusted
24 hours of the onset of rash
î Vesicular rash (‘dewdrop on a rose petal appearance’) that begins on
trunk; spreads to face and extremities (centrifugal) with lesions of Ramsay-Hunt Syndrome:
different stages Valacyclovir
î Complications: Pneumonia, Encephalitis, Reye’s syndrome, Prednisone
Cerebellar ataxia, secondary bacterial infection
POSTEXPOSURE PROPHYLAXIS:
HERPES ZOSTER / SHINGLES Active vaccine can be given
î Unilateral painful vesicular eruption with a dermatomal distribution within 5 days of exposure to
(thoracic and lumbar) modify course
î Debilitating pain (postherpetic neuralgia) à most common complication Anti-VZV Ig: given within 96h

after exposure; for pregnant,
RAMSAY-HUNT SYNDROME / HERPES ZOSTER OTICUS
newborns exposed to maternal
î Reactivation of latent VZV residing within geniculate ganglion
varicella, and
î A triad of ipsilateral facial paralysis, ear pain, and vesicles on the face, on
immunocompromised
the ear, or in the ear is the typical presentation.


CONGENITAL VARICELLA
î Fetuses infected at 6-12 weeks’ AOG: maximal interruption with limb
development (short and malformed limbs covered with cicatrix – skin
lesion with zigzag scarring associated with atrophy of the affected limb)
î Fetuses infected at 16-20 weeks’ AOG: eye and brain involvement
 VIRUS MORPHOLOGY TRANSMISSION PATHOGENESIS / SPECTRUM OF DISEASE DIAGNOSIS TREATMENT / PREVENTION NOTES
Cytomegalovirus Enveloped icosahedral Human body fluids - Immediate early proteins Cultured in shell tubes Drug-of-Choice:
Double-stranded linear DNA o Translated from premade mRNAs Ganciclovir
(CMV) / HHV-5
Transplacental o Impair assembly of the MHC class 1-viral peptide complexes Negative heterophil test - CMV is largely resistant to

CONGENITAL CMV INFECTION acyclovir

Organ î Most common infectious cause of congenital abnormalities
Giant cells with owl’s-eye
transplantation î Most common intrauterine viral infection DOC for prevention of CMV disease
nuclear inclusion in solid-organ transplant patients is
î Most common when the mother is infected in first trimester
valganciclovir
î Microcephaly, seizures, deafness, jaundice, and purpura

owl’s-eye nuclear inclusion

î Periventricular calcifications

HETEROPHIL-NEGATIVE MONONUCLEOSIS Periventricular

î Monospot-negative Calcification is seen
î Fever, lethargy, and abnormal lymphocytes in blood smears Cytomegalovirus

SYSTEMIC CMV INFECTIONS

î Pneumonitis, hepatitis, colitis
î AIDS retinitis: hemorrhage, cotton-wool exudates, vision loss
Epstein-Barr Virus Enveloped icosahedral Saliva - Infects mainly lymphoid cells, primarily B-lymphocytes through CD21 Differential white blood cells MONONUCLEOSIS
Double-stranded linear DNA - Elicits EBV-specific antibodies and non-specific heterophil antibodies count will show elevated Heterophil-Positive:
(EBV) / HHV-4 “atypical lymphocytes” à î Epstein-Barr Virus

INFECTIOUS MONONUCLEOSIS Downey cells

î ‘Kissing disease’ Heterophil-Negative:

î Monospot-positive/heterophil-positive î Cytomegalovirus
î fever, sorethroat, lymphadenopathy î Toxopasma
î splenomegaly à rapid increase in size produces a tense, fragile, splenic
capsule à splenic rupture is a rare complication (Avoid contact sports!)

MALIGNANCIES
î Burkitt’s lymphoma (in African people) Use of amoxicillin in
î B-cell lymphomas mononucleosis can cause
î Nasopharyngeal carcinoma (in Chinese people) characteristic
î Hairy leukoplakia (in AIDS patients) maculopapular rash.
Human Herpesvirus 6 Enveloped icosahedral saliva ROSEOLA / EXANTHEM SUBITUM / SIXTH DISEASE
Double-stranded linear DNA - rose-colored macules appear on body after several days of high fever;
(HHV-6)
can present with febrile seizures; usually affects infants
- Nagayama spots: erythematous papules on soft palate and base of the uvula

Human Herpesvirus 8 Enveloped icosahedral Sexual KAPOSI SARCOMA Surgical excision

Double-stranded linear DNA î most common AIDS-related malignancy Radiation
(HHV-8)
Organ î malignancy of the vascular endothelial cells
transplantation î Dark/violaceous plaques or nodules representing vascular proliferations

POXVIRIDAE: Largest DNA virus; the only DNA virus that is complex (not icosahedral); the only DNA virus that replicates in the cytoplasm (not in the nucleus)
Variola virus Enveloped complex Aerosol SMALLPOX HP: Guarnieri bodies:

î Only disease that has been eradicated from the face of the earth intracytoplasmic
Brick-shaped poxvirus Contact î Incubation Period: 7 – 14 days
containing linear double- eosinophilic inclusions
î Prodrome of fever and malaise followed by centrifugal rash
stranded DNA î Classic smallpox lesions: deep-seated, firm/hard, round well-circumscribed

Replicates in the cytoplasm vesicles or pustules; as they evolve, lesions may become umbilicated or

confluent Guarnieri bodies
î Lesions with same stage of development
Molluscum Direct contact MOLLUSCUM CONTAGIOSUM HP: Henderson-Patterson Cifodovir
Contagiosum virus î flesh-colored dome-shaped papules with central umbilication bodies: intracytoplasmic
eosinophilic inclusions
 VIRUS MORPHOLOGY TRANSMISSION PATHOGENESIS / SPECTRUM OF DISEASE DIAGNOSIS TREATMENT / PREVENTION NOTES
HEPADNAVIRIDAE
Hepatitis B Virus Enveloped virus with Blood transfusion - the only DNA virus that produces DNA by reverse transcription with Acute diagnosis: Entecavir The virus is one of the
incomplete circular double- mRNA as the template; not a retrovirus but has reverse transcriptase HBsAg, IgM anti-HBc smallest enveloped animal
Tenofovir
stranded DNA Needlestick injury - hepatocellular injury due to immune attack by cytotoxic T cells viruses, and the 42 nm
Interferon-alpha virions, which are capable of
Ø HBV has no cytopathic effect Chronic diagnosis:
Sexual Lamivudine infecting hepatocytes, are
HBsAg, IgG anti-HBc
VIRULENCE FACTORS: referred to as "Dane
Across the placenta î Surface antigen (HBsAg) Markers of replication: PREVENTION: particles" à the complete
î Core antigen (HBcAg) HBeAg, HBV DNA HEPATITIS B VACCINE infectious form of Hepatitis
Perinatally î e antigen (HBeAg): used as marker of potential infectivity - First vaccine to prevent a B virus
Liver Biopsy: Granular human cancer
HEPATITIS B INFECTION eosinophilic “ground - 1st dose should be given first
î Incubation Period: 10-12 weeks 12 hours of life and counted Age at the time of
î Fever, anorexia, and jaundice glass” appearance
as part of 3-dose primary infection is the best
î Dark urine, pale feces, and elevate transaminase levels
series predictor of chronicity.
î Can lead to cirrhosis and hepatocellular carcinoma - Subsequent doses are given at
î Extrahepatic manifestations: Councilman body: least 4 weeks apart
The younger the age at the
eosinophilic globule of cells time of HBV infection, the
o Aplastic Anemia - 3rd dose preferably given >24
that represents a dying higher the probability of
o Membranous à Membranoproliferative glomerulonephritis weeks of age chronicity.
hepatocyte often surrounded
o Polyarteritis nodosa (autoimmune vasculitis) by normal parenchyma

SEROLOGIC EVOLUTION INTERPRETATION OF SEROLOGY Complications:
Time Period HBsAg Anti-HBs Anti-HBc HBeAg HEPATORENAL SYNDROME: functional renal failure without renal
Incubation Period (+) (-) (-) (+) pathology
Acute Infection (+) (-) (+) IgM (+)
Window Period (-) (-) (+) IgM (-) HEPATOPULMONARY SYNDROME: vascular dilatations cause
Complete Recovery (-) (+) (+) IgG (-) overperfusion relative to ventilation, leading to V/Q mismatch and
Chronic Carrier (+) (-) (+) IgG (-) hypoxemia
Chronic Active (+) (-) (+) IgG (+)
Vaccinated (-) (+) (-) (-) PORTAL HYPERTENSION


HEPATIC ENCEPHALOPATHY
The only positive during window period: Anti-HBc IgM
The only positive among vaccinated patients: Anti-HBs

What can differentiate chronic active infection from chronic carrier: HBeAg

Chronic infection is characterized by the persistence of HBsAg for at least 6
months.

Persistence of HBsAg is the principal marker of risk for developing chronic
liver disease and liver cancer (hepatocellular carcinoma) later in life.

 DNA VIRUSES RNA VIRUSES

HHAPPPPy DNA Viruses: Hepadna, Herpes, Adeno, Pox, Parvo, Papilloma, Polyoma

All DNA viruses have double stranded DNA EXCEPT: PARVOVIRUS (single-stranded) All RNA viruses have single stranded RNA EXCEPT: REOVIRUS (ROTAVIRUS) (dsRNA)
All DNA viruses have linear DNA EXCEPT: PAPILLOMAVIRUS (circular, supercoiled) All RNA viruses have replicate in the cytoplasm EXCEPT: INFLUENZA VIRUS
POLYOMAVIRUS (circular, supercoiled) RETROVIRUSES
HEPADNAVIRUS (circular, incomplete)
All DNA viruses are icosahedral EXCEPT: POXVIRUS (complex)
All DNA viruses replicate in the nucleus EXCEPT: POXVIRUS (cytoplasm; carries own DNA-dependent RNA
polymerase)








 VIRUS MORPHOLOGY TRANSMISSION PATHOGENESIS / SPECTRUM OF DISEASE DIAGNOSIS TREATMENT / PREVENTION NOTES
NAKED RNA VIRUSES
PICORNAVIRIDAE
Poliovirus Naked (+) ssRNA Oral-fecal - replicates in motor neurons in anterior horn of spinal cord, causing HP: Cowdry type B PREVENTION: ENTEROVIRUSES
Naked icosahedral symmetry paralysis intranuclear inclusions Vaccination
- Poliovirus
- host range is limited to primates SALK SABIN
Three serologic (antigenic) - Limitation is due to the binding of the viral capsid to a receptor found - Echovirus
IPV OPV
types based on different only on primate cell membrane Killed Live, attenuated - Coxsackie virus
antigenic determinants on the

outer capsid proteins POLIOMYELITIS AND MENINGITIS RNA viruses with

î Inapparent, asymptomatic infection icosahedral symmetry
The oral vaccine or Sabin vaccine
î Abortive poliomyelitis which is a live attenuated vaccine § Flaviviruses
- Most common clinical form is preferred over the Salk vaccine § Caliciviruses
- Mild febrile illness with headache, sore throat, nausea, and vomiting or killed vaccine because it § Reoviruses
î Non-paralytic poliomyelitis interrupts fecal-oral transmission § Picornavirus
- Aseptic meningitis by inducing secretory IgA in the
î Paralytic poliomyelitis § Togaviruses
GIT; killed vaccine does not.
- Flaccid paralysis, permanent nerve damage § Hepevirus

Coxsackie virus Naked (+) ssRNA Oral-fecal Coxsackie A viruses Coxsackie B viruses NOTE:
î Herpangina (vesicular pharyngitis) î Pleurodynia (Bornholm disease, Pleurodynia is pain due to
Classification is based on î Acute hemorrhagic conjunctivitis “devil’s grip”) an infection of the
pathology in mice î Hand-foot-and-mouth disease î Severe generalized disease of intercostal muscles
(vesicular rash on hands and feet infants (myositis), not of the pleura.
and ulcerations in the mouth) î Myocarditis, pericarditis (Most
î Aseptic meningitis commonly identified causative
agent of heart disease in humans)
î Aseptic meningitis

ECHO virus Naked (+) ssRNA Oral-fecal ASSOCIATED DISEASES: Orphan virus means a
î Aseptic meningitis virus that is not associated
(Enteric Cytopathic
î Upper respiratory tract infection with any known disease.
Human Orphan) î Febrile illness with and without rash Even though Echoviruses have
î Infantile diarrhea since been identified with
various diseases, the original
î Hemorrhagic conjunctivitis name is still used.

Rhinovirus Naked (+) ssRNA Aerosol droplets - replicate better at 33°C than at 37°C à affect primarily the nose and Common cold: most
conjunctiva rather than the lower respiratory tract common human infection
More than 100 serotypes Hand-to-nose - acid-labile à they are killed by gastric acid when swallowed à do not
contact infect the GIT (unlike the enteroviruses)
- Host range is limited to humans and chimpanzees

Hepatitis A virus Naked (+) ssRNA Oral-fecal - The virus replicates in the GI tract and then spreads to the liver during a Anti-HAV IgM: most useful PREVENTION: There is no antigenic
brief viremic period. test to diagnose acute Vaccine contains killed virus. relationship between
(aka Enterovirus 72)
Virus has a single serotype - The virus is not cytopathic for the hepatocyte. infection Hepatitis A and other
- Hepatocellular injury is caused by immune attack by cytotoxic T cells. Administration of immune hepatitis viruses.
globulin during the incubation
HEPATITIS A INFECTION period can mitigate the disease
î Children most frequently infected
î Self-limited hepatitis
î Short incubation hepatitis
î Anicteric hepatitis: asymptomatic or only mildly ill, absence of jaundice,
with positive serologic evidence of infection
 VIRUS MORPHOLOGY TRANSMISSION PATHOGENESIS / SPECTRUM OF DISEASE DIAGNOSIS TREATMENT / PREVENTION NOTES
HEPEVIRIDAE
Hepatitis E virus Naked icosahedral (+) ssRNA Oral-fecal î Causes outbreaks of hepatitis (epidemics), primarily in developing Liver Biopsy: Hepatitis E
countries Patchy necrosis - Expectant (pregnant)
î no chronic carrier state, no cirrhosis, and no hepatocellular mother
carcinoma - Enteric
î Infection is frequently subclinical
- Epidemic
î Fulminant hepatitis in pregnant women

CALICIVIRIDAE
Norwalk virus Naked icosahedral (+) ssRNA Oral-fecal VIRAL GASTROENTERITIS RNA viruses with
î Most important cause of epidemic viral (nonbacterial) gastroenteritis icosahedral symmetry
(Norovirus)
in adults § Flaviviruses
î Sudden onset of vomiting, diarrhea, accompanied by fever and abdominal § Caliciviruses
cramping § Reoviruses
§ Picornavirus
§ Togaviruses
§ Hepevirus
REOVIRIDAE: only RNA virus with a double-stranded RNA (dsRNA) genome
Rotavirus Naked double-layered capsid - Rotavirus is resistant to stomach acid and hence can reach the small ROTAVIRUS VACCINE SEGMENTED GENOME
with segmented double- intestine î 1st dose: 6 weeks of age Bunyaviruses
stranded RNA (10 or 11 - Villous destruction with atrophy à â absorption of Na+ and loss of K+ î Last dose: not later than 32

weeks of age Orthomyxoviruses
segments) VIRAL GASTROENTERITIS
î Monovalent (RV1)/Rotarix: 2- (influenza)
î Most common cause of childhood diarrhea
dose series Arenaviruses
î Severe cases: stools are clear (“white stool diarrhea”) î Pentavalent (RV5)/RotaTeq: 3-
Reoviruses
dose series
î Min interval: 4 weeks

To God be the Greatest Glory!



















 VIRUS MORPHOLOGY TRANSMISSION PATHOGENESIS / SPECTRUM OF DISEASE DIAGNOSIS TREATMENT / PREVENTION NOTES
ENVELOPED RNA VIRUSES (NEGATIVE SENSE)
ORTHOMYXOVIRIDAE
Influenza Virus Enveloped virus with a helical Respiratory droplets Influenza A worldwide epidemics (pandemics) Oseltamivir (DOC) Antigenic Shift vs
nucleocapsid and segmented, each year, influenza is the MCC of respiratory and Zanamivir Antigenic Drift
ss-negative RNA infections Sudden Shift is more deadly
î used for both the treatment
has 16 antigenically distinct types of hemagglutinin and prevention of influenza than GraDual Drift
and 9 antigenically distinct types of neuraminidase; Shifts cause PANDEMICS
î neuraminidase inhibitors,
some of these types cause disease in humans but most of Drifts cause EPIDEMICS
which act by inhibiting the
the types typically cause disease in other animal species
- Many species of animals (e.g., aquatic birds, release of virus from infected
such as birds, horses, and pigs
chickens, swine, and horses) have their own cells
Influenza B Major outbreaks of influenza A for Amantadine
influenza A viruses. î effective against both influenza
Does NOT lead to pandemic effective only against
- These animal viruses are the source of the RNA A and B viruses
segments that encode the antigenic shift variants Influenza C Mild respiratory tract infection Influenza A
Does NOT cause outbreaks of influenza
that cause epidemics among humans.
The envelope is covered with two different types of spikes (which are also
Amantadine and Rimantadine
§ E.g., if an avian and a human influenza A virus
considered as the virus’ major antigens): î effective only against influenza
infect the same cell (e.g., in a farmer’s A NEGATIVE-STRAND
respiratory tract) àreassortment ànew variant o HEMAGGLUTININ
• bind to the cell surface receptor (neuraminic acid, sialic acid) to
î no longer used due to RNA VIRUSES
of the human A virus, bearing the avian virus widespread resistance Always Bring Polymerase
hemagglutinin, may appear initiate infection of the cell
Or Fail Replication
- There is evidence that aquatic birds (waterfowl) are • the target of neutralizing antibody
Arenaviruses
a common source of these new genes and that the • most important antigen
PREVENTION:
reassortment event leading to new human strains o NEURAMINIDASE
î The main mode of prevention
Bunyaviruses
occurs in pigs. • cleaves neuraminic acid (sialic acid) to release progeny virus from the Paramyxoviruses
infected cell is the vaccine, which contains
- Pigs may serve as the “mixing bowl” within which
• degrades the protective layer of mucus in the respiratory tract à both influenza A and B viruses Orthomyxoviruses
the human, avian, and swine viruses reassort.
enhances the ability of the virus to gain access to the respiratory (annual vaccination) Filoviruses
§ Waterfowl: H1 to H16, N1 to N9
§ Humans: H1 to H3, N1 and N2 epithelial cells. Rhabdoviruses

ANTIGENIC SHIFT ANTIGENIC DRIFT

Influenza B virus (Pandemics) (Epidemics)
- is only a human virus
- Major changes based on the - Minor changes based on
§ there is no animal source of new RNA segments
reassortment of segments of the mutations in the genome RNA
- does not undergo antigenic shifts
genome RNA
- undergo enough antigenic drift that the current
- Example: when human influenza
strain must be included in the new version of the
A virus recombines with swine
influenza vaccine produced each year
influenza A virus
- no antigens in common with influenza A virus
- Sudden change in the molecular - Slow and progressive change in
structure of a microorganism à the composition of
new strain à little or no microorganisms à altered
acquired immunity to these immunological responses and
NOVEL strains à new epidemics susceptibility
or pandemics

SPECTRUM OF DISEASE
î Incubation period: 24-48 hours
î Fever, myalgia, headache, sore throat, and cough
î Complications:
- Fatal bacterial superinfection
• S. aureus
• S. pneumoniae
• H. influenzae
- Reye’s syndrome

 VIRUS MORPHOLOGY TRANSMISSION PATHOGENESIS / SPECTRUM OF DISEASE DIAGNOSIS TREATMENT / PREVENTION NOTES
PARAMYXOVIRIDAE
Measles Virus Enveloped, helical, non- Respiratory droplet Measles virus infects the cells lining the URT à enters the blood à infects HP: Multinucleated î Vitamin A supplementation:
segmented ss-negative reticuloendothelial cells à spreads via the blood to the skin à cytotoxic T-cells attack the can reduce morbidity and
RNA
giant cells (Warthin-
measles virus-infected vascular endothelial cells in the skin à rash à virus can no longer be mortality from measles,
recovered à patient can no longer spread virus to other Finkelday bodies), particularly in malnourished

which form as a result of children

Can transiently depress cell-mediated immunity

the fusion protein in the


Infection confers lifelong immunity spikes, are characteristic PREVENTION Warthin-Finkelday bodies

of the lesions. Measles Vaccine
SPECTRUM OF DISEASE
- live attenuated vaccine
î aka red measles, rubeola, “first disease” - Given subcutaneously Cardinal Manifestations

C
î Incubation Period: 10-14 days - Age: 9 months of Measles
î Period of communicability: 4 days before and 4 days after the onset of the rash - may be given as early as 6 ough
î Pathognomonic enanthem: Koplik’s spots (bright red lesions with a white central dot on months of age in cases of oryza
the buccal mucosa) outbreaks onjunctivitis
î Timing of appearance of rash: Height of the fever oplik spots
î Cephalocaudal appearance of maculopapular rash (face – trunk – extremities – MMR Vaccine
palms/soles) - Given subcutaneously
ENVELOPE SPIKES OF PARAMYXOVIRUSES
î Rash fades in the same sequence in which it appears à branny desquamation and - Given at 15 months
Virus Hemagglutinin Neuraminidase Fusion Protein disappears within 7-10 days - 2 doses recommended PaRaMyxoviruses
Measles (+) (-) (+) î Complications: Parainfluenza virus
Mumps (+) (+) (+) o Otitis Media POSTEXPOSURE PROPHYLAXIS
RSV (-) (-) (+) o Giant cell Pneumonia, Secondary Bacterial Pneumonia î Measles Ig for prevention & RSV
Parainfluenza (+) (+) (+) o Higher rate of activation of PTB attenuation within 6 days of Measles
Hemagglutinin: binds sialic acid and promotes viral entry o Subacute Sclerosing Panencephalitis (SSPE) / Dawson disease exposure
Neuraminidase: promotes progeny virion release - neurodegenerative disease caused by persistent infection of the brain by an altered î Measles Active Vaccine can
Mumps
form of the measles virus; manifests 5-7 years after initial infection be given to susceptible children
î Final common pathway to a fatal outcome is the development of bronchiolitis obliterans >1yo within 72 hours
Mumps virus Enveloped, helical, non- Respiratory droplet - The virus infects the URT à spreads through the blood à infects the: PREVENTION Three MCC of viral
segmented (-)ssRNA o parotid glands à Parotitis (increase in pain when drinking citrus juices) MMR Vaccine (aseptic) meningitis
o testes à Orchitis - live attenuated vaccine
- Given subcutaneously î Mumps virus
o ovaries
o meninges à aseptic Meningitis - Given at 15 months î Coxsackie virus
o pancreas à Pancreatitis - 2 doses recommended î Echovirus

- Infection confers lifelong immunity

Respiratory Enveloped, helical, non- Respiratory droplet - Surface spikes are fusion proteins, not hemagglutinins or neuraminidase Ribavirin
segmented (-)ssRNA - Fusion protein causes cells to fuse, forming multinucleated giant cells (syncytia)
Syncytial Virus

Palivizumab (monoclonal
(RSV) Humans are the
VIRAL PNEUMONIA
î RSV is the most important cause of pneumonia and bronchiolitis in infants antibody against F protein)
natural hosts of prevents pneumonia caused by
î Severe disease in infants due to immunologic cross-reaction with maternal antibodies
RSV. RSV infection in premature
RSV is also an important cause of otitis media in children and of pneumonia in the elderly
infants.
and in patients with chronic cardiopulmonary diseases.

Parainfluenza Enveloped, helical, non- Respiratory droplet LARYNGOTRACHEOBRONCHITIS / CROUP Racemic epinephrine
segmented (-)ssRNA î results in a “seal-like” barking cough and inspiratory stridor
virus 1 and 2
î Narrowing of upper trachea and subglottis à steeple sign on x-ray
î Severe croup can result in pulsus paradoxus secondary to upper airway obstruction.

In addition to croup, these viruses cause a variety of respiratory diseases such as the
common cold, pharyngitis, laryngitis, otitis media, bronchitis, and pneumonia.

VIRUS MORPHOLOGY TRANSMISSION PATHOGENESIS / SPECTRUM OF DISEASE DIAGNOSIS TREATMENT / PREVENTION NOTES
RHABDOVIRIDAE
Rabies virus Bullet-shaped Animal Reservoirs: - When a human is bitten, the virus replicates locally at the wound site for a few days, then HP: Negri bodies Pre-exposure:
enveloped, helical, non- Dogs, cats, skunks, migrates (15-100 mm/day) up to nerve axons to the CNS (retrograde transport) (cytoplasmic, round to Vaccine
segmented, (-)ssRNA raccoons, and bats oval, eosinophilic inclusions (PVRV or PDEV or PCEV – D0, D7,
SPECTRUM OF DISEASE and D21/28)
that can be found in
Transmission by Incubation 2 weeks to 6 years (depending on the site of the bite)
pyramidal neurons of the
animal bite Period The only time when vaccination is effective hippocampus and Purkinje Post-exposure:
Prodrome Nonspecific symptoms of fever, headache, sore throat, fatigue, nausea cells of the cerebellum, Vaccine +/- Immunoglobulin Negri bodies
1st rabies symptom: pain / itchiness / paresthesia sites usually devoid of
Acute ENCEPHALITIC / FURIOUS RABIES WHO GUIDELINES FOR POST-EXPOSURE PROPHYLAXIS
inflammation
neurologic - Phobic spasms: hydrophobia, aerophobia Category I Touching or feeding animals, No Treatment

period - Fluctuating consciousness licks on intact skin
Immunofluorescent Category II Minor scratches or abrasions Vaccine
- Autonomic instability
antibody test without bleeding or licks on

PARALYTIC / DUMB RABIES (IFAT): gold standard in broken skin and nibbling of
- Percussion myoedema: mounding of the muscles at the percussion site the detection of rabies uncovered skin
which disappears after a few seconds specific antigen Category III Single or multiple transdermal Vaccine +
Coma Follows the acute neurologic period, regardless of the presentation bites or scratches; Immunoglobulin
Death occurs secondary to respiratory center dysfunction contamination of mucous
Rabies has the highest case fatality ratio of any infectious disease membranes with saliva from
licks; exposure to bat
bites/scratches
All Category II exposures on
head and neck areas
FILOVIRIDAE: longest viruses
Ebola virus Enveloped, helical, non- Natural Host: fruit - targets endothelial cells, phagocytes, hepatocytes ELISA Supportive care, no definitive Ebola virus is named for the
segmented, (-)ssRNA bats of the - Incubation period: 2- 21 days treatment. river in Zaire that was the site
Pteropodidae family - abrupt onset of flu-like symptoms, diarrhea/vomiting, high fever, myalgia Antigen tests of an outbreak of
thread-like viruses - can progress to DIC, diffuse hemorrhage, shock Strict isolation of infected hemorrhagic fever in 1976.
Transmission: - high mortality rate (100%) RT-PCR individuals and barrier practices
direct contact with for health care workers are key
bodily fluids, to preventing transmission
fomites (including
dead bodies),
infected bats or
primates (apes/
monkeys)
 VIRUS MORPHOLOGY TRANSMISSION PATHOGENESIS / SPECTRUM OF DISEASE DIAGNOSIS TREATMENT / PREVENTION NOTES
ENVELOPED RNA VIRUSES (POSITIVE SENSE)
CORONAVIRIDAE
Coronavirus Enveloped, helical, non- Reservoir: SPECTRUM OF DISEASE
segmented, (+)ssRNA Horseshoe bat COMMON COLDS
with prominent club- î Second to rhinovirus as the most common cause of common colds

shaped spikes form a Immediate host: SEVERE ACUTE RESPIRATORY SYNDROME
“corona” (halo) Civet cat î Incubation Period: 2-10 days (mean, 5 days)

î Receptor for SARS-CoV on surface of cells is angiotensin-converting enzyme-2 (ACE-2)
Two serotypes: Transmission:
î Binding of the virus to ACE-2 on the surface of respiratory tract epithelium à dysregulation
229E and OC43 Respiratory Droplet
of fluid balance à alveolar edema
î Severe atypical pneumonia rapidly progressing to ARDS
î Leukopenia and thrombocytopenia are seen
î CXR: interstitial “ground-glass” infiltrates that do not cavitate

MIDDLE EAST RESPIRATORY SYNDROME

î MERS-CoV binds to CD-26 on the respiratory mucosa (not ACE-2)
î clinical findings of MERS are similar to those of SARS
FLAVIVIRIDAE
Dengue virus Enveloped, icosahedral, Bite of female DENGUE FEVER (BREAKBONE FEVER) • NS1 Antigen: to detect PREVENTION: Dengue is the most
non-segmented, Aedes aegypti î Influenza-like syndrome characterized by biphasic fever, myalgia, arthralgia, rash, gene product (NS1 î Insecticides common insect-borne viral
(+)ssRNA mosquito, Aedes leukopenia and lymphadenopathy glycoprotein) from day 1 î Draining stagnant water disease in the world.
albopictus
until day 6 from the î Mosquito repellent
Four serotypes: DENGUE HEMORRHAGIC FEVER
onset of fever î Dengue Vaccine FLAVIVIRUSES
DEN-1, 2, 3, 4 î severe, often fatal, febrile disease characterized by capillary permeability, abnormalities of
- Dengvaxia® (CYD-TDV)
hemostasis and a protein-losing shock syndrome î West Nile virus
(Each serotype Aedes aegypti is • RT-PCR: to detect dengue - first licensed in Mexico in
provides specific lifetime recognized by white î Hemorrhagic shock syndrome is due to the production of large amounts of cross-reacting î Hepatitis C and G virus
viral genes (RNA) in December 2015 for use in
immunity, and short- markings on its legs antibody at the time of a second dengue infection (antibody-dependent enhancement) acute phase serum î Yellow fever virus
individuals 9-45 years of
î Japanese enceph virus

term cross-immunity) and a marking in DENGUE WITHOUT DENGUE WITH samples which coincide age living in endemic areas
the form of a lyre SEVERE DENGUE with the onset of î Dengue virus
WARNING SIGNS WARNING SIGNS - live recombinant
on the upper Probable dengue: Lives in or travels to dengue- Lives in or travels to a viremia tetravalent dengue vaccine î Zika virus
surface of its thorax Lives in or travels to dengue- endemic area, with fever dengue-endemic area - given as a 3-dose series on
endemic area, with fever, plus any lasting for 2-7 days, plus any of with fever of 2-7 days and • Dengue IgM: marker of a 0/6/12-month schedule
two of the following: the following: any of the above clinical recent infection RNA viruses with
• Headache • Abdominal pain or tenderness manifestations for dengue icosahedral symmetry
• Body malaise • Persistent vomiting with or without warning • Dengue IgG: marker of
• Myalgia • Clinical signs of fluid signs, plus any of § Flaviviruses
past infection; a fourfold
• Arthralgia accumulation the following: § Caliciviruses
increase confirms the
• Retro-orbital pain • Mucosal bleeding • Severe plasma leakage, § Reoviruses
diagnosis
• Anorexia • Lethargy, restlessness leading to: § Picornavirus

• Nausea • Liver enlargement - Shock § Togaviruses
• Vomiting • Laboratory: increase in Hct - Fluid accumulation with • CBC-PC: Characteristic
• Diarrhea and/or decreasing platelet respiratory distress findings are § Hepevirus
• Flushed skin count • Severe bleeding thrombocytopenia with
• Rash (petechial, Herman’s sign) • Severe organ leukopenia. A
AND Confirmed dengue: impairment hematocrit level
• Laboratory test, at least CBC • Viral culture isolation - Liver: AST or ALT >1000 increase >20% is a sign
(leucopenia with or without • PCR - CNS: e.g., seizures, of hemoconcentration
thrombocytopenia) and/or dengue impaired consciousness and precedes shock.
NS1 antigen test or dengue IgM - Heart: e.g., myocarditis
antibody test (optional) - Kidneys e.g., renal failure

Confirmed dengue:
• Viral culture isolation
• PCR
 VIRUS MORPHOLOGY TRANSMISSION PATHOGENESIS / SPECTRUM OF DISEASE DIAGNOSIS TREATMENT / PREVENTION NOTES
FLAVIVIRIDAE (continued)
Hepatitis C virus Enveloped, icosahedral, Humans are the PATHOGENESIS: Anti-HCV antibodies: ACUTE HEPATITIS C: A chronic infection is
non-segmented, reservoir for HCV. - Replication of HCV in the liver is enhanced by a liver-specific micro-RNA called miR-122. screening Peginterferon alfa characterized by elevated
(+)ssRNA
This micro-RNA acts by increasing the synthesis of HCV mRNA. - significantly decreases the transaminase levels, a
HCV is the most
- Death of the hepatocytes is probably caused by immune attack by cytotoxic T cells Recombinant immunoblot number of patients who positive RIBA, and
prevalent blood-
Has at least six - Alcoholism greatly enhances the rate of hepatocellular carcinoma in HCV-infected assay (RIBA): confirmatory become chronic carriers detectable viral RNA for at
borne pathogen in
genotypes and multiple individuals. test
least 6 months
the United States. CHRONIC HEPATITIS C:
subgenotypes based on - Rate of chronic carriage of HCV is much higher than that of HBV
differences in the genes
• PCR–based test that combination of
Major mode of î Peginterferon alfa-2a
that encode one of its SPECTRUM OF DISEASE: detects the presence of
transmission:
two envelope - Incubation period: 8 weeks HCV-RNA (viral load) in î Ribavirin
blood-borne
glycoproteins. - Acute infection: milder than infection with HBV the serum should be If genotype 1, add:
Setting: IV drug
This genetic variation - Hepatitis C resembles hepatitis B as far as the ensuing chronic liver disease, cirrhosis, and performed to determine î Protease inhibitor
users
results in a the predisposition to hepatocellular carcinoma are concerned whether active disease - Boceprevir, Simeprevir,
“hypervariable” region
- HCV infection also leads to significant autoimmune reactions and extrahepatic exists. Telaprevir
Minor modes:
in the envelope manifestations, including:

Needle-stick
glycoprotein. o Thyroiditis o DM Cirrhosis resulting from chronic

injuries, during
birth, sexual o Autoimmune hemolytic anemia o leukocytoclastic vasculitis HCV infection is the most
Genotype 1: most
common in US o ITP o á risk of B-cell NHL common indication for liver
o MPGN o lichen planus transplantation
o porphyria cutanea tarda
- HCV is the main cause of essential mixed cryoglobulinemia
Zika virus Enveloped, icosahedral, Aedes mosquito - Causes conjunctivitis, low-grade pyrexia, muscle and joint pain, malaise, headache, and Supportive care, no definitive Zika virus was first identified
non-segmented, bites itchy rash in 20% cases treatment. in Uganda in 1947.
(+)ssRNA - These symptoms are usually mild and last for 2-7 days.
Sexual and vertical
transmission Complications:
possible î Microcephaly
î Guillain-Barre Syndrome

Yellow Fever virus Enveloped, icosahedral, Reservoir: - characterized by jaundice and fever May see Councilman PREVENTION: Arbovirus is an acronym for
non-segmented, monkey or human - severe, life-threatening disease that begins with the sudden onset of fever, headache, bodies (eosinophilic î mosquito control arthropod-borne virus and
(+)ssRNA myalgias, and photophobia apoptotic globules) on liver î vaccine containing live, highlights the fact that these
- After this prodrome, the symptoms progress to involve the liver, kidneys, and heart biopsy attenuated yellow fever virus viruses are transmitted by
- Prostration and shock occur, accompanied by upper gastrointestinal tract hemorrhage arthropods, primarily
with hematemesis (“black vomit”) mosquitoes and ticks. Most
arboviruses are classified in
West Nile virus Enveloped, icosahedral, Bite of Culex - bird-mosquito-man cycle
three families, namely,
non-segmented, mosquito - Virus transmitted via blood from bite site to brain.
togaviruses, flaviviruses,
(+)ssRNA

Reservoir: Wild - Initial self-limited febrile illness with progression to neuroinvasive disease
and bunyaviruses
birds - The most important clinical picture is encephalitis with or without signs of
meningitis, typically in a person over 60 years of age.

Humans are
dead-end hosts - Asymptomatic in 80%; fever and headache in 20%; encephalitis in 1%
Japanese B Enveloped, icosahedral, Bite of Culex - most common cause of epidemic encephalitis PREVENTION:
non-segmented, mosquitoes - most prevalent in Southeast Asia JE vaccine
Encephalitis virus
(+)ssRNA - Thalamic infarcts on CT scan - live attenuated recombinant
Principal vector: monovalent viral vaccine
Culex - given 0.5ml subcutaneous for
tritaeniorhynchus children 12 months and above
summarosus - primary series: single dose
- booster dose: 12-24 months
after the 1st dose
 VIRUS MORPHOLOGY TRANSMISSION PATHOGENESIS / SPECTRUM OF DISEASE DIAGNOSIS TREATMENT / PREVENTION NOTES
TOGAVIRIDAE
Rubella virus Enveloped, icosahedral, Respiratory RUBELLA / GERMAN MEASLES / 3-DAY MEASLES PREVENTION: 5Bs of Congenital Rubella
non-segmented, droplets î Incubation period: 14-21 days MMR Vaccine Syndrome
(+)ssRNA î Period of communicability: 1 week before up to 1 week after the appearance of rash - live attenuated vaccine Bulag (cataracts)
Transplacentally î Prodrome: malaise, fever and anorexia for several days; may be accompanied by mild - Given subcutaneously
Only one known coryza and conjunctivitis (children may not have a prodrome) - Given at 15 months
Bingi (SN deafness)
serotype î Cephalocaudal appearance of maculopapular rash - 2 doses recommended Bobo (mental retardation)
î Postauricular lymphadenopathy: most characteristic clinical feature - should not be given to Butas puso (PDA)
î Enanthem: Forchheimer’s spots (petechiae on soft palate; not pathognomonic) immunocompromised patients Blueberry muffin rash
î polyarthritis caused by immune complexes (especially in adult women) or to pregnant women

î Natural infection leads to lifelong immunity.



CONGENITAL RUBELLA SYNDROME
î Risk is greatest early in fetal development when cell differentiation is at a peak (first

trimester)
î Rubivirus infected human embryo cells demonstrate chromosomal breakage and inhibition
of mitosis.
î Body areas affected in congenital rubella include:
o Heart: patent ductus, interventricular septal defects, pulmonary artery stenosis, etc.
o Eye: cataracts, chorioretinitis, etc.
o CNS: mental retardation, sensorineural deafness, microcephaly
î “blueberry muffin” appearance due to dermal extramedullary hematopoiesis

To God be the Greatest Glory!

 RETROVIRIDAE p24
î Distinguished from all other RNA viruses by the presence of an î Group-specific antigen
unusual enzyme, reverse transcriptase à which converts a î Located in the core
single stranded RNA viral genome into a double-stranded viral î Not known to vary
DNA (ssRNA à dsDNA) î Antibodies against p24 do not neutralize HIV infectivity but
serve as important serologic markers of infection
HUMAN IMMUNODEFICIENCY VIRUS (HIV)
gp120
CHARACTERISTICS: î Interacts with the CD4 receptor
î Enveloped virus with two copies (diploid) of a single-stranded î Gene mutates rapidly à many antigenic variants
positive polarity RNA genome î V3 loop: most immunologic region of gp120
î Most complex of the known retroviruses î Antibody neutralized HIV infectivity, but the rapid appearance
î Many serotypes of variants à difficult to prepare vaccine
î High mutation rate may be due to lack of an editing function in
STRUCTURE: the reverse transcriptase

gp41
î Mediates the fusion of the viral envelope with the cell
membrane at the time of infection

GENOME:
Gene Proteins Function
Structural genes found in all retroviruses
p24, p7 Nucleocapsid
gag
p17 Matrix
Reverse Transcribes RNA genome into DNA
transcriptase
pol Protease Cleaves precursor polypeptide
Integrase Integrates viral DNA into host cell DNA
Attachment to CD4 protein
gp120
env Antigenicity changes rapidly
gp41 Fusion with host cell à Inhibited by INFUVIRTIDE
î Transmembrane protein, TM (fusion protein, also called gp41), Regulatory genes found in HIV that are required for replication
which is linked to a surface protein, and SU (attachment Activation of transcription of viral genes
tat Tat
protein, gp120)
Transport of late mRNAs from nucleus to
î Cone-shaped, icosahedral core containing the major capsid rev Rev
cytoplasm
protein (CA also called p24)
Regulatory genes found in HIV that are not required for replication
î MA (outer matrix protein, p17) – directs entry of the double-
Decreases CD4 proteins and class I MHC
stranded DNA provirus into the nucleus, and is later essential
for the process of virus assembly. There are two identical
nef Nef proteins on surface of infected cells; induces
death of uninfected cytotoxic T cells
copies of the positive sense, single-stranded RNA genome in
Enhances infectivity by inhibiting the action
the capsid (that is, unlike other viruses, retroviruses are diploid)
î The RNA is tightly complexed with a basic protein, NC vif Vif of APOBEC3G (an enzyme that causes
hypermutation in retroviral DNA)
(nucleoprotein, p7), in a nucleocapsid structure that differs in
morphology among the different retrovirus genera. Transports viral core from cytoplasm into
vpr Vpr
nucleus in non-dividing cells

vpu Vpu Enhances virion release from cells

HIV Proviral Genome

Transmission: Pathogenesis:
î Original source: chimpanzees î Virus binds CD4 as well as a coreceptor, either CCR5 on
î Transfer of body fluids macrophages (early infection) or CXCR4 on T cells (late infection)
î Transplacental o The drug MARAVIROC is a CCR5 receptor antagonist.
î Perinatal î Preferentially infects and kills helper (CD4+) T lymphocytes
î Needlestick o Loss of cell-mediated immunity
o High probability of opportunistic infections
î also targets a subset of CD4+ cells called Th17 cells, which are
important mediator of mucosal immunity
o Th17 cells produce IL-17, which attracts neutrophils to the site
of bacterial infection.
o loss of Th17 cells à bloodstream infections by bacteria in the
normal flora of the colon (eg., E.coli)


î Main immune response consists of cytotoxic (CD8+) lymphocytes

STAGES OF INFECTION















Phase 0 Infection HIV acquired through sexual DIAGNOSIS
intercourse, blood, or perinatally î Presumptive diagnosis: detection of antibodies in the
Phase 1 Window Rapid viral replication but HIV test is patient’s serum to the p24 protein of HIV using ELISA.
Period negative o There are some false-positive results with this test
î Definitive diagnosis: Western blot (aka Immunoblot) analysis
Phase 2 Seroconversion Peak of viral load o Viral proteins are displayed by acrylamide gel electrophoresis,
Positive HIV test transferred to nitrocellulose paper (the blot), and reacted with
Mild flu-like illness lasting 1-2 weeks the patient’s serum.
Phase 3 Latent Period Asymptomatic o If antibodies are present in the patient’s serum, they will bind to
the viral proteins (predominantly to the gp41 or p24 protein).
CD4 goes down
o Enzymatically labeled antibody to human IgG is then added.
Lasts 1-15 years o A color reaction reveals the presence of the HIV antibody in the
Phase 4 Early CD4 500 to 200 infected patient’s serum.
Symptomatic Lasts 5 years ELISA WESTERN BLOT
Mild mucocutaneous, dermatologic, Presumptive diagnosis Definitive diagnosis
and hematologic illnesses sensitive specific
high false positive rate low false positive rate
Phase 5 AIDS CD4 <200 low threshold high threshold
Lasts 2 years rule out test rule in test
AIDS-defining illnesses develop
î HIV can be grown in culture from clinical specimens, but this
AIDS-DEFINING ILLNESSES procedure is available only at a few medical centers.
CD4 ETIOLOGY CLINICAL SYNDROME
î The PCR is a very sensitive and specific technique
M. tuberculosis Disseminated tuberculosis o can be used to detect HIV DNA within infected cells
HSV HSV esophagitis o Some individuals who do not have detectable antibodies
<500
C. albicans Esophageal candidiasis have been shown by this test to be infected.
HHV-8 Kaposi sarcoma o The amount of viral RNA in the plasma (i.e., the viral
P. jiroveci PCP pneumonia load) can also be determined using PCR-based assays.
T. gondii Cerebral toxoplasmosis
<200 C. neoformans Meningoencephalitis TREATMENT
C. immitis Coccidioidomycosis î Highly active antiretroviral therapy
C. parvum Chronic diarrhea
M. avium Invasive pulmonary disease

<50 H. capsulatum Histoplasmosis

CMV CMV retinitis


AIDS-DEFINING ILLNESS: Prevalence
P. carinii pneumonia (PCP) 42.6%
Esophageal candidiasis 15.0%
Wasting 10.7%
Kaposi sarcoma 10.7%
Disseminated MAC 4.8%

COMMON OPPORTUNISTIC INFECTIONS
Site of Infection Disease or Symptom Causative Organism
Lung 1. Pneumonia Pneumocystis jiroveci, CMV

2. Tuberculosis Mycobacterium tuberculosis
Mouth 1. Thrush Candida albicans

2. Hairy leukoplakia Epstein-Barr virus
3. Ulcerations HSV-1, Histoplasma capsulatum
Esophagus 1. Thrush Candida albicans
2. Esophagitis CMV, HSV-1
î Immune reconstitution inflammatory syndrome (IRIS)
Intestinal tract Diarrhea Salmonella sp., Shigella sp,
CMV, Cryptosporidium parvum, describes a collection of inflammatory disorders associated
Giardia lamblia with paradoxical worsening of preexisting infectious processes
Central nervous 1. Meningitis Cryptococcus neoformans (HBV, HCV, MAC, MAI, etc) following the initiation HAART in
system 2. Brain abscess Toxoplasma gondii

HIV-infected individuals
3. Progressive multifocal JC virus
leukoencephalopathy
Eye Retinitis CMV PREVENTION
Skin 1. Kaposi's sarcoma HHV-8 General Prevention:
2. Zoster Varicella-zoster virus î Condoms, not sharing needles, proper blood disposal,
3. Subcutaneous nodules Cryptococcus neoformans
Reticulo- Lymphadenopathy or Mycobacterium avium complex,
postexposure prophylaxis
endothelial system splenomegaly Epstein-Barr virus
Perinatal Prevention:
The two most characteristic manifestations of AIDS are Pneumocystis î Perinatal Prophylaxis, cesarean delivery, breastfeeding
pneumonia and Kaposi’s sarcoma. cessation



HIGHLY ACTIVE ANTIRETROVIRAL THERAPY (HAART):
î Often initiated at the time of HIV diagnosis.
3
î Strongest indication for patients presenting with AIDS-defining illness, low CD4+ cell counts (< 500 cells/mm ), or high viral
load
î Regimen consists of 3 drugs to prevent resistance: 2 NRTIs (zidovudine and lamivudine) and protease inhibitor (indinavir)










































HEPATITIS VIRUSES

Number Other names for the disease Etiology(ies)

First disease Rubeola Measles virus
Measles
Hard measles
14-day measles
Morbilli
Second disease Scarlet Fever Streptococcus pyogenes
Scarlatina
Third disease Rubella Rubella virus
German measles
3-day measles
Fourth disease Filatow-Dukes' Disease Some say the disease does not exist. Others
Staphylococcal Scalded Skin Syndrome believe it is due to Staphylococcus
Ritter's disease aureus strains that make epidermolytic
(exfoliative) toxin
Fifth disease Erythema infectiosum Erythrovirus (Parvovirus) B19
Sixth disease Exanthem subitum Human Herpes Virus 6 or Human Herpes
Roseola infantum Virus 7
"Sudden Rash"
Rose rash of infants
3-day fever

 MEDICAL PARASITOLOGY

BIOLOGICAL RELATIONSHIPS MODES OF TRANSMISSION
Symbiosis Process of living together of two different Contact Transmitted • Enterobius vermicularis
species of organisms Infection is transmissible directly from • Trichomonas vaginalis
Commensalism One organism gains but the other is not harmed nor person to person • Sarcoptes scabei
affected nor helped • Pediculus capitis
Phoresy if used for transport Soil-transmitted
• Ascaris lumbricoides
Inquilinism if used for housing/shelter The infective stage becomes infective
• Trichuris trichiura
Mutualism Reciprocal benefit after a period of incubation in the soil.
• Ancylostoma duodenale
Parasitism one organism (the parasite) gains food and shelter
• Necator americanus
from another (the host) which suffers from the • Strongyloides stercorales
relationship
Arthropod-transmitted

Infective stage develops in the • Plasmodium spp.
TYPES OF PARASITES ACCORDING TO ITS LOCATION
arthropod intermediate host which • Wuchereria
Endoparasite Ectoparasite
transmits the infection by biting or • Trypanosoma
Lives inside the body of the host Lives outside the body of the host when ingested by man
Presence in host connotes Presence in host connotes
Snail-transmitted
infection infestation Infective stage develops in the snail
Ex: Plasmodium, Giardia, Taenia, Ex: mites, lice, ticks • Schistosoma
intermediate host or second
Ascaris • Echinostoma
intermediate host after partial
development in the snail
TYPES OF PARASITES ACCORDING TO HOST RELATIONSHIP Food/Animal-transmitted • Trichinella spiralis
Obligate Parasite Facultative Parasite Infective stage develops in animals • Taenia solium
Need a host at some stage of their May exist in a free-living state but whose flesh is an important food item of • Capillaria philippinensis
life cycle to complete development becomes parasitic when the need man • Paragonimus westermani
and propagation arises Water-transmitted
Infective stage of the parasite develops
TYPES OF PARASITES ACCORDING TO SITE OF INFECTION • Giardia lamblia
in the external environment and usually
Accidental/ Establishes itself in a host it does not ordinarily live • Entamoeba histolytica
reaches man through ingestion of
Incidental contaminated water.
Permanent Remains on host for life Sexual intercourse • Trichomonas vaginalis
Temporary Lives on host for short period of time Congenital transmission • Toxoplasma gondii
Spurious Free-living organism that passes through digestive tract Inhalation of airborne eggs
with infecting the host Skin penetration


TYPES OF HOSTS
SOME DEFINITION OF TERMS IN THE LIFE CYCLE OF PARASITES
Definite / Final organism in which the adult or sexually PROTOZOA
Host mature stage of the parasite lives TROPHOZOITES CYSTS
Intermediate organism in which the parasite lives • Motile • Nonmotile
Host during a period of its larval or asexual • Feeding • Nonnmetabolizing
development • Reproducing form • Nonreproducing form
Paratenic Host reservoir of infection in transmitting the • surrounded by a flexible cell • surrounded by a thick wall
parasite without undergoing any membrane • survives well in the environment
development inside this host and so is often involved in
Reservoir Host Allow life cycle to continue and become additional transmission
sources of human infection • Flagellated forms à promastigotes or trypomastigotes

• Non-flagellated forms à amastigotes
TYPES OF VECTORS HELMINTHS
Vector: living invertebrate carrier (e.g. an arthropod) that transmits a • Many helminths have a life cycle that progresses from egg à larva à
pathogenic organism from an infected to a noninfected host adult.
Biologic Vector Mechanical Vector • Regarding the laboratory diagnosis of these infections, examination of the
harbor the parasitic organism merely transfer parasitic organism stool for ova and parasites (O&P) is often done. Ova refers to the eggs,
internally with further from one host to another by their and parasite refers to the larval or adult forms.
development appendages • Eosinophilia is associated with several helminth infections, especially

when roundworm larvae migrate through tissue; seen in:
EXPOSURE AND INFECTION
o Roundworms: Ascaris, Strongyloides, Trichina, Toxocara
Exposure Process of inoculating an infective agent
o Hookworms: Necator and Ancylostoma
Infection Establishment of infective agent inside host
o Flatworm (fluke): Schistosoma (a trematode)
Incubation Period Between infection and evidence of symptoms
• Eosinophils are an important component of the host defense against
(Clinical)
these parasites.
Pre-patent Period Between infection and demonstration of infection

(Biological)
PARASITES OF MEDICAL IMPORTANCE
SPECIAL TYPES OF INFECTION
Autoinfection Infected individual becomes his own direct
source of infection
Hyperinfection/ Infected individual is further infected with same
Superinfection species leading to massive infection

EFFECTS OF THE PARASITE ON THE HOST
Enzymatic E. histolytica trophozoites secrete cysteine
interference proteases which digest cellular material
Invasion and Plasmodium invades RBCs and causes rupture
destruction
Nutrient Diphyllobothrium latum competes with host for
deprivation available supply of Vitamin B12


MECHANISMS OF IMMUNE INVASION

Immune E. histolytica produces suppressor factor the

suppression inhibits monocyte movement

Antigenic Surface protein variation in T. gambiense

variation

Host mimicry E. granulosum carries blood group antigen

Intracellular T. gondii multiplies inside macrophages
sequestration
 Balamuthia
Sarcodina Entamoeba
(move by pseudopodia) Acanthamoeba
Naegleria
Sarcomastigophora
Giardia
Mastigophora Leishmania
(move by flagella) Trypanosoma
Trichomonas

Plasmodium
Babesia
Protozoa Apicomplexa Sporozoa
Cytoisospora
(no organelle of locomotion) (no locomotory organ)
Cryptosporidium
Toxoplasma

Ciliophora
Balantidium
(move by cilia)

Microspora
Enterocytozoa
(spore-forming)

Metazoa




ASCHELMINTHES PLATYHELMINTHES


(Round worms) (Flat worms)
Appear round in cross-section Dorsoventrally flattened
With body cavities No body cavity
With straight alimentary canal and an And if present, the alimentary canal is

anus blind-ending



NEMATODES CESTODES TREMATODES
Elongated cylindrical worms - Adult tapeworms are found in - Non-segmented, usually leaf-

Sexes are separated, unsegmented the intestine of their host shaped, with two suckers but no
Reproduce by oviparous and - Have a head (scolex) with sucking distinct head
viviparous organs, a segmented body but no - They have an alimentary canal
alimentary canal and are usually hermaphrodite

- Each body segment is - Schistosomes are the exception.
Ascaris (roundworm)
e hermaphrodite (They are threadlike, not leaf-
Trichuris (whipworm)
shaped, and have separate sexes)
Enterobius (pinworm/threadworm)
Ancylostoma (hookworm)
Necator (hookworm)
Diphyllobothrium Paragonimus
Strongyloides
Taenia (Tapeworm) Schistosoma
Capillaria
Echinococcus Fasciolopsis
Dipylidium Echinostoma
Hymenolepis Fasciola
Clonorchis
Opisthorchis


PROTOZOA PARASITE BIOLOGY TRANSMISSION INFECTIVE STAGE DIAGNOSTIC STAGE PATHOGENESIS/VIRULENCE FACTORS SPECTRUM OF DISEASE TREATMENT NOTES
INTESTINAL PROTOZOA
Entamoeba î Pseudopod-forming Fecal-oral Mature Cysts Trophozoite î Lectin: mediates adherence ASYMPTOMATIC CYST CARRIER STATE ASYMPTOMATIC CYST
nonflagellated protozoa CARRIER STATE

histolytica - found in diarrheal stools î Amebapores: for penetration

and within the intestinal AMEBIC COLITIS î Diloxanide furoate

à Brownian movement î Cysteine proteases: for cytopathic

and extraintestinal lesions effect
î Dysentery without fever (DOC)
î Most invasive parasite î Flask-shaped colon ulcer î Iodoquinol
- characteristically contain
among Entamoeba î Paromomycin
ingested red blood cells

î Eukaryotic organism that (erythrophagocytosis) à Ingestion of cysts AMEBOMA

lack membrane-bound hematophagous Ü î granulomatous lesion that may form in AMEBIC COLITIS Trophozoites (with
organelles cyst produces trophozoites in the the cecal or rectosigmoid areas î Metronidazole engulfed RBCs in the
- nucleus has a small central
nucleolus and fine
intestine î associated with dystentery î Tinidazole cytoplasm)
Ü
chromatin granules along amebic dystentery in the colon

AMEBIC LIVER ABSCESS î Diloxanide furoate
the border of the nuclear Ü
î Most common extraintestinal form
î Paromomycin
membrane spread to the liver (MC), lung, brain
î Usually in the posterosuperior aspect
AMEBIC LIVER ABSCESS
Cyst of the right lobe
- This is according to majority of î Metronidazole
- predominates in non-
diarrheal stools references. But according to Schwartz, î Tinidazole
- smaller than E. coli it is the superior-anterior aspect. î Percutaneous drainage
- has four nuclei (E. coli has 8) î Anchovy paste-like aspirate (thick for nonresponders
chocolate brown in color)

Giardia lamblia î Flagellate that lives in the Fecal-oral Cysts Trophozoite î Adhesive disc and lectin facilitate ACUTE INFECTION î Metronidazole
duodenum, jejunum, and - found only in diarrheal attachment to avoid peristalsis î abdominal pain

upper ileum stools î Villous flattening, crypt î watery, foul-smelling diarrhea

- pear-shaped with two hypertrophy and disruption of î excessive flatus, smelling like rotten
î Falling leaf motility nuclei, four pairs of flagella, cytoskeleton eggs

î Simple asexual life cycle and a suction disk with î Ultimately leads to enterocyte î No fever and non-bloody (does not

which it attaches to the apoptosis invade the mucosa and does not enter the
î Covered with variant bloodstream)

intestinal wall î trophozoite causes inflammation of Multinucleated

surface proteins
the duodenal mucosa à trophozoites
CHRONIC INFECTION
Cyst malabsorption of protein and fat. î constipation, weight loss, and

STRING TEST: swallowing

- found in diarrheal and a weighted piece of string
steatorrhea
formed stools à trophozoites adhere to

the string and can be
visualized after
withdrawal
Cryptosporidium î Opportunistic infection Fecal-oral Thick-walled Thick-walled oocysts î The oocysts excyst in the small î Self-limited nonbloody diarrhea in î Nitazoxanide:

oocysts - using a modified Kinyoun intestine, where the trophozoites immunocompetent patients DOC for immuno-
hominis / parvum î Undergoes schizogony and
acid-fast stain (and other forms) attach to the gut î Severely debilitating prolonged diarrhea if competent patients
gametogony wall. CD4 <200 (due to autoinfection)


î Invasion does not occur. î NO effective drug
î Autoinfection in
î The jejunum is the site most heavily therapy for severely
immunocompromised
infested. immunocompromised
patients
patients, but Oocysts on acid-fast
î Acid-fast organism paromomycin may be stain
useful in reducing
diarrhea.

î HAART for HIV patients
 PROTOZOA PARASITE BIOLOGY TRANSMISSION INFECTIVE STAGE DIAGNOSTIC STAGE PATHOGENESIS/VIRULENCE FACTORS SPECTRUM OF DISEASE TREATMENT NOTES
INTESTINAL PROTOZOA (continued)
Balantidium coli î only ciliated protozoan Fecal-oral Cysts Diagnosis is made by finding BALANTIDIASIS / î Tetracycline:
that causes human large ciliated BALANTIDIAL DYSENTERY treatment of choice
disease (i.e., diarrhea) trophozoites or large î B. coli is locally invasive, causing
î Largest protozoan cysts with a characteristic V- colonic ulcers (round-based, wide- î Metronidazole
parasite of humans shaped nucleus in the stool necked intestinal ulcers)
î extraintestinal lesions do not occur
î Pigs are the main reservoir
(unlike the case with E. histolytica)
à diarrhea among
slaughter house workers

UROGENITAL PROTOZOA
Trichomonas î Exists only as Sexual intercourse Trophozoites Trophozoite TRICHOMONIASIS î Metronidazole 2g
trophozoite (“ping-pong” (seen in wet mount of î Watery, foul-smelling, greenish single dose
vaginalis
î Pear-shaped flagellated transmission) vaginal fluid) discharge accompanied by itching and - Treat both the
trophozoite with jerky burning patient and the
î Strawberry cervix partner
motion

î cannot exist outside human

because it cannot form cysts
Motile Trophozoites


Life cycle of Entamoeba histolytica, showing the sites of action of amebicidal drugs


THE COMMENSAL AMOEBA
- non-invasive and do not cause disease
- reproduce by binary fission
- cysts pass through the acidic stomach unscathed, protected by their cyst wall
- excystation occur in the small intestine

Entamoeba dispar morphologically similar to E. histolytica but their DNA and ribosomal RNA are
different
Entamoeba hartmanni similar to E. histolytica but is much smaller and does not ingest RBC, sluggish
Entamoeba coli cosmopolitan in distribution, harmless inhabitant of colon, has a larger cyst and
greater number of nuclei than E. histolytica
Entamoeba polecki parasite of pigs and monkey, cyst is uninucleated
Entamoeba gingivalis has no cyst stage and does not inhabit the intestines, found in the mouth,
moves quickly and has numerous blunt pseudopodia, transmission is via kissing
or droplet spray
Endolimax nana small size, sluggish movement
Iodamoeba butschlii no peripheral chromatin granules on the nuclear membrane

 PROTOZOA PARASITE BIOLOGY TRANSMISSION INFECTIVE STAGE DIAGNOSTIC STAGE PATHOGENESIS/VIRULENCE FACTORS SPECTRUM OF DISEASE TREATMENT NOTES
BLOOD AND TISSUE PROTOZOA
Plasmodium î Most important parasitic Bite of infected Sporozoites Trophozoite (ring forms) î Most of the pathologic findings of î Paroxysmal fever with malaise and bone PREVENTION BUZZ WORDS
disease in man female mosquito malaria result from the destruction pains î Chemoprophylaxis
species Infected RBC with 1-2
(Anopheles of RBCs. î Hemolytic anemia, jaundice, î Insecticide-treated nets
splenomegaly î Insect repellants with small chromatin dots
î ASEXUAL life cycle consists minimus DIAGNOSTIC TESTS FOR MALARIA - enlarged spleen characteristic
à P. falciparum
of schizogony and flavirostris) î Thick and thin smears with Giemsa stain of malaria is due to congestion of î Parasitic pneumonitis DEET
î Cerebral malaria î Biological modification
gametogony - Thick smear: to screen for the presence of sinusoids with erythrocytes,
coupled with hyperplasia of - Malarial or Durck granulomas à cultivation of snails infected RBC
transmission organism
lymphocytes and macrophages î Acute Renal Failure (Blackwater fever) that eat up mosquito with presence of ring
î SEXUAL life cycle involves across the - Thin smear: for species identification
placenta, in blood î Septic shock (algid malaria) larvae form stage only à P.
sporogony - HIGHEST YIELD WHEN BLOOD SAMPLES
falciparum
transfusions, and TAKEN DURING FEVER OR 2-3 HOURS AFTER î People with RBC defects ( G6PD

by intravenous PEAK deficiency, sickle cell) are SPECIAL CLINCAL OUTCOMES
Areas of High Areas of Chloroquine infected RBC
Endemicity Resistance
drug use also protected against the severe effects î RECRUDESCENCE
occurs of falciparum malaria - Recurrence of symptoms after a with presence of
î Palawan î Palawan
temporary abatement (2-4 weeks) band form stages à

î Kalinga- Apayao î Davao del Norte - Seen in P. falciparum and P. P. malariae
î Partial immunity based on humoral
î Ifugao î Campostela Valley malariae
antibodies that block merozoites
î Agusan del Sur from invading the red cells occurs in
infected individuals (premunition) î RELAPSE
- Return of disease after its apparent

COMPARISON OF SPECIES - Results to low level of

parasitemia and low-grade cessation (1-6 months) due to
P. falciparum P. malariae P. vivax P. ovale
symptoms reactivation of hypnozoites
Asexual cycle 48 hours 72 hours 48 hours 48 hours
- Seen in P. ovale and P. vivax
Periodicity Malignant Benign Benign Benign

tertian quartan tertian tertian
RBC preference All ages Old RBC Young RBC Young RBC
Parasitemia Highest Lowest Low Low Clinical Setting Drug Therapy Alternative Drug
Merozoites 0 6-12 12-24 8 Chloroquine-sensitive P.
Gametocytes Banana- Large Small falciparum and P. Chloroquine
Compact malariae infections PROPHYLAXIS
shaped round round Drug Prophylactic Use
P. vivax and P. ovale
Cerebral Chloroquine + Primaquine
Yes No No No infections Chloroquine Areas WITHOUT resistant P. falciparum
Malaria
Recrudescence Yes Yes No No Malarone (Atovaquone- Malarone
Uncomplicated Areas WITH chloroquine-resistant P. falciparum
Relapse No No Yes Yes Proguanil)
Infections with Quinine + Doxycycline/ Mefloquine
Drug Resistance Many Few Few Few OR Mefloquine
chloroquine-resistant P. Clindamycin
Malarial Dots Maurer Ziemann Schuffner Schuffner falciparum OR Co-Artemether + Doxycycline Areas with MULTIDRUG-resistant P. falciparum
Lumefrantine
Terminal prophylaxis of P. vivax and P. ovale
MALARIAL DOTS PRESENT IN INFECTED RBCs: Primaquine

Artesunate + Doxycycline/ infection; alternative for primary prevention
SCHUFFNER MAURER ZIEMANN Severe or complicated Clindamycin Artemether +
Punctate Coarse
infections with P. OR Mefloquine/Malarone Doxycycline/Clindamycin
Fine dots falciparum OR Mefloquine/Malarone
granulations granulations OR Quinidine gluconate
P. vivax SPECIAL SITUATIONS
P. falciparum P. malariae
P. ovale Chloroquine-resistance Mefloquine + Doxycycline
Eradication of hypnozoites Primaquine
Severe cases or pregnant Quinidine or Quinine







Action of chloroquine on the formation of hemozoin by Plasmodium species.

 PROTOZOA PARASITE BIOLOGY TRANSMISSION INFECTIVE STAGE DIAGNOSTIC STAGE PATHOGENESIS/VIRULENCE FACTORS SPECTRUM OF DISEASE TREATMENT NOTES
BLOOD AND TISSUE PROTOZOA (continued)
Toxoplasma î Tissue protozoan Ingestion of cysts Fecal oocysts Trophozoites (Bradyzoites) Two Types of Trophozoites: î IMMUNOCOMPETENT: Treatment of Choice: MONONUCLEOSIS
in raw meat, TACHYZOITES - Usually asymptomatic Sulfadiazine + Heterophil-Positive:
gondii
î Domestic cat is the contaminated - rapidly multiplying - some resemble infectious Pyrimethamine î Epstein-Barr Virus
definitive host food - cell-mediated immunity usually mononucleosis, except that the
limits the spread of tachyzoites heterophil antibody test is negative For patients who cannot Heterophil-Negative:
î Humans and other Transplacentally î Cytomegalovirus
LABORATORY DIAGNOSIS: - seen in body fluids in early, receive sulfa drugs,
mammals are î For the diagnosis of acute acute infections î IMMUNOCOMPROMISED: clindamycin can be î Toxopasma
intermediate hosts and congenital infections,
- encephalitis
added to
BRADYZOITES - brain abscesses usually seen as
an immunofluorescence pyrimethamine.
- slowly multiplying multiple ring-enhancing lesions on CALCIFICATIONS in
assay for IgM antibody is - contained in cysts in muscle and MRI TORCH INFECTIONS
used.
brain tissue and in the eye Intracranial:
î Microscopic examination of
î CONGENITAL TOXOPLASMOSIS î Toxoplasmosis
Giemsa-stained
- Can result in abortion, stillbirth or

preparations shows Periventricular:

neonatal disease with
crescent-shaped î Cytomegalovirus
trophozoites during acute hydrocephalus, encephalitis,

infections. chorioretinitis, and

î Cysts may be seen in the hepatosplenomegaly

tissue. - Fever, jaundice, and intracranial
calcifications are also seen

Leishmania î Flagellate protozoa Bite of the female Promastigotes Amastigote LEISHMANIASIS Conventional Therapy:
sandfly of the CUTANEOUS MUCOCUTANEOUS VISCERAL Sodium
species
genus Causative L. tropica stibogluconate
L. braziliensis L. donovani
Phlebotomus or Agent L. mexicana (Pentavalent antimonial)
Lutzomyia LABORATORY DIAGNOSIS
Local Name Oriental Sore Espundia Kala-azar
Examination of Giemsa- Second-line agents:
Presentation ulcerating single or parasite attacks infects macrophages
stained tissue and fluid Amphotericin B
multiple skin sores tissue at the à migrate to the
samples for the Pentamidine
mucosal-dermal spleen, liver, and
nonflagellated form junctions of the bone marrow à

(amastigote), which is the nose and mouth à parasite rapidly

Macrophages containing only form that occurs in multiple lesions multiplies à
L. donovani amastigotes humans and other mammals. hepatosplenomegaly

Babesia microti î Sporozoan Bite Ixodes tick Giemsa-stained blood smears î Babesia infects RBCs, causing them BABESIOSIS Mild to moderate
(same as Borrelia reveal intraerythrocytic to lyse, but unlike plasmodia, it has î Influenza-like symptoms begin gradually disease:
burgdorferi of ring-shaped trophozoites no exoerythrocytic phase. and may last for several weeks Atovaquone +
Lyme disease) are often in tetrads in the î Hepatosplenomegaly and anemia occur Azithromycin
î Asplenic patients are affected
form of a Maltese cross
more severely. Severe disease:

Quinidine +

Clindamycin “Maltese cross”

Cyclospora î Coccidial sporozoa Fecal–oral Spherical oocysts in a causes watery diarrhea in both Trimethoprim-
(contaminated modified acid-fast stain of a immunocompetent and Sulfamethoxazole
cayetanensis
water supplies) stool sample immunocompromised individuals

Isospora belli î Coccidial sporozoa Fecal–oral Oocyst typical oocysts in fecal The oocysts excyst in the upper small The disease in immunocompromised Trimethoprim-
transmission of specimens intestine and invade the mucosa, patients presents as a chronic, profuse, Sulfamethoxazole
oocysts causing destruction of the brush watery diarrhea
border
 PROTOZOA PARASITE BIOLOGY TRANSMISSION INFECTIVE STAGE DIAGNOSTIC STAGE PATHOGENESIS/VIRULENCE FACTORS SPECTRUM OF DISEASE TREATMENT NOTES
BLOOD AND TISSUE PROTOZOA (continued)
Trypanosoma î Blood and tissue protozoan Feces of Reduviid Metacyclic Trypomastigote in blood î Many cells can be affected, but CHAGAS’ DISEASE / AMERICAN Drug of choice for the
î All four forms: bug (“kissing trypomastigote smear myocardial, glial, and TRYPANOSOMIASIS acute phase:
cruzii
- Amastigote bug,” triatoma, reticuloendothelial cells are the î ACUTE PHASE: Nifurtimox
- facial edema
- Promastigote or cone-nose) most frequent sites.
- Epimastigote
- nodule (chagoma) near the bite Alternative Drug:
deposited in a î Cardiac muscle is the most
- Trypomastigote painless bite LABORATORY DIAGNOSIS: - fever, lymphadenopathy, Benznidazole
î a stained preparation of a frequently and severely affected hepatosplenomegaly
(Kiss is supposedly
tissue

painless) bone marrow aspirate - unilateral palpebral swelling

or muscle biopsy î neuronal damage leads to cardiac (Romaña’s sign) There is no effective
specimen (which may arrhythmias and loss of tone in the - resolves in about 2 months drug against the
reveal amastigotes) colon (megacolon) and esophagus
chronic form.
î CHRONIC FORM:
î culture of the organism on (megaesophagus)
- myocarditis, dilated cardiomyopathy
Trypomastigote in special medium
with apical atrophy
blood smear î Xenodiagnosis: allowing - megacolon, megaesophagus
an uninfected, laboratory- (secondary achalasia)
raised reduviid bug to feed - Death is usually due to cardiac
on the patient and, after arrhythmias or congestive heart
several weeks, examining failure
the intestinal contents of
- leading cause of CHF in Latin
the bug for the organism
America
Trypanosoma î Blood and tissue protozoan Tsetse fly Metacyclic Trypomastigote in blood î Trypomastigotes spread from the skin à blood à lymph nodes à brain Suramin for
î Only two forms: (Glossina), a trypomastigote î The typical somnolence (sleeping sickness) progresses to coma as a result of a bloodborne disease
brucei
- Epimastigote painful bite demyelinating encephalitis (ARAS, brainstem)
Melarsoprol for
- Trypomastigote î In the acute form, a cyclical fever spike (approx. every 2 weeks) occurs that is
î exhibit remarkable related to antigenic variation. CNS penetration

antigenic variation of
Morula cells of Mott
their surface glycoproteins AFRICAN TRYPANOSOMIASIS / AFRICAN SLEEPING SICKNESS

î initial lesion: indurated skin ulcer (“trypanosomal chancre”) at the site of the

Trypanosoma brucei gambiense Trypanosoma brucei rhodesiense fly bite
î causes the disease along water courses î found in the arid regions of east Africa î intermittent weekly fever and lymphadenopathy
in west Africa î enlargement of the posterior cervical lymph nodes (Winterbottom’s sign) MELlow music will
Trypomastigote in î deep hyperaesthesia (Kerandel's sign) SURely put you to
î runs a low-grade chronic course î causes a more acute, rapidly SLEEP.
blood smear î Encephalitis à excessive somnolence
over a few years progressive disease that, if untreated, is
• Morula cells of Mott: plasma cells with cytoplasmic immunoglobulin
usually fatal within several months MELarsoprol and
globules
î Transmitted by Glossina î Transmitted by Glossina SURamin for African
î Untreated disease is usually fatal as a result of pneumonia.
palpalis (or riverine tsetse) morsitans (or savannah tsetse) SLEEPing sickness

î Treatment: î Treatment:

Stage 1 Stage 2 • Suramin (to clear parasitemia)
Pentamidine Eflornithine followed by Melarsoprol
Suramin Melarsoprol

Acanthamoeba î free-living amebas carried into the Trophozoites Occur primarily in î KERATITIS: most common disease Pentamidine, î MC parasite that
î Most common protist in soil skin or eyes immunocompromised individuals associated with Acanthamoeba infection ketoconazole, or contaminates
castellani
during trauma î GRANULOMATOUS AMEBIC flucytosine contact lenses
ENCEPHALITIS

Naegleria fowleri î free-living amebas Swimming in Trophozoites occur in otherwise healthy persons î PRIMARY AMEBIC Amphotericin-B
freshwater Trophozoites can penetrate the nasal MENINGOENCEPHALITIS
lakes mucosa and cribriform plate
 PROTOZOA PARASITE BIOLOGY TRANSMISSION INFECTIVE STAGE DIAGNOSTIC STAGE PATHOGENESIS/VIRULENCE FACTORS SPECTRUM OF DISEASE TREATMENT NOTES
DINOFLAGELLATES
Dinoflagellates î Flagellated marine protists Eating bivalve î Filter feeders accumulate toxins produced by dinoflagellates î Gastric lavage with
î Algal blooms cause red mollusks

activated charcoal
SHELLFISH POISONING SYNDROMES
tide (mussels, clams, î Supportive fluid
Syndrome Toxin Incubation Clinical presentation
î Most common in the oysters, and resuscitation
Philippines is Pyrodinium scallops) and fish Facial paresthesia, total
Paralytic Saxitoxin

obtained from red paralysis, respiratory failure î Endotracheal

bahamense var. 15 mins
compressum tide Facial paresthesia, slurred intubation for
Neurotoxic Brevetoxin
speech, ataxia, diarrhea respiratory failure

Diarrhea, nausea and vomiting,
Diarrhetic Okadaic acid î Neostigmine and
abdominal pain
30 mins edrophonium to
Diarrhea, short-term memory improve muscle
Amnesic Domoic acid
loss, seizures weakness

PLATYHELMINTHES
Species Transmission Intermediate Host Site Affected Treatment
CESTODES / TAPEWORMS
Eggs/larvae in undercooked
Taenia solium Pigs Intestine Praziquantel
pork
Taenia saginata larvae in undercooked beef Cattle Intestine Praziquantel
Diphyllobothrium latum larvae in undercooked fish Fish Intestine Praziquantel
Eggs in food contaminated
Echinococcus granulosus Swine Liver Albendazole
with dog feces
TREMATODES / FLUKES
Schistosoma japonicum Penetrate skin Snail Blood Praziquantel
Pargonimus westermani Ingested with raw crab Snail and crab Lung Praziquantel
Clonorchis sinensis Ingested with raw fish Snail and fish Liver Praziquantel

ASCHELMINTHES / NEMATODES
Location Species Disease Transmission Treatment
Ascaris lumbricoides Ascariasis Ingestion of eggs Albendazole
Ancylostoma duodenale
Hookworm Larval penetration of skin Albendazole
Necator americanus
Intestines Trichuris trichiura Whipworm Ingestion of eggs Mebendazole
Enterobius vermicularis Pinworm Ingestion of eggs Pyrantel pamoate
Strongyloides stercoralis Strongyloidiasis Larval penetration of skin Ivermectin
Capillaria phiippinensis Capillariasis Eggs in undercooked fish Albendazole
Wuchereria bancrofti Diethylcarbamazine
Filariasis Mosquito bite
Tissue Brugia malayi (DEC)
Trichinella spiralis Trichinosis Eggs in undercooked meat Thiabendazole



CESTODES / FLATWORMS Taenia solium Taenia saginata Diphyllobothrium latum Echinococcus granulosus
Parasite Biology / Scolex: has four suckers and circle of hooks arranged around a rostellum Scolex: has four suckers but, longest of the tapeworms composed of a scolex and only three
Characteristics Gravid proglottids: have 5 -10 primary uterine branches no hooklets (no rostellum) Scolex: has two elongated sucking proglottids à one of the smallest
Gravid proglottids: have 15-25 grooves for attachment; no hooks tapeworms
T. solium T. saginata
Suckers 4 4 primary uterine branches Proglottids: wider than they are long; Scolex: circle of hooks and four
Rostellum (+) (-) gravid uterus is in the form of a rosette suckers (similar to T. solium)
Uterine Branches 5-10 15-25 Have oval and operculated eggs
Intermediate Host Pigs Cattle Copepods (first IH) and fish (second IH) Sheep / Humans (accidental IH)
Infective stage Larvae (cysticerci) Eggs Larvae (cysticerci) Plerocercoid / sparganum larvae Eggs
Mode of Transmission Ingestion of larvae (cysticerci) in Ingest eggs in food or water Ingestion of larvae (cysticerci) in Ingestion of plerocercoid larvae in Ingestion eggs in food contaminated with
undercooked pork contaminated with human feces undercooked beef undercooked fish dog feces (Dog is the definitive host)
Stage in Humans Adult tapeworm in intestine, Cysticercus, especially in brain; Adult tapeworm in intestine, Adult tapeworm in intestine can cause Larva causes unilocular hydatid cyst
Associated with Disease causing taeniasis causing cysticercosis causing taeniasis diphyllobothriasis disease, especially in liver and lung
Sites Affected Intestine Brain and eyes Intestine Intestine Liver, lungs, and brain (hydatid cysts)
Signs and symptoms Mild intestinal symptoms Brain (neurocysticercosis): Abdominal pain Abdominal pain Liver cysts à hepatic dysfunction
headache, vomiting, seizure Weight loss Diarrhea Pulmonary cysts à erode into a bronchus
Pruritus ani Vitamin B12 deficiency caused by à bloody sputum
Eyes: uveitis or retinitis, larvae in Intestinal obstruction preferential uptake of the vitamin by Cerebral cysts à headache and focal
viterous the worm à megaloblastic anemia neurologic signs.
Rupture of cyst à anaphylactic shock
Diagnosis/Diagnostic Stage Gravid Proglottids in stool Biopsy, CT scan Gravid Proglottids in stool Unembryonated operculated eggs in Biopsy, CT Scan, serology
stool
Treatment Praziquantel Praziquantel, Albendazole, or Praziquantel Praziquantel Albendazole, or surgical removal of cyst
surgical removal of cysticerci PAIR procedure: Puncture, Aspiration,
Injection, Reaspiration
Pathogenesis Ingested larvae (cysticerci) in small Ingestion of eggs in food or water Taeniasis similar with T. solium See diagram on the next page Worms in the dog’s intestine liberate
(see diagrams on the intestine attach to gut wall contaminated with human feces thousands of eggs
Ü Ü
next page) Ü
eggs hatch in the small intestine T. saginata does NOT cause Eggs ingested by sheep (or humans)
Grow into adult worms à taeniasis
Ü Ü cysticercosis in humans. Ü

Gravid proglottid containing eggs detach oncospheres burrow through the wall into Oncosphere embryos emerge in the small
intestine
daily a blood vessel
Ü Ü
Ü
Eggs are passed in the feces disseminate to many organs, especially the migrate primarily to the liver but also to
Ü
eyes and brain the lungs, bones, and brain
Eggs eaten by pigs (intermediate host) Ü Ü
Ü
Six-hooked embryo (oncosphere) encyst to form cysticerci Embryos develop into large fluid-filled hydatid
Ü
emerges from each egg in pig’s intestine cysts, the inner germinal layer of which
Ü
cysticercosis generates many protoscoleces within “brood
Embryos burrow into blood vessel and
capsules.”
carried to skeletal muscle Living cysticerci do not cause
Ü
inflammation Cyst acts as a space-occupying lesion
Develop into cysticerci in muscle
Ü

Eaten by human (definitive host) Cysticerci can become space- Cyst fluid contains parasite antigens,
occupying lesions in the brain which can sensitize the host.

















































Praziquantel




Albendazole





Praziquantel





Praziquantel
Praziquantel

CESTODES OF MINOR IMPORTANCE
Echinococcus multilocularis Hymenolepsis nana Hymenolepsis diminuta Dipylidium caninum
• Definitive hosts: FOXES • Dwarf tapeworm • Rat tapeworm • most common tapeworm of dogs and cats
• Intermediate host: RODENTS • most frequently found tapeworm in developed • Transmission: ingestion of RAT FLEA cysticercoid • Transmission: ingestion of DOG OR CAT FLEAS
• Transmission: accidental ingestion of food countries larvae carrying cysticerci
contaminated with fox feces • Ingestion of cysticercoid larvae from infected • Accidental parasite • Diagnosis: “barrel-shaped” proglottids in stools
• larvae form multiloculated cysts (honeycomb RICE or FLOUR BEATLE • Drug-of-choice: NICLOSAMIDE
vesicles) • eggs are directly infectious for humans
• Treatment: ALBENDAZOLE; surgical cyst removal • eggs either pass in the stool or can reinfect the
small intestine (autoinfection)
• Eggs: 8-10 polar filaments and six-hooked larva
• Treatment: PRAZIQUANTEL

TREMATODES ARTHROPRODS OF MEDICAL IMPORTANCE

▫ Phylum: Platyhelminthes Organism Scientific Name Disease Features
▫ Flattened, leaf-shaped or cylindrical worms (Schistosoma) Lice Pediculus humanus Pruritus of the scalp or trunk
▫ Unsegmented Nits seen of hair shaft
▫ Hermaphroditic / Monoecious except SCHISTOSOMA Treatment: topical ivermectin lotion, lindane, and malathion
▫ All flukes are transmitted by ingestion of METACERCARIA except SCHISTOSOMA which is Phthirus pubis Pruritus in pubic area
transmitted by skin penetration of CERCARIA. Nits seen on hair shaft
▫ All fluke eggs are operculated except SCHISTOSOMA. Flies Dermatobia hominis Pruritic, painful, and erythematous nodule
Larva may be seen emerging from nodule
SPECIES: Pruritic, erythematous wheal
Bedbugs Cimex lectularius
▫ Paragonimus (lung fluke)
Mites Sarcoptes scabei Pruritic, erythematous papules and linear tracks
▫ Schistosoma (blood fluke) Treatment: permethrin cream, washing/drying
▫ Fasciolopsis all clothing/bedding, treat close contacts
▫ Echinostoma Ticks Dermacentor Ascending paralysis
Small intestinal flukes
▫ Metagonimus

▫ Heterophyes
Mechanisms of Action of Anti-mite/Anti-Louse Therapy
▫ Fasciola î Permethrin: neuronal membrane depolarization via Na+ channels
▫ Clonorchis Liver flukes
î Malathion: acetylcholinesterase inhibitor
▫ Opistorchis
î Lindane: blocks GABA channels à neurotoxicity
▫ Eurytrema pancreaticum (pancreatic fluke)
▫ Gastrodiscoides (large intestinal fluke)

CLASSIFICATION OF TREMATODE EGGS
LARGE UNEMBRYONATED MEDIUM, UNEMBRYONATED SMALL / MINUTE, EMBRYONATED
▫ Echinostoma ▫ Paragonimus ▫ Clonorchis
▫ Fasciolopsis ▫ Heterophyes
▫ Fasciola ▫ Opisthorchis
▫ Metagonimus

CLASSIFICATION OF FLUKES ACCORDING TO SECOND INTERMEDIATE HOST
WATER PLANT-
ANT-BORNE
SNAIL-BORNE
FISH-BORNE

BORNE (MOLLUSKS)
▫ Faciolopsis buski ▫ Eurythrema ▫ Echinostoma ▫ Clonorchis sinensis
▫ Fasciola hepatica pancreaticum ilocanum ▫ Heterophyes heterophyes
▫ Opisthorchis spp.
▫ Metagonimus yokogawai
 TREMATODES / FLUKES Schistosoma japonicum S. mansoni S. haematobium Paragonimus westermani Clonorchis sinensis
Parasite Biology / î Oriental fluke; Blood flukes î Japanese lung fluke î Chinese liver fluke / Oriental liver fluke
Characteristics î Reside in the mesenteric and portal veins î Hermaprodite î Hermaprodite
î Adult schistosomes exist as separate sexes (other trematodes are hermaphrodite)
î Evade host defenses by coating themselves with host antigens
î Can cause schistosomiasis (aka bilharzias, bilharziasis, or snail fever)
Intermediate Host Snail: Snail: Snail: Snail: Antemelania asperata Snail: Parafossarulus
Oncomelania hupensis quadrasi Biomphalaria glabrata Bulinus truncatus Mountain crab: Sundathelphusa philippina Fish: Cyprinidae
Infective stage CERCARIAE LARVAE (metacercariae) LARVAE (metacercariae)
Mode of Transmission SKIN PENETRATION BY CERCARIAE INGESTION of raw crabmeat/crayfish INGESTION of undercooked fish
Stage in Humans
Associated with Disease
Adult flukes living in mesenteric or bladder veins lay eggs that cause granulomas Adult flukes live in the lungs Adult flukes live in the liver
Sites Affected Veins of small intestine, liver Veins of colon Veins of urinary bladder Lung Liver, especially the common bile duct
Spectrum of Disease Intestinal Schistosomiasis Urinary Schistosomiasis Paragonimiasis Clonorchiasis
ACUTE SCHISTOSOMIASIS: î Within the lung, the worms exist in a fibrous î Inflammatory response can cause
î Cercarial dermatitis (swimmer’s itch) capsule that communicates with a bronchiole à hyperplasia and fibrosis of the biliary
î Katayama fever: systemic hypersensitivity; serum sickness-like syndrome provokes a granulomatous reaction tract
CHRONIC SCHISTOSOMIASIS î Secondary bacterial infection frequently occurs
î Main symptom: chronic cough with bloody ACUTE DISEASE:
î Pseudopolyps in the colon î Painless hematuria and î Fever, eosinophilia, lymphadenopathy,
î Liver granulomas (due to delayed hypersensitivity) lead to sputum
fibrosis of the bladder tender hepatomegaly
presinusoidal obstruction, hepatomegaly, and portal î CXR: ring shadow opacity
î Hydronephrosis
î Closely resembles tuberculosis CHRONIC DISEASE:
hypertension î Associated with squamous
î Hepatobiliary disease
î gastrointestinal hemorrhage, massive splenomegaly cell carcinoma of the î Pancreatitis
î Liver UTZ: clay pipestem fibrosis with lacelike pattern bladder î Cholangiocarcinoma (Klatskin tumor)
î MCC of death: exsanguination from ruptured esophageal
î Neurocirculatory dystonia
varices
Diagnostic Test Fecalysis (Kato-Katz technique): demonstration of parasite eggs 3% NaOH preparation Direct fecal smear
Circumoval precipitin test (COPT): detects circulating schistosome antigen Potassium permanganate stain
Rectal imprint: biopsy of rectal tissue with the aid of proctoscopy - showing melon-like ridges with
abopercular protuberance
Diagnostic Features of Eggs Large, prominent Operculated / unembryonated egg in Operculated / embryonated egg in
Small lateral spine (‘knob’) Large terminal spine
lateral spine sputum or feces feces
Treatment PRAZIQUANTEL PRAZIQUANTEL PRAZIQUANTEL
Others AREAS OF ENDEMICITY: Sorsogon, Samar, Leyte, Oriental Mindoro, Bohol, ASIAN LIVER FLUKES:
all of Mindanao EXCEPT Misamis Oriental • Clonorchis sinensis
• Opistorchis viverrini (Southeast Asian liver fluke)
The single most important epidemiological factor in schistosomiasis is human waste in water
containing the intermediate host.
TREMATODES/FLUKES OF MINOR IMPORTANCE
Fasciola hepatica Fasciolopsis buski Heterophyes heterophyes
î sheep liver fluke î giant intestinal fluke î intestinal parasite of people living in Africa, the Middle East, and Asia
î Humans are infected by eating watercress (or other aquatic plants) î intestinal parasite of humans and pigs that is endemic to Asia and India. who are infected by eating raw fish containing cysts
î Symptoms are due primarily to the presence of the adult worm in the î Humans are infected by eating aquatic vegetation that carries the î Pathologic findings are due to inflammation of the intestinal
biliary tract. cysts. epithelium as a result of the presence of the adult flukes.
î In early infection, right-upper-quadrant pain, fever, and hepatomegaly î Pathologic findings are due to damage of the intestinal mucosa by î Mimics peptic ulcer disease
can occur, but most infections are asymptomatic. the adult fluke. î Praziquantel is the treatment of choice.
î Months or years later, obstructive jaundice can occur. î Most infections are asymptomatic, but ulceration, abscess
î Halzoun is a painful pharyngitis caused by the presence of adult flukes formation, and hemorrhage can occur.
on the posterior pharyngeal wall. î Gland abscesses
î The drug of choice is triclabendazole. î Worm intoxication: anasarca and coma resulting from
accumulation of toxins
î Praziquantel is the treatment of choice.


Schistosoma

Paragonimus






















Clonorchis

Ascaris

Necator &
Ancylostoma

lemon-shaped or
barrel-shaped eggs
with bipolar plugs /
football-shaped eggs

Trichuris

NEMATODES Necator americanus Strongyloides
Ascaris lumbricoides Trichuris trichiura Enterobius vermicularis Capillaria philippinensis
Ancylostoma duodenale stercoralis
Common Name or Giant Roundworm / Ascariasis Hookworm Whipworm Pinworm / Seatworm / Strongyloidiasis Pudoc Worm / Capillariasis
Disease Miners’ anemia, “tunnel disease”, Wakana disease, Mystery Disease / Wasting Disease
Enterobiasis / Oxyuriasis
“brickmaker’s anemia” “Egyptian chlorosis”
Parasite Biology / î Most common and largest nematode î Soil-transmitted helminth (STH) î Soil-transmitted helminth î Soil-transmitted helminth î Soil-transmitted helminth î intestinal nematode
Characteristics î Soil-transmitted helminth (STH) î Blood-sucking nematodes î Life cycle is confined to humans î Facultative parasites î only nematode whose life cycle
î Differentiated based on character of buccal î MC STH in developed countries î only helminth that causes involves a migratory bird
spears of filariform larvae à a cosmopolitan worm greater pathology in AIDS
patients
Habitat Small intestine Small intestine Large intestine Large intestine Small intestine Small intestine
Transmission Ingestion of embryonated eggs Skin penetration by filariform larva (L3) Ingestion of embryonated eggs Ingestion of embryonated eggs Skin penetration by filariform ingestion of infected fish with
Inhalation of eggs larva (L3) L3 larvae
Infective Stage Embryonated egg L3 / Filariform larva Embryonated egg Embryonated egg L3 / Filariform larva L3 larvae
Diagnostic Stage Fertilized egg Eggs in feces Unembryonated egg Eggs on perianal folds Rhabtidiform (L1) Unembryonated egg
Diagnostic Test Direct fecal smear Direct fecal smear Direct fecal smear Graham’s scotch/cellulose Harada-Mori culture Direct fecal smear
Kato-katz technique Kato-katz technique Kato-katz technique tape test Kato-katz technique
Harada-Mori culture - lemon-shaped or barrel- (distinguished by their - Peanut-shaped eggs with
- D-shaped ovum with thin
shaped eggs with bipolar prominent genital primordium flattened bipolar plugs
colorless cell wall
plugs / football-shaped eggs and a pointed tail)

Pathogenesis î Major damage occurs during larval î The major damage is due to the loss of î Burrow their hairlike anterior î Female releases thousands of î Larvae penetrate intestinal î Embryonated eggs can cause
migration blood at the site of attachment in the ends into the intestinal mucosa fertilized eggs on perianal skin wall directly without leaving autoinfection and
î Principal site of tissue reaction is the small intestine (0.1-0.3 mL/worm/day) î Does NOT cause significant - Eggs develop into larvae, host and migrate to the lungs hyperinfection
lungs, where inflammation with an î Blood is consumed by the worm and oozes anemia causing anal pruritus (autoinfection) î ulcerative and compressive
eosinophilic exudate occurs from the site in response to an î Autoinfection can occur degeneration of enterocytes à
î Heavy worm burden à malnutrition anticoagulant made by the worm. severe malnutrition
Spectrum of LUNG PHASE: CUTANEOUS PHASE: î Diarrhea î Pruritus ani CUTANEOUS PHASE: ACUTE DISEASE:
Disease î L3àL5 î Penetration of L3 to the skin î Rectal prolapse (from î Eosinophilic enterocolitis î Penetration of L3 to the skin î Borborygmi
î Hypersensitivity pneumonitis î Ground itch increased peristalsis to expel the î Vulvovaginitis î Acute: Ground itch î Fever, abdominal pain,
(Loeffler’s Syndrome) î Cutaneous larva migrans (creeping worms) î Salpingitis î Chronic: serpiginous track eosinophilia
INTESTINAL PHASE: eruption) î Appendicitis (oxyuriasis) (larva currens)
î L5 à adult worms LUNG PHASE: LUNG PHASE: CHRONIC DISEASE:
î Acute intestinal obstruction î Lung migration of L3 (no development) î Lung migration of L3 î Chronic watery diarrhea
î Malabsorption syndrome î Simple lung eosinophilia (Loeffler’s î Acute: Loeffler’s syndrome î Edema, wasting

î Nutrient deficiencies syndrome) î Chronic: Paradoxical asthma î Protein-losing enteropathy
WANDERING WORMS: INTESTINAL PHASE: INTESTINAL PHASE: î hypogammaglobulinemia
î Due to erratic behavior of adult worms î L3 à L5 î Mild watery diarrhea
î Hepatobiliary ascariasis î Up to 200mL of blood may be lost per day î burrowing into the mucosa and
î Pancreatitis, appendicitis î Iron-deficiency (microcytic submucosa à ulceration and
hypochromic) anemia à weakness and sloughing à duodenitis
pallor DISSEMINATED
î Protein malnutrition (hypoalbuminemia) STRONGYLOIDIASIS:
î Hyperinfection syndrome
(in immunocompromised)
Treatment Albendazole (has greater larvicidal Albendazole Mebendazole Pyrantel Pamoate Ivermectin Albendazole
activity than mebendazole)


D-shaped ovum

Strongyloides

Enterobius

Wuchereria

Capillaria

 Wuchereria bancrofti
NEMATODES Trichinella spiralis
Brugia malayi
Disease Filariasis Trichinosis
Trichinella
Parasite Biology / î blood and tissue nematode î Tissue nematode
Characteristics î most debilitating nematode infection î Intermediate host: pigs
î Usual scenario: farmer from abaca plantation

Characteristics Wuchereria Brugia

Appearance Smoothly curved Kinky
Terminal nuclei Absent Present
Prevalence Widespread SEA only
Mosquito vector Culex, Aedes, Anopheles Mansonia
Preference Scrotal lymphatics Limb lymphatics
Clinical picture Hydrocele Elephantiasis
Severity More severe Less severe
Transmission Mosquito bite Undercooked pork
Infective Stage Third-stage larva (L3) Encysted larvae
Diagnostic Stage Microfilariae (L1) Encysted larvae
Diagnostic Test î Thick blood smear: curved or kinky microfilariae î Muscle biopsy: most definitive; larvae within
î Specimen collection best done at night between 8PM and striated muscle
4AM à NOCTURNAL PERIODICITY î Elevated CPKs
î DEC Provocation Test î Xenodiagnosis
î Bentonite Flocculation test
Pathogenesis Adult worms in the lymph nodes à inflammation à INTESTINAL STAGE: liberated from pork by gastric juices
lymphatic obstruction à lymphedema MUSCLE STAGE: disseminated hematogenously to
striated skeletal muscle àencysted within a host-
derived cell (nurse cell)
Spectrum of ACUTE DISEASE: MILD DISEASE:
Disease î Acute adenolymphangitis î Fever, muscle pain (myalgia)
î Filarial fever î Periorbital edema
î Nocturnal wheezing (tropical pulmonary eosinophilia) î Eosinophilia
- Small epithelioid granulomas (Meyers-Kouwenaar î Hemorrhagic phenomena (subconjunctival
bodies) splinter)
î Expatriate syndrome

SEVERE DISEASE:
CHRONIC DISEASE: î Myocarditis
î Hydrocele î Encephalitis
î Elephantiasis î Pneumonia
î Milky urine (chyluria) î Respiratory myositis
Treatment Diethylcarbamazine Thiabendazole
Others LOCAL EPIDEMIOLOGY
BANCROFTIAN FILARIASIS MALAYAN FILARIASIS
Sorsogon Albay Eastern Samar
Samar Mindoro Agusan del Sur
Leyte Marinduque Palawan
Palawan Rombon Sulu
Camarines All of Mindanao
 NEMATODES OF MINOR IMPORTANCE

Ancylostoma caninum, Angiostronglyus
Onchocerca volvulus Loa loa Dracunculus medinensis Toxocara canis Anisakis simplex
A. braziliense cantonensis
î Transmitted by female î African eye worm î Guinea fire worm î Dog ascaris î Dog and cat hookworm î Transmitted in î Zoonotic roundworms
blackfly (Simulium) î Transmitted when copepods î Visceral larva migrans
î Transmitted by deer fly or î Creeping eruptions undercooked seafoods î Transmitted in raw
î Clinical findings: mango fly (Chryops) are swallowed in water î Ocular toxocariasis (cutaneous larva î Eosinophilic meningitis seafoods
- Dermal nodules î Clinical findings:
î Loaiasis characterized by - Ocular larva migrans migrans) î Most common cause of î Causes eosinophilic
- Hanging groin deformity - Pruritic painful papule parasitic meningitis
- Subcutaneous edema - Uveitis gastroenteritis
- Lizard skin (calabar swellings) - Live worm in skin ulcer - Endophthalmitis
- River blindness - Worm crawling across

î DOC: Ivermectin the conjunctiva
- Lysis of worms à î DOC: Diethylcarbamazine
Mazzotti hypersensitivity
reaction




PARASITE HINTS ANTIMICROBIALS TO AVOID DURING PREGNANCY





















REFERENCES:
î TOPNOTCH Medical Board Prep Microbiology Handout by Pacifico Eric E. Calderon, MD
î TOPNOTCH Medical Board Prep Microbiology Supplemental Handout by Pacifico Eric E. Calderon, MD
î FIRST AID for the USMLE Step 1 2017
î LANGE Review of Medical Microbiology and Immunology 13th edition
î Clinical Microbiology Made Ridiculously Simple 6th edition
î Board Review Series Microbiology and Immunology 5th edition
î Lippincott’s Illustrated Reviews: Microbiology 3rd edition
î DLSHSI College of Medicine Department of Microbiology and Parasitology Lectures (AY 2013-2014)
î Various internet sources

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