MICROBIAL WORLD VIRUS

Microbe/Microorg (mikros: small; scopein: too see) - only seen w/electron microscope; acellular; adapt to immune response
- bacteria, fungi (yeasts, molds), protozoa, microscopic algae; virus - reproduce only by using other org’s cellular machinery of other organisms (considered as
- marine & freshwater microbes basis of food chain in ocean; soil microbes break down living when they multiply within host cells they infect)
waste & incorporate N from air into org comp; intestine microbes digest & make vit Component: genetic material/core- DNA/RNA; surrounded by capsid
- photosynthesizers, decomposer, recycler capsid- protein coat
- classified acc to evolutionary relationship, scientific name, specific characteristic envelope- lipids; only on some virus
- process where microbes produce acetone/butanol discovered in 1914 by Chaim spikes- glycoproteins; attach to cell; only on virus w/envelopes
Weizmann, In August of WWI, acetone production became important for making
cordite (smokeless form of gunpowder used in munitions) MULTICELLULAR ANIMAL PARASITES
- fermented food; microbe enzyme can be manipulated to cause them to produce - eukaryotes; collectively called helminths (microscopic)
what they don’t normally make (cellulose, digestive aids, drain cleaner, insulin) - require more than 1 host to complete life cycle
Classification: Ectoparasite- on surface of host (mice, lice) Endo- live inside
- minority are Pathogenic (disease-producing)
Kind: platyhelminth- flat worm cestode (tapeworm, 5-20mm) trematode (fluke, 1mm-3 cm)
Microbiology- deals w/small things seen only w/magnification Nematode- round worm (1mm-1m)
- “ “: genetics, physiology, disease/benefits, interaction w/env;
interaction w/mammalian host, uses in industry & agriculture Classification (1978, Carl Woese)
Characteristics: Easy- reproduce rapidly, quickly grow large proportions in lab Bacteria- cell walls w/peptidoglycan Archaea- cell walls lack peptidoglycan
Difficult- can’t be seen directly
Eukarya: Protists (slime molds, protozoa, algae)
Taxonomy Fungi (unicellular yeasts, multicellular molds, mushroom)
- formal system for organizing, classifying, naming living things Plants (moss, ferns, conifers, flowering plants)
3 primary concerns: Classification- orderly arrangement into groups Animals (sponges, worms, insects, vertebrates)
Nomenclature- assign names to taxonomic rankings per species
Brief History of Microbiology (refer to Bio notes)
Identification- discover & record traits for taxonomic scheme
Classifications (refer to BIO notes) Phylogeny- relatedness in groups Debate over Spontaneous Generation
- after van Leeuwenhoek’s discovery, scientific community became interested their origins
Nomenclature
- 150-200 yr gap: many believed that life forms spontaneously arise from nonliving matter
- 1735 by Carolus Linnaeus to avoid chaos in scientific studies & for future identific
- (1168) Francesco Redi showed that maggots didn’t generate spontaneously. He filled 2
- binomial/2 names: genus (genera); specific epithet (species name)
jars w/decaying meat: 1st was unsealed, so flies to laid eggs & formed to larvae.
- scientific names describe organism, honor a researcher, identify habitat of a species.
- Staphylococcus aureus, bacterium on human skin (Staphylo- describes clustered - skeptics claimed that fresh air was needed for spontaneous generation. So Redi set up a
cell arrangement; -coccus- shaped like spheres; specific epithet aureus- Latin, golden) 2nd exp where he covered a jar w/fine net instead of sealing it. No larvae appeared in
gauze, even tho air is present. Many still believed that small org like “animalcules,”
- genus of Escherichia coli is after Theodor Escherich,; specific epithet coli- in colon)
were simple enough to generate from nonliving materials.
Types - (1745) spontaneous generation strengthened when John Needham found even after he
BACTERIA heated chicken & corn broth before pouring into covered flasks, cooled solutions
- simple, unicellular; since their genetic material isn’t enclosed in nuclear membrane, now w/ microorganisms, claiming that microbes developed from fluids
they’re prokaryotes (Greek: prenucleus) - 20 yrs later, Lazzaro Spallanzani: microorg from air entered Needham’s solutions after
- shapes: Bacillus (rodlike), coccus (spherical/ovoid), spirillum (corkscrew, curved); they’re boiled. Nutrient fluids heated after being sealed didn’t grow microbes. Needham
some Starshaped/square responded that “vital force” for spontaneous generation were destroyed by heat.
- individual may form pairs, chains, clusters (formations are characteristic of genus) - Spallanzani was criticized that there wasn’t enough O2 in sealed flasks to support life.
- enclosed in cell walls w/carbo & protein complex peptidoglycan
Theory of Biogenesis
- reproduce by binary fission; for nutrition, most use organic chemicals/ manufacture
own food by photosynthesis; derive nutrition from inorganic substances. - (1858) Rudolf Virchow challenged SG w/biogenesis where cells arise only from
preexisting living cells.
- swim by flagella
- (1861) Louis Pasteur resolved SG; formed basis of aseptic techniques
ARCHAEA (domain; kingdom: Archaebacteria) - He showed that microorgs are present in air & can contaminate sterile solutions, but air
- unicellular prokaryotic; cell walls lack peptidoglycan; live in extreme env itself doesn’t create microbes. He filled flasks w/beef broth & boiled it. Some were left
- don’t cause human disease; cell membrane w/unusual lipid not found in others open & cooled, which were contaminated. The sealed ones were uncontaminated. He
3 groups: methanogens- produce methane as waste from respiration showed that microbes in air were agents for contaminating nonliving matter
halophiles (halo: salt)- live in extremely salty env (Great Salt Lake, Dead Sea) - Pasteur placed broth in open, long-necked flasks bent into S-shaped. The contents were
thermophiles- live in hot sulfurous water (hot springs) boiled & cooled: broth didn’t decay & no life after months. His unique design allowed
FUNGI air to pass into flask, but curved neck trapped airborne microorg.
- uni/multicellular; large multicellular (mushrooms) may look like but can’t - microorg can be present in nonliving matter. Microbial life can be destroyed by heat.
photosynthesize; walls have chitin; external heterotrophs
- unicellular (yeast) are oval & larger than bacteria Golden Age (1857-1914))
- most typical fungi (molds) form visible masses mycelia, w/hyphae (long filaments) - by Pasteur & Robert Koch led to establishment of microbiology.
that branch & intertwine (cottony growth on bread)
Fermentation & Pasteurization (LOUIS PASTUER)
- reproduce sexually/asexually; nourish by absorbing solutions of org material
- slime molds have characteristics of fungi & amebae - relationship of microorg & disease: French merchants asked Pasteur why wine & beer
soured. At the time, many believed that air converted fluid sugars to alcohol.
PROTOZOA/PROTISTS - yeasts convert sugars to alcohol w/o air. Spoilage caused by bacteria (change alcohol into
- means “original”/first”; discovered by Leeuwenhoek; 2-200 micron meters acetic acid w/air)
- unicellular eukaryotic; move by pseudopods (false feet), flagella, cilia
- live as free entities or parasites that absorb org compounds Germ Theory of Disease
- reproduce asexually/sexually; Euglena are photosynthetic - yeasts play in fermentation was 1 st link between microorganism activity & physical &
chem changes in organic materials
3 types: Amoeboid- gliding motion due to pseudopods
- resisted at first bc disease believed to be punishment for one’s crimes or misdeeds.
Ciliates- vibrating motion by cilia through water
Flagellates- propelling motion by flagella - (1865) Pasteur fought silkworm disease. Earlier, Agostino Bassi proved that another
silkworm disease was caused by fungus. Pasteur found that more recent infection
ALGAE was caused by protozoan
- aerobic photoautotrophic eukaryotes; as/sexually; cell walls w/ cellulose - (1860s) Joseph Lister applied germ theory to medical procedures. He’s aware that in
- abundant in fresh & saltwater, soil; associated w/plants; w/mitochon. & chloropl 1840s, Ignaz Semmelweis showed that physicians transmitted infections. He used
- don’t generally require org compounds from env; “pond scum” phenol (carbolic acid) to kill bacteria/treat surgical wound ; heat for sterilization
- (1876) 1st proof that bacteria cause disease is Robert Koch, Pasteur’s rival to discover Prepare Specimens for Light Microscopy
cause of anthrax. He found rod-shaped bacteria Bacillus anthracis in cattle blood that - mount sample on glass slide;
died of anthrax. He found that 2 sets of blood cultures has same bacteria. He - depend on specimen condition (living/preserved), aims of examiner, type of microscopy
established Koch’s postulates (relate specific microbe to specific disease; standard in
identifying pathogen) Fresh, Living- prepare wet mounts for near observation of natural state
- cells suspended in water, broth, saline for temporary maintenance of
Observing Microorg through Microscope viability, space, locomotion
Hans & Zacharias Janssen (1590) (Dutch eyeglass makers) Fixed, Stained Smears- permanent mount for longterm study; by Robert Koch
- 1st compound microscope (2 lenses), tube w/lenses at each end - air-dry & heat fixation (kill specimen & secure to slide; preserve)
- smear dev’t creates contrast & make inconspicuous feature stand out
Robert Hooke (1635-1703) (English chemist, mathematician, physicist)
- compound microscope improvement STAINING- apply colored chemical/dye; impart color to cell by affixing by chem reaction
Antonie van Leeuwenhoek (1632-1723) (wine assayer, cloth merchant, public official) - enhance morphological structure
- simple microscope (1 lens) - basic dye (cationic): bind (-) cells; acidic dye (anionic): bind the background
Proper care Simple Staining
- start w/lowest objective to focus; store w/lowest object locked in place POSITIVE- dye sticks to cells & give it color
- clean oil off of oil objective; use fine adjustment w/100x & oil objective Simple stain: single dye; dye sticks to specimen; w/ready binding of bacteria cell to
malachite green, crystal violet, basic fuchsin, safranin dyes
Magnification & Microscope Design
- appear as same color but still reveal bacterial characteristics
Characteristics: Magnification- make object appear enlarged - methylene blue (stain granules of Corynebacterium)
Resolving Power- show detail
Differential “ - 2 dyes (primary & counterstain); distinguish cell types/parts
SIMPLE- 1st microscope; 1 magnifying lens; no objectives (magnifying glass, hand lens, - additional chem reagents; dye combi: red-purple, red-green, pink-blue
Leewenhoeks tool) - pinpoint size, shape, arrangement
COMPOUND- 2 magnifying lenses: oculars/eyepiece & objectives
- 2nd magnifying lens system: lamp at base to illuminate; condenser to focus NEGATIVE- dries on outer boundary, forming silhouette
- nigrosin (blue-black), India ink (black suspension of carbon particles)
rays of light to single point
- cells don’t stain bc dye is anionic & repelled by anionic cell surface
Principles of Light Microscopy - value: simplicity & reduced shrinkage/distortion of cell as smear isn’t heat fixed
Magnification- 1st lens (close to specimen): objective (real image) - quick asses for size, shape, arrangement; accentuate bacteria/yeast capsule
- 2nd lens (close to eye): ocular/eyepiece (virtual image) Differential Staining
Resolution/Resolving power- distinguish magnified object clearly Gram- by Hans Christian Gram; 130-y/o technique; ready differentiation based on color
Clarity of Image- resolving power (limits clarity) reaction of cell (structural variations of bacteria cell wall);
- reagents: crystal violet (30 sec), grams iodine (60 sec), ethanol, safranin
Variations on Optical Microscope
- base for taxonomy, cell wall structure, identification, drug therapy
Optical Microscope- w/lenses, condensers, light source
Gram-positive- purple stain Gram-negative- red stain
BRIGHTFIELD- specimen absorbs light; the rest to ocular
- specimen’s image darker than illuminated field Acid-fast- differentiate acid-fast bacteria (pink) & nonacid-fast bacteria (blue)
- multipurpose (live, unstained, stained material) - detect mycobacterium tuberculosis from Hansen’s disease (leprosy) &
Nocardia (agent of lung/skin infection)
DARKFIELD- special disc stop to condenser (blocks all light from entering objective
- impervious outer wall that hold fast to dye carbol fuchsin even when washed
except peripheral light from sides of specimen)
w/acid alcohol
- brightly illuminated specimen around dark/black field
- visualize living cells distorted by drying/heat/cant be stained; outline shape; Endospore/Spore- dye forced by heat into resistant survival cell (spore)
rapid recognition of swimming cells - distinguish spores & vegetative cells that make them
- endospore cell wall impermeable to chemicals; bacillus & clostridium
PHASE-CONTRAST- transform subtle change in lightwaves passed through specimen
genera cause anthrax, gangrene, tetanus
into differences in light intensity
- # of internal detail visibility > bright/darkfield; observe intracellular structure Special Staining
DIFFERNTIAL INTERFERENCE CONTRAST Structural Stain- emphasize special cell parts (capsule, endospore, flagella)
- detailed view of unstained, live specimen by manipulating light Capsule staining- observe microbial capsule (unstructured protective layer around
- refinements: 2 prisms (contrast color to image); 2 beams of light cells of bacteria/fungi); cryptococcus (fungal meningitis in AIDS patient)
- extremely defined image vividly colored & appear as 3D Flagellar “ - reveal flagella; determine flagella presence, number, arrangement
FLUORESCENCE- specially modified compound w/UV radiation source & filters - flagella invisible on light microscopy, identifying helps in knowing pathogen.
- name based on use of dyes (Acridine & Fluorescein) & minerals
- specimen coated/placed w/fluorescence cause to emit visible light to produce intense
blue, yellow, orange, red image against black field
- to diagnose caused by bacteria, protozoans, virus MICROBIAL DIVERSITY (ACELLULAR & PROKARYOTIC MICROBES)
- w/staining technique, it detects mycobacterium tuberculosis Microbe: Cellular (bacteria, archaea, algae, protozoa, fungi)
- fluorescent dyes bind to specific antibodies Prokaryote (bacteria, archaea) Eukaryote (algae, protozoa, fungi)
- fluorescent antibodies detect causative agents in syphilis, chlamydiosis, Acellular (virus, viroids, prions)
trichomoniasis, herpes, influenza
- fluorescent nucleic acid stains differentiate live & dead cells/uncultured cells ACELLULAR: VIRUS- Virion (extremely small, use electron microscope)
- locate microbes in complex mixtures since only cells will fluorescence - 10-300 nm diameter; aka oncogenic virus/oncovirus (specific
cancer: lymphoma, carcinoma, leukemia)
CONFOCAL- laser beams of light to scan depths; sharp image focused in single plane
- used on fluorescently stained specimen; visualize live unstained cell/tissue Properties: has DNA/RNA, unlike living cells which has both
Can’t replicate on own, directed by viral nucleic acid once introduced to host
ELECTRON- tiniest details; origin: study metals & small electronic parts
Don’t divide binary fission, mitosis, meiosis
- used in early 1930s; provide resolution; image formed w/beam of electrons
- magnify in stages by: 2 lens systems, condensing lens, specimen holder, Lack genes & enzymes for energy production
focusing apparatus Depend on host’s ribosomes, enzyme, metabolites (building blocks) for
protein & nucleic acid production
Forms: transmission EM- detailed cell/virus structure; transmit electrons in specimen
- item stained w/metals to increase contrast & sectioned into thin slice Origin: 1st Theory- virus existed before cells
- cant view living specimen 2nd “ - cells came first, virus represent ancient derivatives of degenerate cells
scanning EM- most dramatic/realistic image; create detailed 3D of all bio - scientists: virus lack most of basic cell features & not composed of cells, so they’re
- image produced when it bombard surface of whole, metal-coated nonliving entities.  acellular microbes / infectious particles
specimen electrons while scanning back & forth; cant view living specimen
Basic morphology Shingles- painful nerve disease caused by herpes virus
a. COMPLEX: poxvirus (large DNA virus), flexible-tailed bacteriophage - after chickenpox, virus remain latent for years; when immune defense
b. ENVELOPED: weakens, latent chicken pox resurface to cause shingles
w/helical nucleocapsid (mumps virus, rhabdovirus)
- flexi & arranged as looser helix within envelope
- human virus (influenza, measles, rabies)
w/icosahedral “ (herpesvirus, HIV/AIDS)
c. NAKED:
Helical capsid (plum poxvirus)- very rigid & tightly wound into cylinder
- virus infecting plant
Icosahedral capsid (poliovirus, papillomavirus)

basic parts:
Capsid- protein coat/outer shell; most prominent geometric feature
- made w/identical protein subunits capsomeres
- capsomeres: spontaneous self-assemble; results in helical & Icosahedral
Helical: rod-shaped bind together to form discs that link & form continuous helix
into which nucleic acid strand is coiled
Function: introduce DNA/RNA into host cell (bind to cell surface, help to penetrate NA)
Stimulate immune sys to make antibodies to neutralize virus & protect host
cell’s against future infection
Nucleic Acid- DNA/RNA
Envelope- coating made of lipid, protein, carbs
Function: when released from host, virus take w/them its membrane sys Antiviral Agent
w/protein mol spikes/peplomers to attach to host - antibiotic inhibit metabolic act of cellular pathogen, but virus aren’t cells
more supple than capsid, so virus are pleomorphic (envelope assume dff - “ may be prescribed to prevent secondary infection for those w/colds/flu
forms) & shaped spherical to filamentous - interfere w/virus-specific enzymes & virus production by disrupting critical phase in viral
 found only in some virus that infect animal cells cycle/inhibit viral DNA/RNA/protein synthesis
Classification acc to Characteristics ONCOGENIC VIRUS/ONCOVIRUS- cause cancer
a. type of genetic material (DNA/RNA) Epstein-Barr (herpes virus)- cause infectious mononucleosis (not cancer) but cause 3
b. capsid shape c. capsomere # d. capsid size cancers: nasopharyngeal carcinoma, Burkitt lymphoma, B-cell
e. envelope presence/absence f. type of host g. disease type it produces lymphoma, Kaposi sarcoma (common in AIDS patient)
h. target cell i. immunologic/antigenic properties Human papillomavirus (wart virus)- cause cervix/genital tract cancer
4 Categories acc to type of genome Retrovirus- closely related to HIV; cause AIDS human T-lymphotropic virus type 1 (HTLV-
a. Genome- DNA (double-stranded), RNA (single-stranded) 1), cause rare type of adult T-cell leukemia
b. Capsid- shapes & symmetry VIROIDS
c. Envelope derived from host’s nuclear membrane/cell membrane
- smaller & less complex infectious agents
d. Viral Disease
- short, naked fragment of RNA (300-400 nucleotides length) which interfere w/plant cell
metabolism & stunt their growth, killing it
BACTERIOPHAGE/PHAGE
- potato spindle tuber (produce small, cracked, spindle-shaped potato); citrus exocortis
- virus infecting bacteria; enter bacterial cell to replicate
(stunt citrus tree); chrysanthemum, coconut palm, tomato disease
Acc to shape: Icosahedron- spherical w/20 triangular phages (smallest: 25 nm diam)
Filamentous- long tubes formed by capsid proteins assembled to helix PRIONS
(900 nm long) - smaller infectious protein causing neurological disease (Scrapie in sheep/goat)
Complex- icosahedral heads attached to helical tails; may have base - Bovine spongiform encephalopathy (BSE) “mad cow disease”
plate & tail fibers - Kuru- ate human brains as part of ritualistic cannibalism
- Kuru, Creutzfeldt-Jakob disease (C-J) & Gertsmann-Straussler-Scheinker disease (GSS)
Acc to nucleic acid: single/double-stranded DNA phage are fatal spongiform encephalopathies where brain is riddled w/holes/spongelike
Single/doubled-stranded RNA phage
- Gertsmann-Straussler-Scheinker disease (GSS) involve loss of coordination & dementia
Acc to events after invasion:
Virulent- cause lytic cycle (ends w/lysis destruction of bacterial cell)
- attachment to lysis takes 1 hr
Temperate/Lysogenic- inject nucleic acid into cell
- don’t immediately initiate lytic cycle but their DNA remains
integrated into bacteria chromosome in generations
ANIMAL VIRUS
- infect humans & animal; DNA/RNA virus
- made of solely nucleic acid surrounded by capsid/complex
Latent Virus Infection- limited by body’s phagocytes & antiviral proteins (interferons)
produced by virus-infected cells
Herpes- (cold sores/fever blister) fever, stress, sunlight trigger viral genes to take
over cells & produce more virus; cells are destroyed
PROKARYOTIC Basic type:
BACTERIA- rod-shape; w/peptidoglycan (polysaccharide & peptide chains) in cell walls CELL WALL STRUCTURE- shape; structural support (osmotic pressure)
Appendage (sprout from surface): Motility- flagella & axial filaments - gains strength & stability from unique macromol peptidoglycan made of
Attachment/Channel- fimbriae & pili repeating fragments of long glycan cross-linked by short peptides
FLAGELLA- “organelles of locomotion”; long, thin; flagellate (flagellated protozoa) a. Gram + Wall- thick, homogenous peptidoglycan (20-80 nm thickness)
- self-propulsion; swim freely; outside cell wall / different arrangement - w/acidic polysaccharides
- attached to protein hook, anchored to wall & membrane by basal body Teichoic acid- ribitol/glycerol & phosphate polymer embedded in PG sheath
Parts: filament- helical w/flagellin protein; inserted into curved, tubular hook Lipoteichoic acid- attached to lipids in plasma membrane
Hook- anchored to cell by basal body b. Gram – Wall- more complex due to outer membrane (OM) & thinner peptidoglycan
Basal body- stack of rings (2-4) firmly anchored into cell wall to cell membrane OM: Lipopolysaccharide- lipid bound to polysaccharide; project from lipid surface
- poly form somatic antigen in gram – pathogens for identification
Lipoprotein- lipid forms matrix of OM top layer
- lipid become toxic when released during infection
Protein-protein inserted in OM upper layer; selective permeability
gram + & gram – (gram staining)

acc to # & arrangement:

Polar Arrangement- flagella attached to 1 or both ends of cell
Monotrichous (1 flagellum) Lophotrichous (small tufts of flagella from same site)
Amphitrichous- flagella at both poles of cell
Peritrichous- flagella dispersed randomly over cell surface
Presence of Motility- used in lab for bacteria identification
Special Stains/Electron M Preparation- see flagella arranegement
Flagellar Response- to chemical signals (chemotaxis)
Positive- movement in direction of favorable chem stimulus
Negative- “ away from repellent/harmful compound
 flagella guides in direction due to detecting chemicals where receptor clusters at cell
membrane bind specific mol (transmit signals to flag & sets rotary motion)
Run- counterCW, smooth linear direction to stimulus & interrupted by tumbles
Tumbles- due to flagellum reversing direction

CELL MEMBRANE STRUCTURE- beneath cell wall

Fluid Mosaic Model- by S.J Singer & GL Nicolson
- membrane as continuous bilayer formed by lipids w/polar heads outside
& nonpolar heads at center
- embedded globular protein; dynamic due to lipid & protein
- fluidity as engulfment/discharge/secretion by cells
- selective permeability; capacity to regulate transport mol
Fx: site for energy reaction, nutrition processing, synthesis
Regulate transport (nutrient passage into cell & waste discharge)
CILIA- organelle of locomotion; shorter/hairlike, thinner, more numerous than flag Selective permeability (mol passage)
- ciliates (ciliated protozoa); beat w/coordinated, rhythmic movement Secretion (metabolic product release to extracellular env)
Bacteria Shape, Arrangement,
Fimbriae & Pili- interaction w/cells but not for locomotion, except for specialized pili Size
FIMBRIAE- small, bristlelike fibers from surface of bacterial cell
PILUS/SEX PILUS- elongate, rigid tubular structure made of special protein pilin
- linked to mating between conjugation (DNA transfer; genetically produced,
happen only in compatible gram-negative cells)
- pilus from donor cell unites w/recipient cell, providing connection for
making transfer

Cell Envelope- boundary layer; chemically complex external covering of most bacteria
lying outside cytoplasm
Main layers: cell wall- stacked together, tightly bound into unit
Cell membrane- maintain cell integrity (quality of complete membrane in
perfect condition)
 MICROBIAL GROWTH
2 Categories:
a. PHYSICAL
Temperature- psychrophile (cold-loving); mesophile (moderate-temp)
thermophile (heat-loving); hyperthermophile/extreme thermophile
bacterial growth: minimum growth temp -lowest
optimum “ “ - best temp
maximum “ “ - highest temp possible
pH- acidity/alkalinity; bacteria best grow: 6.5-7.5; acidophile (acid-tolerant)
Osmotic Pressure- isotonic, hypotonic, hypertonic
- plasmolysis (osmotic water loss causing cytoplasm)
b. CHEMICAL
Carbon- backbone of life; needed for organic comp
Nitrogen, Sulfur, Phosphorus- synthesize cell material; protein synthesis (N, S)
- DNA/RNA synthesis (N, some S)
Trace Elements- Fe, Cu, Mo, Zn; for cofactor function
Oxygen- aerobe (use molecular O2); anaerobe (don’t use O2)
- obligate aerobe (require O2 to live; cant use molecular O2 for reactions)
Prokaryotic Groups w/Unusual Characteristic - facultative anaerobe (can grow even w/o O2)
PHOTOSYNTHETIC BACTERIA- independent w/light-trapping pigments - microaerophile (aerobic; grow only in O2 conc lower than those in air)
- use sunlight energy to make nutrient from simple inorganic comp Organic Growth Factor- some bacteria lack enzymes for vitamin synthesis
Types: produce O2 during photosynthesis - amino acids, purines, pyrimidines
“ substances like sulfur granules/sulfate
BIOFILM- thin, slimy layer encasing bacteria to adhere; live in communities
CYANOBACTERIA- blue-green Function: cell-to-cell commu (quorum sensing)- to coordinate together for benefits
- 1-10 μm; colonial/filamentous groupings; oldest type on earth Characteristic: share nutrients & sheltered from harmful factors in env
- freshwater & seawater (algal bloom); some are pollution-resistant Facilitate transfer of genetic info (conjugation)
- biological indicators of polluted water; thylakoid have chlorophyll (adaptation)
Features: gas inclusion- float on water surface & increase light exposure CULTURE MEDIA- inoculum (microbe introduced into culture media to initiate growth)
Cysts- convert nitrogen gas into form usable by plants - culture (microbes that grow & multiply in culture media)
Phycocyanin- blue-green pigment - agar media (solidifying agent from marine alga used for growth)
(in test tubes (slant/deep)/petri dish (petri plates when filled)
GREEN & PURPLE SULFUR BACTERIA
CHEMICALLY-DEFINED MEDIA- whose exact chemical compound is known
- photosynthetic; bacteriochlorophyll; doesn’t give O2 as product of photosynthesis
- sulfur springs, freshwater lake, swamps COMPLEX MEDIA- w/nutrients from yeast, meat, plants, protein digests
- liquid (nutrient broth); w/agar (nutrient agar)
GLIDING, FRUITING BACTERIA Functional types
- mixed collection of gram – bacteria in water & soil; glides over moist surface
Selective & Differential- cleverest & most inventive; for special microbes
- gliding property (filament rotation under outer membrane of cell wall); no flagella
- slime bacteria (myxobacteria); fruiting body (survival structure) - w/extensive applications in isolation & identification
- permit preliminary identification of genus/species
Unusual forms of Medically Significant Bacteria Selective- 1/more agents inhibiting growth of other microbes
RICKETTSIAS - for primary isolation of specific microbe
- distinctive, tiny, gram - ; can’t survive/multiply outside host cell - hasten isolation by suppressing unwanted background microbe
- can’t carry out metabolism completely on own so they’re closely attached to host - mannitol salt agar (MSA) (w/7.5% NaCl as inhibitory)
- Rocky Mountain spotted fever (Rickettsia rickettsia, ticks) - MacConkey Ag ar & Hektoen enteric agar (HE) (w/bile salts as selective/inhibitory
- Endemic Typhus (Rickettsia typhi, lice) Differential- show visible differences: chemicals in media & ways microbe react to them
- dyes: for differential agents bc its pH indicators coloring due to acid/base
CHLAMYDIA
- Chlamydia & Chlamydophila; require host cell for growth & metabolism Enriched- w/blood, serum, hemoglobin, growth factors
- Chlamydia trachomatis (cause eye infection leading to blindness & most common STD) Growth Factor- vitamins & AA microbes can’t synthesize
- Chlamydia pneumoniae (agent in lung infection) - “fastidious” for bacteria need GF & complex nutrient
Blood Agar- made by adding sterile animal blood (sheep) to sterile agar base
ARCHAEA- single-celled; archaea/archaeons; domain: Archaea; genetic seq in RNA Enrichment Culture- used when few bacteria can be missed; if others are in large #
- extremophile: metabolically show adaptation deadly to other org
- multiple adaptation combo: temp, salt, acid, pH, pressure, atmosphere Obtaining Pure Cultures
- methane producers, hyperthermophiles, extreme halophile, sulfur reducers Pure Culture/Axenic- for single species/colony; for lab study: precise exam & control
- can have 2nd level culture subculture (from well-isolated transferred
ARCHAEBACTERIA
into separate media & incubated)
Methanogen- convert CO2 & H2 to methane gas; anaerobic mud & bottom sediment
of lake isolating pure cultures:
- gas made as fuel; greenhouse effect (maintain earth temp, global warming)
- found in oral cavity, human large intestine
Extreme Halophile- need salt to grow; high salt tolerance (multiply in NaCl solu)
- halobacteria: use red pigment to synthesize ATP using light)
Hyperthermophile- flourish at 80-121 C; can’t grow at 50 C
- volcanic water, soil, submarine vent; acid & salt tolerant
- hyperthermophilic (archaea at high temps)
a. Streak Plate Method FILTRATION- liquid/gas pass in screen to retain microbes; for vaccine, antibiotic
- isolate single bact type; small droplet sample (parent) spread over medium’s surface - high-efficiency particulate air (HEPA) remove 0.3 μm diameter
- pattern thins out sample & separate cells; after incubation; 4th quadrant has dots LOW TEMP- depend on microbe & intensity of application
- small dots are indiv colonies w/millions bact High Pressure- alter protein & carb, causing rapid inactivation of vegetative bact cell
Bacterial Division (Binary Fission) Desiccation-can’t grow but still viable; lyophilization/freeze-dry preserve microbes
OSMOTIC PRESSURE- use salt (cure meat), sugar (preserve fruit)
RADIATION- depend on wavelength, intensity, duration
Ionizing- gamma, X-ray, electron beam; wavelength shorter than 1 nm
Nonionizing- WV 1 nm longer; UV

Control of Microbial Growth

Sterilization- destroy all living microbes; sterilant (agent)
Heating- most common; for most resistant endospores
Filtration- sterilizing liquids/gas
Disinfection- destroy non-vegetative (≠ sterility) ; use chemicals, UV, H2O, steam
Biocide/Germicide- microbes (except endospore)
Fungicide- kills fungi Virucide- inactivate virus Chemical
 -cide (“kill”); -stat/-statis (“stop/steady”) (inhibit growth/multiplication)
DISINFECTION (to evaluate its effectiveness:)
Use-dilution test- metal/glass cylinder dipped in standardized culture in liquid
Physical Methods media, removed, dried 37 oC, which are placed into disinfectant for
HEAT- sterilize media & glassware; kill microbes by denaturing enzymes 10 min 20 oC
Concepts: thermal death point (TDP)- lowest temp where microbes in liquid - transferred to medium; disinfectant effectiveness acc to # cultures
suspension is killed in 10 min Disk-diffusion method- evaluate chem agent efficacy
Thermal death time (TDT)- min temp for it to die in liquid culture - use disk of filter paper (soaked w/chemical & placed inoculated &
Decimal reduction time (DRT/D value)- bacterial heat resistance incubated agar plate w/test organism)
Moist Heat- coagulate proteins/denaturation - after incubation, chem is effective; clear zone (inhibit growth around)
Boiling- kill vegetative bact, almost all virus, fungi, spores in 10 min Disinfectants:
Autoclaving- pressured steam in healthcare env Phenol & Phenolics
Pasteurization- mild heat; pasteurized milk (remove microbes & lower # ) Phenol- control sewage odor; antiseptic but w/undesirable odor
- high temp short-time (HTST)- 72oC 15 sec (lower bacteria count) - throat lozenge bc local anesthetic effect but w/little antimicrobial eff at low conc
Sterilization- ultra high temp (UHT) 140 oC 4 sec to store for months w/o ref Phenolics- phenol derived; ↓ irritating quality/↑ antibacterial act w/soap/detergent
- exert antimicrobial act by injuring lipid plasma membrane, leaking cell contents
Dry Heat Sterilize: Flaming- inoculating loop
Incineration- sterilize & dispose contaminated bag/dressings Biphenol- phenol derive; hexachlorophene (lotion); pHisoHex (surgical microbial control)
Hot-air- oven; 170 oC 2 hrs - triclosan (antibacterial soap & toothpaste)
Biguanide- affect bacterial cell membrane MORBIDTY
- chlorhexidine (control for skin & mucous membrane; for surgical hand scrubs
MORBIDITY MORTALITY
& patient preop skin preparation when paired w/alcohol/detergent - someone being unhealthy - someone being dead
Halogen- iodine+chlorine (antimicrobial agent) iodine (oldest/most effective antiseptic - morbidity rate (examine how many got - mortality rate (# death in a year per 1000
- chlorine (disinfectant; germicidal bc of hypochlorous acid that forms when disease in specific population, at specific people. Paired w/birth rate)
chlorine is added to water geographical during specific time - incidence of deaths in population
- proportion of illness in population
Alcohol- bacteria & fungi but not endospore & nonenveloped virus
- bad antiseptic in wounds (coagulate protein where bacteria grow)
Ethanol- optimum conc is 70%
Isopropanol- slightly superior to ethanol as antiseptic & disinfectant
EXAMPLES EXAMPLES
- system provides direct community influenza - infant mortality are high & upper class not
morbidity data otherwise unavailable exempted
- morbidity for hospitalized w/measles is - poor hygiene led to high mortality in children
reduced - mortality from lung cancer is increasing
- result shows that incidence of myopia - mortality in immigrants higher than avg
morbidity is 44.84% - city’s most shocking statistic is its high infant
- falls are linked to increased morbidity & mortality rate
higher healthcare cost

PREVALENCE/POINT PREVALENCE
- total # of disease cases in population in a time; proportion of total # of persons in popu
- all current cases (old & new); counts existing diagnosis
2 types: Point Prevalence- popu proportion diseased in single time point; single snapshot
In a population at 1 point in time: # cases / # persons
Period ‘ - “ “ diseased in specific time period
INCIDENCE- counts new disease diagnosis in defined time period
 both are fundamental distinction in epidemiology
OUTBREAK- sudden ↑ in disease occurrence; constitutes 4 linked case of rare infectious d
- waterborne/foodborne
Spread of Disease
SPORADIC- occur in popu of geographic area
ENDEMIC-constant presence; # cases fluctuate over time, but disease never dies completely
- steady frequency in long time
EPIDEMIC- occur in greater than usual # cases rapidly in region in short time
PANDEMIC- epidemic across continents/worldwide

EPIDEMIOLOGY & PUBLIC HEALTH

Epidemiology- study of factors determining frequency, distribution, determinants of
disease in human population; how to prevent, control, eradicate these
COMMUNICABLE DISEASE- infectious disease is transmissible person to person
CONTAGIOUS “ - communicable disease easily transmitted in persons EPIDEMIC PANDEMIC
ZOONOTIC ‘ / ZOONOSIS- infectious d humans acquire from animal sources - grew out of control
- global; disease widely spread geographically
- (medicine) illness actively spreading
Incidence- # new cases of specific illness diagnosed/reported in a time EXAMPLES
Incidence Rate- incidence & divided by #`people at risk for disease EXAMPLES - AIDS will surpass Black Death as worst
Formula: during a given time period - flu in Moscow - all countries must activate preparedness
- yellow fever as providential act to discourage - malaria is still pandemic in some countries
INCIDENCE = ------------------------------------------ x 1000
urban growth - HIV: worst, since 1982
Population at risk during period - CHOLERA: 1816-1824 in Asia & Europe
- flu caused huge strain in health service

Pandemic Diseases
HIV & AIDS
HIV- damage immune system by killing CD4 cells
AIDS- last stage of HIV; HIV # ↑ as CD4 ↓; w/o medicine, HIV advance to AIDS in 10-12 yrs
CD4 Cells-immune system; its loss makes it hard to fight infection
Modes of HIV Transmission Strategies to Break Chain of Infection
a. BROAD: eliminate/contain reservoirs; curtail pathogen persistence at source
prevent contact w/infectious substance from exit pathways
eliminate means of transmission
block exposure to entry pathways
reduce/eliminate host susceptibility
b. SPECIFIC: effective hand hygiene; good nutrition, sleep, reduce stress
immunization from common pathogens; insect & rodent control
patient isolation; decontamination of surface & medical instrument
use gloves, gown, mask, respirators; needle safety device in blood collection

RESERVOIRS OF INFECTION
- source; site where pathogen multiply/merely survive until transferred to host
- living/inanimate objects/hosts
TUBERCULOSIS Living:
- caused by Myobacterium tuberculosis; 2nd leading killer of adults & w/HIV a. Human- colonized by pathogen that doesn’t currently cause disease in host
- if untreated, person infect 10-15 people a year Passive- carry pathogen w/o having disease
MALARIA Incubatory- can transmit during incubation of infectious disease
- most important tropical parasitic disease; kill more than others except TB Convalescent- harbor & transmit while recovering from disease
Active- completely recovered but continue to harbor pathogen indefinitely
Interactions in Pathogens, Hosts, Env b. Animals-zoonotic disease: humans acquire from animals
1. Factors pertaining to PATHOGEN c. Arthropods- insects/arachnids; vectors
a. Virulence- ability to cause damage to host
b. Portal of Entry c. # Organisms entering body Nonliving
2. Factors pertaining to HOST a. Air- contaminated by dust/respiratory secretions by humans (breath, talk, sneeze, cough)
a. Health status c. Host susceptibility (lifestyle, work, travel, hygiene) b. Soil- spores of Clostridium causing tetanus, botulism, gas gangrene by open wound
b. Nutritional Status c. Dust- bacteria spores & dried human/animal excretions
d. Food & Milk- by careless handling
3. Factors pertaining to ENVIRONMENT
e. Water
1. Physical (geographic location, climate, humidity, season, heat, cold)
f. Fomites- can transmit pathogen; healthcare settings (bedding, gown, utensils, towel)
 availability of reservoirs & vectors
- hospital equipment (bedpan, stetho, latex gloves, thermo, electrocardiographic
 sanitary & housing condition; waste disposal; healthcare
electrodes)
 availability of potable water
Modes of Transmission
Breaking Chain of Infection
1. CONTACT (direct/indirect) 4. VEHICULAR (food, water, dust, fomites)
2. DROPLET (cough, sneeze, talk) 5. VECTOR (bites from insect/arachnids)
3. AIRBORNE
‘
Public Health Agencies
WHO- by UN started in 1948; promote technical cooperation for health on nations, carry
out programs to control/eradicate disease, & improve human life quality
CENTRES FOR DISEASE CONTROL & PREVENTION (CDC)
- assist state & local health dept in applying epidemiology
- microbiologist: most dangerous pathogens known to science due to facilities
Travel during epidemic to investigate & control it
Bioterrorism & Biological Warfare
Biological Warfare use microorg BW Agents- microbes involved
Bioterrorism Agent- people as biological terrorist & pa thogen they use
BW & BT Agents;
1. Bacillus anthracis (anthrax)
1. - fatal intoxication by botulinal toxin produced by C. botulinum (gram +, which enter by
spores in open wounds), which is added to water/food, odorless/tasteless, tiny # is
ingested to cause fatal case
- nerve damage, visual difficulty, respiratory failure (usual cause of death), flaccid paralysis
of voluntary muscle, coma, death in a week if untreated
2. Smallpox virus (Variola)- serious, contagious, fatal
3. Yersinia pestis (Plague)- gram – coccabacillus; predominantly a zoonosis ADHERANCE
- by flea bite Adhesins (ligand)- pathogen surface projection adhering to complementary host receptors;
Bubonic Plague/Black Death- killed 1/3 Europe; hit city dwellers due to glycoprotein/lipoprotein; associated w/fimbriae
overcrowding & lack of sanitation Mannose- most common receptor
4. Clostridium botulinum (botulism) Biofilm- attachment & resistance to antimicrobial agent; resist disinfectant & antibiotic

MICROBIAL MECHANISMS OF PATHOGENECITY

Pathogenicity- ability to produce disease by overcoming host defenses
Virulence- degree of pathogenicity
How Microorg Ener Host- specific route where pathogen gains access to body
PORTAL OF ENTRY
- microorg penetrate mucous membrane of conjunctiva & respiratory, gastrointestinal,
genitourinary tracts
Respiratory Tract-easiest & most frequently traveled; microbes inhaled in nose/mouth
in drops of moisture/dust
- common cold, pneumonia, TB, flu, measles
Gastrointestinal- microbes destroyed by stomach hydrochloric acid & enzymes/small How Bacterial Pathogens Penetrate Host Defense
intestine bile & enzymes; those survived cause disease CAPSULE- increase virulence; streptococcus pneumoniae (pneumococcal pneumonia)
- these are eliminated w/feces & transmitted by contaminated water, - we make antibodies against capsule which destroy them by phagocytosis
food, finger - nonpathogenic bacteria produce capsule; virulence of some isn’t related to capsule
Genitourinary- sexually contracted; microbes cause STI & penetrate unbroken mucous CELL WALL
membrane, some need cut/abrasion - streptococcus pyogenes make heat- & acid-resistant M protein (mediates attachment
- HIV, genital wart, chlamydia, herpes, syphilis, gonorrhea of bacteria to host epithelial cells & help bacteria resist phagocytosis by WBC)
Others: most can’t penetrate intact skin, they enter hair follicles & sweat duct - Neisseria gonorrhoeae grow in human epithelial cells & leukocytes; use fimbriae &
Some enter tissues by inoculation through skin & mucous membrane in bites, outer membrane protein Opa to attach to host cell
injection, wounds (parenteral route: route of penetration) - Myobacterium tuberculosis use its waxy lipid (mycolic acid) cell wall & increase
virulence by resisting phagocyte digestion
ENZYMES
Coagulase- bacterial enzyme that make fibrin clot to protect local infections]
- coagulate fibrinogen in blood
Fibrinogen- plasma protein made by liver; converted by coagulase into fibrin
(threads forming blood clot) which protect bacterium from
phagocytosis & isolate it from host defenses
Bacteria spread from local infection by:
Kinase- destroy blood cell
Fibrinolysin/Streptokinase- by Streptococcus pyogenes
Staphylokinase- by Staphylococcus aureus
Hyaluronidase- destroy mucopolysaccharide holding cells together; by streptococci
Collagenase- hydrolyze connective tissue collagen; by Clostridium
IgA protease- destroy IgA antibodies; by N. gonorrhoeae, N. meningitidis
(meningococcal meningitis), & others that infect CNS
ANTIGENIC VARIATION
Adaptive Immunity- specific defensive response of body to infection/antigen
- body make antibodies as response to antigens to inactivate/destroy them
Antigenic Variation- where pathogens alter their surface antigens before body responds,
making it unaffected by antibodies
CYTOSKELETON
Actin- major component; some use to penetrate host cells/move between host cells
- salmonella strains & E.coli make contact w/host cell plasma membrane
- used by Shigella & Listeria species to propel through host cytoplasm in host cells
Invasins- surface proteins by microbe that rearrange near actin filaments
Membrane Ruffling- result of disruption in host cytoskeleton
Preferred Portal of Entry
- most cause infection only when entering specific POE Cadherin- glycoprotein used by bacteria to move between cells
Salmonella typhi (Typhoid Fever)- swallowing (preferred), rubbed on skin (no reaction, How Bacterial Pathogens Damage Host Cells
slight inflammation) SIDEROPHORES- small org secreted by bacteria & fungi released to medium where they
Streptococci (Pneumonia)- inhalation (preferred); swallowing don’t cause symptoms take Fe away
Yersinia pestis (Plague) & Bacillus anthracis (Anthrax)- > 1 portal of entry - once Fe siderophore complex is formed, it’s taken by siderophore
receptors on bacteria surface
Numbers of Invading Microbes - free Fe conc in human body is fairly low
- Virulence expressed as: LD50 (lethal dose for 50% of inoculated host)
DIRECT DAMAGE- pathogens metabolize & multiply in cells which usually rupture
ID50 (infectious dose for 50% “ ‘ )
- pathogen that rupture cells spread to other tissues in greater numbers
- if few microbes enter body, they’ overcome host defenses. If many, it cause disease. - most damage by bacteria is done by toxins
- ↑ likelihood of disease = ↑ number of pathogens
TOXINS- poisonous produced by microbes; toxigenicity (capacity to produce toxins)
- toxemia (toxin in blood); intoxication (due to toxin, not microbial growth)
Effects: damage enzyme & ↓ body prevention of free radical damage that speeds aging
Inhibit protein synthesis, destroy blood cell & vessel
 Promote disease by directly damage host tissue & disable immune system
Types (based on position relative to microbe cell) PORTAL OF EXIT
Exotoxins- made in bacteria as part of growth & metabolism - secretion, excretion, discharge, shed tissue; relate to infected part
- protein & enzyme catalyzing certain biochemical reactions - let pathogen spread in popu by moving between susceptible hosts
- Antitoxin- antibodies made by body for immunity to exotoxin Respiratory Tract- droplet formed from mucous discharged from mouth & nose
- destroy cell/dirupt normal cell metabolism; highly potent & cause major damage - cause TB, whooping cough, pneumonia, measles, scarlet fever,
A-B Toxin- 1st to be studied; polypeptides & have most exotoxins chickenpox, meningococcal meningitis, mumps smallpox, flu
- enter host cell by endocytosis & harm by ADP-ribosylation of host cell protein Gastrointestinal- in feces contaminated w/pathogen associated w/salmonellosis,
Membrane-Disrupting- cause lysis to host cell by disrupting plasma membrane cholera, typhoid fever, shigellosis, amebic dysentery, poliomyelitis
- contribute virulence by killing host cell - in saliva w/pathogen causing rabies, mumps, infectious mononucleosis
- form pores/disrupt phospholipid layer in cell membranes
Genitourinary- microbes for STI in secretions from penis & vagina
Superantigen-bacteria proteins; cause high severe immune reaction
- urine have pathogen causing typhoid fever & brucellosis
- nonspecifically promote proliferation of T-cells by interactions w/immune
Others: yaws, impetigo, ringworm, herpes simplex, warts from skin
sys cells
Infected blood removed & reinjected by biting insect (yellow fever, plague,
Genotoxin- gram – (Haemophilus ducreyi & Helicobacter spp) that damage DNA
tularemia, malaria) & contaminated needle & syringe (AIDS, hepatitis B)
Endotoxin- within bacteria cell; released in bacterial multiplication & when gram – die
& cell wall undergo lysis SUMMARY
PLASMID- small, circular DNA not connected to main bacteria chromosome & can a. How Microbes enter Host
independent replication; carry info determining pathogenicity
R (resistance) factor- plasmid group for resistance to antibiotics
LYSOGENY- bacteriophage remain latent & don’t lysis of bacteria
- lysogenic (cell w/prophage) are medically important bc bacterial
pathogenesis is caused by prophages
- Lysogenic conversion (change microbe traits bc of prophage), where
bacteria cell is immune to infection by same phage
b. How Bacterial Pathogen penetrate Host defenses
Pathogenic Properties of Virus
a. Viral Mechanisms for Evading Host Defense
- virus penetrate & grow in host cell where immune system cant reach
- some enter host cell bc attachment site mimic substance useful to cells -
b. Cytopathic/Cytopathogenic Effects (CPE) of Virus
- structural change in host cell bc of viral invasion
- virus cause host lysis/when cell dies w/o lysis due to inability to reproduce
- Inclusion Body, Cytoplasmic Mass
- virus produce cytopathic effects:
c. How Bacterial Pathogen Damage Host Cell
 macromolecular synthesis; host cell lysosome; inclusion body; adjacent infected cell
 viral infection result in antigenic change; chromosomal change in host cell
 Cause cancer transform host cell; virus-infected host make alpha & beta interferons

Pathogenic Property of Fungi, Protozoa, Helminths, Algae

FUNGI- heterotrophs; ecosystem’s nutrient cyclin
- spore-bearing; reproduce a/sexual; uni/multicellular by dev’t of long-branch filament
- acquire nutrient by absorption but lack chlorophyll; mycoses (disease by fungi)
Effects: poisoning, parasitic infection, allergic reaction, asthmatic disease
Eye infection resulting in blindness
PROTOZOA- informal term for single-celled, free/parasitic eukaryotes feeding on
organic matter (tissue/debris)
- called flagellates; locomotory organelle are flagella in adults; body covered by pellicle
- binary fission is longitudinal; autotrophic/autotrophic d. Pathogenic Properties of Virus
Effect: malaria; trypanosoma protozoa (genus Trypanosoma) cause sleeping sickness
Giardia cause giardiasis; enter body by food/water contaminated by feces
HELMINTH- class separated by external form & host organ; hermaphrodite & bisexual
- final classific based on ext/internal morphology embryo, larval, adult stage
- (> 1mm/>1 m); well-developed organ system & most are active feeders
- body flattened & covered w/plasma membrane (flatworm)
- body cylindrical & covered w/cuticle (roundworm)
- some are hermaphrodites, others have separate sexes
Effect; simplest is by accidental ingestion of eggs (Ascaris, Echinococcus, Enterobius,
Trichuris) or larvae (hookworm)
Other w/larvae actively penetrate skin (hookworm, schistosome, strongyloides) e. Pathogenic Properties of Fungi, Protozoa, Helminths, Algae
Extensive migration in tissue, damage directly & initiate hypersensitivity reaction
that infect Skin, lungs, liver, intestine
ALGAE- photosynthesis; seaweed (kelp/phytoplankton), pond dung, algae blooms
- uni/multicellular; lack well-defined body (absent roots, stems, leaves)
- asexual (spore)/sexual; free-living, some form symbiotic relationship w/others
Effects: dangerous toxins; blue-green algal toxin in drinking water cause tumor f. Portal of Exit
- algae-affected water unsuitable for drinking, recreation, agricultural use. Contact cause
skin irritation, mild respiratory effect, hay-fever symptoms
- ingest toxins cause gastroenteritis symptom (vomiting, diarrhea, fever, headache)
 Parasitic Life Cycles
- 3 common components: mode of transmission
infective stage (morphologic form that invades human
diagnostic “ (1/more forms detected in lab retrieval method)
- can have definitive host/1 or more intermediate host
2 phases
a. Route when in/on body- understands parasite symptomatology & pathology
- insight on best diagnosis method & selection of appropriate
antiparasitic med
b. Route followed independently of body
- provide crucial info pertinent to epidemiology, prevention, control

Generic Parasite Life Cycle

INTRODUCTION TO PARASITOLOGY
Parasites- live & obtain nutrient from other organisms
Parasitology- epidemiology, parasite-host relatioship, parasitic life cycle, disease
process & symptoms, treatment, prevention/control
Historical Perspectiive
- documentation of its existence by ancient Persians, Egyptians, Greeks (prehistoric)
- human progressed through years in age of civiliztion, as well as parasites
- knowledge on: parasite are problem & realization that the’re responsible for Diseases Processes & Symptoms
infection (invasion IN body); infestation (invasion ON body)
- entire body/parts may affect by the parasite disease
Disease (process w/haracteristic symptom, emerged, determine - major body areas: 1. Gastrointestinal (GI) & Urogenital (UG) Tracts
effective means of healing infected person is a priority) 2. blood & tissue 3. Liver, lung, major organs
- as parasitic life cycle is discovered, vectors are responsible for transmission, parasite 5. miscellaneous locations (CSF, eye, skin, extremities)
control & elimination were priorities
Elephantiasis- enlarged breast, leg, scrotum bc of parasite
- medical & biologic science expanded our knowledge on makeup & host relationship
- anemia, vit deficiency, bowel obstruction, edema, skin lesion, blindness
- today:practitioners have knowledge to gain high expertise on parasite identification &
treatment as # * diversity of parasites increases
Enhanced preservation of speciment allow parasite to remain viable
in laboratory diagnosis, promise to be exciting
measures to protect practitioner in handling samples

PARASITE-HOST RELATIONSHIP
- human host is normally in contact w/microbes (normal flora), only few cause disease
(primary & opportunistic pathogens)
- aka INTERACTION, characterized by fighting to invade body & body defending itself
Host- larger, supports survival & growth of smaller microbes
Parasite- metabolically dependent on host; any that cause a disease)
Adaptation to parasitism
- morphological adaptation to way of life
- organs unecessary to parasitic existence are lost/degenerated Treatment
- reproductive sys very highly developed together w/increased reproductive capacity - antiparasitic med
- specialized attachment organs (suckers, hooks) are developed - diet change
- physiological & biochemical adaptation; immune evasion - vit supplements
- fluid replacement
- blood transfusion
- bed rest

Prevention & Control

- massive chemo; improve sanitation, education, cook/freeze pork & inspect meat
- manage pigs by treating/vaccinating
- control source of infection (treatment of patient, carrier, reservoir hosts)
- intervention at routes of transmission (manage feces/water, vector, intermediate host)
- protect susceptible host (personal hygiene, change diet, medicine taking)
- develop & implement parasite awareness educ programs
- use insecticides, protective clothes, netting, water treatment
- avoid unprotected sexual relations, handle, cook, protect food

Specimen Processing & Laboratory Diagnosis

- crucial to parasite recovery; for reliable diagnosis of infection:
a. Knowledge of Patient- travel history, daycare attendance, refugee
b. Appropriate Specimen- number frequency, time of collection
c. Use Appropriate Procedure- flotation, sedimentation, staining
d. Adequate training of Technologist- college curse, workshop, education
- specimen types for parasite exam
 c. px w/heavy worm burden w/other health problems are more likely to have severe
a. STOOL- most common sample for macroscopic & microscopic technique symptom/complication
- involve traditional parasite recovery method O&P (O=eggs, P=parasite) - life cycle involves intestinal tract
- nematodes cause intestinal infection symptoms during invasion:
b. OTHERS- blood, tissue biopsies, CSF, sputum, urine, genital material
Abdomen pain, diarrhea, nausea, vomiting, fever, eosinophilia
- other traditional & new parasite recovery techniques Skin irritation, skin blisters, muscle involvement
a. CELLOPHANE TAPE PREPARATION- to recover pinworm eggs
b. ENTEROTEST/STRING TEST- recover several parasites Nematode Classification
c. OTHER: Direct Fluorescent Antibody (DFA), Enzyme Immunoassay (EIA),
Indirect Fluorescent Antibody (IFA), Latex Agglutination (LA),
Polymerase Chain Reaction (PCR), Rapid Immunochromatography Technique

Parasite Nomenclature & Classification ENTEROBIUS VERMICULARIS/PINWORM/SEATWORM

Science Nomenclature- each has: phylum, class, order, family, genus, species - parasitic only to humans; adults inhabit in ileocecus (cecum & adjacent ascending colon &
- “King Philip Come Over For Good Spaghetti distal ileum)
1. Parasite classified acc to Int’l Code of Zoological Nomenclature - infection causes ENTEROBIASIS; worldwide, found in 30% kinder & primary school
2. Major divisions of animal kingdom: phylum. Class, order, family, genus, species students & 16% adults in US; most common worm in US
3. Main criteria: morphology & genetic structure of parasites - adults live in large intestine & cecum. Female go to anal region at night & lay eggs (itching)
4. Each parasite is designated under binomial system (genus & species) - scratching anal region contaminates hands & bedclothes
- eggs develop rapidly & become infective in 6 hrs at body temp
- when swallowed, eggs hatch in small intestine & mature in large intestine

Morphology

Laboratory Diagnosis
- recover eggs; Individual eggs are visible to naked eye & low-power microscope
- light-yellowish thread-like adults are clearly visually detectable during night/toilet paper
- transparent adhesive tape on anal area picks up eggs to be used for diagnosis
- egg microscopic identification by cellophane tape method (Graham Scotch) or anal swabs
(done in morning before defecation & washing)
- detection of adult on anal skin

PHYLUM NEMATODA
Morphology
- multicellular; round in cross section Life Cycle
- basic forms: eggs (female sex cells after fertilization) -
Juvenile worm/larva (long & slender)
Adult worms
- developing larvae inside fertilized eggs emerge & continue to mature

Life Cycle
- in individual nematodes, it’s similar but organism-specific
- exact means where each enter host & migrate into intestinal tract vary by species
- eggs/larvae, depending on species, continue develop into adulthood.
- adults reside in intestine where to concentrate on obtaining nutrition & reproduction
Pinworms- infected eggs ingestion transmit disease
Hookworm- its larvae burrow through foot skin & make way to intestinal tract

Laboratory Diagnosis
- by recovery of eggs, larvae, occasionally adult worms
- specimen of choice vary & include cellophane tape preparation around anal opening,
stool sample, tissue biopsy, infected skin ulcers
- serologic test are available for diagnosis of select nematodes

Pathogenesis & Clinical Symptoms

- 3 possible factors contributing to ultimate severity of nematode infection:
1. # of worm present 2. Time length infection persists 3. Host overall health
- nematode infection:
a. last for 12 mos or longer depending on species
b. Occurrence increase time to years; some remain asymptomatic/minimal pain
 Prevention & Control
Epidemiology
- highly prevalent; infect 10% of population in developed countries (children higher)
- US: E. vermicularis is most common of helminthic infection (42 mil cases in 1980s;
prevalence 15-50% in children)
- common in children, institutionalized group, household; not associated
w/socioeconomic level

Clinical Symptom
TRICHURIS TRICHIURA
Morphology
- thin whip-like anterior (3/5 of worm) & thick fleshy posterior (2/5 length)
- male: 3-4.5 cm long; posterior end is coiled & possess single cubicle
Female: 4-5 cm; posterior end is straight
Infective Stage & Mode of Infection
- by egg ingestion w/larvae on contaminated raw vegetables

Treatment
- pyrantel pamoate, albendazole, mebendazole (secondary dose may necessary)
- cure only after 7 perianal smears
- egg reduction rate is hard to know bc eggs are from perianal area, not feces
- contraindication to drugs: pregnancy & hypersensitivity Pathogenesis & Laboratory Diagnosis
- effects: GI disturbance, headache - though adult burrow their hairlike ends into intestinal mucosa, they don’t cause
Prevention & Control significant unlike hookwoms
- wash hands w/soap & water (after toilet, before eating) - cause diarrhea, but most infections are asymptomatic
- trim nails regularly & avoid biting nails; don’t scratch anal area - cause rectal prolapse in children with heavy infection
- shower at morning & wash anal area to remove eggs; cleanse bathroom & toilet - lab diagnosis: based on finding typical eggs (barrel-shaped w/plug at each end) in stool

Life Cycle

ASCARIS LUMBRICOIDES
Morphology

Epidemiology
- 800 mil infected worldwide; children in poverty in tropics & subtropics
- common in poor rural places; many people harbor infection of both Trichuris & Ascaris
- 10% of px in endemic areas, worm burden is high (200 worms/pts)
- genetic studies: 25% of variation in infection susceptibility is due to genetic factors
Laboratory Diagnosis
STOOL- specimen; adults recovered in small intestine, gallbladder, liver, appendix Clinical Symptoms
- adults may be in feces, vomit, external nares
- Enzyme-linked Immunosorbent Assay (ELISA) is available
Egg: unfertilized & fertilized detected by stool exam
Larva: during early pulmonary migratory phase, it’s found in sputum/gastric aspirate
Adult: by x-ray of GIT

Epidemiology
- egg production is very heavy (240,000 eggs/day), which embryonate in external env
& infective in 2-3 wks
- on ingestion, they hatch in small intestine & move to liver & lungs via blood. In lungs,
they molt twice, break alveoli, reach bronchioles where they’re coughed & swallowed Treatment
- on reaching intestine, it mature to adults in 60-80 days, Avg lifespan 6-12 mos Mebendazole (Vermox)- by selectively & irreversibly blocking glucose uptake & nutrients in
susceptible adult intestine; take 2nd course if px not cured in 3-4 wks
Clinical Symptoms Albendazole (Albenza)- decrease whipworm ATP making, causing energy depletion,
immobilization, death
Prevention & Control
- prevent soil contamination in feces; construction of latrines
- wash hands before eating (children, soil worker); wash veggies & fruits
- don’t use night soil as fertilizer

TRICHINELLA SPIRALIS
Treatment- albendazole & mebenazole Morphology
Female- 3-4 mm, Male- 1.5mm  both have single set of reproductive organs
 Juvenile- 124x6 um; 1 or more coil in a cyst in skeletal muscle fibers

Laboratory Diagnosis
- blister formation; outline of worm under skin (enhanced reflected light)
Adult: gravid female show at skin surface; after death, it calcifies & detected radiologically
Larva: in water, many larvae discharge; microscopic exam
- Serology: antibody seen in serum by ELISA & Fluorescents Antibody Test
- Skin Test: antigen is injected in intradermal to see wheal reaction

Life Cycle
Laboratory Diagnosis

Life Cycle

Epidemiology
- in 1986, there’s 3.5 mil cases of Guinea worm in 20 endemic nations in Asia & Africa.
Number of cases is reduced by 99% to 3190 in 2009, 3185 of it in 4 remaining endemic
Epidemiology
nations of Africa: Sudan, Ghana, Mali, Ethiopia

Clinical Symptoms
- disease: DRACUNCULOSIS; clinical features develop 1 year after infection following worm
migration to subcutaneous tissue of leg
- blister formation: blister rupture when in water (ulceration- larva release by female)
- secondary bacterial infection of ulcer
- female release metabolic waste causing toxemia (cause rash, nausea, diarrhea, dizziness)
- female produce substance causing inflammation, blistering, ulceration on lower
extremities. Inflamed papule burn & itch, ulcer can become secondarily infected
- no s/s until 1 year of infection; hours before worm emerges, person have fever, swelling
Clinical Symptoms
- >90% of worms come out at legs & feet; wound develop secondary bacterial infection

Treatment
Worm Removal- twisting it around; weeks to months
Metronidazole, Niridazole, Mebendazole, Surgical Removal

Treatment
- plenty of rest w/adequate fluid intake, fever reducers, pain relievers
- px w/severe infection treated w/prednisone
- thiabendazole but its effectiveness is questionable
Mild: supportive treatment like bedrest, analgesics, antipyretics
Moderate: albendazole (400mg BID 8 days)
Mebendazole (200-400mg TID 3 days, then 400mg for 8 days)
Prevention & Control
Severe: glucocorticoids like prednisolone to albendazole/mebendazole
- main way: educate those prone to: drink uncontaminated water from underground
Prevention & Control Don’t enter drinking water sources w/ulcer
- proper cooking of pork; regular inspection by trichiniscopy Use filter for drinking water to remove copepods
- freeze pork at -15C for 20 days to kill larva; control of rodents Unsafe water is boiled/treat w/larvicide to kill copepods
- cook fish properly; encourage dog owners to keep out infected dogs

DRACUNCULUS MEDINENSIS/GUINEA WORM

- white worm emerging from skin lesion; 60-120.cm (1m) long
- infection occurs when person drinks water w/infected water fleas (Cyclops)
Morphology
 CESTODES
TAPEWORMS IN DOGS
characteristics:
- flat, segmented bodies w/scolex, neck, proglottids/strobila
scolex- organ of attachment w/4 suckers, rostellum, hooks (others)
- new segments produced at neck; older segments pushed back & grow larger
- person can have only 1 tapeworm inside intestines
- hermaphroditic; each mature segment has male & female sex organs
- lack body cavity/digestive system; adults inhabit small intestine of definitive host
- need intermediate host (except Hy. nana)
- grow by proglottids/body sections

Laboratory Diagnosis
- stool for recovering Taenia eggs & gravid proglottids
- scolex seen after px treated w/antiparasitic meds
- cellophane tape preparation in perianal result for very high recovery rate of Taenia eggs
- eggs must be identical; to speciate, gravid proglottid/scolex must be examined
Life cycle

Laboratory Diagnosis
- stool as primary specimen
- eggs, some partially degenerated gravid proglottids, scolex after treatment
- tissue biopsy infected w/atrial E. granulosus examined for presence of org
- serologic test for select organism
Pathogenesis & Clinical Symptom
- most px are asymptomatic, others complain vague, nondescript GI discomfort,
diarrhea, abdominal pain, develop nausea, dizziness, headache, weight loss
- intestinal obstruction & vit B12-induced macrocytic anemia in px
w/Diphyllobothrium latum
- liver & lung involvement in px w/E. granulosus, w/persistent cough, localized pain, Epidemiology
eosinophilia. anaphylactic shock (produce many histamine which can be fatal) - present in places w/ unsanitary condition & beef/pork diet on routine basis
- T. saginata in cosmolopitan areas, T. solium worldwide
Classification - both require an intermediate host (cow/pig)
Clinical Symptoms
- px w/TAENIASIS (Taenia infection) are asymptomatic
- nondescript symptoms (diarrhea, abdominal pain, appetite change, slight weight loss
- dizziness, vomiting, nausea
- lab tests reveal moderate eosinophilia; prognosis is usually good

TAENIA SAGINATA/BEEF TAPEWORM & TAENIA SOLIUM/PORK TAPEWORM Treatment

Total scolex eradication- most important; difficult
Praziquantel- effective (adult worm) except when there’s ocular/CNS involvement
Paramomycin & Quinacrine hydrochloride (Atabrine)- alternative treatment
Prevention & Control
- proper sanitation, thorough cooking; prompt treatment of infected px

HYMENOLEPIS DIMINUTA/RAT TAPEWORM

Morphology

morphology
Laboratory Diagnosis Praziquantel- choice treatment
- stool for eggs except for proglottids since these disintegrate in human gut Niclosamide- alternative; not readily available in USA
- scolex rarely seen
Life Cycle
DIPYLIDIUM CANINUM/DOG/CAT/PUMPKIN SEED TAPEWORM
morphology

Epidemiology
- worldwide; those where grain/cereal aren’t protected from rat/insects
Clinical Symptoms
- asymptomatic
- HYMENOLEPIASIS (mild symptoms like diarrhea, nausea, abdomen pain, anorexia)
Treatment
Praziquantel- choice of treatment Laboratory Diagnosis
Niclosamide- alternative; but not readily available in USA - stool for egg packets/gravid proglottids; single egg in stool is extremely rare
Prevention & Control Life Cycle
- rodent control measures to prevent rats from gran/cereal
- protect food from rat dropping & intermediate host insect
- inspect potentially contaminated food before consumption

HYMENOLEPIS NANA/DWARF TAPEWORM

morphology

Epidemiology
- worldwide; children most susceptible
Clinical Symptom
- asymptomatic to light symptoms
- DIPYLIDIASIS: heavy worm burden; appetite loss, diarrhea, abd discomfort, indigestion
: anal pruritus by gravid proglottids migrating out of anus
Treatment
Praziquantel- choice treatment
Niclosamide & Paromomycin- alternative
Laboratory Diagnosis Prevention & Control
- stool for eggs - dogs & cats regularly checked by deworming & periodic prophylactic antihelminth med
Life Cycle - treat & protect against flea infestatiodn regularly
- children must not be licked in/near mouths by dog/cat

DIPHYLLOBOTHRIUM LATUM/BROAD FISH TAPEWORM

morphology

Epidemiology
- most common in southeastern USA, tropical, & substropical climates
- preschool/day care center; contaminated human feces/rodents as source of infection
Clinical Symptoms
- light infection; asymptomatic
- HYMENOLEPIASIS (GI symptom- abdomen pain, anorexia, diarrhea, dizzy, headache)
Laboratory Diagnosis
Treatment
 - stool for eggs/proglottids; intact scolex from untreated px is rare
- stool from infected px after drug treatment must have scolex & no new proglottids
Life Cycle

Epidemiology
- temperate regions worldwide; USA, Alaska, Great Lakes region Epidemiology
- endemic areas in South America, South Asia, Central Africa, Baltic region, Finland - sheep/herbivores raised in close contact contact w/dogs/wild canines
(raw/freshwater fish consumption) - Great Britain, South America, Australia, Africa, Asia, China, Middle East
- fish-eating animals also as definitive hosts - Alaska (US), West & Southwest USA

Clinical Symptom Clinical Symptom

- asymptomatic - ECHINOCOCCOSIS (HYDATIDOSIS)
- DIPHYLLOBOTHRIASIS: digestive discomfort, overall weakness, weight loss, abd pain - discomfort acc to cyst size & location; symptom show 1 year after ingesting eggs
: vit B12 deficiency (when adult worm attaches to proximal - lung infection chest pain, coughing, shortness of breath
jejunum) mimics pernicious anemia - liver involvement result in obstructive jaundice
Treatment - symptom related cyst dev’t in other body organs are site-specific
Praziquantel & Niclosamide- choice - as cyst enlarge: necrosis of infected tissue, death, cyst rupture naturally/during biopsy,
Prevention & Control anaphylactic shock, eosinophilia, allergic reaction, cyst fluid spread & form new cyst
- human fecal disposal, avoid raw/undercooked fish, proper cooking of fish

ECHINOCOCCUS GRANULOSUS/DOG TAPEWORM/HYDATID TAPEWORM

Morphology

Laboratory Diagnosis
- hydatid cyst fluid on biopsy for scolex, daughter cyst, brood capsule, hydatid sand
(note: careful since infected px can have anaphylaxis if fluid exits from hydatid cyst)
- serologic test
- hydatid cyst by radiography, computed tomography (CT), ultrasound scan technique’

Life Cycle Human Use of Microorganisms

 BIOTECHNOLOGY- food, drug, vaccine; yeast for bread & wine/beer recombinant DNA technology revolutionized research & practical applications
GENETIC ENGINEERING- manipulate genes to make product; Recombinant DNABACTERIOLOGY
technique (of bacteria)- began w/ van Leeuwenhoek’s 1st exam of tooth scraping
- bacteria & fungi first to be genetically engineered - Pasteur looked bacteria’s roles in food & env
- use microbes to make proteins for drugs, hormones, enzymes - 1997, Heide Schulz discovered Thiomargarita namibiensis seen
BIOREMEDIATION- “bios”(life), “re”(again), “mederi”(to heal) w/naked eye, lives in mud on African coast. It consumes hydrogen
- use living org to treat environmental problem sulfide (toxic to mud-dwelling animals)

Microbes & Human Disease MYCOLOGY (of fungi)- fungal infection rates accounted for 10% of hospital infections.
Climatic & env changes increased Coccidioides immitis infections in Cali
- microbes make up normal microbiota/flora in body
PARASITOLOGY (of protozoa & parasitic worm)- medical symbol, rod of Asclepius,
- microbes’ disease-producing properties & host’s resistance determine disease contraction
- biofilms are bacterial communities that form slimy layers on surface represent removal of parasitic guinea worms (Asclepius was Greek
- infectious disease is where pathogens invade susceptible host physician who practiced 1200 B.C. & deified as god of medicine.
- emerging infectious disease (EID) is new/changing, show increase in incidence on - clearing of rain forests exposed laborers to undiscovered parasites. Parasitic
past/future disease were found In patients whose immune sys were suppressed by
organ transplants, cancer chemotherapy, AIDS.
- these 3 branches are going through “golden age”
- advances in genomics (of organism’s genes) classify bacteria & fungi acc to their genetic
Vaccination relationships w/ other bacteria, fungi, protozoa.
- 70 yrs before Koch’s discovery, Edward Jenner experimented smallpox after milkmaid
told that she couldn’t get smallpox bc she already got cowpox, He collected scrapings IMMUNOLOGY (of immunity)
from cowpox blisters & inoculated healthy 8 y/o volunteer w/cowpox by scratching - vaccines for measles, rubella (German measles), mumps, chickenpox, pneumococcal
their arm w/pox needle. It turned into raised bump. He became mildly sick but pneumonia, tetanus, tuberculosis, influenza, whooping cough, polio, hepatitis B
recovered & never again contracted cowpox/smallpox (Immunity from vaccination) - its major advance in 1933, when Rebecca Lancefield proposed that streptococci (sore
- after Jenner’s, Pasteur discovered why vaccines work. Bacterium causing fowl cholera throat/strep throat, streptococcal toxic shock, septicemia/blood poisoning) be classified
lost its virulence/become avirulent after growing in lab for long periods. However, it & acc to serotypes (variants within species) based on cell wall’s component
other microorgs w/decreased virulence can induce immunity against subsequent - 1960, interferons (made by body’s immune system) were discovered; these inhibit virus
infections by its virulent counterparts. Pasteur used vaccine for cultures of avirulent replication
microorgs used for preventive inoculation. (vacca, Latin: cow); vaccine honored
VIROLOGY (of virus)- from Golden Age
Jenner’s earlier cowpox inoculation work
- (1892) Dmitri Iwanowski: organism that caused mosaic disease of tobacco was small
- Je
that it passed through filters fine enough to stop all known bacteria. He wasn’t aware
nner’s experiment isn’t 1st time a living viral agent (cowpox virus) was used to that this was a virus
produce immunity.
- (1935), Wendell Stanley showed that tobacco mosaic virus (TMV), was diff bc it’s
- (1500) physicians in China immunized patients from smallpox by removing scales simple & homogeneous that it crystallized like chemical compound.
from drying pustules of a person suffering from smallpox mild case, ground these to - since dev’t of electron microscope in 1940s, microbiologists observed virus structure
fine powder & inserted into nose to be protected.
- some produced from avirulent microbial strains that stimulate immunity to related
virulent strain.
- others are made from killed virulent microbes, from isolated components of virulent
org/by genetic engineering

Birth of Modern Chemo: “Magic Bullet”

Chemotherapy- treat disease by chemicals; treat noninfectious disease
Synthetic drug- chemotherapeutic agents prepared from chemicals in lab
Antibiotics- chem produced naturally by bacteria/fungi to act against other microorg
First Synthetic Drug
- Paul Ehrlich (fired 1st shot in chemotherapy revolution). He speculated about “magic
bullet” that hunt & destroy a pathogen w/o harming infected host
- (1910) after testing substances, he found a chemotherapeutic agent salvarsan
(arsenic derivative effective against syphilis) named as such since it offers salvation
from syphilis & contained arsenic
- before this, only known chemical in Europe was quinine (extract from bark of South
American tree) used by Spanish conquistadors to treat malaria.
- (late 1930s) researchers developed drugs derivatives of dyes since dyes synthesized &
manufactured for fabrics were tested for antimicrobial qualities by microbiologists
looking for a “magic bullet.”; sulfonamides (sulfa drugs) were synthesized
Antibiotics
- Alexander Fleming almost tossed culture plates w/mold. He noticed its pattern—
clear area where bacterial growth inhibited encircled mold Penicillium chrysogenum,
its inhibitor was penicillin. So, penicillin is an antibiotic produced by fungus. By 1940s,
it was tested clinically & mass produced
- however, antimicrobial chemicals kill pathogenic microbes & damage host. Toxicity to
humans is a problem in drug dev’t to treat viral diseases. Viral growth depends on life
processes of normal host cells. There’s successful antiviral drugs which interfere
w/viral reproduction would also affect uninfected body’s cells.
- Drug resistance results from genetic changes in microbes that allow them to tolerate
amount of antibiotic that normally inhibit them
- appearance of vancomycin-resistant Staphylococcus aureus & Enterococcus faecalis
alarmed us bc it indicates that previously treatable bacterial infections may soon be
impossible to treat w/ antibiotics

Modern Developments in Microbiology

- Golden Age of Microbiology provided basis for achievements
- new branches of microbiology developed like immunology & virology