Mietzner Wisdom:

● Need to take at least once, prob next semester: chap 9 (boards questions), 44, 45
(vaccines), 57 (bioterrorism)
● Viruses: mietzner will always ask about how they escape the immune system
● Chapters Mietz Mietz recommends next semester (Ch. 9 bacterial toxins close to
boards, Ch. 45 vaccines next semester or in third block of this semester, Ch. 57
biological agents of warfare and terrorism
● Pregnant: no MMR, yes DTTP
__________________________________________________________
Chapter 8
▪ Don’t need to know specific little details, know only about the ones talked
about in the case
▪ Know how organisms get in and compete
▪ Know for organisms the adhesisns and recepteors (like fibronectin binding
protein)
● Bacteria that produce fimbriae that help stick to the walls to
overcome the inherent negative charges between the cells that will
usually repulse
▪ Know tropism, why certain organisms like certain places
▪ –chelin or –bactin are always iron binding molecules produced from the
bacteria to try and grab the free Fe
▪ Figure 8-1 is important (breaking down C3b…) Which is a mechanism to
avoid complement deposition? - example questions
● Don’t need to know the speicif cthing about strep that’s mentioned
here…peptidase?
▪ Subverting phagocytosis: production of –lysin (like streptolycin) pore
forming toxin produced by that bacteria
▪ Inhibition of phagosome lysosome fusion. Don’t worry about the specific
examples. Won’t ask speicifc organism unless it was in the case.
▪ Refresh yourself with table 8-3 but don’t get too crazy with it
▪ Know shigella: changes intracellular environment without change in
extracellular?
▪ Superantigens: staph, strep – bind T cells and MhC independent of
antigen to set off a cytokine storm and end with system problems
▪ Antigenic variation, might need to know surface protein antigen that is
variable in a certain type of bacteria (gram + or -)
▪ Proteolysis and antibodies, know IgA proteases clip at hinge region of IgA.
▪ Latency is mentioned…not too important

Chapter 9 Microbial Toxins

● AB type toxins, A = active, B = binding
● Type III cytotoxin, think injectosome; the molecular syringes (example:
diphtheria)
● Will never ask a question about Exo S, Exo Y cytotoxins
● TLRs and PAMPs:
○ TLR 2 recognizes Gram (+) teichoic acids
 ○ TLR 4 recognizes Gram (–) LPS
○ TLR 5 recognizes flagella
Exotoxins
● Pathogenicity islands-genomic areas where virulence factors collect
o Usually on mobile elements like phages
o diphtheria phage, cholera toxin is on a phage
▪ Eg Diphtheria toxin regulated by low iron
● Know how endotoxin activates macrophages
o Pattern recognition receptors
● Toll-like receptors-know TLR4 recognizes LPS/LPS binding protein
● LPS: activates complement (alternative pathway), macrophages, B
lymphocytes-> Past question twice
● Pyrogenic
● End-stage of endotoxin toxicity is DIC
o Humans are + sensitive vs other species to LPS
o Shock, Waterhouse – Friderichsen
Superantigen
● Does not require peptide stimulation-nonspecifically links MHC
● Set off a "cytokine storm"
●
● Table 9-1:
Bacillus anthracis: 2AB, EF, LF
Pertussis: adenocylcase (AB exotoxin); pertussis toxin AB5 that riboosylates
Gas to increase cAMP (and insulin production, neutrophil dysfxn, and increased
sensitivity to histamine)
Botulinum toxin: know mechanism of action, flaccid paralysis
C. diff: glucosylates (NOT GYLCOSYLATES) Rho proteins
C. perfringens: Lecithinase (phospholipase C-degrades membrane
phospholipids to cause cell death and Gas gangrene), enterotoxin
Tetanus toxin: causes spastic paralysis
Diphtheria and pseudomonas: ADP ribosylates EF-2 (to inactivate it) and
inhibit protein synthesis and cause cell death.
- Diphtheria presents in developing countries as sore throat with mild fever and
LAD. Pharyngeal exudate with coalescing pseudomembrane (grayish exudate from cell
necrosis due to toxin). Can obstruct respiratory tract and cause dyspnea. If systemic,
toxin can cause myocarditis/HF and neurologic toxicity.
E. Coli (EHEC) and Shiga toxin: inactivates 60S ribosome to kill cell
Listeria: listerlysin O, a pore forming toxins, pokes holes in endosomes,
allows organism escape
Staph: pore forming antigen
Scaled skin: exfoliative toxin – cross links
Heat stable/labile enterotoxin, P Aeruginosa/Exotoxin A is fair game

● Look at Figure 9.3

○ Can be subunit toxins or on the same protein
 ■ Eg Diphtheria toxin is A/B domain-B binds and translocates the A
subunit across the cell (all on the same molecules)
■ Diphtheria=Exotoxin A (from pseudomonas)-SAME TOXIN, even
though antigenically distinct-> ADP Ribosylate EF-2
○ Cholera toxin-A B5, a "subunit toxin", no covalent association
● Tetanus/Botulinum toxin-KNOW THE MECHANISM OF ACTION w/ blocking of
Ach-stimulating (botulism) versus inhibiting (tetanus) neurotransmitters via
GABA
● Know figure 9.4 – TNF, IL-1, IL-6
● Know figure 9.5
Membrane-Damaging Toxins
● C Perfringens-gas gangrene via a lecithinase and lipase; spores in muscle
germinate
○ Grows anaerobically
● Pore-forming toxins
○ Eg Alpha toxin S Aureus, Streptolysin O (holes in eukaryotic membranes)
● Spreading factors-important for necrotizing fasciitis
○ Hyaluronidase, DNASe, Streptokinase
Toxoid vaccines
● eliminates enzymatic activity, retains immunological activity
● Eg dTaP
● Passive vs. active immunization

Chapter 10

Chapter 11
Staph saph, epi, aureus
Leading cause of osteomyeltisi, arthiritis
READ the cases- Osteomyelitis and faruncle formed
Pg 154, attaches are fibronectin binding proteins and collagen
Staphylolysin – pore forming toxins
o Ch. 11: staph
▪ Not all green boxes are as good as others, but they’re mostly good.
▪ Table 11-1: know aureas, epidermis, saphrophyticis (just know connection
with UTI)
▪ Know pink box on pg 150
● Furuncles, impetigo, endocarditis, aspiration pneumonia,
osteomyeltitis/arthritis, TSS, scalded skin syndrome, food
poisoning
▪ Fomites: things that exist on doorknobs, droplets, touching.
▪ The nose is the tropical rainforest of the body for diversity. Staph likes it
there too
▪ Uses lipases, gylcorol, phospholases (?) to eliminate competition- degrade
skin lipids.
▪ Colonize skin + mucosal associated w bacterial cell surface protesins
(MSCRAMMS)- microbial surface components recognizing adhesive
matrix molecules). also Binds with fibronectin binding protein (allows to
 invate epithelial/endothelial cells . Mscrams bind to collagen. Just know
these are associated with staph areus
▪ Know that they cause damage by being able to penetrate, pyogenic,
▪ Figure 11-4 is incredibly important: produces , neutrophils, leukocydin,
hemolysins (actually works on all types of cells). Produces a coagulase
which will form clotting and blocks the immune system that way.
▪ Protein A works by turning the antibodies around and bingind to the Fc
portion- reduce opsonization, lyse neutrophuls and rbc that have entered
infection area via leukocidis and hemolysins- pour out lyosomal tissue-
damage surrounding tissue
▪ Also has a capsule kind of
▪ Produce leichotoicc acids or whatever
▪ Panton valentine leukocydin (damage neutrophils), leukocydin, produces a
hylauronitase (hydrolyzes the matrix of connective tissue and spread
bacteri
▪ Know methicillin resistance is mediated by a penicillin binding protein,
different than vancomycin resistance. Don’t really need to know about
others
▪ Epdiermis likes to grow as a biofilm - endocarditis, grows on catheters,
● Slime layer produced is a glycocalyx. This covers the entire colony
rather than each specific bacterium
▪ Saphrophyticis is common UTI, 2nd or 3rd to e. coli.
▪ Staph Auerues only: scalded skin, exfoliated toxin clips desmosomes to
peel back the skin
● Know TSS: superantigen
● Staph-enterotoxin: staph food poisoning. Intoxication rather than
an infection. Toxins produced have to be resisitant to acids,
proteases, and somehow has to make it to emetic centers of the
brain
▪ For treatments, just know the methicillin and vancomycin. Pretty much
ignore the rest of the table
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All Staph are Catalase+, the Coagulase test will distinguish between S Aureus and S.
Saprophyticus/Epidermidis
Other identification buzzwords: "Grape-like clusters", "yellow colonies" (Aur=gold)
Dz to associate w/ S Aureus:
● Osteomyelitis
● Hospital-Acquired Pneumonia
● Food poisoning
● MRSA-Necrotizing Fasciitis
Specific clinical scenarios mentioned:
● Skin infx: Gymnast/Wrestler gets a scrape from a mat, gets the MRSA
o Key terms: Abscesses, Boils, Furuncles, Carbuncles
o Jordan note: furuncles are boils; carbuncles are furuncles connected under
the skin
● Food poisoning-timing is important. This is an intoxication
 o Get it at a picnic, eating chicken/potato salad
o Onset: 4 hours as opposed to days
o Jordan note: not heat labile
● Toxin-related dz: TSST (toxic shock syndrome toxin, see below)
o Classic scenario: extra-absorbent tampon, but can happen w/ a boil
● Not mentioned, but hella boards: pt is recovering from Influenza/Parainfluenza
and then gets a bacterial infx: it's Staph Aureus
Table 11-1: Know S epidermidis: common dz, coag -, white colonies, does not ferment
mannitol, novobiocin sensitive
S Aureus loves the nasopharynx, colonizes epithelial surfaces by sticking to
fibronectin (see p 154)
        Colonize via MSCRAMMs that bind to host ECM proteins
● Fibronectin-binding proteins
● Collagen binding (colonize connective tissue, bones, joints)
● Fibrinogen-binding proteins "clumping factors" (important for clot formation,
responsible for the coagulase test)
Causes nec fasc-("spreading dz")-degrades cells/junctions between cells via lipases
and glycerol hydrolases
High Yield Fact: Pts with chronic granulomatous dz are particularly susceptible to S
Aureus (because they can't make enough H202 to set off oxidative killing pathways)
Virulence Factors:
● Encapsulated
● Protein A binds the Fc portion of IgG, reducing opsonization
● Leukocidin
● Hemolysins (α,β,ᵞ)-lyses RBCs, pore forming toxin
o Exception: β toxin is not a pore former, but a sphingomyelinase that
prepares RBCs for lysis (temp-dependent); may have role in biofilms
● Collagenase= clot-dissolving
● Panton Valentine Leukocidin-also a pore former, along w/ α,ᵞ toxins damages
neutrophils
● Peptidoglycan-activates complement via the alternative pathway
o Lipoteichoic Acid activates TLR2, stimulating cytokines (gram - like
response)
● Slime layer (common to other Staph spp)
● Catalase-produces free radicals (common to other Staph spp)
● Coagulase: converts fibrinogen->fibrin, can help prevent phagocytosis since
WBCs suck at penetrating clots
● Hyaluronidase-hydrolyzes connective tissue, facilitating bacterial spread along
tissue planes
o Lipases, Proteases, DNAses do the same thing
Mechanism of methicillin resistance- altered PBPs (does produce B-lactamase, not as
important)
Virulence factors coag neg staph: "slime layer"-forms biofilm, capsule-like
● Think of infection of a central line/prosthetic joint
S. Saprophyticus-UTIs
Toxin-mediated dz
 ● Staph Scalded Skin Syndrome
o Caused by exfoliative toxins A and B (proteases that degrades
desmosomes)
● TSST
o Superantigens-nonspecifically link MHC II w/ T cell receptor, sets off
cytokine storm (term is ringing bells)
o Sign of recovery: peeling skin
o Associated w/ tampons because of O2 requirement
o IFN gamma prevents neutralizing antibodies, so you can get toxic shock
multiple times
● Food poisoning
o diarrhea-HELLA peristalsis by acting directly on the vomiting center of the
brain
o Do not require active bacterial infx, an intoxication
Dx- selectively grow on CNA agar (not actually mentioned in the chapter)
Rx-
● Don't need to know specific anti-staph therapy
● Mechanism of Vancomycin Resistance: D-Ala D-Ala-> D Ala-D Lac
● (unlikely question) Big guns: Linezolid, Daptomycin
Prevention: Don't be gross, wash your hands

Chapter 12 strep
- Gram + tell apart with catalase→ -
- Table 12-1
o Group A, B, D, lump together all viridans
- Differentiate via hemolytic patterns
o B, a, or y hemolytic
o viridans=green=alpha
o AB test for polysaccharide in cell wall
- Only humans, aerisolization
- Causes lots, most important is phayingitis in yound and skin in old &
immunologic sequelae
- Attaches using M protein (only in group A) on surface, binds proteins that make
immune system hard to recognize
o Middle portion (semi conservative)→ rheumatic fever
o Hypervariable region→ cause repeated infections
- Streptokinase & streptolysin (lysin = pore forming toxin)
- HA capsule to avoid immune
- Toxin
o Scarlet fever- sandpaper rash, strep pyrogenic extoxin, superantigens =
nonspecific cross with T cells Rc with MHC.--> cytokine storm
o Toxic shock, another superantigen
- Local infection
o Strep throat, fasc nec
- Systemic
- Immunulogic sequelae
o Cross react with heart→ rheumatic fever
o Post strep glomerulonephritis- crosslink complex get in kidney→ complement
hurt glomeruli
- Group a are all sensitive to penicilin
- Vag & kid meningitis from birth canal, something about 6 month
- Strep mutans= dental caries
- Enterococci- gram +, been around a lot of bacteria genomes, taken up a lot of
genes, high AB resistance, happen when get in blood from perf colon
- Vancomycin resistance- change in terminal d-ala to d-lac
o Ch12: strep
▪ This is the only one we use the hemolysis tests
▪ Can also speciate by group specific antigens. Antibodies to the specific
components in…
▪ Speciatino also using enzymes and genes
▪ Group A and B: beta hemolytic
▪ Strep pyogenase is group A strep, B hemolytic
▪ Table 12-1: skip 3rd row, include group D, skip everythting except last 4
rows and just call those
● Streptococcus mutans
● Relatively wimpy organisms
▪ Have growth requirements that staph doesn’t have
▪ Figure 12-2: pharyngitis, impetigo, necrotizing fasciitis, osteomyeltitis,
TSS, psot strep glomerulonephritis, scarlet fever, acute rheumatic fever
▪ They have to stick by their adhesins
● Group A: use M protein to adhere in conjuction with lipoteichoic
acid forms a bridge with fibronectin. Evades immune system by the
capsule
o Produce number of toxins that allow spread (pg 183 on the
right side) like streptokinase, streptolycin,
deoxyribonuclease, and know about pan-miphra big brown
myocitis streptodornase pg163)?
o Produces hyaluronic capsule
o M protein is its own structure, not a pilli. It is 2 coiled things
attached to membrane. Has a hypervariable region.
Semiconserved region might produce immune response that
cross reacts with the heart that leads to rheumatic fever (this
is not the same as endocarditis!!).
o Scarlet toxin and TSS toxin are both superantigen. Know
scarlet fever rash is a sandpaper like rash. Pyogenic exotoxin.
Doesn’t care about ABC or specifics
o Rheumatic fever response is called non-suppartive immune
sequeling?
o psot strep glomerulonephritis: antigens get into blood
stream, immune complex binds to glomerula, produces
 complement which then destroy the membrane basically by
just getting stuck there.
o Rapid strep test is for the cell wall components of a group A
strep. It’s 80% sensitive.
● History of strep: can see if they had antibodies antistreptolysin O or
streptodormase if they have murmurs, rheumatic fever
● Group A are not resistant to penicillin
▪ Group B: no M protein, a leading cause of bacterial meningitis in neonates
because it is common in the vaginal flora
▪ Viridans strep (the last 4 of that one table): normal flora of the mouth. Can
be causes of bacterial endocartitis. Only have to know strep mutans (or
butans?)
▪ Enterococci: Live in the gut, resistant to salt and bile. Other strep can’t
grow in presence of bile (??). These are opportunistic, very resistant but
not very aggressive. Can use synergy: cellw all synth inhibitor with a
ribosomal synth inhibitor to treat. Don’t need differences between facalis
and fasesium??
Speciation:
● Alpha, Beta, Gamma hemolysis
● Lancefield (Group A/B)
● Name (Pyogenes, pneumoniae)
Group A Strep= Beta hemolytic strep= S Pyogenes
Leading cause of pneumonia, acute pharyngitis, otitis media; common cause of
osteomyelitis . Cause of necrotizing fasciitis
Fig 12-2: could categorize into 3 classes
● pyogenic (++white cell response)
● toxin-mediated (Scarlet fever, toxic shock syndrome)
● Immunological sequelae (post-strep glomerulonephritis, rheumatic fever)
Unique to humans, spread human-human; local flora is protective
Know the virulence factors, bold in p 163:
● M protein- ONLY FOUND IN Group A Strep
o Analogous to fimbriae/pili because it facilitates attachment
o 2 copies of one protein (a dimer)- has 3 regions
▪ Highly conserved membrane anchoring
▪ Semiconserved middle part
▪ Induces an immune response in heart tissue, causing
rheumatic fever "rheumatogenic strain"
▪ Hypervariable region
▪ Can cause repeated infx with strep
o Uses lipoteichoic acid to bind fibronectin
o Attaches to serum proteins (albumin etc) so it can disguise itself
o Hyaluronic acid capsule AND a hyaluorinidase (facilitates invasion of host
cells)
o Poorly immunogenic because humans have hyaluronic acid
● Streptococcal toxins
 o Pyrogenic toxins: Superantigens nonspecifically cross T cells to MHC->
causes toxic shock syndrome/scarlet fever  and creates a cytokine
storm
▪ Spe A, B, C not important
● Post-streptococcal glomerulonephritis-antigen/antibody complexes deposit on
glomerulus, stimulating complement and fcks the kidney
o Rapid strep: detects antigens
o Culture: beta hemoylsis on blood agar
o Why do we put kids on penicillin? No documented cases of penicillin-
resistant streptococci
▪ Prevent rheumatic fever
▪ Prevent contagiousness
▪ Alternative tx: macrolides (azithromycin, erythromycin, etc)
● Group B strep: normal vaginal/lower GI flora strep, also B hemolytic
o One of the leading causes of neonatal meningitis (acquired in birth canal
or caregiver inoculation, not a problem after 6 weeks of age)
o Tx: penicillin
o Polysaccharide capsule
▪ Note: most organisms causing meningitis will have a capsule
● Viridans Strep
o Alpha hemolytic (will turn agar green)
o Normal oral flora, introduced into mouth during toothbrushing
o Invade heart valves and escape immune system, forming a biofilm-
vegetative growth
o Causes dental caries-S mutans
● Enterococci
o Normal GI flora, only cause a problem during trauma
o Big issue: antibiotic resistance

o Analogous to fimbriae/pili because it facilitates attachment

o 2 copies of one protein (a dimer)- has 3 regions
▪ Highly conserved membrane anchoring
▪ Semiconserved middle part
▪ Induces an immune response in heart tissue, causing
rheumatic fever "rheumatogenic strain"
▪ Hypervariable region
▪ Can cause repeated infx with strep
o Uses lipoteichoic acid to bind fibronectin
o Attaches to serum proteins (albumin etc) so it can disguise itself
o Hyaluronic acid capsule AND a hyaluorinidase (facilitates invasion of host
cells)
o Poorly immunogenic because humans have hyaluronic acid
● Streptococcal toxins
 o Pyrogenic toxins: Superantigens nonspecifically cross T cells to MHC->
causes toxic shock syndrome/scarlet fever  and creates a cytokine
storm
▪ Spe A, B, C not important
Chapter 13
- Know quellung rxn: capsules can be visualized by adding an antibdoy that causes
an antibody- antigen precipitation in the normally transparent zone
- S. pneumoniae produces an IgA protease along w/ H. influenza & Neisseria-
three bacteria along undergo transformation
- Major virulence factor of S. pneumoniae is a capsule
- Produces autolysin
- Humans are the only reservoir for S. pneumoniae, normal part of respiratory
tract flora that is held back by host defenses
- Most CF patients are infected w/ pseudomonas, not Strep pneumo as in the case
- Know the three stages of pneumonia on pages 173-175
o 1st- alveoli fill w serous fluid + inflammatory cells
o 2nd- early consolidation the alveoli are infiltrated by neutrophils and rbc-
strong chemotactic signals + complement
o 3rd- late consolidation – hepatitization
o 4-th – resolution, scaveging macrophages
- Diagnosis- look for G+ cocci
- Strep is catalase negative- how to differentiate b/t two different G+ cocci
- Alpha hemolytic on blood agar
- Sensitive to optochin (antibiotic that targets G+ bac)
- Becoming resistant to penicillin- alter the PBP or produce beta lactamase
- Strep pneumo produces an altered PBP
- Vax against strep pneumo using the capsule
------------------------------------------------------------
- Pneumococcus
o Strict diplococci, catalase -
o Alpha hemolytic
o Know the case on 170
▪ Leading cause of CAP- 500,000 cases a year
▪ Need to know for path: lobar pneumonia. Typical pneumonia
▪ Productive cough that will have the organisms in the sputum,not
diagnostic though, lots of contamination
o Catalase negative and it produces a bunch of H2O2
▪ This decreases mucociliary escalator function
o Produces pneumolysin which is a pore-forming toxin
o Autolysin degrades its self to release its DNA. It undergoes natural
transformation (just like Neisseria and Haemophilus). On page
176- emergence of resistance, selective pressure, organism
adapts and takes dna from env’t
o Capsule is the main virulence factor
 o Specific to strep pneumo is the Quellung reaction (add antibodies
specific to the capsule and you see the capsule swell)
o Diver disease: babies (pneumonia and meningitis), young people (otitis
media and conjunctivitis) and elderly (CAP, can lead to meningitis)
o Don’t really need to know list of organisms on paradigm box on 172
o Humans are the only reservoir
o Inhalation pneumonia (bypass epiglottis): mycobacterium, legionella, s.
pneumo
o Host defenses: cough reflex, epiglottis (prevents secretions from getting
down), mucociliary escalator, alveolar macrophages
o Spread: 173-175 hits pathology of pneumonias, will be a question on the
stages
▪ 1. Alveoli fills w serous fluid containing many organisms but few
inflammatory cells
▪ 2. Early consolidation, the alveoli are infiltrated by neutrophils and
red blood cells – strong chemotactic signals – fight bw phagocytes
and bacteria- resisted by phagocytosis due to capsule
▪ 3. Late consolidation – alveoli are packed w victorious neutrophils
▪ 3. Resolution, neutrophils replaced by scavenging macrophages-
clear debris resulting from inflammatory process
o When grown on blood agar they are a-hemolytic. Also Optochin
sensitive
o Resistance to penicillin, alteration of PBPs
o Know pneumo vaccine (based on capsule, but there are over 90 different
capsules of it)
▪ Multivalent vaccine (has several of most common forms of
capsules)
▪ It’s also a conjugate vaccine, so the carbohydrate is attached to
protein to get the T cells involved

Chapter 14
- Only significant gram neg diplococci
- These are the 2 bad neisseria (there are good ones too)
- Gono and menging- 80% related, 20% in gonno is due to antigenic variation ,
meninges devotes its 20% to making a capsule
- Produce an IgA protease
- Pg 183- how gon causes disease thru sex contact, via pili it attaches to pili of non
ciliated cells – goes to lamina propria, white cells- grows invade inside insidious
immune response
- Oxidase +. Gon can only ferment glucose. Menin can ferment both glucose and
maltose
- 33% of women are asymptomatic- men is symptomatic
- There are some good Neisseria that are part of local mouth/vaginal flora
- Concept: LOS
o LOS is LPS except that it lacks an O antigen. No repeated sugar on it
- Grown on Thayer-Martin medium
- Gonococcus and meningococcus are 90% identical but gon = STD, men =
meningitis
o 10% diff: Gon has antigenic variation of cell surface protiens
▪ Menin has a capsule
- Gon most commonly causes cervicitis and urethritis. Can ascend up genital tract
(not the urinary tract) and can move to endometrium, fallopian tubes, and then
to blood stream to cause DGI (disseminiated gon infect) and then can go to the
joints to cause septic arthritis
o People that are defective in making terminal complement proteins (C5-9)
are especially susceptible
o Leading cause of pharyngitis on college campuses. Can also cause proctitis
- Know the gram stain pic at the top of 180 (fig 14-1. Little dots inside of white cell
are the gonococci) This is diagnostic in areas not in the vagina/mouth due to the
presence of the “good” Neisseria
- 30% of females have subclinical symptoms so they have asymptomatic infections
of Gonorrhea. Best prevention is contact-tracing (Who they’ve been sleeping
with)
- Paradigm box on pg 181-3:
o Gon is kidney bean shaped with surface pili (made up of millions of
subunits of pilin). Pili have a receptor on its tip for long interactions. Opa
protein is involved with intimate attachment.
o Phase variation is when the promoter region (for protein synth) can be
turned on and off, used for both Pili and Opa.
o Antigenic variation is when cassettes downstream of pilE loci that can add
onto the second half of the pilE that changes the surface presentation of
the pili on the Gonococcus and makes it Quasi-species
- They produce IgA protease that clip IgA1 at the hinge region.
- Neisseria is one of 3 organisms that undergo natural transformation
- Know the attachment to ciliary stasis to yadayada. Ciliary stasis – motility of
ciliated cells slows and ultimately ceases Intracellular traffic + exocytosis =
transcytosis
o Gonococci can be transported to the base of the nonciliated cell where the
bacteria-laden vacuoles fuse w the basement membrane
o Excotysosis : the phagocytic vacuoles discharge gonocci into the
subepithelial connective tissue. From there- organisms cause local
inflammation or enter blood vessels to cause disseminated disease
- Damage due to white cells degranulating in the area
- Don’t worry about proteins involved with DGI, but you should know that sialic
acid addition lets it blend in in the blood stream. There are never antibodies to
sialic acid.
- It is a leading cause of tubal infertility due to scarring of the fallopian tubes
- 50% of all gonococcal infections have comorbid chlamydia infections and vice
versa.
- Meningococcus
o Know demographic of the meningitis (mostly adolescents)
 o Grows in pharynx first, goes to lung, then to blood, and then to meninges
o Serogroup B meningococci have a polysialic acid so it is unable to make a
capsular vaccine for it. But there is a vaccine, just uses surface protein
antigens
- Treatment:
o Meningococci are susceptible to all antibiotics so you can just use
penicillin
o Gonoccocus is highly resistant so use high dose ceftriaxone (need higher
dose because the resistance is use of B-lactamases) and azithromycin for
concurrent chlamydial infection
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Two differences between gon and meningitis:
Men is encapsulated and ferments maltose, gon does neither of these things
Gon
Virulence factors: pili, Opa proteins
Don't know the paradigm boxes, know that gon is a quasispecies because of
frequent replication mistakes, so we have no vaccine
● Growth on Thayer-Martin/Martin-Lewis/"chocolate" agar
● Typically localized to cervix/urethra
● Women often asymptomatic, cause scarred fallopian tubes and PID
● *Complement deficiencies C5-9 cause disseminated gonococcal infx
● Gonococcal arthritis= leading cause of arthritis in sexually active people
● All neisseria produce an IgA protease
● Know that gonococci can become resistant due to addition of sialic acid residues
(which humans have)
(Hem, Neisseria, S pneumoniae= mucosal pathogens that have an IgA protease)
Know entry, spread, multiplication
        >Attached to non-ciliated cells, LOS
        >Cilia stop beating, die
        > +white cell response w/degranulation
*know that there are highly resistant gonococcal strain, cotreat with chlamydia
Meningitis
Group B doesn't have a (polysaccharide) vaccine because it is coated in poly-sialic acid
Polysacch: T-independent antigens
Time from initial disease symptoms->death= 24 hours
Purpura fulminans

(FYI
Meningitis in infants: H flu, Strep pneumo, E coli (K1-polysialic acid capsule)
adolescents: N meningiditis
Mg in elderly: Strep pneumo)
Vaccine B- polysach acid its on our nerve tissues we don’t want a vaccine for that
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--------------------
Two differences between gon and meningitis:
Men is encapsulated and ferments maltose, gon does neither of these things
Jordan note: you need a capsule to cause meningitis (usually)
Gon
Virulence factors: pili, Opa proteins
Don't know the paradigm boxes, know that gon is a quasispecies because of
frequent replication mistakes, so we have no vaccine-former PBL question
● Growth on Thayer-Martin/Martin-Lewis/"chocolate" agar (sheep’s blood)
● Typically localized to cervix/urethra
● Women often asymptomatic, causes scarred fallopian tubes and PID
● *Complement deficiencies C5-9 cause disseminated gonococcal infx-HELLA
BOARDS
● Gonococcal arthritis = leading cause of arthritis in sexually active people
● All neisseria produce an IgA protease
● Know that gonococci can become resistant due to addition of sialic acid residues
(which humans have)
● Jordan note: sialic acid is what our cells use to prevent complement activation.
Think of it as a passport or writ allowing safe passage.
● Opa Proteins-Strains that lack 'em are not engulfed by neutrophils (past
question)
(Hem, Neisseria, S pneumoniae= mucosal pathogens that have an IgA protease)
● Know entry, spread, multiplication
o >Gonorrhea attach to microvilli of non-ciliated cells, LOS
o Jordan note: LOS is the same as endotoxin
o >Cilia stop beating, die
o > +white cell response w/degranulation
● *know that there are highly resistant gonococcal strain, cotreat with
chlamydia
Jordan note:
Gonorrhea attach to NONciliated cells. These cells use microvilli to phagocytosize the
gonorrhea. The gonorrhea then multiplies within the phagolysosome.
● Nonciliated cells: When they interact with nonciliated cells they cause the cilia to
stop beating, leading to that cells death. Ciliated cells slough off. No cilia means
no clearance of bacteria from fallopian tubes.
● "Parasite-directed endocytosis"
Meningitis
● Group B doesn't have a (polysaccharide) vaccine because it is coated in poly-sialic
acid
● Polysacch: T-independent antigens
● Time from initial disease symptoms->death= 24 hours
● Purpura fulminans-was a question, literally just recognize what this is
o purpura fulminans causes widespread purpua, and can lead to DIC and
skin necrosis
● FYI
o Meningitis in infants: H flu, Group B Strep, E coli (K1-polysialic acid
capsule)
o Adolescents: N meningiditis
o Meningitis in elderly: Strep pneumo
Chapter 15
Bacteriodes- gram – rods
Most abundant in the intestines
Anaerobes only grow in anarobe conditions
Digest our food
Give us nutrients, when they come uncontained- problems, leave our
alimentary canal – surgical interventions, nick the intestine, perforation of
gut, diverticulum
Fluora is complex but theyere all anaerobic gram – rods, bacterialis fragilis
15-1 know how many species are there- polymicrobic- a bunch of diff species
, might not be sensitive to the antibiotic
bacilis, clostridia – 2 major anaerobes , pg 190 , why anaerobes are –
catalase required for detoxification of oxygen, if you don’t have those you
cant luve
-densley packed, exchange their dna
pg 191 leackage of bacteria into peritoneum
will ask if youd use metranizadole – works on anarerbobic bacteria
● G-, anaerobe
○ Bacteriodes: Gram negative obligate or facultative anaerobes
● Flora of intestines in healthy people→ only cause disease when not contained (burst
appendix or perf colon), → seed into peritoneum to make cysts(poor space for immune
response)→ dec blood
○ Example of a gram- facultative anaerobes in an abscess-E COLI
○ Abscesses are via fibrin deposition
● From table on pg. 190, only need to know B. fragilis
○ When have “bacteroides infection” usually polymicrobial→ difficult to treat
w/ a single antibiotic
● Oxygen is toxic to them
○ difficult to culture in the lab→ hard to diagnose→ use PCR
○ Makes toxic radicals bc they don’t make superoxide dismutase and
catalase
■ Fragilis is different→ more pathogenic becuse it has both
● Virulence factors
○ Produce a lipopolysccharide and polysaccharide A which undergoes phase
variation
■ Not very potent LPS (not that much sepsis)-> Different lipid A
■ Polysaccharide A-important for abscess formation
■ exhibits phase variation (turn gene expression off/on)
● Treat w/ metronidazole b/c works on anaerobes
○ But actually… (Treat with something systemic if you have perforation bc
metronidazole it can go systemic and met isnt good systemically)
○ cotreat for E coli (imipenem)
● Know about B. fragilis toxin- pg. 193 (BFT)
○ Metalloprotease, Disrupts tight junctions in enterocytes-> colon cancer
● Causes opportunistic infections
● If have a case of bac. intestinal infection leading to sepsis think, bacteroides
Chapter 16

- Dysentery = bloody diarrhea caused by an invasive organism

- Watery diarrhea due to toxins
- G- rods that grow MacConkey agar that are oxidase negative = def of
entereobacteracea
- G- rods that grow on MacConkey agar that are oxidase positive = vibrionaceae
- Vibrios exist in brackish waters (coastlines)
- Toxin co-regulated pilli = pilli necessary for Vibrio to attach to enterocyte, after
binding produce cholera toxin
- Know the mechanism of action of cholera toxin
- W/in enterobacteracea, distinguish w/ lactase presence or absence
- The type of disease E. coli cause depends on the virulence factors they have-
know the types of E. coli- add uropathogenic E. coli (virulence factor = gal-gal
pilli) & E. coli k1 (have a K antigen that is a polysialic acid also found on nerves =
don’t make an AB against it)
- Antacids make you more susceptible to E. coli infection
- ETEC uses CFA pilli to stick to the enterocyte, then produces LT which is
mechanistically identical to cholera toxin
- Know the mechanism of action of LT
- ETEC also produces ST which is a peptide that increases cGMP
- Travel to places with poor sanitation = suspect ETEC
- EPEC = leading cause of infantile diarrhea in developing countries
 - EPEC has bundle -forming pilli to attach to enterocyte & induces the bac. to
produce a type III secretion system that allows it to inject molecules (TIR)
directly into the enterocyte
- Shigella is acid-resistant (takes very few shigella to cause an infection vs. E. coli
due to the stomach acid)
o human-human
- Know fig. 16-2 on pg. 200
- TIR molecule travels to the cell surface & becomes a receptor for intimin on the
bac. surface, cause pedestal formation b/c uses cell’s actin to get to the surface
(attachment & effacement) = villus rearrangement & malabsorption
- Culture on MacConkey agar (importance of lactase)
- Treat watery diarrhea w/ oral rehydration, not antibiotics
----------------------------------------------------------------------------------
- Ch16: secretory and invasive diarrheas: e. coli
o Can be wate`ry or dysentery (or on the spectrum)
o Mostly gram negative rods.
o Table 16-1
▪ Definintion of an enterobacteriacie – gram neg rod, grow in MAC,
oxidase negative
▪ Vibrioneciae….Gram negative rods, grow in MAC, oxidase positive
▪ E coli si lactase + and salmonella/shigella are lactose –
▪ MAC incorporates bile and lactose into the agar.
▪ Just know the top 3. Escherichia, salmonella, shigella
o Don’t know table 16-2, just know organisms in text
o Next 2 pages: differences between eschericiah and vibria, who gets
infection
▪ Vibria is in brachish waters (where salt and fresh water meet) so
will be found mostly in costal areas
▪ E coli is a zonar infection, found in animals and humans
▪ E. coli can cause a lot of different infections. So for UTI – upex
strain (uropathogenic) had a p. fimbriae.
▪ Table 16-3, don’t know about EAggEC
o E. coli is sensitive to acid so you need to ingest a shit ton, and once they get
to the intestine they have to stick.
o Really need to know Fig 16-2
▪ V. cholera attaches with TCP to enterocyte which will then make it a
factory for the toxin. Binding site. Facilitates translocation of A
subunit across the membrane. ADP ribosylates adenylase cyclase
complex. cAMP only
▪ E. coli: Colonization factor of association. Produce HLT (heat labile
enterotoxin) which acts the same as cholera toxin. Also makes heat
stabile toxin (HST) stimulates cGMP activity and cAMP too.
o Moctozuma’s revenge.
o Enteropathogenic e coli. Not mediated by a major toxin but just
interaction with the cell itself. Clinical scenario you’d see it with is usually
3rd world, no sanitation in water. Kids less than 1 year of age
 ▪ Figure 16-3. IT sticks with bundle forming pili. Once it sticks it fkips
switch in bacteria to produce type 3 secretion system (injectosome)
– syringe that llows bacteria access to eukaryote. TIR goes inside
the eukaryotic cell, gets presented on surface of enterocyte (by
recruiting actin and allows it to bind to intamin on the cell to form a
pedestal formation- attachment and effacement)
▪ P. 212 of next chapter, bottom left pic shows it on the pedestal.
EHEC = EPEC +shiga toxin
o Know that there are other vibrios and e colis. Usually infected via breaks in
the skin or oysters.
o Know treatment: oral rehydration therapy, no antibiotic
--------------------------------------------------------------------------------------------------------
1. Watery diarrhea are toxin-mediated
2. Know the molecules used for attachment!
3. Table 16-1 not important for the exam, know for boards
4. Know:
5. Table 16-3 (ETEC, EPEC, EHEC. EIEC and EAgg are not as important to Meitz)
6. Fig 16-2
7.

8. Vibrio
9. basically the same pathogenesis as ETEC
10. Epidemics-brackish waters
 11. Epidemic strains: Toxin-Coregulated Pili and Cholera toxin (mediated by a
phage)
12. Cholera toxin
a. Binds GM1 Ganglioside
b. is a pentamer and w/ A (active) and B (binding) subunits-ADP
Ribosylation of Gs causes a decrease in Na absorption and an increase in
Cl secretion
13. ETEC:
14. Zoonotic
15. Cfa for attachment
16. ADP Ribosylation of adenylate cyclase
17. Know heat labile= cAMP and heat stabile=cGMP
18. EPEC:  water-borne, zoonotic, leading cause of diarrheal deaths in younguns in
3rd world countries
a. does not produce a toxin
19. FIG 16-3
20.know TIR AND INTIMIN
21. Type III secretion
22. Bundle-forming pilus
23. Tir is the receptor for intimin
24. Actin rearrangement within the cell=pedestal formation
25. "Attachment and effacement"
26. Other bugs: vibrio cholera, enterogenic and enteropathogenic ecoli
27. V haemolyticus/parahemolyticus cause skin ulcers= live in the water, shellfish
eaters or processers get this
28.Inoculum size: Shigella has a low inoculum, acid resistant

Chapter 17 Shigella, EHEC, Salmonella

-fig 17-1 , shigella can’t invade thru apical side, they have to go through M cell or invades
through the lateral junction. While shigella was inside eukaryotic cell, it produced
shigotoxin (nuclease that clips 60s ribosome- inactivates it, blocks protein synthesis-
cells die, you get white cell into lumen of gut and you get dysentery)
ICS- intercellular survival gene
- Dysentery
o worst of diarrhea spectrum
o invasive, has WBCs & RBCs
- Shigella
o acid resistant, invasive
o Cannot invade apical epi
▪ lateral have tight junction
 ▪ Invade M cells & go through tight junctions→ lamina prop→ white cell
response
● Recruits immune cells to the area
▪ Replicate on basal side & invade enterocytes from here
o Make actin comets that propel into adjacent cells
▪ Bacteria grabs the cellular actin & uses it to propel it through cell
and to the next cell
o Shiga toxin cleaves 60s ribosome→ stop protein synthesis→ kill
▪ Toxin causes ulceration of colon→ bloody diarrhea
▪ White & red cells in lumen
▪ Can look for shiga toxin in stool
o Human-human
▪ Diarrhea not contained→ can spread
o Treatment- oral rehydration, if severe→ antibiotics
▪ General principle of AB: facultative intracellular→ need it to penetrate
eukaryotic cell→ fluoroquinolones & macrolides
▪ Need an AB to get to that site of action
- T3 secretion system
o contact-dependent secretion
o Capacity of bacteria to make protein protrusion from cell surface
(injectisome) to transfer contents into eukaryotic cytosol
o Transmitting proteins from the microbe to the host cell
o Yersina, shigella, EPEC
- EPEC
o T3 secretion
▪ Bundle forming pilli that attach to enterocyte
▪ inserts tir receptor into host→ goes to surface of enterocyte = receptor for
EPEC to connect via intimin
▪ Tir recruits actin to make pedestal→ attachment & effacement
- EHEC (EPEC with shiga toxin)
o Zoonotic (contaminated meat & animal feces)- hamburgers
▪ hamburgers
o Noninvasive- makes the pedestal & toxin
o LPS produced by e coli potentiates shiga toxin
▪ Shiga-like toxin has a predisposition to kidney tissue
▪ children get HUS, shut down kidneys
▪ Adults- thrombotic thrombocytopenicpurpura
o O157:H7
▪ O & H antigens
o Grows on macconkey agar
▪ Uses lactose→ grows pink on macconkey
▪ Doesn’t use sorbitol, sorbutol
o Treatment
▪ Oral rehydration
▪ Antibiotic bad because releases toxins in bacteria
- Salmonella
o Transcytosis
▪ Bacterial mediated endocytosis
● Cause ruffling of host membrane when comes in contact
● invade apical side of enterocytes and M cells
▪ move through cell→ lamina propria→ white cell response
o Non-typhoid strain
▪ die locally (cannot grow in macros)
o Typhoid strains
▪ invade macrophages→ transport throughout body→ typhoid fever
▪ Vi antigen antiphagocytic capsule in typhoid strain→ get to different
tissue (liver, spleen, GB)
▪ septicemia (fever due to endotoxin via IL1, IL6, TNFa)
● Treat with ABs
▪ Can invade & live in bile→ colonize gallbladder (carrier state)
▪ Has ability to attack the heart→ endocarditis
o Salmonella & E.Coli req more bacteria bc not acid resistant
▪ Million organisms to cause disease in healthy stomach (antacids &
PPIs lowers this #)
o Lactase - neg→ white on macconkey
o Zoonotic- over easy eggs & turtles
o Vaccine for travelers only
 ● Case 1: 22mog, low income, near mexico, febrile, no appetite, watery dia. Next day: no dia,
stools mucous and blood→ inc→ vomit. ED: fever, gen seizure, dehydration, hyperactive bowel.
Leukocytosis, dec in Na & glucose. Fluids & Abx. Shigella grew. Got better
● Case 2: 85yom, nursing home. 3yo grandaughter visit--shared hamburger.
○ Grandpa: Ab cramps RLQ, watery dia, blood. Progressed to pure blood stool w/in 24 hr.
Nausea, no vomit. Barium enema: edema of colon with spasm. Cuture neg for salmonella
& shigella. Sorbitol nonfermenting E.coli→ O157:H7 EHEC. IV fluid
○ Grandaughter: 2 day later, watery dia, inc over 2 day→ blood. Vomit, urine output
diminish. Pale lethargic, low consiousness. Dec platelets, RBC. HUS.
● Case 3: asian in US, goes home, cared for aunt with fever & dia. 3wk later: chill, fever,
headache, muscle pain, no appetite. Fever inc over days. Ill & confused, tender
abdomen, hepatosplenomeg, no jaundice, pulse low, WBC low, monocytosis. Typhoid
fever. Ceftiraxone. Blood grow salmonella typhi. Got better. 6wk later recur. SMX-TP

Chapter 18 pseudomonas aeruginosa

- It’s everywhere, water
- Causes diesse when in the wrong place→ can cause a lot of thing bc its everythere
- Opportunistic: CF, burn pt, conjunctivits, hot tub folliculits, UTI in hospitals
- classic scenario: osteomyelitis from stepping on a nail
- Gram neg rod→ oxidase positive; Catalase+
- Read cystic fibrosis case
- Green colony & grape smell
- Virulence factors
o Water borne→ flagella
o Has to stick→ type 4 pili (cause twitching motility→ allows to retract and pull
bacteria closer to the cell)
o Need to grow→ need iron→ pyoverdin & pyocyanin (colors media
green)= Pyocyanin and pyoverdin: siderophores that grab Fe from
environment; pyocyanin also generates ROS
o Grow as biofilm- city with stacks of bacteria that need communication→
autoinducers to make alginate
o Needs protect itself→ alginate (capsule/glycocalyx), coats entire surface to
biofilm (instead of each single bacteria)
▪ Quorum sensing: produce autoinducers known as homoserine
lactones- induces alginate formation
o Pseudomonas endotoxin A→ kills cell by binding to host cell and ADP
ribosylating EF-2 so it halts protein synthesis (can halt all protein sythn in the
cell, just like diphtheria toxin)
o Elastase (CF pt- decrades lung→ cant expand and collapse→ going to need
transplant) & other proteases
o Fever → LPS
- Grow them on anything
- Treat: 100x more genome capacity→ more diversity→ highly antibiotic resistant
o efflux pumps are involved
-------------------------------------------------------------------
- Table 18-2
o Siderophores: pyochelin and pyoverdin scavenge iron. Pyoverdin turns
agar green and is a dead giveaway.
o Don’t need to know pyocyanin
-------------------------------------------------------------------------------------------
General characteristics:
● do not ferment lactose
● Alginate
o super important adhesin in CF "mucoid strains"
o equivalent of a capsule (immune evasion)
o slime layer coating (important in biofilms)
● Endotoxin (b/c gram neg)
Attachment
● Makes love to Asialo GM1 present on host cells (via flagella/pili)
o May be increased more on epithelia of CF pts
● Grow as a biofilm, recruiting neutrophils
o Protection from dehydration
● TLR5+Flagella-> wakes up inflammatory response
● TLR4+Lipid A of LPS
● Type III secretion systems and exoenzymes-don't worry about it

Chapter 19 Bordetella
● Gram neg coccobacillus, fastidious
○ Related to Hemoph,
○ obligate human mucosal pathogens, we are transiently colonized w/
○ Not going to ask about the other bordatellas, just pertussis
● Clinical
○ whooping cough/croup- "diarrhea of the lungs"
● Toxins
○ Endotoxin: mucosal, short chain LPS-LOS
■ Responsible for host immune response/fever
○ Adenylate cyclase toxin- similar to heat-labile enterotoxin/Cholera toxin
○ Pertussis toxin-AB5 toxin, assoc w/ lymphocytosis, ADP-ribosylating
toxin (Gi), produces adenylyl cyclase
○ Other ADP-ribosylaters (he loves his ADP ribosylation!): cholera,
diphtheria, exotoxin A of pseudomonas
○ Tracheal cytotoxin (he asked a question about this before)- a component
of peptidoglycan layer of pertussis; if you were to isolate this it could do
damage to tracheal cells
■ Similar to gonorrhea's mechanism of damage
● Virulence
○ Fimbriae-adherence
○ FimHagglutin-like pili
○ Pertactin- assoc w/ cell surface
● Ddx
 ○ Bordet-Gengou agar selects for it (starts the same way as the bacteria!)
● Illness:
○ First stage:Cattharal stage: mucosal secretions, "cold like"
■ If you don't tx in this stage....recovering can take 6 months
○ Paroxysmal: One week after beginning dz, classical "whoop", ppl faint,
lasts 2-8 weeks
● Vaccine-DtaP->  was definitely a question on preventing pertussis in infants via
vaccination (at birth? vaccinate mom? etc)
○ acellular pertussis= 2-4 pertussis toxins rather than the whole, killed
bacteria
○ "Homeschool"- keyword for not vaccinated
○ Older adults might have waning titers, even if vaccinated-can have bad dz
if not tx'd (macrolides/TTC)
○ Diptheria/Tet: purified toxins: "Toxoids"-thermically inactivated the
enzymatic activity, retain antigenicity
○ Kids would get fevers b/c of endotoxin that remained in the vaccine; led to
ppl not vaccinating and caused new cases of pertussis
○ Because it is a killed vaccine, you need boosters (10 year boosters, 3*)
○ *These virulence factors listed above are required for the vaccine; you
also need the adenyl cyclase toxin and the pertussis toxin in the vaccine
● Boards, not PBL exam- *Know the HACEK organisms for boards
● Kingella "pitting of the agar"
Chapter 20 Clostridia
- Gram pos rod, anaerobic, spore forming
- C diff
o Antibiotic associated diarrhea, antibiotic suppresses normal
flora of gut.
o Pseudomembranous colitis
▪ Cause malabsorption
▪ Often the colitis is so bad you need to resect the colon
o Antibiotic associated
▪ (especially broad-spec that acts on anaerobes like
CLINDAMYCIN)
o Ingestion of clostridial spores in context of antibiotic therapy
▪ Part of flora, spore repopulates
▪ Toxogenic strains in hospitals have spores
o Toxins
▪ A&B Glucosylate (put a glucose on) Rho GTPases→ inactivate→ loss of
structure & die→ pseudomembrane
▪ Just like cholera and E coli, the bacteria themselves do not invade
the mucosa-it's the toxins
o Diag
▪ C. diff infection usually diagnosed by detecting toxins in feces
o Treatment
▪ anaerobe→ treat metronidazole
▪ Oral vancomycin
- C. perfringens
o Food borne illnesses
o Gram +, spore formers
o 4th leading cause of diarrhea in US!!!!!!
▪ Watery diarrhea, self-limiting
▪ Between 8-14 hours, food is infected by the spores, germinate and
secrete a enterotoxin
▪ Enterotoxin itself is pore-forming that pokes holes in enterocytes
▪ Causes pigbell in the germans (bloody diarrhea) associated with pok
o Gas gangrene, loose limbs
▪ Deep wound (anaerobic)--> germinates
● Also likes calcium and areas of poor perfusion
▪ Produce lecithinase
● phospholipase C-degrades membrane phospholipids to cause
cell death and Gas gangrene & myonecrosis
● Allow it to spread through tissues
● Anaerobic fermentation→ produce gas
● Tissue necrosis and crepitus
● Muscle poorly vascular→ cant get ABs in there→ debridement
o Diagnosis:
▪ For wounds: gram stains and culture under anaerobic conditions
 - C. tetani
o Rusty nails, wound infections w/ contact to soil
o Tetanus toxin
▪ Spastic paralysis via gaba & glycine inhibition
▪ Lock jaw
o Vaccine: tetanus toxoid (DTaP)
▪ Take toxin, treat with chemical to make enzymatic activity gone,
retains antigenicity
- C. Botulinum
o ingestion of preformed clostridial neurotoxin in contaminated food
(does not necessarily change appear or taste of food)
▪ classically in home-canned food
▪ Spore in cans→ no o2 & energy→ germinates and makes botulism toxin
▪ Not an infection, = intoxication
o Descending flaccid paralysis via inhibition of Ach release at
peripheral cholinergic junctions
▪ Diplopia
▪ Dysphagia
▪ Keeps going down
▪ Cant breath
o Babies
▪ High spore count in honey
▪ Can infect & grow in the Gi bc no competing bacteria
▪ Floppy baby syndrome
▪ Kills babies by getting into umbilical cord
o Treat with antitoxin
▪ "passive immunization"
▪ pregos, infants, children
- Know the difference between how botox/tetanus toxins work
- Case 1: 79yow, diabetic, nursing home. Persistent leg ulcer→ debried, cephalosporins &
ampicillin. Fever, watery dia, low ab pain. Stool + for toxin A & B of c.diff, oral
metronidazole. 3wk later: return, oral vancomycin

Chapter 21 Legionella
● Gram stains variably
● Lung infection, immunocomproised (old smoker exposed to water source)
● Facultative IC bacteria
○ Environment- lives in amoebas
○ When hangs out, exists as a biofilm in pipes & water stuff
○ Infected water gets aerosolized→ lung infection
○ Likes to hang out near ER (p244)
○ Don't need to know transmitted and replicated forms
○ Live in water so have flagella
○ Block phagosomal fusion so can live in cell
○ Don't need to know about secretion system
○ Cytokines reacto to lipopolysaccharide→ Fever, SOB, watery diarrhea
 ○ Can grow outside, but would rather not
● Don't worry about paradigm box
● Pneumonia with diarrhea
● Diag: culture (need special lab), urine antigen test (legionella buzz word)
● Need drug that gets inside the cell
○ Macrolides
○ Fluoroquinolones
---------------------------------------------------------------------------
Facultative intracellular bacteria; 2 obligate are chlamydia and ; can live outside but
prefers to be inside. Its a gram neg rod, it gram stains variably; p. 243 when you hear of
something with plumbing and pneumonia think legionella. It likes to hang out in
nature-ameba; when it gets inside cells it gets into alveolar macrophages. During its trip
into our body, it escapes ameba or ameba dies and it grows on pipes forming a bile film,
staying indefinitely. Highly resistant to chlorine and highly heat resistant. See
outbreaks, typically infects older immunocompromised people. Conventional
legionaires, infected these old smokers, exposed to aerosols from pipes. Gains access by
aeorolization ,comes into lungs, picked up by alv mac, inhibits phag lys fusion. Key
factor: programs endosome to head toward ER. Dont care about replic. Trans. Stringent
Response. Dont get down in the weeds about paradigm box, Rab 1. Disease itself is the
immune response to infection, TNF alpha . Symptoms typical of pneumonia, fever cough
SOB, chest pain. One thing you need to know, whenever you see pneuominia with
diarrhea think legionella. Young people can get it as well if it is in high enough doses.
These org are diff to grow. For boards, not for his q’s: when you see agar media with
charcoal and cysteine, theyre talking about growing up Legionella. Treatment: need to
ID source and can use UV light, problem with hospitals- cant just turn up temp of water,
do it by wings, incorporate ionizing tank in water producing copper and silver to inhibit
growth. Dont worry about pther diseases assoc. Like pontiac fever
Treatment: need to think about these org being inside cell, abx needs to penetrate into
cells; 2 classes: macrolides and fluoroquinolones
---------------------------------------------------------------------
- Gram neg rod, facultative intracellular (so you need macrolide or
fluoroquinolone)
- Likes to hang out in amoebas and macrophages
- Difficult to grow but they can be grown
- Poor gram strainers, they cause pneumonia. So if you gram stain someone with
pneumonia and nothing is there, then think legionella
- Like to grow as biofilms in plumbing and can aerosolize in the environment
- Not transmitted person to person
- Needs to be aerosolized, inhalation pneumonia, not aspirated. Atypical
pneumonia
- Enveloped by endoplasmic reticulum similar to autophagy in resident alveolar
macrophages. Don’t need to know tramissible form or stringent response. Don’t
really need to know other inctracellular stuff
- Don’t worry about paradigm
- Damage due to cytokines. Atypical pneumonia, long term low grade fever. Person
with pneumonia + diarrhea is likely for legionella
 - Urine antigen is a way to diagnose
- Best prevention is better water treatment. Need higher concentrations of chlorine
to kill and much higher heat (above 70 degrees)
- Don’t worry about other pegionella diseases
--------------------------------------------------------------------------------------------------------
--------------------
Gram (-) rod, but stains poorly
Example patient: 65 year-old, immunocompromised, with history of water contact,
atypical pneumonia AND diarrhea
Live in two places: facultative intracellular pathogen, can live outside a cell but want to
be inside a cell
Difficult to grow in lab, need CHARCOAL AGAR
Also lives as a biolfilm, think plumbing pipes
Point source spread via aerosol, NOT spread person to person
Resistant to chlorine and heat, but need high levels to kill legionella
Legionella into macrophages
Get into cytoplasm and then into ER and feed off the proteins being made there
Skip the paradigm box
Host cell-mediated response causes the damage
Urine antigen test can confirm presence of Legionella
Antibiotic must get access to microbe inside cell macrolides and fluoroquinolones
--------------------------------------------------------------------------------------------------------
--------------------
Fastidious gram- rod (requires charcoal/cysteine/iron)
Facultative intracellular bacteria- does not get consumed by a phagolysosome,
enters the endoplasmic reticulum instead, causing differentiation into the replicative
form
Once legionella has chewed the macrophage/amoeba up, it converts to a
transmissible form (mediated by the stress response known as the stringent reponse)
The transmissible form has flagella
Don't worry about the paradigm box
Environmentally, they are harbored in the H20 in amoebae- not transmitted
person-to-person
No toxin, induces an immune response
Can cause pneumonia, diarrhea
Dx: culture (unique requirements, see above), urine antigen test (has been a
question), no PCR
Clinical pearls/potential buzzwords for clinical scenario: was a question in the past
-old building (eg, VA hospital w/ low budget, retirement home, etc)
-air conditioner
-immunocompromised/older
-smokers
-old pipes-grows as a biofilm
Getting rid of it in the environment: Begin w/ a heat flush,  Copper/silver ionization
system, resistant to chlorine
Tx/prevention: B/c facultative intracellular-Fluoroquinolones/Macrolides
Other strains: know pontiac fever, not the others
Chapter 22 H. pylori
● Key concepts area
● Gram -, helical (although really comma) shaped
● Colonized 60-70% of stomachs
○ Can carry with no prob
○ Get ulcer
● Increased cell replication→ Maltoma- MALT lymphoma → gastric cancer
● Makes urease- clips urea into NH4 & CO2→ ammonia cloud around bacteria→ can
survive acit
● flagella→ motile; goes from lumen to mucosa to get at the low pH
● Figure 22-3 (Focus on)
○ Adhere (dont need to know bab or sab)
○ 2 toxins: CagA (-->morphologic changes in mucosa) VacA (--> apoptosis)
■ Alter shape & kill→ immune response
○ T4 secretion (injectisome)
● Diagnosis
○ steiner stain (specific for H. pylori) after endoscopy
○ Urea breath test- radiolabeled urea→ exhale radiolabeled CO2
○ Elisa for ABs but less specific
● Treatment
○ Triple or quad therapy (know both)
■ Include PPI
■ 1-2 AB (one should be good for anaerobes)
■ Neutralizing agents (bismuth)
○ Long term 14d treatment
● BTW: metronidazole & clarithromytacin work great on anaerobes
----------------------------------------------------------------------------------
- Pathogen: Gram negative, helical shaped microbe with high degree genetic
diversity
- Encounter:
o Infects half of the world, acquired in childhood. Fecal-oral or oral-oral
routes.
- Entry:
o Able to survive in highly acidic environment of the stomach. Produces
urease that buffers the acid by producing ammonium (NH4+) from
urea.
- Spread and multiplication:
o Colonizes the mucus layer and epithelial surface of the stomach.
o It evades host immunity via vacuolating toxin (VacA) that suppresses T-
Cell responses
- Damage:
o VacA – causes cell death of the gastric epithelium
o CagA- disrupts tight junctions between cells
o Gastritis- via low levels of inflammation
 o Chronic infection-10% chance of developing gastric/duodenal ulcers,
atrophic gastritis, and gastric adenocarcinoma, or gastric MALT
lymphoma
- Diagnosis:
o Rapid urease test, histology and microbial culture on endoscopic
biopsy.
o H.Pylori specific serology and stool antigens by immunoassay- stool
antigen is highly accurate.
- Treatment and prevention:
Triple therapy- two antibiotics with a proton pump inhibitor

Chapter 23 Mycobacterium
- Mycobacteria - does not Gram stain; use acid-fast stain
o Acid-fast = Ziehl-Neelson = fluorochrome stain
o Different from Mycoplasma, which lack cell wall
- Two pathogenic strains
o Tuberculosis and leprae
- Also have Mycobacteria Avian complex
- Very fastidious and slow-growing, obligate aerobes
o Extremely slow-growing; generation time is 20 hours in contrast to 20
minutes for E. coli
- Similar to Gram-positive organisms even though they don’t Gram-stain
o Have cytoplasmic membrane, cell wall with mycolic acids, doesn’t have
outer membrane, making it Gram-positive-like
o Mycolic acid provides waxy coating on cell surface, so Gram-stain reagents
won’t penetrate

- Page 258 - Case of Ms. A

o Recurrent TB
o Localization of TB to upper lobes
- Waxy cell coat - organism is resistant to drying and can persist in environment
for long time
- Transferred from human to human
- Can’t grow M. leprae in culture
- Page 260
 o In US, don’t have M. tuberculosis for respiratory infections, but worldwide
it’s a huge problem
o Because we have healthy immunocompetent population
- Spread by droplets
o Inhalation infection → inhalation pneumonia; vs aspiration infection
o Breathe it in and it gets into alveoli
o Gets into lungs to cause primary infection
▪ Recruits alveolar macrophages and it gets inside them
▪ Inhibit phagolysosome
▪ Secretes cytokines, recruiting lymphocytes to the area to surround
infected alveolar macrophage, giving rise to Ghon complex
- Ghon complex - lymphogranuloma
- Lack of robust T-cell response makes you more susceptible to disease
- Tuberculoid tuberculosis - immunocompetent immune response forming a
granuloma
- Immunocompromised patients - organism exists within macrophage, is transferred
throughout the body → miliary tuberculosis; can have meningitis
- Endogenous TB - main cytokines are TNF-alpha and IL-1
o Take toll on body
o Causes a wasting disease → fever, weight loss, night sweats
- Key test - tuberculin test, PPD
o Injection underneath skin + await immune response
o Outside US, they use live attenuated vaccine → BCG vaccine
▪ Shown to be about 70% protective in population, so not perfect, but
it’s better than nothing
o US - incidence is so low that we don’t vaccinate; we’d rather screen
- Localized infection, low-grade, not debilitating
o Osteomyelitis in adults, infecting vertebral bodies (Pott’s disease)
o Can cause meningitis
- Diagnosis
o Sputum sample if you have active infection
▪ Gram-stain and look for acid-fast bacilli
o Skin test
o Gold standard is culturing, which takes weeks
- Treatment
o Anti-TB drugs are very selective, but resistance develops
o Initially use 3-4 drugs till we isolate the strain and find what it’s resistant
to
▪ INH, rifampin (for RNA polymerase), pyrazinamide, ethambutol
- Prevention
o Screening in US
- M. leprae
o Only found in humans
o Armadillo
 o Optimal temperature of 35 degrees, so localized to the extremities
o Like TB, it depends on immune status
o If T cells don’t work, you get lepromatous leprosy
o Lepromin is the equivalent of tuberculin
---------------------------------------------------------------------
- Obligate aerobes, resistant to drying (live for a long time in the air), grow very
slowly (doubling time is 15hrs), and they are acid-fast staining
- Only need to know M. tuberculosis and M. leprae from 23-1
- Can’t grow M. leprae in vitro but we do know that it’s optimum growth temp is 35
C which is why it stays in the extremities
- Exclusive human pathogens, just like pneumococcus
- Taken up by alveolar macrophages, where it can stop phagolysosomal fusion so it
can stay alive inside of it while also stimulating the macrophage to release
cytokines to bring lymphocytes to area that will form granulomatous Ghon
complexes (tuberculoid tuberculosis)
- If immune system wanes, then the granuloma falls apart. This is the
Reactivation/secondary TB.
- The case is secondary TB, which tend to exist in the upper lobes because
there is a lot of air and lymph nodes for spread
- Immunocompromised: no granuloma is formed and then this goes to become
miliary tuberculosis which can lead to Pott disease
- (treatment p266) Isonazid, pyrazinamide, and ethambutol are specific
for TB
- BCG vaccine is a live vaccine, efficacy is only 7% effective
- M. leprae – very poorly spread
o Localized to extremities because it likes 35 C instead of 37 C
o Poor immune response leads to lepromatous is analgous to miliary in TB
--------------------------------------------------------------------------------------------------------
●
● Grow extremely slowly (doubling time= a day)-> you don't culture
o Tx pts empirically (rifampin, isoniazid, ethambutol, pyrazinamide)
● Know BCG, M Tuberculosis, M Leprae
o BCG- attenuated mycobacterium that is used as the vaccine
● Entry: aerosolization
o p 258- "pulmonary TB", normally see it in the upper lobes
o Infects macrophages, impairing phagolysosomal fusion
● Normally: macrophages induce cytokines/lymphocytes, forming a granuloma
● Cell wall component: purified protein derivative (basis for the test)
o If you are infected, T-cell response-> you get the bump
o + PPD-> looking for granulomas on CXR
o Neg CXR-pt had exposure, cleared it
● Immunocompromised
o Miliary TB (encephalitis) because you can't get a good T cell response

Leprosy "Hansen's disease"

 ● Grows at low temperature/35 degrees (skin)
● Can have tuberculoid (TH1 response)-> granulomas in nerve endings
o Loss of sensation in extremities, susceptibility to infx
● Miliary equivalent: (Th2 response) Lepromatous leprosy (lepromatous is lethal)
o "Lion face"
Tx:
● Rifampin, Isoniazid, Pyrazinamide, Ethambutol "RIPE"
o Rifampin= RNA polymerase inhibitor
● INH, Pyrazinamide, Ethambutol-> selective for TB
o Start on 3 of these drugs, then discontinue 2 when sensitivities are
determined
● Drug resistance=huge problem
Lots of TB now because of HIV pts

Chapter 24 Syphilis
Spirochetes-doesn't gram stain, more like a gram -
● Flagella is internal in the periplasmic space- endoflagella
o Corkscrew-like movement
o Other spirochete dz: Lyme, Relapsing fever (Borrelia), Leptospira
o "Non sexy" syphilis-yaws, pinta-> will give you + syphilis tests, but rare in
U
● Dx: dark field microscopy
● Lacks LPS
First stage: organism enters microabrasions, causes a painless chancre
● "1/3 rule"-If untreated, 66% of cases will self-resolve (our book says 50%)
o The rest, 2 months later-> secondary syphilis
▪ Rashes on palms/soles, flu-like symptoms, lymphadenopathy
● 1/3 of these 2ndary syphilis will proceed to symptoms after latent/tertiary
syphilis
o Know the dz involved in tertiary syphilis
▪ gummas-fatty lesions on the bones/liver
▪ Heart dz-endarteritis of the vasa vasorum,aortic insufficiency,
aortic aneurysms/rupture
▪ Neurosyphilis-tabes dorsalis (lost proprioception), Argyll-
Robertson pupil (accommodates, doesn't react to light)
▪ "Charcot Joint"
▪ Lesions contain few treponemes -he didn't say this but it has
come up on practice questions
● Congenital syphilis-know the buzzwords
o Hutchinson incisors, mulberry molars, saber shins, deafness, arthritis
● Dx w/ serology
o VRDL/RPR uses bovine cardiolipin (a mitochondrial lipid)
▪ Lots of false +
▪ Things like virus, lupus, some drugs
o FTA is confirmatory
 ● Tx w/ Penicillin G (injectable-1 week for primary, secondary and 3 weeks for
tertiary)
● Not that many cases of syphilis-less than HIV
o Note that according to our STD chapter, the incidence of syphilis is rising
o Increased incidence in MSM

Chapter 25 Lyme disease (borrelia burgdorferi – spirochete)

- Can be observed by dark field microscopy
- Takes 3 days for transfer of ticks midgut contents to blood stream.
- Localized spirochetemia (bullseye rash – erythema migrans, only occurs in 50%
of infected)- 48 hours to get to skin from tick
- Mice association, mice take over- from lyme
- Know table 25-1, pretty helpful, don’t worry about treatment part
--------------------------------------------------------------------------------------------------------
● Cause of arthritis in young people
● Spirochetes are gram negative "like" because they have outer cytoplasmic
membrane, but they don't gram stain
● Kinky periplasmic flagella=endoflagella
● know Borrellia burgdorferi
● Has a Linear chromosome w/ 22 linear plasmids
o Outer surface proteins=Osps (lipoproteins); cause cross-reactivity w/ host
tissues and the autoimmune neuro sequelae
o Didn't mention this,but I would note the lack of LPS
● OspA/OspC outer surface proteins that can be switched on/off depending on
where they're growing
o Osps can be used as vaccines
o Important for colonization and protection from antibodies
o Phenotypic changes brought on by + temperature (cos they drank blood,
yum): OpsA->C
● Fig 25-1- Know the stages
o 1st: local infx+rash (erythema chronicum migrans)
▪ In the past, he has written this question: clinical scenario where
someone removed a tick from their hair so the rash was not seen
▪ If not treated, moves to stage II: spirochetemia all up in the
bloodstream (penetrates endothelium)
o 2ndary lyme dz
▪ rashes EVERYFUCKINGWHERE
▪ Myocarditis+AV block
▪ Bell's palsy
▪ Meningitis
▪ Eye stuff: Conjunctivitis, Iritis, Choroiditis, Panopthalmitis
▪ Arthritis
o Tertiary lyme dz- KNOW THESE
▪ Progressive arthritis
▪ lyme encephalopathy
 ▪ Can have post-lyme syndrome complications years later, assoc w/
HLA times that are the same as rheumatoid arthritis; autoimmunity
implied
● Rx w/ doxycycline (won't be asked on PBL exam)
● Zoonotic infection, lives in animal reservoir (deer or white footed mouse,
different for each animal). Comes from the deer tick (oxoides). Localized to
certain parts of US
● Fig 25-5 -Seasonality=know peak is summer (bit less in the fall)-> because of tick
life cycle (doesn't sound like we need to know details)
● Know that B Bg likes to bind to Glycosaminoglycans (GAGS) in the ECM
(past question, though may have been removed from bank)
● One way B Bg avoids the immune system is via antigenic variability: VlsE is
an important outer surface protein for this job
● Be familiar w/ geographic distribution (25-6)
● Dx:Mostly clinical
o Analogous to syphilis; use ELISA to screen and confirm w/ Western blot
o Possible false + tests if pt has had past infx from other spirochetes (like the
Syph!)
o Don't worry about treatment
For boards, not PBL: Know the other spirochete dz
Prevention: Anti-OpsA antibody based vaccine don't help the person (or dog :( ) clear
the dz; rather it introduces the antibodies into the tick, kills existing spirochetes in the
tick, and prevents further spread *withdrawn from market according to book

Chapter 26

Gram -
Transmission:
● B Henselae: Cats
● B Quinata: Humans/Louse (humans=reservoir)
● B Bacilliformis: Sandfly (humans=reservoir)
General characteristics:
● Attach to RBCs and cause malformations in the blood vessels
● Cytokines cause proliferation of blood vessels-> bacillary angiomatosis
● Entering the erythrocytes causes a relapsing fever
● Difficult to grow
 ● read the case is Mietzner code for "this has an 80-90% chance of being a clinical
vignette on the PBL test"
● B Quinata and B Henselae assoc w/ AIDS
B bacilliformis-deforms erythrocyte membranes and multiplies within erythrocytes,
leading to a hemolytic anemia
Won't ask about treatment

Chapter 27 Chlamydia
-microbio slides
-elementary body engulfed in endosome , differentiates into reticulate body (becomes
active and replicates)- obligate energy parasites get it from the cell
● One of 2 obligate intracellular bacteria. Chlamydia and rikettsia
● Because so small even if gram stain can't see them.
● What’s the architecture, most like?
○ Like gram neg because has outer membrane and cytoplasmic mem.
○ Chlamydia and mycoplasma in pharm book says don't have cell wall, at
that time was true, but can treat chlamydia with cell wall synthesis
inhibitor- chlamydia dilemma.
○ Sequence genome of chlamydia and see homologs of PBPs found in
genome and so it does have a cell wall not amenable to visual techniques.
Like other gram neg they have LPS.
○ In contrast to rickettsia, chlamydia are energy parasites. Require host cell
ATP.
● Main disease: STD’s chlamydia trachomatis.
○ STD prevalence morbidity- # times it occurs in pop, 800 cases per
100,000 in pop.
○ Can be the cause of infertility in women.
● Table 27-1. Have to know first 4 rows and psitacci.
● P. 294 Trachomatis- serotypes
 ○ A-c. org with propensity for eye.
■ Leading cause of bac blindness in world.
■ A-c can still cause STD’s just higher propensity for eye.
○ D-k type see in STD’s.
■ STD presents as urethritis(male) or cervicits (female).
■ It moves up to endometritis, getting into fallopian tubes
salpingities.
■ Doesnt ascend like gonorrhea where it gets into blood and joints.
■ Because its so prevalent, gives rise to reactive arthritis- reiter’s
syndrome, dont call it anymore because he was nazi and discovered
this on jews- can’t see can’t pee can’t climb a tree. Can cause bac
neonatorum- give baby erythromycin eye drops.
○ L strains
■ Assoc. With warm weather and poor,.
■ Go into lymph node, strangulates them and becomes sore and
painful, visible on inspection.
● C. pneumonia-
○ form of atypical, walking pneumonia,
○ characteristics: interstitial pneumonia, not lobar,
○ only animal reservoir: human, so its maintained in population.
○ Most are asymptomatic.
○ Need to know, on boards and meitz: unknown if its causation or
correlation but atherosclerosis of plaques assoc 80% with c. pneumonia.
■ C. trachomatis 5% diff genome.
● Psittaci
○ Zoonotic pneumoniae- endemic to tropical birds. Parrot fever.
○ Have parrot, clean out its cage, aerosol dust, breathe it in, pneumonia.
● Life cycle:
○ either through aerosol or body fluids (sex),
○ the organism outside of cell exists as EB.
■ Outer mem proteins have high cysteine residue concentrations.
■ In oxygen becomes disulf bonded, shell is covalently bonded- small
dot on p. 296.
■ Particle is not met act not sensitive to abx.
■ Person with active chlamydia infection can autoinoculate their eyes.
■ Its the infectious form.
○ Finds eukaryotic cell, taken up into endosome, endosome escapes fusion
phag lys.
○ In cell it converts into RB,
■ larger, met act, dividing form, non infectious.
■ RB in endosome begins to double. Fig 27-2.
■ Inclusion body is when chlamydia is inside the cell.
■ The energy it needs is a membrane away from where it is.
■ The org produces a type 3 sec system,
● like a straw instead of injecting, its sucking nutrients up to
feed organism as it grows in endosome.
 ○ Eventually ATP and other nutrients exhaust themselves, org senses time to
move on, RB convert to EB,
○ endosome lyses and spreads EB to adjacent cells to repeat infectious cycle.
● Fig 27-1. Portrays persistence.
○ In women, 99% men have urethritis assoc with chlam,
■ 33% are asymptomatic.
■ One possibility: they have persistent infections, have immune
response kind of holding infection in check, still there, gives rise to
inflamm response.
● Even though have silent symptoms, immune response still
there and thats what damages the fallopian tubes and so
forth.
● Dont get down on weeds about CD4 and CD8 cells.
● Damage is result of inflamm resp to presence of org.
■ Gives rise to sym sim to gonorrhea.
■ Urethral, cervical exudate, nothing but white cells.
■ In women, causes urethritis, cervicitis, endometritis, salpingitis.
■ In men, rarely goes to prostate.
● P. 298 concept of damaging fallopian tubes: when egg goes down tube, gets stuck,
fertilized in tube, grown in tube, ectopic preg- life threatening;
● C. pneumoniae can be assoc. With CAD
● Most labs dont culture org because don’t have euk cells needed to culture obl int
bac.
● Dx via NAATs.
● Need to know: Comorbidity of gonorrhea with chlam; 50% of chlam coinf with
gon; 50% of gon with coinf of chlam.
● Treatment:
○ consider treating gon and chlam.
○ need to think about these orgs being inside cell, abx needs to penetrate
into cells;
■ 2 classes: macrolides and fluoroquinolones; won't ask what abx but
will ask the class, to see if you know that it's an intracellular.
-----------------------------------------------------------
One of 2 obligate intracellular bacteria. Beccause so small even if gram stain can't see
them. What’s the architecture, most like? Like gram neg because has outer membrane
and cytoplasmic mem. Chlamydia and mycoplasma in pharm book says don't have cell
wall, at that time was true, but can treat chlamydia with cell wall synthesis inhibitor-
chlamydia dilemma. Sequence genome of chlamydia and see homologs of PBPs found in
genome and so it does have a cell wall not amenable to visual techniques. Like other
gram neg they have LPS. In contrast to rickettsia, chlamydia are energy parasites.
Require host cell ATP.
Main disease: STD’s chlamydia trachomatis. STD prevalence morbidity- # times it
occurs in pop, 800 cases per 100,000 in pop. Can be the cause of infertility in women.
Table 27-1. Have to know first 4 rows and psitacci.
P. 294 Trachomatis- serotypes A-c. org with propensity for eye. Leading cause of bac
blindness in world. A-c can still cause STD’s just higher propensity for eye. D-k type see
in STD’s. STD presents as urethritis(male) or cervicits (female). It moves up to
endometritis, getting into fallopian tubes salpingities. Doesnt ascend like gonorrhea
where it gets into blood and joints. Because its so prevalent, gives rise to reactive
arthritis- reiter’s syndrome, dont call it anymore because he was nazi and discovered
this on jews- can’t see can’t pee can’t climb a tree. Can cause bac neonatorum- give baby
erythromycin eye drops.
Assoc. With warm weather and poor, L strains. Go into lymph node, strangulates them
and becomes sore and painful, visible on inspection.
C. pneumonia- form of atypical, walking pneumonia, characteristics: interstitial
pneumonia, not lobar, only animal reservoir: human, so its maintained in population.
Most are asymptomatic. Need to know, on boards and meitz: unknown if its causation or
correlation but atherosclerosis of plaques assoc 80% with c. pneumonia. C. trachomatis
5% diff genome.
Zoonotic pneumoniae- psittaci endemic to tropical birds. Parrot fever. Have parrot,
clean out its cage, aerosol dust, breathe it in, pneumonia.
Life cycle: either through aerosol or body fluids (sex), the organism outside of cell exists
as EB. Outer mem proteins have high cysteine residue concentrations. In oxygen
becomes disulf bonded, shell is covalently bonded- small dot on p. 296. Particle is not
met act not sensitive to abx. Person with active chlamydia infection can autoinoculate
their eyes. Its the infectious form. Finds eukaryotic cell, taken up into endosome,
endosome escapes fusion phag lys. In cell it converts into RB, larger, met act, dividing
form, non infectious. RB in endosome begins to double. Fig 27-2. Inclusion body is
when chlamydia is inside the cell. The energy it needs is a membrane away from where
it is. The org produces a type 3 sec system, like a straw instead of injecting, its sucking
nutrients up to feed organism as it grows in endosome. Eventually ATP and other
nutrients exhaust themselves, org senses time to move on, RB convert to EB, endosome
lyses and spreads EB to adjacent cells to repeat infectious cycle.
Fig 27-1. Portrays persistence. In women, 99% men have urethritis assoc with chlam,
33% are asymptomatic. One possibility: they have persistent infections, have immune
response kind of holding infection in check, still there, gives rise to inflamm response.
Even though have silent symptoms, immune response still there and thats what
damages the fallopian tubes and so forth. Dont get down on weeds about CD4 and CD8
cells. Damage is result of inflamm resp to presence of org. Gives rise to sym sim to
gonorrhea. Urethral, cervical exudate, nothing but white cells. In women, causes
urethritis, cervicitis, endometritis, salpingitis. In men, rarely goes to prostate.
P. 298 concept of damaging fallopian tubes: when egg goes down tube, gets stuck,
fertilized in tube, grown in tube, ectopic preg- life threatening; C. pneumoniae can be
assoc. With CAD
Most labs dont culture org because don’t have euk cells needed to culture obl int bac. Dx
via NAATs. Need to know: Comorbidity of gonorrhea with chlam; 50% of chlam coinf
with gon; 50% of gon with coinf of chlam. Treatment: consider treating gon and chlam.
Treatment: need to think about these org being inside cell, abx needs to penetrate into
cells; 2 classes: macrolides and fluoroquinolones; won't ask what abx but will ask the
class, to see if you know that it's an intracellular.
-------------------------------------------------
- Obligate intracellular (Ricketsiae are the other ob intracellulars)
- Energy parasites (can’t make own ATP) and are auxotrophic (can’t make certain
amino acids)
 - Too small to gram stain but it is gram negative like in structure
- Has a cell wall but it’s just too small to see
- 2 types:
o Mucosal surface infections (Chlamydia)
o Respiratory diseases (Chlamydophila)
- Table 27-1 know
o C. trachomatis A-C (blindness), D-K (STDs)
▪ These aren’t exclusively limited to blindness or STDs tho
o L1-3 associated with LGV
▪ Clog lymphatic flow that can lead to swelling of lymph nodes
o Chlamydophila pneumonia
▪ Walking pneumonia, intersitital pneumonia.
▪ Associated with atherosclerosis
o C. psittaci is from parrot poop and other birds. Atypical pneumonia
- Life cycle of chlamydia (fig 27-1 pg 196)
o Elementary body, not sensitive to antibiotics because they can’t replicate
or grow. Infectious form. When put into vesicles/vacuoules, Oxygen levels
drop and then the cysteine residues loosen and the EB becomes a RB.
o Reticulate body. Uses type 3 secretion system to get nutrients from outside
the vacuole without having to leave it.
o Asymptomatic infections are due to immune system freezing chlamydia in
a reticulate body state even tho its doing damage
- Can ascend urinary and genital tracts
- Reiter’s syndrome (reactive arthritis) especially for HLA-B27 allele (?)
- NAATs is a more accurate way to test for chlamydia
- Number of cases are not going down
- Treated with macrolides or fluoroquinolones because its intracellular

Chapter 28 Rocky Mountain Spotted Fever

General Features
● obligate intracellular→ do not gram stain, but are gram negative-like
● membrane transporter for acquiring ATP
 o not strictly energy parasites, because can both make their own
ATP in addition to stealing it from host cells (unlike chlamydia)
● Dz of the endothelium-(explains the rash)
o free-radical induced damage to the cell membrane
● R Rickettsii-RMSF
o not a zoonotic infx
▪ tick (Dermacentor) is the reservoir AND the vector
▪ requires 24 hr to transmit blood meal
o enter the cell and spread from cell-cell using actin filaments; make
pseudopodia

● R Typhi
● Ehrlichiosis
o Infection in leukocytes
o Ehrlichiosis+Anaplasmosis-> coinfx w/ Lyme (that pesky Ixodes tick also
carries Babesosis!)
● Coxiella
o Q fever in cattle, sheep goats
o Aerosolized
o domestic animals giving birth (said this 3 times)
o invades macrophages and can be granulomatous
● Diag via: Clinical presentation & Weil-Felix test
 ● Case 1: 9yog mobile home, North Carolina, plays in grass & weeds. Removes ticks
from body every day. fever, severe headache, muscle pains. Then nausea, vomit,
ab pain. Then erythematous rash of 2-4mm macules w/ areas of pink
discoloration on wrists & ankles. Progressed to arms, legs, trunk; many became
maculopapular (red & raised) w/ petechiae. Neg Rocky mtn in blood, CSF, &
urine. Stuporous, edema of face & extremities. Docycycline for rocky mtn. Better.
Titer of AB to rickettsia rickettsii.

Chapter 29 Mycoplasma
Freak of nature: one bacteria lacks cell wall!
○ Extracellular pathogen
○ “Requires” sterols for growth (doesn’t really require it but can incorporate
exogenous cholesterol it into its membrane)
● Confined to Upper respiratory tract or genitalia
● Mycoplasma Pneumoniae
○ Analogue to chlamydiae pneumonia
○ Not lobar

○ “Fried egg” colony formation

■ This is for all Mycoplasma!
○ Takes a long time to grow up on agar
● M. Pneumoniae
○ Person to person by aerosol
○ Prolonged asymptomatic colonization period
■ 2 weeks to a month
○ Organism is confined to Upper Resp tract, does not disseminate
● CARDS toxin
○ Associated with M. Pneumoniae
○ Don’t need to know the mechanism of it
● Cold Hemagglutinin
○ Induce nonspecific IgM molecules which can agglutinate RBC
 ● KNOW THE CASE WELL!!
○ Symptoms!
● Would you treat this person with cell wall synth inhibitor?
○ NO because there is no cell wall
-----------------------------------------------------------------------------------------
● Maintained within human pop spread from person to person.
○ Not considered zoonotic.
● There is some association with mycoplasma and having immunodeficiency issues.
● Walking pneumonia- low grade fever, dry cough, for long period of time.
● Causes atypical pneumonia. P. 311
● Toxin CARDS also decreases ciliary activity. P. 312 what does that mean?
● Real prob with mycoplasma infections- sets you up for secondary bout of
pneumonia from another bug
● Dx: grows poorly, PCR dx, can culture, look for fried egg
● Treatment: can you treat with cell wall synthesis inhibitor? No because lacks cell
wall
● STD is rare and benign, don't need to know much outside of that
----------------------------------------------------------------------
Atypical or walking pneumonia
Slows down mucociliary escalator – CARDS toxin
Produces a lot of H2O2

Chapter 30

Chapter 31 Viruses
Won't ask about
 ● classification (dsDNA, ssRNA, +/- sense etc) unless it was an assigned virus (like
the hepatitises)
● icosahedral/helical/etc not important
● Table 31-1 (virus families)-know for boards
● Hep B replication
● Influenza (segmented) replication
Know if a virus is enveloped-naked viruses will survive in the stomach
Viruses have 2 minimum components: genome (DNA/RNA) and a capsid (protein shell)
Rabies is bullet shaped
Replication Steps: important for knowing where antivirals act
Note: most RNA viruses replicate in the cytosol (except influenza viruses), most DNA
viruses replicate in the nucleus
● Attachment- (where neutralizing antibodies would act)
● fusion/entry
● uncoating (removal of capsid)
● genome replication (early genes)
● capsid construction (late genes)
● egress/release
Fig 31-8
+stranded RNA= mRNA (do not have to physically carry an RNA-dep RNA polymerase)
- ssRNA= needs its own RNA dep RNA pol
DNA viruses can take in their own DNA polymerases and use host machinery
Retroviruses: RNA->DNA->RNA-proteins (reverse txn)
        Don't worry about replication cycle of HBV-> just know it has a reverse
transcriptase
Fig 31-9-> just know:
● Time context to the replication (know terms like eclipse phase, when progeny are
being produced)
● Not in the book: Herpes replication: Immediate early: things that make virus go
latent; genome construction (polymerases), late genes-> capsids
● Early transcripts encode regulatory proteins and enzymes required for dna
replication. Late transcripts encode mainly structural proteins of the virion –
initiation of dna synthesis precedes transcription of the late genes
Hep D virus: defective virus- cannot replicate autonomously, needs a helper virus , hep
D needs hbv
Table 31-2-Don't worry about it
Know: host response to viral infx (cell will undergo apoptosis, etc)
● TLR, intracytosolic receptors respond to things like dsRNA
● NK/CTLymph, MHC presentation (important)
o Lysis of infected cells mediated by Cytotoxic T lymphocytes express mhc
class I
● Neutralizing antibodies would block attachment phase, penetration and
uncoating virus – enhance opsonization . participate in lysis via antibody
dependent cell mediated cytotoxcity , binds to fc of igg
● Interferons- block replication + protein synthesis machinery
Diagnosis: don't worry about it (ELISA/PCR)
Chapter 32 Picornavirus
- need to know: genome do they have envelope
- 32-1, enterovirus + hepatovirus – need to know these two
● + sense ssRNA, non-enveloped, acquired by ingestion
○ non-enveloped b/c stomach acid would degrade it anyway = don’t need it
● High Yield Picornavirus members:"PERCH"
○ Poliovirus, Enteroviruses/Echovirus, Rhinovirus, Coxsackievirus, Hep A

○ hep A is identical to polio but with tropism for liver instead of neural
○ hepatovirus- hepatic cells
● Poliovirus
○ Gain access to host through ingestion or inhalation
■ Spread fecal-oral in poorly sanitized places
○ + RNA acts as own messenger RNA→ replicate in cytosol
○ Bind to host cell receptor: CD155 (lot of cell types, but tropism for
nervous tissue)
○ Replicates by bringing in its own RNA depended RNA polymerase (not
present in eukes)
○ Virus is Translated into one large (genome length) polypeptide from
ribosome
■ Autoproteolyzed into many components
● capsid protein
● RNA dep RNA poly
○ Lytic
■ Poliovirus can cause variable disease depending on where the virus
replicates
● Asymp infection, paralytic diz, encephalitis, meningitis,
herpangina, resp tract diz
■ Neurotropism
● Enter CNS directly or through retrograde transport
● Tropism is due to host immune responses
● Receptor CD155 is important but does not fully explain
neurotropism
■ Lyse cells in the nervous system→ flaccid paralysis
● Anterior horn cells→ spinal paralysis
● Medulla oblongata→ Bulbar Poliomyelitis (resp
arrest)
○ People who have had it & been cured, can have post polio virus symptoms
■ Can live off left over neurons until get older & the regeneration
buffer wares off & symptoms appear
○ Only cases now come from immunocompromised with live vaccine
○ Still endemic in pakistan & afghanistan
○ No treatment, only prevention:
○ Polio Vaccines- salk and sabin vaccine
■ Know advantages and disadvantages of each
■ Salk is Inactive/dead
● Heat killed; IPV: inactivated polio vaccine
● Doesn’t induce mucosal response bc doesnt have as strong
IgG
● Have to give it 3 times (boosters)--> compliance
■ Sabin is live, attenuated vaccine
● OPV=oral polio vaccine (on a sugar cube)
● can be shed in environment to spread immunity
● Mucosal response (IgA) and … IgG
● Disadvantages
○ advent of immunocompromised ppl
○ it can revert to pathogenic form
■ If you were in charge of vaccinating a population, which one would
you give→ LIVE bc need to give to a lot of ppl
● Sacrifice immunocompromised ppl
● Coxsackie- hand foot & mouth
○ + strand RNA
○ Highly contagious
○ Type A: hand, foot, and mouth dx
■ Sloughing and blistering of skin, esp in children
○ Type B: causes heart to be enlarged and flaccid
■ Chief viral cause of myo and pericarditis
○ Correlation with getting T1 DM (make ABs that cross-react with
pancreas)- coxsackie B virus can lead to T1 DM
○ PCR with reverse transcriptase (to get the DNA for PCR)
● Rhinovirus
○ Confined to upper resp tract because it grows at 33 degrees C
■ Can survive acid, can’t grow at core temp
○ Common cold
○ Over 75-100 serotypes→ no vaccine
○ Spread person-person (aerosol, contact)
○ ICAM-1 receptor mediated entry→ infect cells→ lytic infection like
polio→ Cytokine response to activate neutrophils (runny nose) that
cause vasodilation → edema
■ damage/symptoms are due to host response
○ Self-limited disease→ no treatment
○ Sets resp up for secondary infection (otitis media & pneumonia)
○ Exasperates Asthma bc location
○ Causes 50% of all common colds in US
■ Mucopurulent discharge
● Coronavirus
○ + sense single RNA
○ Endogenous to animals (where they are usually asymptomatic)
■ Occasionally can get into human (jump species)
○ SARS (severe acute resp synd)
■ Starts in animal and gives rise to new viruses in humans
■ Ppl monkeying around with monkeys
■ Spread human to human, but poorly
● Just had to contain it
○ MERS
○ Crop up every 10 years
 ○ Enveloped + RNA
● Case 1: 11/130 students in CT diag with paralytic poliomyelitis. 9/11 were boys
age 12-17, all on football team. Clinical hist: flu-like, fever, sore throat, muscle
pain; then stiff neck, inc muscle pain & fever; then flaccid paralysis of legs from
minot to incapacitating. Diag via serum titer of ABs to type 1 poliovirus (not T2 or
3); confirm with isolation from feces & throat. None had vaccine. Contact with
kids from other school who had vaccine.
● Case2: 28yow, scratchy throat, sneeze, nasal discharge, low fever, malaise.
Worsened: nasal discharge thickened & yellow. Max at 48 hr, slowly subsided,
resolve at day 7. Got from 7yo kid

Chapter 33 Arthropod-borne viruses

- Zoonotic infections spread by mosquito (Aedes aegypti carries most of them)
o Humans are dead end host
o In static animals that get human contact & migratory birds
▪ Horses, cows
▪ Birds brought West Nile Virus
- RNA viruses, enveloped because dz in the bloodstream
o Cause encephalitis, rash, & hemmorhagic fever (classic presentation)
- Toga and Flavi: + RNA
- Bunya: - RNA
- diagnosis by viral RNA reverse transcriptase PCR
- No treatment, can only prevent by ridding mosquitos

- Don’t need to know families

- Chikungunya
o rash, arthritis of all joints (debilitaing for 2 yrs)
o + RNA, envelope
- West Nile Virus
o + RNA, envelope
o associated with corvid Birds (crow, raven, vultures)
▪ eat meat
▪ Note dead birds around springs/ponds
o Example
▪ Need lots of mosquitos→ Middle of summer, damp climate, near animal
reservoir (Central Park in NYC)
▪ need compromised person, old person near horse shed
▪ Symptoms: Fainting, dizziness, lightheadedness, fever
o CSF: normal protein, glucose -> virus infection
o Encephalitis
▪ more in elderly
▪ prolonged headache that doesn’t respond to meds, low grade fever,
neuro deficit (coordination, sight, speech)
- Yellow Fever
o + RNA, envelope
o liver component: Associated with Hepatitis
o Go to panama/amazon and come back with jaundice, sudden onset headache &
stiff neck→ lungs, start to get blood
- Dengue
o + RNA, envelope
o hemorrhagic fever: capillaries eventually open and bleed→ bleed in lung & can’t
breathe
o Bone & lumbosacral pain: lay down bc back hurts so much
o Rash, flu like symps
- Encephalitis – WNV
- Rash/arthritis – chikunguya
- Hemorrhagic fever – dengue
- Yellow fever – disease in liver
- Case 1: 72yow, early september. Several days fever, headache, cog decline, difficult
walk. Hospital: high fever, tachycardia, altered mental status, weak left leg, WBC
normal, CSF mononuclear cells, glucose high, protein high. Abx, no response. 5 day
later: 2 gen seizure, coma w/ mech vent, no muscle tone or DTRs. No signs of
improvement→ support withdrawn. CSF + for IgM AB to West Nile Virus & RNA
detected by RT-PCR, serum + IgG AB to WNV.
- Case 2: 20yom, trip to amazon basin. 2wk later: abrupt onset fever, chills, back pain,
headache, N/V, face flushed. Malaria neg, treat for gastroenteritis, felt better. 2 day later:
Headache and back pain back, bloody dia & too weak to walk, high fever, jaundice, renal
fail, creatinine and bilirubin high, albuminuria, urine output declined→ hemodialysis. PT
prolonged→ bleed from injection sites & mucosal surfaces. Transfused, died from
massive GI bleed & hypovolemic shock. RT-PCR + yellow fever RNA
Chapter 34 Paramyxovirus: Measles, Mumps, and RSV
- - ssRNA, enveloped (bc cause disease in blood)
- Must bring its own RNA-dep RNA poly (bc needs to make +RNA strand)
- Spread via respiratory droplets
- Measles
o Hemagglutinin (attaches to cell) and a F (fusion) protein (fuses
with membrane) and M (matrix) protein between envelope and capsid
o Life cycle
▪ Hemagglutinin binds to CD46→ fusion protein fuses envelope with
eukaryotic membrane→ injects caspid into cell
● Lots of hemagglutinin so can attach mult cells & fuse them together→
multinucleate giant cells⇒ rash associated with measles

● Syncytia= multinuclear giant

cells
o Replication in the cytosol
o Spread by aerosol
▪ Highly infectious
o Invades cells and causes viremia
o Then gets in blood→ systemic infection→ make more viruses
o 10 day incubation period, then get symptoms:
▪ 2-3 days in there is fever and the 3 C’s: conjunctivitis, coryza
(runny nose), cough
▪ then form Koplik spots appear on buccal mucosal surfaces
(ulcerated lesions- small bright red spots with bluish centers w/ giant
epi cells in submucosal glands)
▪ Day 2 or 3→ last the rash progresses cephalocaudal (and starts as
maculopapules and evolves to confluence), from giant cells in
epithelium
▪ Run fever throughout
▪ Symptoms for wk to 10 days
 o People who are vitamin A deficient are highly susceptible
o Usually self-limiting disease
▪ Cause subsequent bacterial pneumonia
▪ BUT 1/1000 children develop ADEM (acute demyelinating
encephalomyelitis)
● autoimmune mediated demyelinating disease
● Profound neurological disability
● Present abruptly with fever and altered mental status 2 weeks
after
▪ SSPE (subacute sclerosing panencephalitis-) extremely rare
● 7 to 10 years after primary infection
● Present with mental impairment and myoclonus, then progressive
deterioration until death
o No way to treat; vitamin A to help
o Vaccinating
▪ live attenuated virus in MMR vaccine
▪ requires cold temperature "maintenance of the cold chain"
- Mumps
o basically the same virus but targets the parotid glands
o “Kissing cousin”
- Respiratory Syncytial Virus
o Limited to upper respiratory→ Bronchiolitis, croup Enveloped so can get through
stomach; but can’t live at core temp
o Pathogenicity
▪ Slows down mucociliary escalator
● Cytotoxic to resp epithelium so it damages the ciliary fxn
 ▪ Major surface glycoproteins
● G protein- similar to hemagglutinin, provides antigenic variance
● F (fusion) protein
o DEMOGRAPHICS
▪ URI in Kid <2 year old
● Kids still developing immune & elderly loosing
▪ winter or rainy season (come together--resp droplet sharing)
▪ Develop immunity
o symptoms= immune response
▪ Lymphokines and cytokines produced (immunopathology)
o Gives rise to secondary infections
o Linked w/ asthma (etiology unclear)
o No Tx for it
o no vax bc too many serotypes
- Case 1: 7yom, unvaccinated, visit switzerland. 1 wk later: Fever, sore throat. Then cough,
coryza, conjunctivitis. Continued at school, Neg strep pyo test. Blood measles AB test,
high fever, generalized rash. No isolation precautions. + for measles IgM→ ID 839
exposed ppl
o 11 secondary cases at hospital (infants <12m)
▪ Infant had prolonged convalescence
▪ Another infant traveled & caused more exposures
o 10% classmates unvaccinated
o 48 infants quarantined
o Some given measles immunoglobulin as prophylaxis

- Case 2: 2mom, cough, poor feeding, rhinorrhea, tachypneic, subcostal

retractions, diffuse exp wheezes, pulse ox low. Given o2 & bronchodilator w/ little
effect, IV hydration. Unable to eat bc breathing. Rapid antigen test + RSV. CXR
hyperinflation with peribronchial thickening. Hosp & weaned from o2. Better but
coughed for 2 more wks.

Chapter 35 Rabies
- (-)ssRNA, enveloped. Brings its own RNA dependent RNA pol
- Zoonotic disease, seen in developing countries in dogs
- Tropism for neuronal tissues – Negri bodies (intracytoplasmic
inclusion in neurons, pathognomonic-mass of nucleocapsids)
- 1 – 3 month incubation period
- Closer the bite to the brain, the shorter the incubation period
o Moves from bite to PNS to CNS
- Virus likes salivary glands as they are highly innervated
- Clinically:
o Start with fever, headache, difficulty swallowing, and increased
muscle tone
o Hydrophobia (contraction of muscles involved in swallowing) may occur
at sight or sound of liquids
 o Eventual extensive damage to CNS, coma, and death
- Must treat for it, if infected its lethal (aside from 2 cases)
- Passive treatment with human rabies globulin

o Period of shedding is concomitant with illness or a few days before (up to a

maximum of 10 days), so if a person is bit and the animal doesn’t get sick
until the 11th day, no need for prophylaxis
o If needed, Prophylaxis is 3 steps
▪ Local wound treatment
▪ Passive administration of antibody (anti-serum or rabies
immunoglobulin)
▪ Vaccination (series of 4 doses, extra if immunosuppressed or higher
risk of exposure)

Chapter 36 Flu
○ Common for viruses
○ Replication
 ○ RNA virus, you tend to rep in cytosol,
○ DNA-nucleus
○ exception= influenza rep in nucleus
○ Envelope
○ Typ viruses infecting(growing) in bloodstreams have envelope
○ those that don't cause infect/grow in bloodstream (like rota, adeno)
don't have envelope
○ Envelope no good in gut, because acid destroys the envelope
○ Influenza causes a systemic disease so it’s gotta travel through
blood and so it has an envelope
○ Genome
○ Early proteins, viral genes, typ involve maint and dup of genome
○ Influenza virus is unique because its genome is segmented, like
rotavirus
○ Rather than have one piece of dna/rna in which all genes
lined up, you have 8 different segments
○ Each seg encodes a single gene, critical to antigenic shift
○ The genome is a neg sense ssRNA
○ There are 3 types: A,B,C. A is most important because it
infects animals and humans.
○ Segmented virus
○ Negative sense RNA; 8 segments
○ Each segment is discrete→ encodes for important protein in virus
○ proteins hang onto lipid envelope:
○ Hemagglutinin
○ Neuraminidase
○ M2 protein (target of amantadine)
○ The rest are for RNA polymerase and whatnot
● Anatomy of influenza
○ Pb1 and PB2… are the segments of rna
○ The blue is the capsid protein
○ The white is the envelope
○ On the envelope there are 3 critical proteins to inf cycle: HA, NA, M2-
fusion.
○ Infectious cycle
○ Attach via hemagglutinin
○ Makes RBCs clump→ how we detect it
○ Binds salicylic acid→ close to cell surface
○ Virus gets close and M2 protein fuses membranes together and allows for
injection of capsid (everything in the envelope) into cytosol
○ Transported to nucleus
○ only RNA virus that goes to nucleus
○ Replicates
○ Has to transcribe from each segment
○ Built in cytosol
○ Make caspid protein
○ Create a virus that egresses to the cell surface
○ Buds on host membrane but it’s HA sticks to membrane
Neuraminic acid (salicylic acid)
 ○ Neuraminidase
○ clips its salicylic acid attachments from the membrane and allows it
to go to other cells
○ Surface proteins most prominent are HA & NA
○ If have antibodies→ resistant
○ Antigenic Drift
○ HA & NA mutate over course of year
○ Due to segmented genome
○ Flu is seasonal (fall & winter) (in east, in the spring and summer)
○ Makes its way around the world
○ Antigenic shift
○ Segmented genome is the culprit
○ Give another animal the flu while it is infected with the flu→ superinfection
○ Reassort when infecting→ can mix
○ change a few AA to change antigenicity
○ If the animal flu has the HA or NA that allows to get in human, you have a
new epidemic
○ Ex: A kid with flu plays with a chicken with avian flu, chicken becomes
superinfected, both strains rep in nucleus, segments segregate out and sometimes
mix→ human virus picks up chicken segment→ antigenic shift
○ H1N1 (HA is type 1 & NA is type 1)
○ Spread- aerosolization
○ Damage- Stay in upper respiratory epi → secondary bact infection → death
○ Superinfection w/ S.aureus, Pneumococcus, and Hflu
○ Ion channel something for amantadine and another -adine
○ Clinical Manifestations (know, not just feeling bad)
○ Malaise, chills, resp symptoms, etc.
○ Feeling those interferons
○ Diagnosed based on symptoms
○ Reportable disease
○ Can use RT-PCR or grow in culture
○ Treatment & prevention
○ Vaccine
○ CDC sends people to the east & look at major types
○ Chose 2 As and 1 B (trivalent)
○ Inject chicken eggs with virus
○ Inactivate the virus
○ Can’t have if you have egg allergy
○ alt vaccine in cell culture that’s monovalent to A type
○ $100 -- more expensive
 ○ 3 types
○ most predominantly isolated= A
○ B only infects humans
○ Type A virus can infect humans and animals
○ does have animal reservoir- scary
○ B is isolated at lower freq, no animal reservoir
○ Live attenuated virus “flu mist”
○ Grow it in the cold- 35 deg
○ Adapt it so at 37, it doesn’t work
○ Don’t use it because efficacy = zero
○ only has 1 type
○ Know Reye’s syndrome
○ KNOW THE DRUGS
○ Have to be given 24 hrs before symptoms
○ Amantadine, rimantadine
○ Inhibit uncoating and genome release
○ target m2 fusion protein→ block its channel opening to prevent H+
mediated uncoating
○ Only effective against flu A
○ Neuraminidase inhibitors
○ Prevent removal of salicylic acid, hence release of virus from host
membrane→ can’t infect further
○ Good for A and B, and as prophylaxis
○ Tamiflu (Oseltamivir), Zanamivir, and
○ Peramivir for emergency use for H1N1 only
 Ask about rimantidine and tamiflu
● Case 1: 2yom, early january, sibling had high fever, sore throat, muscle aches.
Developed runny nose, cranky. antipyretic & antiviral against flu virus for him
and rest of his family.

Chapter 37 Rotavirus
● dsRNA, segmented, can get antigenic variation
● Causes a gastroenteritis (ROTA= "right out the anus")
● Seasonal distribution, wintertime
● Fecal-oral spread
● enteric adenovirus brings in own RNA-dep RNA pol
● Infect enterocytes-
○ disruption gastric mucosa -for some reason this is ringing a bell
"shortening and atrophy of the villi, denuded villi, and
mononuclear cell infiltration of the lamina propria"
○ watery diarrhea
○ no  intense immune response
● Don't worry about the dx
● Vaccine: live, attenuated (old vaccine=intussusception; has come up on a couple
of board ?s)
 ● Norwalk viruses- won't ask about being a calicivirus
○ cruise ships- basically, if the question stem has someone on a cruise w/
gastroenteritis, this is your answer
○ blood type B has protection- was a question, and yes the prompt
included a cruise ship

Chapter 38: Retrovirus

● 2 major retroviruses in humans is HIV-1 and HTLV-1
● HIV
o envelope that looks like host cell membrane except for
▪ GP120 - binds to CD4 on T cells, facilitated by CCR5 or CXCR4
▪ GP41 - allow for fusion of envelope and host membrane→ capsid is
released inside the cytosol & dissolves to release the ssRNA & RT
▪ (need a protease to cleave from a precursor GP160)
▪ gp41 is the inside membrane and gp120 is the outside
o capsid w/ P24 protein
o 2 + ssRNA strands
o RT - acts as an RNA-dependent DNA polymerase =DNA-RNA hybrid
▪ 1)Reverse Transcriptase: RNA-dep DNA polymerase
▪ 2) RNAse H removes the RNA-now you have ssDNA
▪ 3) DNA dependent DNA polymerase, makes a dsDNA
o Integrase - Inserts ds DNA into the host genome = provirus
o Go from RNA -> DNA -> mRNA -> protein
o Virus buds off & is released
o Genome encodes:
▪ Gag (group-specific antigen P24)
▪ Pro (protease)
▪ Pol (RT)
▪ Env (envelope) proteins
▪ Tat & rev (transcriptional activators) allow the virus to become
latent- turn off when mRNA is going to be transcribed
▪ Nef protein which downregulates expression of MHC-I to avoid
immune response form CTLs

▪ Gag, Pro, Pol, & Env = retrovirus motif

▪ Group specific antigen is the gag and matrix protein
▪ Pol is the protease and polymerase
 ▪ Env: gp160 is the polyprotein that gets cleaved by the viral
encoded protease into gp120 and gp41 (takes place in ER)
o RT lacks effective proofreading
▪ highly error-prone
▪ variations in the surface proteins of the virus
▪ quasispecies disease
▪ Diagnosis
▪ Primary screen - ELISA for ABs to P24 antigen = prelim diagnosis
of HIV
▪ Takes a month before seroconversion (need to have virus
long enough to induce immune response & develop ABs to
P24)
▪ p24 positive usually good 99% of the time
▪ Secondary screen - must do a western blot to confirm positive
ELISA results
▪ Takes purified HIV virulents and puts them on a gel
▪ Check for antibodies to gp160, gp120, gp41, p24
▪ In initial period before ABs for, can diagnose w/ RT PCR (1-2 weeks
post-infection)
▪ Looking for ssRNA
▪ Have to convert DNA into RNA
● Timeline
○ Infection
○ Viral load increases in weeks at expense of CD4 cells
○ CD4 count > 1000, but begins to decrease
○ CD4s eventually brings down viral load & returns back to > 1000
○ But reverse transcriptase (RT) makes a lot of mistakes→ mutations of the
virus surface antigens
○ Over time (years), chronically infect T cells
○ Viral load begins to rise & CD4 count begins to plummet
○ CD4 < 200 + AIDS-defining illness
■ Thrush, recurrent herpes, lymphadenopathy
● HIV categories
○ Category A - flu-like symptoms (?)
■ what happens in acute infection
○ Category B - Herpes Zoster, candidiasis
○ Category C - PCP, Myco. TB, Myco. Avian Complex disease,
dementia
■ what happens in late stage, AIDS
● CD4 counts & viral load vary over the course of an HIV infection
○ early HIV - seborrheic dermatitis, psoriasis, kaposi sarcoma,
molloscum contagiosum etc
○ early AIDS-will ask about thrush
○ Intestine infx-salmonella, shigella, cryptosporidium
○ CD4 count < 200 = AIDS, get opportunistic infections
○ CD4 count super low (50)- Mycobacterium Avium complex
○ JC virus-only in HIV pts (progressive multifocal encephalopathy)
 ● Treatment
○ RT inhibitors: Zidovudine (AZT)
○ Non-nucleoside RT inhibitors: nevirapine
○ Protease inhibitors (end in -vir): ritonavir
○ Integrase inhibitors: Raltegravir
○ HAART:

● Prevention
○ Protect yoself

Chapter 39: Adenoviruses

○ Pathogens:
○ Large, nonenveloped, dsDNA viruses with icosahedral symmetry
○ Encounter:
○ Respiratory serotypes: exposure to aerosols or infected fluids (saliva)
○ Enteric types: contamination with fecal matter
○ Clinical Scenario:  point-source spread from a water-borne illness or a
nosocomial infx from an optometrist's office
○ Initial site of replication in most cases is probably oropharynx
○ Disease:
○ Most often cause mild infection of respiratory and GI systems
○ Severe infections can cause keratoconjunctivitis and acute, severe
pneumonia
○ Cause pink eye, swimming pool/keratoconjunctivitis, common cold,
adenitis, URI
○ Adenovirus- different serotypes→ different diseases
 ○ Attach via CAR receptor-> taken up in clathrin coated pits→ endosomes carry
into cell
○ difference lies in that the tips of the penton fibers-have tissue tropism
for the eye, or upper respiratory tract, et
○ E1A interacts w/ RB and that E1B/E4 interacts w/ p53 and that it is
similar to HPV

○ Replication:
○ Temporal regulation of gene expression dependent upon viral regulatory
genes
○ Employ both virally encoded and host proteins in the replication process
○ Damage:
○ Evade antiviral host defenses (prevent host cells from expressing
MHC proteins, mediate resistance to TNF, abrogate interferon
response, and antigenic diversity)
○ Infection can be fatal in immunocompromised
○ Interactions w/ defense: know the mechanisms like MHC class I
deregulations, etc
○ Diagnosis:
○ Recognition of clinical features
○ Lab Dx not typically done except life-threatening situations (PCR)
○ Treatment/Prevention:
○ No vaccine available
○ No antiviral drug
○ Case 1: 83 pt to opthalmologist in Erie. Red eye, eyelid swell, discharge, photophobia,
change in vision. Only 2 had fever or dia. All recovered. No further outbreaks after office
instituted preventitive measures (dec use of instruments). CDC studied this epidemic
keratoconjunctivitis→ serotype 37. Diag with immunofluorescence microscopy of
specimens & viral culture. Found in office-- instruments, work surfaces, eye drops, air
conditioning filter. No staff tested pos
Chapter 40 HPV
● Nonenveloped circular dsDNA
● dna virus that has to rep in nucleus
○ uses host dna polymerase
○ HPV cannot replicate w/o host proteins
● Things that don’t go into GI don’t need envelope (waste of energy)
○ Capsid instead→ basis for vaccine
● Where in body = serotype
○ Over a 100 diff serotypes, its a transforming virus
○ High risk for cancer: 16, 18, 31, 33, 35
■ transforming genes: p53 & Rb

● Disease
○ Cutaneous warts
■ Spread through contact (skin to skin), facilitated via microabrasions
■ Need microabrasions in skin to gain access, need to reach basal
layer of epithelium in skin
■ Can cause disease on any mucosal surface (pharyngeal), but
generally on exposed part
■ cutaneous: Can be found on hands and skin dried
■ Condyloma: genital region
○ HPV 6/11-genital warts (little potential for carcinogenesis)
■ Cause of condyloma ACUMINATA, not to be confused w/
condyloma lata of syphilis
○ mostly benign unless high risk serotypes esp cervical cancer
● Exist as viral particles
○ E (early) = replication
■ E1 and E2
○ L (late) = capsid
■ L1 & L2- make the capsid
● package the genome
● Replication facilitated by early genes: E1 & E2
○ Maintain the genome as an episome
■ episome- circular dsDNA that can replicate independent of
chromosomes
 ○ need helicase to replicate
○ When you have episome and you rep, you make an concatemer (long DNA
sequence with many segment repeats, enzyme has to uncouple it (like
topoi and helicase)--> split to partion for progeny
○ Infect basal cell layer, occurs in concert with differentiation of
keratinocytes which will then activate the late proteins
● Packaging of genome via L1&L2
○ make the capsid (part of the vaccine)
○ Determines tissue tropism
■ recognizes the basal cells
○ Ex. 15 and 16 like to bind to genital
● Reproduction in concert with the maturation of keratinocytes
○ basal cells diff into keratinocytes; during, the cells become stimulated and over
synthesize keratin skin layers→ and you get a wart
○ Become crazy-->over replicate cell-->wart
● Paradigm box
○ Protein E6&7 bind host cell cycle proteins (Rb & p53) and can interrupt the cell
cycle→ transforming (why HPV causes cancer)
○ All papilloma viruses produce E6 and E7, but in high risk these can
interact with p53 and Rb in order to increase risk of cancer
■ HPV1 is a low risk serotype, still produces E6 and E7 but does not
efficiently bind to p53 and Rb, and only high risk effectively bind
■ P53 = triggers apoptosis in damaged cells
■ Rb = controls cell cycle via E2F (transcription factor)
● Spread- Anytime you have a wart, you shed virus during process & able to infect
others
● Diagnosis
○ Pap (Papanicolaou) smear- when sex active, look at transformation of epi
cells
○ Now testing for HPV DNA in samples instead of looking at cytology
● Treatment
○ Physical removal of the tissue
■ need to get all the way to the basal layer
■ Liquid nitrogen, Salicylic acid, Surgical ablation, Laser ablation
○ Often can’t get all cells and wart comes back
● Most prevalent STD over course of total population (but not new acquisition)
● Can develop immune response to virus and that can prevent infection
● Prevention
○ Barrier prevention
■ Condoms are permeable to viral particles
○ Vaccine
■ subunit recombinant- Production of virus-like particles
● Take L1 capsid protein from major carcinogenic serotypes &
clone it
● The capsid proteins L1 if expressed in E. Coli self assembles
like HPV capsule and so its a virus like particle
■ Gardasil
 ● Quadrivalent (6, 11, 16, and 18)
● Now vaccines have 9 serotypes
● it incorporates frequency and high risk
■ Bivalent vaccines usually only target high risk
● Case 1: 26yom in panic. Small bump on penish shaft→ ignored, found 2 more. Derm
confirmed genital warts→ liqid nitrogen. Transmissible→ see wife, not at risk for cerv.
cancer

Chapter 41 Alphaherpesvirsues
-envelope status and genome composition (alpha, beta, gamma)
-herpes virus is really large
-they have the ability to go latent, go into the host cell and not cause an apparent
infection- ones entire life
-HSV-1 and 2 are the same virus, 1 is above the belt, 2 is below the belt
Double strand DNA with envelope
o One of largest genomes
- Human human
o HSV is spread by direct contact (sharing fluids, sex), VZV spread by
aerosolization

o Simplex virus 1 & 2 are really identical

o Know the differences btwn HSV & VZV
o Anatomy of envelope virus
o Hsv + vzv attach to cells w heparin sulfate- facilitates binding of virus to
surface
envelope putting 2 membranes together + proteins- that help fusion of viral envelope w
eukaryotic cell membrane, and capsid and then it moves to the nuclues
DNA viruses replicate in nucleus, rna virus replicate in cyotosol (machinery / ribosomes
are in cytosol)
o Replication cycle
▪ Nature of envelope→ picked up from nuclear envelope
- Gen Concept: DNA virus replicate in Nucleus RNA in cytosol (exception is
influenza RNA in nucleus)
- Attachment:
● Heparan Sulfate on cell surface proteoglycans
● Require specific cell surface receptors
- Genes
o Early = replicate genome
o Late = capsid, packaging
o Immediate early = latency, tell cell when to start making dna, regulation of
viral production- activate early genes
 host defence mechanisms- cellular immune response, HIV
- Typical lesion = Fluid filled vesicle with erythematous base, painful
o tell difference in chicken & small pox via distribution & time frame
o painful – cause inflammation at area of nerve , very sensitive, Kanker is
painful
o chicken pox- synchronous , rash and lesions synchronously go throughout
ur body
o small pox- all the vesicular lesions pop up at the same time
o chicken pox + herpes- very common
- Latency
o miRNAs bind viral DNA sequences and messes transcription up→ dz remains
latent
o For boards: could also be called LATs (latency-assoc transcripts)
- VZV
o everyone harbors the virus from infection or vaccine
o Most efficiently spread by aerosolization
o initially systemic but eventually is dormant into a dermatome (DRG) and
will come back out as shingles zoster
▪ 1 = chickenpox
▪ 2 = zoster/shingles
o Systemic spread, because it can infect leukocytes
▪ entire rash b/c spread throughout body
▪ eventually finds a sensory neuron for latency
o VZV causing cerebellar ataxia/encephalitis
o Vaccine
▪ prevents pulmonary chicken pox infections in adults if they never
had chicken pox as a kid
▪ live attenuated form that can cause serious disease in
immunocompromised individuals

- HSV
o 80-90% have AB to simplex
▪ AB to herpes is minor means of detection→ cellular response major (why
in children & old ppl)
o HSV is spread by direct contact
o Primary infx of HSV1/2 may be asymptomatic, subsides into latency:
infects dermatomes
▪ (think trigeminal, thoracic dorsal root or sacral ganglia)
o Herpes attach to glycoproteins with heparan sulfate
o Neural tropism
▪ Painful lesion that generally involves a nerve cell
 ▪ Can go to CNS in children and immunocompromised and can cause
encephalitis
o Latency
▪ persistency as an episome (plasmid-like), w/ minimal txn of viral
genes
▪ episome is a genetic particle that can exist freely or within a
chromosome
o cytotoxic → herpetic lesion in 1 infection
▪ “canker” not chancre
o HSV causing blindness or temporal lobe encephalitis

- Immune response
o Immune status will determine if virus emerges
o T cell immunity important
▪ implication in HIV and transplant pts
o Neonatal HSV infections can be fatal <1 month of age
o Antibodies can prevent dz (think VZV vaccine!)
▪ only have minor role in recovery
o Reactivation also induced by sunburns, menstruation
- Diagnosed clinically usually, not really by PCR
- Treatment
o Acyclovir
▪ guanosine analog→ incorporate into DNA and stop replication
▪ to treat a-herpesviruses, but not against b-herpesviruses
● Alpha herpes viruses (HSV1/2, VZV) produce a thymidine
kinase which activates acyclovir->inhibiting DNA
synthesis
▪ Produg- goes in as monophosphate, only works at triphosphate
● viral thymidine kinase that puts the Ps on the prodrug→ selective
for alpha herpes (HSV1/2, VZV)
● EBV/CMV lack these kinases
 ▪ Treats, doesn’t prevent
● only stops replication, doesnt kill latent
o Gancyclovir
- Prevention
o Herpes: don't kiss anyone ever, don't share drinks, live in a bubble. You
now have only a 50% chance of having the herp.
o VZV: Live, attenuated vaccine
- ??? Super high yield: Act I, Scene 4 of Romeo and Juliet-> HSV reference
- Case 1: 26yom, recent vag & oral sex. Several days after: painful itchy sores on
penis shaft & sore throat. Girl admits to having Genital herpes
-chicken pox is live attenuated vaccine

Chapter 42
- Same presentation as alphaherpesvirus (as well as with toxophasmosis)
- herpes virus: double strand DNA genome, enveloped
- ToRTCMVZ (zika)
- Ebv- mainly caused by mononucleosis > CMV

- Broad tropism
o infect all cells
o CMV- bind a lot of receptors
▪ particularly macrophages
o except EBV particularly likes B cells
▪ EBV- bind in particular to CD21 (CD2) on B cells
▪ EBV likes the tonsils
- Clinical
o Infect most by 5yrs
o CMV
▪ Transplant pts, eye infections "sightomegalovirus", peds
▪ CMV= TORCHES agent: infectious across the placenta
▪ transmitted in bodily fluids, most young kids get it
 ▪ most common congenital disease
▪ causes neonatal hearing loss (other sequelae involve the CNS,
bone marrow, liver)
o EBV: kissing
▪ tonsillar exudates
o Higher socioeconomic classes are less likely to be exposed to CMV/EBV
early on in life, so + likely to get mono when teens

● Replication
o Attach via low-affinity interactions w/ cell-surface glycosaminoglycans
o followed by high-affinity interactions w/ specific receptors (like CD21)
o Early genes: set you up for replication
▪ (eg, DNA-dependent DNA polymerase)
▪ produce the microRNA which help become latent
o Late genes: capsid, viral assembly
- All herpes viruses can become latent
o use Latency Associated Transctipts
o EBV LATs: immediate early gene→ nuclear antigen 1 maintains persistence
▪ → LMP1 and 2- latent membrane proteins- give growth signal to host to
grow
▪ EBV nuclear antigens and MiRNAs
o CMV LATs: small micro RNAs→ bind viral DNA sequences and messes
transcription up→ dz remains latent
- Host response pg 432
o EBV decreases activity of NK cells via downregulating MHC class I/II
o read functions - how they avoid recognition by host
 o CMV encode for functional cytokines = homologues of IL8 & 10
▪ EBV does same thing
▪ Tell immune system to look away
o Also affects DNA degradation, IFN induction, apoptosis

- Diagnose
o heterophile IgM ABs (monospot test)
o heterophile antibodies- when the assay you take serum from someone and
put it in animal red blood cells
▪ EBV has tropism for Bs→ stim B to replicate independent of antigen
stimulation→ more reactive and makes random ABs→ cross-reacts w/
animal blood cells
o CMV- owl eye inclusion
o Blood smear: Atypical Lymphocytes=CD8+ T cells
- Immunocompromised & transplant
- EBV Complications
o Post-transplant
o Oncogenesis b/c transforming cells
▪ Hodgkins
▪ Burkitt lymphoma
- Treat
o Nothing in immunocompetent
o Immunocompromised w/ CMV: gancyclovir
▪ Use this bc dont have thymidine phosphatase
▪ more toxic than acyclovir
▪ phosphorylated by a VIRAL kinase (does not require the cellular
kinase)
o Usually don’t treat EBV
- Case 1: 15yof, dating 19yom. 2mo later, sore throat, white exudate on tonsils,
swollen & min tender lns in neck, slight yellow tinge in eyes. Worsening symp,
 dec appetite, loss energy. BF has no symp. Exudative pharyngitis & icteric sclera,
splenomeg, WBC 9,5000 w/ dif: 30%neutros,55% lymphos, 5% monos, 10%
atypical lymphos. Hepatic transaminases elevated (community acq EBV)
- Case 2: 20yom renal transplant 2nd to end renal diz. Tollerated surgery &
immunosuppressants (dec CD8Ts). 6wk later: fever, dec appetite, cerv
lymphadenopathy, dec WBC. diag via clinical path lab (transplant acq CMV or
EBV)

Chapter 43 (hepatitis)

- There is a vax for HepA & B

- No vax for HepC or E
- Know the structure of HepA & B
- be able to tell the Hep status of a patient based on the AGs they have
- Only thing common about them is that they affect the liver
- Easy questions: which ones are fecal-oral? DNA virus? Which ones have
vaccines?
- macrophages of the liver are Kupffer cells ( this is the main cause of tissue
damage/inflammation,  causing high levels of aminotransferases)
-
- Hep A
o linear pos ssRNA
o doesn’t cause chrnic disease, only acute. Long term sequelae should be yes
for it though.
o know that it is similar to poliovirus (bc picornavirus)
o Know flux of aminotransferases

- Hep B: most of the questions come from here. Most important.

o nicked, circular, mostly dsDNA
o About replication, only know:
▪ Genome is covalently, closed, circular DNA with a nick.
▪ Have to use reverse transcriptase because of the nick.
o HBsAg (envelope), HBcAg (capsid), and HBeAg
 o Chronic Hep B leads to HCC.
o Hep B vaccine is a subunit vaccine so that means it’s to the surface antigen
only
o Treatment can involve reverse transcriptase inhibitors, interferon-a
o Dane particle- empty, non-infectious particle composed of surface
antigens
- Hep C
o linear pos ssRNA
o spread by bodily fluids
o RNA polymerase lacks proof reading so there is a ton of mutations (quasi
species disease), this also makes it hard to have a vaccine.
o More likely to go to chronic Hep
o Treat with interferon
- HepD:
o circular, neg ssRNA
o defective, requires HBV
▪ difference between coinfection and superinfection isn't important
to him
- Hep E:
o linear pos ssRNA
o pregnant ladies die from it (20%!)

Chapter 44
● Questions will still include clinical scenario
● Be somewhat of a pseudoquestion
o “Person comes down with HCV caused by positive sense RNA virus”
▪ Gives you an idea of what to use
▪ Ribavirin
● Best way to study for this chapter is TABLE 44-1 AYEEEEEEEEEEEEEEEEE
o KNOW ALL THE COLUMNS EXCEPT FOR “COMMENTS”
● Also likes figure 44-1
● Look for specific examples in the text
o Just drones on about the drugs
 ● JUST KNOW THE FUCKING TABLE ALL RIGHt
------------------------------------------------------------------------------------------------
● Don't know table 44-1
● Know Fig 44-1
Tamaflu=oseltavamir
All we're going to get from him on this chapter is mechanism of action questions
(especially ribavarin, interferon therapy)
Know that acyclovir is a prodrug that requires a thymydine kinase and that
gancyclovir= activated acyclovir
Fig 44-5

Chapter 45 Vaccines
- Know table 45-1
o Live: MMR, Sabin Polio, Varicella, Vaccinia, BCG
▪ Live vaccines are all viruses pretty much except for BCG and
salmonella vaccine
o Killed: polio (salk), Influenza*, hep A, Pertussis, Rabies
o Subunit: Hep B, Gardasil, Diphtheria, HiB, Meningococcal, Pertussis,
Pneumococcal, Tetanus
▪ usually enveloped/capsulate
o Bacterial: TB, salmonella
o Polio: SALK is killed, SABIN is live
o Rabies: post-exposure vaccination
▪ Can also give to raccoons
o Combinations: MMR, DtAP (a=acellular, got rid of LPS)
▪ CDC recommendation: DtAP first trimester pregnancy
- Importance of herd immunity (70-80%+)
o Just FYI: Different dz have different immunity (measles >90, pertussis
>75)
- Know active (you make your own via toxoid) vs passive (giving preformed
antibodies)
- Toxoid is chemically treating a toxin to inhibit the enzymatic activity of the toxin
but retains the immunogenicity of the toxin.
- 3 types: live attenuated, killed, subunit/recombinant (definitions important)
o Live vaccines: only have to give it once
o Killed vaccines can’t infect anyone but you need multiple does for them to
be effective
o Killed vaccines: In gram-negative bacteria, you can't kill the LPS/toxins
(causes fever etc)
o Unconjugated Carbohydrate vaccines won’t be presented to T-cell from
MHC
▪ Capsular polysaccharides are T-independent antigens (past PBL
question): cant stim helper Ts
o Conjugate carbohydrate to protein for presentation purposes
▪ Make more immunogenic when you conjugate it with a protein
 ▪ Conjugated capsular are T-dependent, increase B-cell response via
CD4 Ts
▪ HiB vaccine is poorly immunogenic without the protein, with it, it
induces a stronger immune response (induces B and CD4+
cells)
▪ Especially true <18 months old
- This will be a question
o Which is most important in a killed vaccine? B cells
o Live? CD8+ (CD4 and B cells also stimulated)
o Capsular polysaccharide: B cells,
- **Influenza (killed vaccine): we get a flu shot every year because of antigenic
drift
o Shot includes 2 most prevalent type A strains, most prevalent B strain
o Can't give to people w/ egg allergies
o Live, attenuated version: flu mist (dries up mucous membranes)
- Code words
o "someone comes from a 3rd world country"= not vaccinated
o Vaccines aren't 100%-antibody titers wane
- Question on the exam: Immunize against the measles (live attenuated), what type
of immune response would you cause? B cells, CD8 Ts, CD4 Ts
o he’s going to ask about a subunit vaccine stimulating B-cells and T-cells,
know the vaccine for the organism and how it induces a response
o Know these, capsular polysaccharides, live attenuated, conjugate vaccines
- Table 45-3 Know the "special population" requirements
o What vaccines elderly get: eg strep pneumoniae, influenza vaccine
▪ Really need to know people over 60 need pneumococcal vaccine
o Healthcare workers: eg Hep B, VZV
o Pregnant women: Hep B, tetanus

Chapter 46
-dimorphic
-yeast or as a mold (temperature dependent)
-yeast in the heat and mold in the cold
list of them and exception
candida only exist as a yeast
fragilis- only exist as a mold

Chapter 47 Endemic mycoses

- Fungi eukaryotic
o Dimorphic:
▪ mold (environment; mycelia)
▪ yeast (in body, 37 degrees)
▪ Exceptions:
● Candida – only exists as yeast
 ● Aspergillosis – only exists as mold

- Clinical
o Histoplasmosis
o Dimorphic
o Ohio or Mississippi delta
▪ Associated with bird droppings
o Ex. Mississippi river, Kid in chicken coup, comes down with mild
pneumonia that doesn’t grow bacteria, find antigens in blood stream.
▪ Think histoplasmosis, he would ask what is the treatment?
▪ You don’t treat it, self-limiting
▪ Avoid anti-fungals bc are TOXIC-- Therepeutic index smaller bc
eukaryotic
o Mold makes spores
▪ = conida→ Breath it in & germinate to form yeasts
▪ mold transform to yeast and taken up by alveolar macrophages
▪ Recruit Ts→ granuloma
● Acts similar to TB in the lungs (walled off by granulomas)
▪ Persist & can reactivate with immunosuppression
● Chronic cavitary histoplasmosis
o Hangs out in macrophages
o Damage
▪ patchy pneumonitis
 ▪ Wheezing, dry cough, fever & sweating
o Older, compromised people get this disease
o Usually dont treat ppl with good immune system
▪ Amphotericin has bad side effects, only for immunocomp
o Dx
▪ grows poorly in lab -- takes too long
▪ look for polysaccharide secreted in urine
o Tx:
▪ Know whether or not it is a fungus
▪ Usually self-limiting
▪ Treat with systemic antifungal if needed
- Blastomycosis
o Dimorphic
o Saint river Lawrence valley down to South Carolina (Appalachia,
mississippi river)
▪ Follows appalachian forest bc grows in tree debris
▪ Decaying wood and soil
o Aerospores
▪ Conida are inhaled→ taken up in alveoli
▪ CD4 cells and macrophage immune response, mixed granuloma
▪ Localized in lungs but can make their way to skin to form lesions
o Gives rise to cutaneous lesions
▪ heaped up borders (size of a quarter) with microabscesses in middle
▪ If scrape & look at under microscope = “broad based bud”
o Tx: Antifungal
- Coccidioides
o Arizona, Valleys in Southern California, Central and South America
▪ Endemic in the animals of the desert (southwest US)
▪ Outbreaks when there is lot of rain→ aerosolized the conida
▪ Called “Sonoran Valley fever” and “desert rheumatism”
o Inhaled into alveoli and spread in macrophages
▪ Cause pulmonary infection – Desert Rheumatism or Valley fever
▪ Finds its way to muscle/tissues→ makes sperioles→ hundreds of
endospores→ seed rest of body
▪ Skin involvement- blister
▪ Immunocomp: Meningitis
▪ Spherules in endospores
o Loves to grow in lab, but too infectious
o Tx: Antifungal
- Case 1: infect diz specialist in histo area saw some cases:
o 14yom from NYC spending summer on farm→ chicken coup. 2 wk later: fever,
cough, chest tightness, malaise. Abx dont work, cough worsen. CXR: hilar
lymphad & patchy low lobe infltrate. Acute convalescent AB titer. No antifungal.
o 58yow ICU, kidney transplant 18mo ago. On prednisone, mycophenolate,
cyclosporine. Acute fever, chills, dysp, cough, pO2 65, WBC low, creatinine
 high, CXR: diffuse B/L infiltrates. Bronchoscopic lung biopsy: tiny oval budding
IC yeast in alveolar maros. Histo antigen pos. Diag sever pulm histo→
amphotericin B
o 66yom hist COPD. 6 mo earlier: fatigue, dysp, fever, night sweat, anorexia,
20lb weight loss, productive cough--> yellow with blood. CXR: upper lobe
cavitary infiltrates. Sputum cult: histo after 5wks incubation; AB titers +,
diag chronic cavitary pulm histo. Itraconazole, improve over months

Chapter 48 Candida
● Opportunistic fungal infections are often associated with HIV or any
immunocompromised patient
● Characteristics of fungi
o Eukaryotic, have 60s ribosome, have cell wall that’s different from
bacteria; is dimorphic (yeast phase which is single-celled, or mold which
has mycelia forming)
o Sabouraud Agar
● Yeast w/ pseudohyphae/hyphae
o Form tough-to-dislodge pseudomembranes
● Decreased cell-mediated immunity
o example: alcoholic/drug user, genetically immunocompromised,
breastfeeding
● Thrush/diaper rash
● Candidiasis
o Typically only found as yeast
o Pseudohyphae on them
o Part of our normal flora on moist mucosal surfaces, like oral or vagina
o Largely held in check by other normal flora
▪ But if you wipe them out, the yeast can take over
o Neutropenia - susceptible to candidiasis
▪ Radiation treatment, alcoholism, drug abuse
o Most common form - thrush (white coating of mouth and pharynx)
▪ Other types: diaper rash
o Overgrowing on host tissues, resulting in disease; rarely disseminate
o Relatively easy to grow
▪ Readily grow on Sabouraud agar
o Treatment
▪ Will not be too specific on treatment
▪ Thrush: what will you use to treat it? Answers would include list of
antimicrobials (AZT, amphotericin B as possible answer choices)
- just be able to connect the disease with the type of medication
● Cryptococcus
o Comes from birds
o Think AIDS → cryptococcal meningitis
o Major virulence factor: capsule (encapsulated budding yeast)
▪ able to cause meningitis
 o Latex agglutination test of the CSF in suspected meningitis
o add India ink (hydrophobic molecule) to solution against hydrophilic
capsule

o Good T cell response important to fight it off

o Diagnosis involves encapsulated budding yeast
o Treatment - antifungal
▪ Mietz Mietz notes that amphotericin B has a lot of side effects =
toxic
● Aspergillus
o Exists as a mold almost all the time
▪ Exists as a mold at body temperature, which is intriguing since
usually the yeast form, not the mold form, exists at body
temperature
o Clinical scenario: bone marrow transplant pt w/ loss of vision in their
eyeball
o Acute angle
▪ "Acutely branching septate hyphae"

o Treatment with antifungal

● Mucorymyocis
● Other opportunistic molds - didn’t really look at them
● pneumocystosis
o foamy proteinaceous material w/ diffuse infiltrates
o Disease itself causes a crackling lung; auscultation sounds like paper sack
being crumpled
o Use bactrim (but he probably won’t ask specifically about it)
● Case 1: 60yow who had perf colon is in ICU. had renal fail & req hemodialysis. Had
ileus & on TPN via central catheter. On ventilator, had CHF. Prior pneumonia→
piperacillin/tazobactam. 8 day later: febrile, BP fell, less responsive, started on
 meropenem & vancomycin. Catheter removed & cultured→ yeast, germ-tube + →
candida albicans
● Case 2: 35yom acute myelocytic leukemia w/ treat chemo→ neutropenia &
thrombocytopenia. Neutro count: 50/mm3. Bacteremia w/ Klebsiella pneumoniae→ Abx.
10 day later: (still on abx) fever, pleuritic R chest pain, cough, SOB. CT: nodular lesion
in R low lobe. Bronchoalveolar lavage→ acute branch septate hyphae, culture ID
Aspergillus

Chapter 49 superficial, cutaneous, subcutaneous mycoses

● Sporothorix
○ Rose garderner disease
○ 488- read case
○ In environment
○ Gets into subcutaneous--needs vector (splinters)
○ Conidia
○ Usually self resolve
○ Topical antifungal will not work
○ Dimorphic
○ Figure 49-2 multiple ulcerated nodules, localized
○ Clinical Scenario: man stuck by plant and come down with localized
granuloma rxn
● Dermatophytes
○ Only infect skin (low temp), only mold
○ Causes Tinea
■ You name it after where it is on the body
○ Ringworm
○ Spread enviro or human-human
○ 3 organisms that cause tinea: Microsporum, Trichophyton,
Epidermophyton
■ Grow as molds even in the skin
■ Localized to the surface of the skin
○ Genetic and hormonal factors are associated with susceptibility
○ Dx: scrapings of lesion and stick under microscope slide with K+ Peroxide
■ Septate Mold
○ Tx: Topical Antifungal
○ Eat the pigment in your skin→ white lesion
● Malassezia causes Seborrhea Dermitits
------------------------------------------------------------------------------------------------
- Subcutaneous: major is sporothorix
o Gain access to subq layers by environmental vector (Rose Gardner disease,
case talks about Christmas tree farmers)
o Dymporphic, exist as mold in environment and yeast in body
o Found in woods and all over environment
o Inoculate self and over several weeks get painful nodular granulomar
lesion that stays localized (unless you aren’t immunocompetent, then it
disseminates)
 o Usually self-limiting, but if persistent then treated with systemic
antifungal
o Don’t worry about other subq mucoses
- Dermatophytes (cutaneous)
o Only on skin, restricted to room temperature
o Microsporum
o Tricophytum
o Epidermophyton
o Named Tinea and wherever they are on the body
o Penetrate skin and digest the keratin and pigments which activates
immune response that leads to flaky skin
o Genetic and hormonal components
o Diagnose by scraping rash and add drop of KOH and look under slide for
branching hyphae
o Treated with topical antifungal
- Will need to know some general antifungal drugs (amphotericin and anything-
azole)
--------------------------------------------------------------------------------------------------------
--------------------
Sporothrix Schenkii
● Rose gardener's disease-spread in the environment, not person to person
● Subcutaneous mycosis
● Dimorphic fungus
● Ascending lymphangitis "lil nodules"-> forms a granuloma
Dermatophytes-microsporum, trichophyton, epidermophyton- Ringworm
● Genetic factors
● Tx doesn't help
● Dx w/ KOH-look for budding yeasts

Chapter 50
● Do need to know the class and the drug and how they work
● “MEMORIZE TABLE 50-1 AND YOU WOULDN’T EVEN NEED TO
READ THE CHAPTER”
○ KNOW CLASS, MECHANISM, ACTION COLUMNS
● Polyenes
○ Membrane of fungi made of ergosterol
○ Binds to ergosterol causing disruption of cell membrane
○ Amophotericin and nystatin
● Echinocandins - inhibit cell wall synthesis
● Azole - block ergosterol synthesis
● Flucytosine - inhibits DNA synthesis
● Griseoflavin - topical that you can use for mycoses

Chapter 51

Chapter 52
● Malaria
○ Organism:
■ Protozoa
■ Malaria caused by P. falciparum, P. vivax, P. ovale, and P.
malariae
○ Encounter and entry:
■ Transmission through bite of infected female anopheline
mosquitoes (saliva)
○ Spread and multiplication:
■ Sporozoite is the infectious form present in mosquitoes that is
transmitted to humans
■ Sporozoites enter liver cells which mature, multiply by
binary fission, and are released as merozoites (form that
invades RBCs – contain schizont)
■ Merozoites divide and mature inside RBCs and release new
infective merozoites; a minority form gametocytes
○ Damage:
■ Fever, chills, anemia
■ Can cause splenomegaly
○ Diagnosis:
■ Giemsa-stain shows trophozoite rings in RBCs
■ P. vivax/ovale have Schüffner stippling (red granules in RBC
cytoplasm)
○ Treatment:
■ Chloroquine
■ Chloroquine resistant P. falciparum can be treated with Malarone,
Coartem, quinine + doxycycline, or quinidine
■ When treating liver: primaquine
○ P. Vivale and Ovax have dormant liver forms (as hypnozoite) that must be
eradicated w/ Primaquine. Look for a resurgence of malaria in someone
who has received adequate treatment. 48 hour cycle (tertian) of fevers
AKA fever on first and 3rd days.
○ P falciparum: severe, irregular fever patterns. Pararstized RBCs can
occlude capillaries in brain, kidneys, and lungs
○ P malariae: 72 hour fever cycle (quartan)
○ Virulence factors- knoblike structures with P something, binds to blood cell &
endo→ block cap→ disease
○ Spleen problems
 ○ schufner dots & concept of differentiation
○ Control via control mosquitos
● Babesia
○ Blood protozoa From rodents (via Ixodes tick-same geographic
location as Lyme).
○ Invade RBCs directly, no intermediate liver stage (unlike malaria)
○ In RBCs, replicate into tetrads, and then lyse the RBC as they mature.
May get back into the Ixodes tick to complete the cycle
○ Spleen is important for removing infected cells
○ Treated with clindamycin + quinine
○ Comorbid with lyme disease because spread by same tick
○ 4 nuclei together= diagnostic= iron cross= tetrad
○ “Summer flu”
● Toxoplasma gondii
○ Encounter:
■ Cats (intestine) are definitive hosts; all other animal (sheep,
pigs, cattle) s develop dormant toxoplasmic cysts in their
muscles and viscera
○ Entry:
■ Ingesting oocytes from cat feces or muscle cysts in undercooked
meat (beef or lamb)
■ Spread and multiplication:
 ■ Enters by active invasion of the cell. Creates parasitophorous
vesicle which becomes invisible to the lysosomes
○ Damage:
■ 3rd leading cause of mono (EBV→ heterophile→ think CMV & toxo) =
primary infection
■ TORCHES: chorioretinitis, congenital infection
■ oocyst in brain in HIV (ring enhanced lesions)
○ Diagnosis:
■ Competent host- elevated toxoplasmosis antibody titer especially
IgM
■ Incompetent Host (ie HIV)- unable to mount immunological
response. Must look for ring-enhancing lesions in Brain MRI.
■ Congenital – Usually chorioretinitis is the first and only
symptoms. May have asymptomatic or have various learning
disabilities.
○ Treatment and prevention
■ Competent Host- Self limited, no treatment
■ Incompetent host- pyrimethamine plus either
sulfadiazine or clindamycin
■ Congenital- screen all pregnant women. Difficult to treat once in
utero. Greatest chances of congenital diseases if they seroconvert in
the 1st trimester. Little effect to the fetus if they convert in the 3rd
trimester.
● Trypanosoma cruzi: Chagas disease
○ Tropanosomes
■ Antigenic variation
● Predominant surface protein (VSG?)
● Kill one variant, immune response, mutates to new variant,
cyclic response and mutation
○ Pathogenesis:
■ Bite of infected reduviid bug (“kissing bug”) (fecal matter)
■ Chancre or tissue and lymph node swelling at bite site
■ Most develop mild disease w/ fever, recover spontaneously, and
remain asymptomatic
■ Small proportion develop complications 10-20 years later
● damage to nerves in GI tract (megaesophagus,
megacolon)
● Conducting tissue in heart (right bundle branch block)
● Heart muscle (cardiomyopathy)
■ Fibrosis is the hallmark of pathology
○ Diagnosis and treatment:
■ Blood culture, positive antibody titer
■ Treat with nifurtimox or benznidazole
■ No treatments for late complications
● Trypanosoma brucei: African sleeping sickness
○ Pathogenesis and diagnosis:
■ Bite of infected tsetse flies (saliva)
 ■ Undergo antigenic variation of its immunodominant surface
antigen (variable surface glycoprotein)
■ Reservoirs are wild game animals in East Africa (takes
only months to reach CNS); humans and domestic animals in
West Africa (takes years to reach CNS)
■ Bouts of systemic illness with fever and swollen lymph nodes; can
eventually reach brain and CNS and infect brain and spinal fluid.
During each bout, undergo surface antigen rearrangement (genetic
rearrangement).
○ Treatment:
■ Eflornithine
 ● Table: lesch and brucei less important
● Entaomeba histolytica
-----------------------------------------------------------------------------------
● definitive host- where the parasite exchanges chromosomes/ have sex
○ Malaria def host: anopheles mosquito
● Know differences in 4 species result in type of red cell it infects, bottom of p. 509.
○ Vivax and ovale can get into the liver and harbor latent- persistence.
○ Anti malarial drugs that target vivax and ovale can enter the liver.
○ Falc cant be treated that way. Makes the red cell less pliable so when it
squeezes capillary cant.
● Dx malaria using a blood smear.
○ Know general pattern of malaria in terms of what they look like and
presence of schuffner dots.
● Treatment: chloroquine and MOA-blocks heme detox and kills parasite.
○ Can gen chloroquine resistance.
○ Prevention: problem- major outer protein antigneically variable
● Babesia- Peopel without spleens are more susceptible because cant get rid of bad
cells.
○ Dx and treatment: quinine and clindamycin.
● T. gondii
○ Exist in cats as oocysts and in humans as cysts.
○ During active infection toxo is taken up in mac and trans into body
deposits in tissues gives rise to body aches, fever and pain, serologically
dx.
○ Can see organisms hanging in white cells.
○ Need to know imp in congenital infections esp chorioretinites can get it 3-7
years after birht.
● Trypanasomes is a flagellate.
○ Theres 2 forms: cruzi and brucei.
○ Both forms demonstrate antigenic variation.
○ Cruzi is localized to S. Americas.
■ Typically found in cattle.
■ You can dx via ab presence, cant grow org, d
○ Brucei endemic to africa causing sleeping sickness.
■ recurrent fevers bc antigenic variation.
■ They have a series of variable surface glycoprotein that studs
surface and they express VSG one at a time, it comes up and you
can get a lot gowing in blood stream, eventually dev immune
respone, you knock it down, then vsg2 expresses and get
 trypanosomes in blood get fever and immune response is sig
enough that you get nerve damag.e
● Amebas- just E. histolytica-->that its a ameba that causes diarrhea and the case.

Chapter 53
● Parasites→ protozoa or worms

○ Also know trichomonas vaginalis

● Entamoeba Histolytica
○ Amoeba (no flagella)
○ Ingested as cyst→ stomach acid wakes it up→ Replicated by binary fusion to
become trophozoite (equilibrium of cysts and trophos)--> excreted again as cyst
○ Flasked shaped ulcers in colon
○ Trophozoite binfs to surface sugars→ form amoeba pores→ water flow out→
diarrhea (can be bloody)
○ parasites→ controlled by eosinophils
○ Paradoxical transmission: Diarrhea aren't infectious because mostly
trophozoites are being excreted
○ Biopsy of intestine, immunoassay in stool, ELISA
○ Treat: anaerobic, parasites treated with metronitazole
○ Person person & environment
■ Ingest from sand of Afghanistan (soldier with chronic,
malabsorption diarrhea)
○ 2 forms: growing trophozoite & resistant cyst
○ Change in structure of intestine→ malabsorption
● giardia is
○ Flagellate
○ Vector is water, reservoir is animals
■ Drink water from stream when hiking; “beaver fever”
■ swimming pool
○ Ingest cyst→ acid conversion→ trophozoite with a moustache→
○ 2 nuclei & Sucker on trophozoite→ attach to enterocyte→ inflam→ alter
structure
○ Mild dia progress to malab (greasy)
○ anaerobe→ metronidazole
 ○ Paradoxical transmision
○ Diagnose with cyst & tropho in stool (won’t ask about immunoasay)
● Cryptosporidium
○ Vector is water, reservoir is animals
○ Zoonotic- livestock, poops in water, people drink
○ Acid fast
■ Do acid fast to stool→ mycobacterium tiny & parasite cyst is much larger
○ Infectious form is oocyte (oocyst--resistant but also sexual)
○ Immunocompromised usually ones infected, but if load enough can infect
healthy people as well
■ Associated with HIV
○ Acid fast cysts
● Trich vaginalis
○ Flagellate in local vaginal flora, can colonize urethra but die out if it dries
out
○ Sex transmitted→ parasitic vaginitis, men can have mild urethritis. But women
pay highest price (vaginitis)
○ Diagnose under microscope--vaginal wet prep exudate on low power→ large
motile organisms: swimmers (a lot bigger than bacteria)
○ Vagina anaerobic→
-------------------------------------------------------------------
● Entaomeba histolytica
○ free living single cell=protozoa
○ entameba- ameobiasis- parasite without flagella
○ trophozoite uses lectin to bind to enterocyte and form amoeba pores which
allow water to flow out
○ controlled by eosinophils typically rather than macrophages
● giardia: ex; hiking, drinking water from stream, “beaver fever” not to be confused
with “bieber fever” which also causes intense diarrhea
● cryptosporidium: livestock pooping in water
○ can multiply in large water sources
○ healthy will not usually show major sympt, immunocomp will have
recurring bouts of diarrhea
● trichamonas vaginalis:
○ one of 3 causes of vaginitis (this is parasitic form)
○ results from a dysruption of flora and growth of thick exudate on wet
mount- large, motile organisms
○ because std- treat both to avoid ping pong relapse
--------------------------------------------------------------------------------------------------------
o Know in case about amoeba and flagellate difference.

Chapter 54
● Minimize life cycles
● Ascaris- longest & largest
○ Places that lack sanitation
○ Secretes eggs in stool→ ingested→ larvae→ blood→ lungs→ swallowed→
intestine
○ Eosinophils critical for control
○ Humans are dead end hosts
○ Look in stool for eggs & works via low power microscopy
○ Treat metronidazole (generic for parasitic infection- albendazole)
● Pinworms (vermicularis)
○ Spread by children to entire family
○ Ingest eggs and stay in intestine
■ Resistant to drying→ transmi with clothes (bedsheets, underwear)
○ Itching and scratching in the area (genitals)
■ Eggs emerge and deposited on perianal skin
○ Diagnose: scotch tape test- tape to anus to pull off eggs→ visualize
microscopically (low power)
 ○ abendazole
● Strongyloides
○ Case: Repeated sepsis cured each time= unusual→ parasite penetrating the
intestine to gain access to blood
○ gut→ peritoneum→ blood→ lung→ swallow→ back to gut
● Tapeworm (solium)
○ Pig tapeworm
○ Undercooked pork (cysts→ only cause intestinal infection)
○ Head, fragments
○ Penetrate into deep tissues→ only from larval form in feces
○ Thinking pig farmer/butcher
○ Affect absorption→ megablastic anemia
○ Look at poop for eggs--low power
○ long and ribbon like attach and penetrate into tissues and form cystic
larval forms
○ ingestion of cysts (pork) intestine causes intenal
○ fecal eggs is worse
○ beef tapeworm is called saginata

Chapter 55
● Trichonella spiralis (roundworm)
○ Helminth (not trichonomiasis--protozoa)
○ Pigs- go into striated muscle to make cysts
○ Causes disease in carnivores
○ Muscle aches from cysts in muscle
○ Infection decreased when pig diet changed to grain
■ No longer ingest trichonella
■ Also nowadays meat is inspected when distributed
○ ingestion→ cysts to muscles, inflam response, aches
○ Can self resolve or last for long time
○ Muscle biopsy to diagnose
○ Antiparasitic to treat
● Schistosomes
○ growth in snails finds host can penetrate skin directly then to cause dz
○ Africa
○ Water, cutaneous, fibrotic→ granuloma (depends on species where it goes)
○ Diag: examine stool for eggs
○ Treat with antiparasitic
● Onchocerca volvulus
■ Black fly that bites near eye→ local infection
● Make antigen→ T3 hypersensitivity
● Filaria/Wuchereria
■ Gets in lymph and clogs→ fluid fills elsewhere→ elaphantiasis
■ Transmitted by mosquito
■ Nocturnal
■ Own microbiome- needs some other organisms→ tetracycline to kill the
symbiotics
Chapter 56 Prions
PrPsc versus PrPc
What prion is specific for cattle, table 56-1
No questions on diagnosis
Maybe a question on damage
--------------------------------------------------------------------------------------------------------
● Infectious protein
● pg 553-PrPc-> PrPsc process alpha helix to beta sheet; amyloid plaques that
disorganize hella proteins
● Will ask questions about the human prion dz (CJD, Kuru)
● Know that scrapie is a sheep/goat phenomenon (not a human dz)
● Myoclonus and Hyperreflexia=symptom buzzwords
● Dx on EEG won't be asked
● No good tx
● Only read the first 4 pages of the chapter; we won't be asked about anything from
p 555
Chapter 57 Bioterrorism
- Encounter with Bio weapons
o Aerosolization
o Ingestion
o Zoonotic delivery (mosquitos released into environment)
- A B C Categorization based on threat level

o Know the ones in gray highlight (Category A)

- Bacillus Anthrax
o Gram + rod, Spore former
o Causes Mediastinitis
o White cells and Box-car shaped rods in CSF
o Found everywhere in the environment
o Pg 564
▪ Virulent strain is associated with 2 plasmids
▪ 1st plasmid: capsule formation
● Made of Polyglutamic acid (polypeptide capsule)
● Does not allowmacrophages to take it up
▪ 2nd Plasmid
 ● Anthrax Toxin formation
● Classic AB motif (A active, B Binding)
● B is protective antigen
● A is edema factor (EF), calmodulin dependent adenylate cyclase→
upsets water balance, leading to mediastinitis
● 2nd A is lethal factor (LF), zinc metalloprotease clips MAP kinase
and basically kills cell
o Clinical manifestations
▪ Cutaneous: Tends to be local and forms eschar!, Self-resolving
▪ Ingestion: Rare! Spore contaminated meat
▪ Inhalation
● Spores are highly charged but too big and if you inhale it doesn’t
go into alveoli, but if you weaponize it and make it small, then it
can go into alveoli and becomes very lethal
● Once in alveoli, macrophages take up bug and travel to
mediastinum to cause hemorrhagic mediastinitis
● This takes about 2 days, so Tx Immediately!!
o Tx: Vaccine for military, but not administered broadly
- Yersinia Pestis
o Gram – rod
o Coccobacilli
o Pg 566: causes plague, produces Envelope Antigen F1 / V and W antigens
▪ YOP, inject into cells and kills them
o Normally zoonotic infection, rodents get bit by flea, flea can introduce it to
humans
o Plasminogen activator: low temperatures, it coagulates blood in the flea
▪ Flea is constipated and rather than taking up blood it vomits into the
human blood
▪ Goes to nearest lymph node
▪ Forms Bubo
▪ This takes about 2 weeks to occur, but without tx, in another 1-2 weeks
disseminates to the lungs and causes Bubonic Plague
▪ Once in lungs, original pt can cough and spread to another pt
▪ The new pt gets it in their lungs and can die within 2 days
- Francisella Tularensis
o Tularemia, Gram -
o Lives in Rabbits, Squirrels
o If hunter kills the animal and handles it, it can get into skin (self-resolving)
o Ingestion: intestinal disease (not lethal)
o Inhalation**: less than 10 organisms will kill you in less than 2 days
- Smallpox
o Vaccine tx’ed
o DNA virus
o Some similarity to chickenpox (what is the difference??)
 o Board exam: Variola (largest)
- Viral hemorrhagic Fevers
o Ebola
● Incubation period of 21 days
o Symptoms: fever, myalgia, headache, retro-orbital pain, prostration
(complete weakness-stuck lying prone). May have hemorrhage in
eyes.
▪ Sepsis localized to the lungs, vessels all open up and blood leaks into
lungs
o Yellow fever and Rift Valley fever have jaundice
- C. Botulinum
o MOA: Zinc metalloprotease that causes Synaptobrevin cleavage-->Ach
inhibition. Descending flaccid paralysis
o 4D’s: Diplopia, dysarthria, dysphonia, dysphagia
o They then move down and can shut down resp system
------------------------------------------------------------------------------
- Bacillus anthracis: Category A (most dangerous)
o Gram (+) boxcar shaped bacteria
o Anthrax causes mediastinitis that goes to meningitis
o Polymorphonuclear leukocytes
 o The spore is the infectious particle
o Anthrax toxin consists of 2 binary exotoxins with protective antigen
subunit that mediates binding and entry of toxins into host cells.
o 3 forms of anthrax
▪ GI antrax is bloody diarrhea and necrotic intestines
▪ Inhalation anthrax is the most lethal way. Single spores so they
can fit into alveoli and germinate: fever, myalgia, malaise,
hemorrhagic mediastinitis with widening of the
mediastinum, and eventually meningitis
o Vaccine is the protective antigen binding subunit
- Plague (Yersinia pestis)
o Gram negative rod with bipolar staining (looks like safety pin)
o 3 important virulence factors:
▪ Plasminogen activator (PLA): coagulates blood to facilitate
spread
▪ V and W antigens: anti-phagocytic, let organism survive in host
cells
▪ Yops (type 3 secretion systems to inject cells)
o bronchiopenumonia that kills in 2 days
▪ So 2 weeks total from infection to death
o Pneumonic plague: comes from bubonic plague people coughing
that aerosolizes the pestis, leads to death in 2 days
- P566 pink box good to know
- Tularemia (F. tularensis):
o Gram neg coccobacillus
o Only takes 10 organisms to kill a person if inhaled
--------------------------------------------------------------------------------------------------------
Class A is worst
Anthrax forms spores
Going to get a question on botulinum toxin, know it’s a zinc metalloproteinase that
works on Ach transmitter
4 D’s: diploplia, dysarthria, dysphagia, dysphonia
--------------------------------------------------------------------------------------------------------
All the bugs discussed in this chapter=category A
Topical Anthrax:
● If you acquire anthrax topically, it has to enter a wound (anaerobic envt). This
forms a spreading eschar (purplish black, indurated sore)
● If untreated, can hop into the bloodstream and enter the macrophages
● CT appearance of widened mediastinum typical
● Hemorrhagic fever sx due to a cytokine storm
GI anthrax:
● rare
● faster course than cutaneous anthrax
● GI tract has ulcerations (like the eschar of the skin manifestation)
Inhalation anthrax
● Wool sorter's dz (not as fast as weaponized anthrax because size not ideal)
 ● Not a true pneumonia because bacilli are not in the lungs
● The spores enter alveoli and are engulfed by phagocytes, then go to mediastinal
and peribronchial lymph nodes
o p 563: for spores to be weaponized, should be between 0.5-5
microns to enter the alveoli-all but promised this was going to
be a question
o Dz is flu-like at first, rapid progression to hemorrhagic mediastinitis
● Plague-Y Pestis
o Produces a type III secretion system
o Death in the pt is from a cytokine storm
● Francisella Tularensis
o Rabbits, coyotes
o Can be intestinal or cutaneous dz; these manifestations doesn't spread well
o Spreads well if in lungs (1 organism to kill ya) and get all sortsa septic
o Antiphagocytic capsule
o Forms a granulomatous dz in people w/ shitty cell-mediated immunity
(misdiagnosed as TB)
● Smallpox
o DsDNA, huge
o Hella infectious once the rash sets in

Chapter 58

Chapter 59

Chapter 60
-host defense mechanisms, what does digestive system do to protect?
-pathology
-a specific organism that’s associated with a pbl case – GIARDIA,
hemorrhagic e coli can cause this too
-architecture of enteric mucosa 60-3, need to know about enterocytes and
how they’re arranged in polar fashion – what do M cells do there, goblet
cells and paneth cells
-if someone has an ulcer what organism involved – h.pylori
-salmonella goes thru bile/intestine
-what are requisites for organism to infect gall bladder- survive in env’t of
detergents
-giardias, and e.coli and types of ecoli to cause diseases –salmonella and
shigella (not emphasized from this chapter)
-bacterial overgrowth syndrome- pathology, what happens, gives rise to
diarrhea- greasy diarrhea you cant absorb fat or vitamins- mal absorption.
What vitamins are you deficient in?
diarrhea (caused by toxin mediated bacteria- causes it to secrete water) vs.
dystenery – invasive diarrhea
enterotoxogenic ecoli- watery diarrhea
hemorhaggic ecoli- invasive diarrhea
pg 606, camplobacter gegunium- vibrio , comma shaped rod- causes bloody
diarrhea
- infections of SI : giardias that’s it
- food poisoning 4-8 hrs after- intoxication
- 24-48 hrs later- infection
- don’t look at table 60-1 or 60-2
- food borne illness is most common cause of infectious diseases-
reactive arthiritis
- gram – rods, gram + cocci
- 610, enterohemoragic ecoli – if they become invasive bloody diarrhea
lasts for a long time
● Barriers to infection - always asks a question on that
○ “What happens if you inhibit bacterial growth in the jejunum” - related to
bacterial overgrowth syndrome
○ Look for broad concepts in terms of test questions
○ If you continue taking tums, you decrease stomach acidity, which is
normally a host defense
○ Question on host defenses
■ Lysozyme in saliva is active against G+
■ Dental Pellicle- sticky coating on teeth that bacteria stick to
● *Figure 60-1 Know how the change in composition of bacteria through the gut,
anareobes in stomach
● Prox duodenum is pretty sterile, important because ++ absorption
here
● Bacterial overgrowth in the duodenum -> malabsorption
● Fig 60-3 know all that shit, what each of the things do
○ M cells sample antigens/microbes and deliver them to dendritic cells and
Peyer's patches
○ Dendritic Cells extend processes between tight junctions to sample
luminal antigens
○ mucus formation and gut motility, hinder adhesion
○ IgA
● Know the sequelae of bacterial overgrowth syndrome (malabsorption,
steatorrhea, etc)
o Bacteroides is the bug to blame
● Know the first 1-2 organisms per system
● Mouth
○ Candidiasis - immunocompromised patient
■ Will present the case and ask for most appropriate tx, will be
general: offer options of antibacterial, antiviral, antifungal like
nystatin
■ For heaven's sake, know pseudomembranes
■ Part of the normal flora, culture is a waste of your time
○ May ask something on S. mutans - dental cavities
● Stomach
○ Normally few bacteria, G+ acid-resistant rods, not anaerobes
○ Low levels of Salmonella in food such as peanut butter or
chocolate
○ Acid sensitive bacteria=Salmonella and Vibrio; if a person is on
a PPI/other antacid + risk of infx
○ Achlorhydria assoc w/ infx by G- enteric rods, like bacterial overgrowth
○ Campylobacter-Most common cause of diarrhea
■ causes Guillain Barre
○ Campylobacter and Yersinia will cause reactive arthritis
○ H. pylori
■ Resistant to acid, can be associated with PUD, giving rise to
adenocarcinoma of the stomach
○ *Know that acid stomach and first part of small intestine-not many
bacteria
○ For some reason, viral infections affecting the enterocytes at the villi but
not the crypts is scratching something in the back of my brain.
● Biliary tree S Typhi has a trophism for Gallbladder and E COLI IS THE
MOST COMMON-past question
○ Organisms have to be pretty resistant to bile, like Salmonella, E. coli
○ E. coli and Klebsiella are what he’s going to focus on
○ Charcot Triad-fever, jaundice, RUQ pain
■ Boards note: Book says cholecystitis, everything else says it's more
specific for cholangitis; yes, cholecystitis has been a wrong answer
choice on board questions
○ Kupffer cells protect liver parenchyma
● Small and large intestine
 ○ Bacterial overgrowth syndrome - what happens when there’s no bacteria
and you can’t absorb certain types of vitamins
○ C. diff
○ Will ask a question about HUS and EHEC
○ Don’t worry about EHEC and other related stuff
○ Most common bacteria in the large intestine: ++bacteroides-past PBL
question, asked more generally as "anaerobes"
● Diarrhea vs. dysentery -
○ Diarrhea - bacteria that produce toxins
○ Dysentery - invasive bacteria
● Table 60-1 - TOO FUCKING DENSE
● Page 607
○ Know the first disease in each bullet point:
○ Viruses taht cause death or dys of intestinal epi: rotaviruses & noroviruses,
cause dia by destroy or alter fxn of enteocytes at villi but dont affect the
crypts
○ Bact that colonize the SI: ETEC & cholera, dia secondary to toxins that activate
enzymes responsible for synthesis of cyclic nucleotide mediators → stom Cl
secretion & inhibit Na uptake→ fluid loss
○ Protozoa in small bowel: Giardia & cryptosporidium, avoid secretory IgA
○ Bact that cause food poisoning: bacillus cereus & s. Aureus, preformed
toxin
● DON’T WORRY ABOUT TABLE 60-2
● Know about reactive arthritis
○ Symptoms: “Can’t see, can’t pee, can’t climb a tree”
● Surgical infections - think anaerobes
○ Anaerobes get access to peritoneum and then the bloodstream → sepsis
● Most E. coli can utilize sorbitol, so they turn pink on MacConkey agar with
Sorbitol (SMAC)
○ EHEC O157-H7 doesn't ferment sorbitol, so they’re white colonies on
SMAC agar
● Treatment for diarrhea - Know that most diarrheas are tx'd with oral
rehydration therapy (as opposed to antibiotics)
○ won't ask specifics on the formula because that'd just be silly
○ Know that Giardiasis-Tx w/ Metronidazole
KNOW THE CASES, ESPECIALLY IF THERE’S A SIMILAR ONE IN THE PBL CASES
● Case1: 7mo girl mid ear infect, amoxicillin, cleared infection, 6th day became iritable,
creamy white curd like patches on tongue, scraped→ bleed, candidiasis, stopped AB,
gave antifungal
● Case2: obese 48yo mom, stomach problems, midepi pain moved to RUQ & R
scapula, vomit, pain subsided, several days of intense attacks, 6th day jaundice,
elevated WBC, serum bili & alk phos up, AB, US showed GB distended & had
stoned, culture= enterococci & E. coli, schedule for surgery
● Case3: 63yo man surg to remove tumor obstructing stomach
outlet...gastrojejunostomy, 2y later chronic dia, weight loss, dia became bulky
smelly greasy, fatigue, SOB exertion, numb & tingle in hands & feet, severe
megaloblastic anemia, leukopenia, vit A and precursor carotene low, vit B12
 absent, intrinsic factor present, malab, ==>bact overgrowth synd (thinking
Bacteroides fragilis), vitamins replaced, ciprofloxacin
● Case4: 46yo woman, missionary in guatemala, low fever, ab pain, dia w/ occasional
blood, ate street food in guatemala, O&P & culture neg, colonoscopy→ flask shaped
ulcerations→ entamoeba histolytica, oral metronidazole & paromycin
● Case5: 24yo backpacker recently in colorado, drank from stream, watery dia, anorexia,
weight loss, stool foul smelling & float, O&P neg, endoscopy w/ biopsy of duo→ giardia
● Case6: 9mo girl in child care, irritable, vomit, low fever, upper resp symp: cough, nasal
discharge, pharyngitis; watery dia w/out blood or leukos→ viral gastroenteritis, ELISA=
rotavirus antigen in stool, oral rehydration
● Case7: 3yo girl cramps, fever, watery dia after hamburger, turned bloody on day 3,
leukocytosis, day 5 isolate E.coli O157:H7, leukocytosis w/ neutos & bands,
thrombocytopenia, anemia, elevated creatinine, RBC fragments on smear→
microangiopathic hemolytic anemia, progressive anemai, thrombo, & uremia w/out
concumptive coagulopathy-->HUS, week of hemodialysis, transfusions
● Case8: 5yo boy, 12yo girl visit a farm, have home cured meat and raw milk, boy gets
watery mucoid dia with flecs of blood, low fever, ab pain, resolve; girl worsened in 3
days, localized pain to RLQ, high fever, leukocytosis→ appendicitis→ surgery found it
normal, & terminal ileum inflamed with enlarged mesenteric lns, stool culture= yersinia
entercolitica; fater got arthralgia and erythem nodosum, tested pos for y. Entercolitica,
treat trimeth/sulfameth
Don't worry about peptostreptococcus

Chapter 61 CNS
-polysach capsule , meningitis have carbohydrate capsule
-question: host defense mechanism, cli/ case we had- neisseria meningitis,
- Find 1 q on immune: how does system maintain sterility/prevent infection
o BBB, astrocytes, microglia
o CNS inflamm response is microglial infiltration and proliferation of
astrocytes
- Tables 61-1:
o Acute meningitis (bacterial)
▪ Streptococcus pneumoniae
▪ Neisseria meningitidis
▪ Haemophilus influenzae type b
▪ Group B streptococci
▪ Escherichia coli
o Acute encephalitis (viral)
▪ Arboviruses
▪ Enteroviruses
▪ Herpesvirus
o Don’t need any chronics
o Brain abscesses – know toxoplasmosis (ring enhanced lesions in
AIDS patients)
o Will ask what is the most common→ know overall disease
- Get to brain via blood or neurons
 o Hematogenous spread→ meninges (bacteria)
▪ Can get to CNS by blood bc capsule & tropism for BBB
● E.coli has K1 antigen in capsule; Polysaccharide rich sialic acid→ bact
adherance & antiphagocytic
▪ Exceptions: listeria (look at listeria handout on portal, facultative IC,
just stays in cells, no traveling) & m. tuberculosis
o neural cells → brain (virus)
- People with AIDS can develop progressive multifocal
leukoencephalopathy (PML) caused by reactivation of JC virus
- Most Common Bugs of Meningitis (Table-61-2)- what causes meningitis and who
gets it
o Neonates
▪ Group B strep (gram + cocci)
▪ Listeria Monocytogenes (gram + rod and invasive to cells, associated
with meningitis in immunocomp people)
▪ E. coli K-1 (gram - rod)
o S. pneumo for everyone else (followed by N. meningitides and
HIB)
o 3-60 Month
▪ Strep Pneumo,
▪ Neisseria Meningitidis
▪ H. flu Type B
o Adolescents: Neisseria Meningitidis
o Cranial surgery – S. aureus
o Immunosuppressed: L. monocytogenes and Pseudomonas
aeruginosa
o Old people
▪ Listeria Monocytogenes
▪ strep pneumo
- Table 61-3: viral encephalitis
o Know nature of genome
o eastern eq- RNA, children
o HSV- DNA, all ages
o WNV- RNA, older adults
o Enterovirus- RNA, infants/children
o Rabies- RNA, all
o VZV- DNA, children/immunocompromised
o HIV- RNA, adults
- (Table 61-4 is money!)
o White cells consume the glucose, not the bacteria
o Acute bacterial meningitis
▪ elevated WBCs (massively), RBCs, and protein
▪ Decreased glucose
o Acute viral meningitis (nuchal rigidity, brudinski sign)
▪ elevated WBCs and protein
▪ Normal RBCs and glucose
o Viral encephalitis
▪ elevated WBCs RBCs (massively), and protein. Normal glucose
o Brain abscess: elevated WBCs, protein. Normal RBCs and glucose.
- Treating Meningitis
o Treat acute bact meningitis right away
▪ BBB penetration→ Ceftriaxone
▪ 2nd gen cephalosporin
▪ Dexamethasone- try to decrease swelling of brain
o Vaccines
▪ Capsular based vaccines for bacteria
- Acute Viral Encephalitis
o Know the Case
o Read the section
o Dx: PCR
- Diagnose wtih MRI
- READ the CASES
o Bacterial Meningitis
▪ Army recruit camp, meningitis, fever, headache, nuchal rigidity, petechial rash on his lower
extremities. On lumbar puncture, opening pressure was slightly elevated. CSF cell count
revealed WBCs 5oo, glucose decreased and protein increased. A smear revealed small Gram-
negative coccobacilli and numerous leukocytes. intravenous vancomycin and ceftriaxone, the
CSF culture grew N. meningitides. Vancomycin was discontinued
o Viral Meningitis
 ▪ fever, severe headache, and some nausea. Nuchal rigidity. very sensitive to bright sunlight.
lumbar puncture was performed. The CSF opening pressure normal range. The CSF 76 WBCs,
protein mildly increased, and glucose normal. enteroviral PCR returned positive 36 hours

o Tuberculous Meningitis
▪ native of South America, chicken pox. recovered uneventfully. headache and again had fever.
lost her appetite and vomited a few times. stupor 4 days later, impaired eye movements. A
chest radiograph showed right upper lobe pneumonia. A cranial CT scan showed enlarged
ventricles suggestive of acute hydrocephalus. A lumbar puncture revealed an opening
pressure highly elevated, and the CSF showed 350 WBCs, protein was increased, and the
glucose was decreased. Gram stain and acid-fast stain of the CSF did not show organisms.
CSF detection of tuberculostearic acid and a positive mycobacterial PCR, M. tuberculosis grew
from her CSF and susceptible to isoniazid, rifampin, pyrazinamide, and streptomycin. urgent
ventricular drainage,ABs, and steroids for 2 months. discharged to receive 10 additional
months of therapy with isoniazid and rifampin
o HSV Encephalitis
▪ 60-year-old man, confusion, right-sided weakness, and fever. he thought “there were devils in
the room.” he smelled roses. Three days previously, he had complained of mild nausea and
vomited once. When he arrived at the emergency department, generalized seizure. A CT scan
of the head was normal, but (MRI) scan documented T1-hypoin- tense and T2-hyperintense
signal in the cortex and gray– white matter junction in the left temporal lobe. CSF obtained by
lumbar puncture contained 50 WBCs, glucose normal range , and elevated protein. (EEG)
revealed periodic high-voltage spike wave activity from the left temporal region. Intravenous
acyclovir was started immediately. HSV PCR was positive. Mr. R. continued to receive intra-
venous acyclovir for 3 weeks, which halted the progres- sion of his neurological symptoms.
However, he had many residual signs of neurological impairment and required extensive
rehabilitation therapy.
o Acute Abscess Caused by a Bacterial Infection
▪ 20yo. complained of earache. many such episodes in left ear, but now associated with a
headache that made her nauseated. She vomited once. large blind spot in her right field of
vision. A CT scan of her head revealed a 4×3-cm mass in her left occipital lobe, consistent with
an abscess. needle aspiration &smear revealed Gram-positive cocci and Gram-negative rods.
broad-spectrum antibiotics, including ceftriaxone, metronidazole, and vanco- mycin, aspirate
grew only S. aureus, which was susceptible to methicillin. intravenous nafcillin (to cover S.
aureus) and metronidazole (to cover anaerobic bacteria) for 6 weeks.
Chapter 62
- Need to know the mucociliary elevator and the types of proteins in secretions
o lysozyme, lactoferrin, and secretory IgA antibodies
- Infections of Nose & throat: Pharyngitis
o Group A strep
o Rhinovirus
o Adenovirus
o Pharyngitis is usually caused by bact of the oral flora
- Infections of the Epiglottis: Epiglotitis
o Upper respiratory tract stops at the glottis, lower is from the epiglottis to
the lungs
o H. flu
o Strep pneumo
- Infections of the Larynx & trachea
o Parainfluenza virus (croup)
▪ must have lower temps so can’t get into the body core, predisposes
to secondary infections
- Infections of the Large Bronchi
o Bac. that cause lower respiratory infections must be encapsulated, those
that infect the upper respiratory tract aren’t
o serotyping w/ antiserum
▪ Typable = has a capsule
▪ nontypable = no capsule
▪ H. influenzae type B produces a capsule & is invasive in the lower
respiratory tract
▪ Strep pneumo is also encapsulated
o Bordetella pertussis (whooping cough)
o Mycoplasma pneumoniae
o Chlamydophila pneumoniae
- Infections of the Bronchioles
o RSV, esp in firs 2 yrs of life
- Infections of the Lungs
o Two ways of acquiring pneumonia- community & hospital
o Community Acq
▪ Strep pneumo
▪ H. influenzae
▪ Mycoplasma pneumonia
o Hospital-acquired
▪ G- rods that are highly resistant
▪ S. aureus
o Q fever caused by Coxiella burnetii, from farm animals
o Chlamydia psittaci from birds (parrot fever), aerosolized
- Won’t ask about treatment or the tables
- Subacute Pneumonias
 o Fungal (Histoplasma capsulatum, Blastomyces dermatitidis, Coccidioides immitis, and
Cryptococcus neoformans)
- Pneumonia in Immunocompromised
o Pneumocystis jiroveci
- Cases
o Group A strep pharyngitis
▪ 5yo fever sore throat, tonsils enlarge & coates qith patchy exudates,
ant cerv nodes enlarged & tender, throat culture +, penicillin
o Acute epiglottitis
▪ 3yo fever, dyspnea, drooling, nasal flaring, endotracheal tube
placed, Xray: swell epiglottitsi, naficillin, culture grew H. flu
o Laryngotracheitis
▪ 19mo runny nose, hoarseness, cough, low fever, barking cough,
noisy breath on insp, croup, humid treatment
o Acute tracheobronchitis
▪ 28yo cough, myalgias, headache, cough, substernal pain,
fever,resolve w/o tratment, culture- influenza
o CAP
▪ 36yo hist smoke, fever, chill, cough, L side pain worse w/ brething, rales
in LLow lung, CXR infiltrate in lllobe→ pneumonia, WBC 16000, CAP→
Abs
o HAP
▪ 52yo chronic alcoholism, appendectomy, postop fever, tachycardis,
cough, green sputum, pulse ox 89%, SOB, left lung base bronchial
breath sounds, CXR L side infiltrate, ox via cannula, broad spect
AB, culture= K. pneumo
o Subacute
▪ 46yo seizure disorder, cough, fever, weight loss, foul breath, amphoric
breath sounds→ lung cavity, CXR cavity w/ inflam, penicillin
o Immuno comp
▪ 53yo HIV, fever, cough, fatigue, pulse ox low on exertion, CXR
diffuse infiltrate, PCR sputum= P. jiroveci, Trimeth-
sulfamethoxalone

Chapter 63
- Host defenses
o Removed with voiding
o ABH blood goup antigens secreted on mucosal surfaces→ prevent bact
attachment
- UTI More in female
o Shorter urethra
o Lactobacillus: flora of vagina maintains acidic pH→ prevent colonization by
uropathogens in vagina
- Bact infect prostate via ascent from urethra
o Cause: turbulent flow from BPH
 - Most common uropathogen
o E.coli
▪ P fimbria- adhesin that binds to galactose residues in UT mucosa
▪ Flagella
▪ Aertobactin- scavenges iron
o Staphy saprophyticus 2nd
- Community acq
o 95% female, UPED e coli then staph sephyticis and then….
- Hosp acq
o antibiotic resistant E coli
o Indwelling catheter, ureteric stent, nephrostomy tube
▪ Biofilms: use Tamm-Horsfall protein
▪ Recurrent infection
- Host Response
o TLR-4 on bladder epi response to LPS
o Inflam response→ IL6, 8, 10
o Limited local IgA & IgG response
o Local immunity – limited, after episode of acute cystitis, doen’t protect
from future episodes
o Progression of UTI to pyelonephritis
o
- Diagnosis
o Symptomatic bacteriuria is 10^5 colony forming units/mL
o Urine culture
▪ Many false + → need Clean cash urine is important
▪ want to know what’s in the middle of urine screen, not stasis
- Treatment
o cystitis due to UTI is short treatment course
o Pyelonephritis is long treatment course
o Recurrent UTI
▪ make sure prophylaxis is appropriate
▪ People susceptible to recurrent UTI have non-secretor of ABH
blood group antigen status
▪ tamhorsefall with galactose residues in biofilms
- Cases
o 39yo male, parapelegic, bladder & leg spasms, culture K. pneumo
▪ 87yo fem nursing home, chronic incontinence, lethargic, cloudy
urine, cultrue E.coli, pyuria

Chapter 64 Infections of the Skin & Soft Tissue (shelby’s book notes/not meitz notes)
● Host defense
○ Flora: gram + (staph epidermidis; s. Aureus, strep pyo)
○ Exfoliation & dryness from sloughing of stratum corneum
○ Low temp
○ Saltiness (staph epidermidis is salt-resistant)
 ○ Lipid content
○ Langerhand cells
● Virulence factors
○ Hyaluronidase (spreading factor)- enzyme in S. aureus & S. pyo
● Infections
○ Exogenous- environment invasion
■ Excess moisture (psudomonas), trauma, percutaneous catheters
■ Staph aureus
○ Endogenous- internal source
■ Abscess from endocarditis
■ Necrosis from meningitis--> purpura fulminans
■ Immunocomp- ecthyma gangrenosum (pseudomonas)
■ Exanthems (rathes): viral= measles & rubella
■ n
○ Toxin-induced- toxin from different site
● Impetigo- spreading infect, children
○ Staph aureus
○ Strep pyo
● Erysipelas- spreading infection involving dermal lymphatics, usually on face
○ Strep
● Cellulitis- spreading infect with major focus in subcut fat
○ Strep- spread via hyaluronidase
○ Staph aureus
○ h. flu - periorbital in unvax kids
● Abscess
○ folliculitis
■ Staph aureus
■ Psuedo
○ boils/furuncles & carbuncles
■ Staph aureus
● Necrotizing infections
○ fasciitis (w/myonecrosis)
■ Strep
■ Anaerobes
○ gas gangrene
■ Clostridia
● S. aureus
○ Localize, form abscesses
○ Exfoliatin destroy desmosomes→ Scalded skin synd
○ Toxic shock synd
● S. pyogenes
○ Spread extensively through tissues→ cellulitis
○ Erythrogenic factor/pyogenic exotoxin → strawberry tongue & desquamation
○ Toxic shock (w/ necrotizing fascitis)
● Cases
 ○ 27yo infect around nail, draines, pus culture= s. Pyo, 5 day later: pain in
forearm, fever, rash on arm & shoulder, lymphadenopathy, diag strep
cellulitis, penicillin, culture s. Pyo
○ 37yo roofer, swell & pain on neck, hist of boils, 3 day prior- iritation in
whiskers→ progress & size of walnut = mass w/ soft center w/ erythema, needle
asp, g + cocci in clusters + neutros, grew s. Sureus, ABs
○ 57yo woman, T2DM, pain in foot, watery discharge btwn toes, ulcer on
sole of foot, fever, foot swollen w/ patchy erythema, cyanosis, signs of
necrosis, crusting & oozing on toes, ABs, infection ascent, OR- necrotic
fascia into thigh removed, culture Bacteroides fragilis
○ 52yo chemo for lymphoma, chills, fever, pain on shoulder, erythematous
round area w/ central vesicle, broad spect ABs, in hours developed
necrotic center & surrounding erythema= ecthyma gangrenosum, biopsy=
infarcted bv teeming with bacteria, culture p. Aeruginosa, antimicrobial
○ 24yp operation for inguinal hernia, 5d after chills, rash on trunk & face,
sore throat, headache, myalgias, vomit, dia, postural dizziness, rash w/
blanching, conjunctivitis, strawberry tongue, wound drained brown, high
WBC & creatinine, gram + cocci in clusters, grew s. Aureus, + for toxic
shock synd toxin 1, desquamation of hands & trunk, ABs

Chapter 65 Infections of Bones, Joints, & Muscles

- Osteomyelitis- staph a.
o Hematogenous
▪ childhood & adolescence
▪ Metaphyses (to active bone)
▪ Infection comes from arteries going into bone → infect at loops between
artery & veins
o Infants
▪ Subperiosteal space-->abscess, invulcrum
o Children
▪ metaphyses; sequestrum
o Adults
▪ Vertebral bodies, spinal epidural abscess, psoas abscess
o Sickle cell--Salmonella
o Diabetes --polymicrobial
o Infectious source
▪ Penetrating trauma
▪ Ortho hardware
o Chronic
▪ May be doemant & asymp
▪ Monitor with c-reactive protein & erythrocyte sedimentation rate
- Joint infections
o Agents-
▪ Staph a
▪ sexually active adults- N. gonorrhea
- Muscle infections
 o Infecting organism isn’t in muscular tissue→ Involvement from acute phase
response accompanying sepsis & trauma
▪ Mediated by products of macros
● IL-1
● TNF
● PGE2
o Direct infection: pyomyositis
o Gas gangrene
▪ Localized and spread from contiguous site
● Crepitus = clostridium perfringens, anaerobic
● Muscle abscess = staph or strep
● Myositis = mixed anaerobic & enteric
▪ Hematogenous spread
● Bacterial = streps, staph
● Fungal = Aspergillus, candida
● Mycobacterial = TB
● Parasitic
● Viral = coxackie
- Cases
o 15yo boy blunt force trauma to thigh, pain, chills, fever, swelling above
knee, normal ROM, boils on neck and chest, diag osteomyelitis

Chapter 66 Sepsis
-definitions!
-how to get sepsis, going thru kids bones
66-1, know the first 3, associated w fever, disemminated vascular coagulation
-process of fever, what tells the body to cause sepsis- fever. Pathogen . molecular
patterns
LPS for gram – bacteria, recognized by tlr pg. 676
Know: tlr-2 : recognized lipotichoic acid, tlr-4: recognizes polysach gram - , tlr-5:
flagellin in flagella- gram +/-
Syndromes Assoc with Disseminated Infection
● Host response
o Proinflam cytokines:
▪ TNFa - mimic sepsis, margination of neutros
▪ IL-1 - fever, inc adhesive of leukos, inc endo procoag
▪ Prostaglandins
▪ Leukotrienes
▪ Toxic oxygen products
▪ adhesion proteins
▪ Proteases
▪ plasma protein systems- complement, coag cascade
▪ Kallikrein-kinin system
o Stimulators of cytokines
▪ cell wall components
▪ Gram neg: LPS, Lipid A
▪ Gram pos: lipoteichoic acid, peptidoglycan
o Innate immune system
▪ Recognize pathogens via pattern recognition receptors on neutros,
monos, macros, & dendritics
▪ toll -like receptors
▪ TLR4
▪ On macros, dendritics, endo cells→ form TLR4 dimers
when receptros engaged
▪ Recognize
▪ LPS + CD14 & fusion protein on microbe
▪ gram neg bact, RSV
▪ Taxol (chemotherapy), fibronectin, hyaluronan
 ▪ Recognize pathogen-associated molecular patterns (PAMPs)
● Damage
o Vasculature: early dilation & pooling in vs→ leak
▪ Dec syst vasc resistance
▪ Inc venous capcitance
o DIC from proinflam neutro-endo cell interactions that activate the coag
cascade→ consumption clot factors, deposit fibrin, clot formation

● Tx for sepsis
o Fluids
o Vasopressors for vasoC & inc cardiac contractility
o Brod-spectrum, IV, cidal ABs
o Other: ventilator, transfustion, dialysis, IV insulin
● Cases
o Infection from a wound
▪ 48yo farmer, cut thumb, skin red, swollen, throbbing, ooze yellow-
white pus, red streaks up forearm, shaking chills, queasy, fever,
flushed, tachycardia, low BP, IV fluid, AB, culture staphy auerus
o Postsurgery infect
▪ 59yo pelvic surg for cervical carcinoma, remove some bowel,
replace bladder, 3rd day after resp rate inc, felt sick, low temp, next
day had inc temp, abdomen tender, flushed, axious, restless, low
 BP, ABs, IV fluid, worsened, SOB, rales, dec IV fluid, vasopressor,
cardiac cath- CO doubled normal, syst vasc resistance low, urine
negligible, mechanical vent, reexploration, attach for ileum to colon
disrupted W/ leakage of bowel contents & abscess formation

Chapter 67 Intravascular infections

- Endocarditis
o Who gets it: ppl w/ shitty heart valves, MVP, artificial heart valves, IV drug
abusers
o types
▪ Acute: high fever, toxic course lasting a few days to weeks
● Usually high virulence like S. aureus and on top of previously
normal valve
▪ Subacute: lower fevers and anorexia, weakness, and weight loss.
Symptomatic for longer than several weeks
● Usually S.viridans (from tooth brushing) and other low virulence
on top of a previous valve injury
o Goes from blood to heart valve
▪ any bacteria that can seed the bloodstream
- Organisms causing endocarditis via access to blood
o S. aureus
o S. epidermidis
o S. viridans
o Enterococci
o HACEK (haemophilus, actinobacillus, cardiobacterium, eikenella, Kingella
o New heart valve/drug abusers: S Aureus
o Heart valve replacement after 6 months: S Epi
o Everybody is susceptible to the viridans strep (alpha hemolytic, look green
on blood agar)
o Sick (aka immunocompromised) people: enteric rods
- Don’t need table 67-2
- Virulence factors
o Help them stick (p683 and 684)
o FimA- allows adherence of strep to fibrim
o Lipoteichoic acid- adherence of enterococci to platelet-fibrin aggregates
o Staph, Strep, and Enterococci bind fibronectin
o Staph binds fibrinogen in vegetations via clumping factor→ acute endocarditis
w/out valvular disease
- Vegetations grow as biofilms. Heart valve is poorly vascularized so there isn’t
good immune response or ability to get antibiotics there well
o Any operations on valves greatly increases risk (due to non-bacterial
thrombotic vegetations of platelets and thrombin), usually need
prophylaxis antibiotics for rest of life if prosthetic
- Diagnosed by vegetations on echo,
 o Develop along the line of valve closure on low pressure surface of the
regurgitant valve or septal defect
- Damage is proteolytic (by the organism) and immunologic
o Septic emboli, AB-bact antigen circulating complexes
o Continuous bacteremia due to constant shedding of bacteria into
blood, leading to constant cytokine release and thus the fever, fatigue,
anorexia, weight loss
o Immune complex deposition in tissues leads to Osler nodes,
petechiae, vasculitis purpura, and glomerulonephritis
o Circulating immune complexes of organism antigen→ deposit→ tissue injury
▪ Osler nodes
▪ Petechiae-
▪ Janeway lesions (vegetations that have clogged up capillaries)
▪ Roth spots
o Post strep Glomerulonephritis associated due to deposits in glomerular BM→
complement stimulation
- Diagnosis
o Difficult to culture, need at least 3 blood cultures with similar
organism over 24-48 hrs
o follow CRP to monitor clinical course
o Most common cause of a culture-negative endocarditis is prior
administration ABs
- Treated with long term and high dose antibiotics due to poor valve
vascularization, prevention is key
- Cases
o 57yo syst ejection murmur & mild aortic stenosis, HTN, diabetes; 6wk
fevers, malaise, weakness, loss appetite, pale, hemorrhages in palpebral
conjunctiva, low hgb, high c-reactive protein, high creatinine, RBC in
urine, echocardiography bicuspid aortic valve w/ moderate stenosis, mild
aortic insuf, & mobile elements consistent with vegetatitons, cultures
strep. Bovis, penicillin, unresponsive w/ dilated L pupil, CT L parietal
hemtoma, died, Autopsy: embolic infarcts in myocardium & spleen, GN &
kidney infarcts, subarachnoid & L parietal intracerebral hemorrhage from
leaking aneurysm (mycotic aneurysm from bact growth in vessel wall)
*He didn't say this, but hella boards shit: S bovis endocarditis=colon
cancer/other colon pathology

Chapter 68 Head and neck

- Host Defenses
o lysozyme, lactoferrin, secretions
- Otitis media
o infants
o H.influenza
▪ Gram neg
▪ Type B has capsule, without capsule they can only cause disease above
the epiglottis
 o Moraxella catarrhalis
▪ Gram neg
o S.pneumo
o Middle ear space fills with fluid which makes the TM less mobile and leads
to conductive hearing loss
o Treated with Amoxicillin, no culture usually done
- Orbital Cellulitis
o Staph A
o Complication of acute sinusitis eroding into subcut orbit→ subperiosteal abscess
- Facial Cellulitis
o H.flu
▪ Prevent with vaccine
o Purplish hue face swelling
- Oropharyngeal abscess
o Peritonsillar abscess, cause trismus (cant open mouth)
o “Hot potato” voice
o Group A strep
▪ Beginis as cellulitis of peritonsillar tissue→ local necrosis→ oral flora
gain access to necrotic tissue → deeper infection
o commensals (s. aureus)
- Conjuctivitis
o Bacteria
▪ h flu
▪ s. Pneumo
▪ M. catarrhalis
▪ staph
▪ Pseudomonas aeruginosa
● Serious infect of ant portion of eye
● Contact lens wearers
o Viral
▪ Adenovirus
● Don’t give treatment
▪ Distinguish from bacterial via URI symps
▪ Herpesvirus
● Serious infect of ant portion of eye→ blindness
● Vesicular lesions on eyelid
- Cervival lymphadenitis
o TB
o S. aureus
o EBV
▪ Test for with heterophile AB
- Cases
o Otitis media
▪ 14mo cold, irritable, stopped eating, fever, ear infection, amoxicillin
o Orbital cellulitis
 ▪ 13yo recurrent allergic rhinitis with runny nose, watery eyes, fullness
in face; one day awoke with headach, cough, foul taste in mouth,
antihistamine & acetaminophen; next day headache sever, cant open L
eye, ill, erythema & swelling aroung eye & exudate from eyelids, fever,
tachycardia, OS deviated inf & lat, limited EOM, otolaryngologist for
orbital cellulitis
o Facial cellulitis
▪ 14mo unvaccinated, fussy, low fever, swelling in R cheek, slight
purplish hue, high fever, ABs for facial cellulitis
o Orophayngeal abscess
▪ 19yo scratchy throat, inc sore, R ear ache, felt feverish, aspirin, 6th day
barely open mouth to eat breakfast, difficult to swallow, voice lower
pitch, reccommended hospitilization & surgery
o Conjunctivitis
▪ 9yo return from summer camp, woke with sensation something stuck
in eye & conjunctival irritation, blured vision in OD, tender,
preauricular ln, runny nose, eyelids looked bloody and tears blood
tinged, patch over eye, viral
o Cervival lymphadenitis
▪ 18yo traveled to outside home town for first time, mild sore throat,
low fever, tender lump beneath angle of jaw, lump grew overnight to
size of walnut, cervical adenitis, CBC with diff & screen for heterophile
AB

Chapter 69 STDs
- know relative rates of infection
● Population dynamics
○ Depends on transmisibility, new partner acquisition, & duration of
infectiousness
○ Most common bacterial STD: chlamydia (14-16 y/o girls)
■ Dx w/ NAAT (nucleic acid amplification techniques)
○ Most common viral (according to the table): Genital Herpes (45 million)
● Damage
○ Acute manifestations
■ Mucopurulent cervicitis and urethritis
● Chlamydia and gonorrhea
■ Genital ulcers
● Herpes, syphilis and chancroid
● Inc risk getting HIV
■ Sexually transmitted systemic diseases
● HIV, hepatitis
○ Chronic infections/complications
■ Fallopian tube scarring
● Ectopic, infertility, chronic pelvic pain
■ PID
● Chlamydia and gonorrhea
● Inc risk getting HIV bc altered mucosa
 ■ Cervical cancer
● HPV
■ Syphilis
■ Recurrent herpes
■ Congenital (can cross placenta)
● Syphilis, herpes, HPV, chlamydia
● Can be part of vaginal flora
● Warts from HPVn
■ PROM (premature rupture of membranes-STDs while pregnant)
● PID
○ "1/3 rule"
■ only 1/3 symptomatic (so women don't seek care until workup for
infertility or have an ectopic pregnancy)
○ Host defenses-Ciliary movement towards uterus, mucous flow, myometrial
contractions during menses leading to sloughing of the endometrium
○ During/near the end of menses=most susceptible time for PID (high
estrogen, low progesterone and reflux of menstrual blood)
○ Adolescents have larger zone of ectopy (extension of columnar epi from
endocervical canal to ectocervix→ unprotected & inc susceptibility
○ Unknown if oral contraceptives affect STD acquisition
○ Gonococcal PID
■ Slows & stops ciliated epi cells
● ciliated cells sloughed off due to toxic lipid A on
lipooligosaccharide
● attach to noncilliated epi via pili→ internalize
● Subepithelial inflam (via lipid A LOS & peptidoglycan)
○ Chlamydia PID
■ obligate intracellular organism
■ Elementary bodies (infectious form) attach to cells and are
endocytosed
● Form Inclusions in phagosomes
● Differentiate into reticulate bodies (metabolic form)
● Incite immune response
■ (elementary="enfectious"/reticulate body=replicative)
■ Elementary bodies can exist outside body for a finite period of time,
auto-inoculation is possible, leading to conjunctivitis
○ Other: mycoplasma, endogenous
○ Empirically tx chlamydia/gonococcal infx together (he probably
won't ask for specific drugs, but hella boards-Azithromycin or Doxy w/
Ceftriaxone)
● Bacterial vaginosis
o Three types: Bacterial, fungal, parasitic
o Good lactobacilli flora reduced & inc Gardernella vaginalis
▪ Also, trich, candida potential etiologies for same symptoms
▪ Trich and BV will increase pH of the vagina
▪ Candida infx have nl pH
o Lactobacillus keeps pH low
 o (douching can lose natural bacilli, causing gardnerella to move in)
● HIV
o Risk transmission 3-5x more with other STDs
▪ Inflammatory STDs (eg gon) and ulcerative dz
▪ HPV: Anogenital warts do NOT put the pt at an increased risk
▪ HIV causes worse manifestations of other STIs (persistent herpes)
● Prevention/Control
o barrier protection
▪ Female controlled
▪ Microbicides- chemical barrier against STDs
o contact tracing- test & treat sexual contacts
o compliance

Chapter 70 Infections of Immunocomp Pt (shelby’s book notes/not meitz notes)

● Host Defense & Dysfunction: Skin & mucous membranes
○ Barrier, pH, temp, normal bact flora, lysozyme
■ Burns: stph a & pseudomonas a
■ C. diff- normal flora killed or altered by AB
■ Cystic fibrosis- Pseudomonas
○ Innate immune syst: neutros
■ Granulocytopenia
● Most common cause: myelosuppressive cancer chemo
● Neutropenia inc risk severe infection from bacteria, viruses,
& fungi
● Gram neg enteric bacilli, staph, candida, aspergillus
■ Chemotaxic dys (congenital)
● S. aureus
■ Chronic granulomatous disease (neutros cant do resp burst)
● Defect in NADPH oxidase→ no H2O2→ risk catalase + organisms
● S. aureus, fungi → granulomas
● Myeloperoxidase convert bacteria’s H2O2 into lethal radicals→
prophylaxis for S. aureus
○ Adaptive immunity
■ CD4 Ts: antigen recognition, cellular immunity
● Th1 = IFN-gamma, IL2→ activate CD8s, macros, NKs
● Th2 = IL4, 5, 10→ differentiation of Bs & secific AB responses
○ Humoral defense: Complement cascade & immunoglobulins
■ Ig def
● Congenital: Bruton X link agammaglobulinemia
● Acquired: Common variable immunofeficiency
● S. pneumo, Hflu
○ encapsulated
■ Complement def
● Neisseria
■ Spleen: has complement & AB producing Bs, & removes opsonized
microbes
 ● S. pneumo, H. flu
○ Cell mediated immunity
■ Severe combined immunodef (SCID)- no Ts
● P. jirovecii, candida, aspergillus, viruses
■ Immunosuppresive drugs, esp corticosteroids - acquited defect in
cell mediated immunity
■ AIDS- no CD4 helper Ts→ uncontrolled opportunistic infection &
malignancy
● P. jirovecii, CMV, mycobacteria

● Treat
○ Colony-stim factor to make neutros
○ Granulocyte infusions
○ Vaccines
● Cases
○ 17yo fever, bruise, diag acute mylogenous leukemia, chemo: cytarabine &
daunorubicin; 7d later burning mouth pain, white plaques, mucosa
sloughed off leaving ulcers in mouth; AML remission, allogenic marrow
transplant; 5d later no circulating WBCs, became febrile, oral pain,
difficult swallow, fatigue, malaise, blood culture E.coli, AB, temp dropped;
8d later febrile blood culture canfifa albicans, antifungal; 19d later WBCs
appear in circulation; 31d after transplant SOB, CXR: difuse pneumonia p.
Jiroveci, trimethpprin/sulfamethoxazole; 10d later herpes zoster, treated,
mild graft vs host; 5mo later SOB, lobar pneumonia, blood & sputum
culture: strep pneumo, penicillin
Chapter 71 AIDS
Mietz Mietz likes this chapter yo because of the cases
Initial infection: Starts with flu-like symptoms + mononucleosis
Sore throat, body aches, lymphadenopathy
Diagnosed using p24 assay + Western blot + RT PCR
Transmission via body fluids
Consequences - Fig. 71-1 - know it
Progression to AIDS
Eczema, psoriasis, herpes
Know the bolded terms in this section
HAART therapy
Two RT inhibitors and a protease inhibitor
Fig. 71-2
Good figure on steps that you can interfere in HIV
Know AIDS-defining illnesses pink box thingy in general on page 716
Rare illnesses that we only typically see in the immunocompromised
Such as CMV in adult, PCP, etc.
Lung infections
Pneumocystis
GI
Multiple bacterial and viral diarrheas
Mycobacterial infections
As CD4 count decreases, a lot of Myco. infections in environment can screw you
over
Opportunistic fungal infections as well
JC virus associated with AIDS dementia of the nervous system - only spot in the book
where it’s mentioned
Try to mount immune response to HIV, resulting in wasting disease in dementia
Oncology - Kaposi sarcoma
Rest of the chapter is common sense stuff and not really testable
-----------------------------------------------------------------
- Figure 71-1 is a good chart to know
- Progression to AIDS on 714: know all the things in bold
- AIDS defining illnesses: Cryptosporidium, CMV, all the other ones we’ve seen
somewhere else
- Nervous system infection: toxoplasmosis, JC virus (in AIDS patients causes
progressive multifocal leukoencephalopathy)
- HIV itself can cause wasting syndrome
- Kaposi sarcoma is caused by human herpes virus 8
- Don’tneed secondary illness to cause neurological problems in HIV

Chapter 72
● Basically know TORCHES
● Nothing for host defense mechanism; just the placenta
● Maternal IgG
 o DTAP vaccine booster
▪ Dead vaccine, bump up the mom’s IgG
o Don't give MMR because it live vaccine
● Table 72-3 congenital infections
o Should add zika to that
● Perinatal
o After baby born, through birth canal
o P 726 Pathogens & microbial agents of watever
▪ E. coli
▪ Meningitis strain
▪ Capsule = K1
▪ Equal in importance with meningitis cases in infants
▪ From intestine→ vag→ baby
▪ Group b strep
▪ Common in vag flora
▪ Monosterioa something
▪ Ghonnorea & chlynida
▪ Bacteria neonatorum→ colonizes eye→ can cause blindness
● Baby can get HIV
o Mom has 33% chance of transmitting in utero
o Find out in 1st trimester→ treat azt→ reduce to something%
o Diag in mother very important
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● Know the cases well
● Table 72-1
● Group B Strep
● Tx CMV w/ Ganciclovir
o Mechanism of action: Chain-terminating rxn
o Ganciclovir + tox (as compared to acyclovir)
o Prevents/reduces hearing loss
● Toxoplasma-from cats and undercooked meat
● Know that IgG crosses the placenta
● Table 72-3, 72-4
● Tx Syphilis w/ penicillin G because can administer IM
● "Mulberry molars, saber shins"on a kid= mom had syphilis (know those
buzzwords)
Most common perinatal infx:
● E Coli (as far as I can see, this isn't in the chapter, but he mentioned this:K1
strain has polysialic acid, like Group B meningococcus. Allows organism to
invade because we don't make immune responses to polysialic acid)
● Group B Strep (tx w/ penicillin)
● Listeria Monocytogenes
o Can multiply at 4 degrees-refrigerator cheese
● 3rd world countries- conjunctivitis caused by N gon, C trachomatis
o Tx w/ erythromycin
 ● HSV
o Tx w/ acyclovir
● Hep B
Prevention
● Pertussis vaccine
● Penicillin-Group B strep
● Handwashing-CMV

Chapter 73

Chapter 74
- Ch74: fever
o Know cytokines associated with fever, TNF, IL1, IL6
o General phys
o No fever on unknown origin
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- P742 Transient receptor family proteins that reset the body thermometer
- Pathophys of fever (cytokines TNF-a, IL-1, and IL-6)
- MOA of antipyretics and leukotriene participation
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Know the case
● Will get? s on specific molecules
● Have a "big picture" view of Fig 74-1 (mentioned an adrenergic ->
vasoconstriction/cholinergic-> sweating)
● Know the bold terms on pg 742 (we will get first order questions, specifically
mentioned OVLT)
o Eg TR Family proteins sensing cold (TRPM1, PA8) vs warm (TRVP 1-4)
● Pathophysiology of fever (IL-1 and TNFa, won't ask beyond that)
o Fever can set off prostaglandin cascades, why pregnant ladies can go
into premature labor if they have a minor infx
● Be familiar w/ the benefits and detriments of fever
o Transferrin levels decrease during fever, making Fe less available
● Don't bother w/ table 74-1 (fever of unknown origin has a lot of different causes,
eg granulomatous dz)

Chapter 75 Healthcare Associated Infx

● Nosocomial-hospital acquired
● Iatrogenic-we did it
● S Marcescens-thought to be innocuous, causes dz
● Know most common organisms for a given nosocomial infx
o Table 75-1 (only take the first organisms from each box like S Aureus or
Klebsiella)
● Skin penetration-S Epidermidis and P Aeruginosa
● CAP-Strep Pneumo; HAP:G- rods and S Aureus
 ● Catheterization-most common way we introduce bugs into the pts
o Selection for lots of antibiotic resistance
● Pay attn to the cases-will steal from the cases
● Know the risk factors for bacteremia/nosocomial pneumonia/wound infx
CLIs will have a lot of media questions

Chapter 76 Foodborne
- Anti bug
o Stomach acid, peristalis
▪ Drugs tha stop this
- Most are infectious, & there are 3 intoxications that need to know (staph,
butlisim, baceilius)
- Listeria
o Grows in refrigeratorn
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- Just know about organisms we’ve seen before
- Know diff between infections and intoxications
- Don’t need table 76-1
- Toxins act faster (4-6 hours) whereas infections are usually days after
- Intoxications
- Staph Enterotoxin resistant to heat and proteases (can survive stomach), causes
disease within 4-8 hours and is finished in 48 hours. Severe vomiting, cramps,
diarrhea
- C. perfringens, 5th leading cause of diarrhea in US. Watery diarrhea
o Gram +, spore formers, germinate and secrete a toxin.
o Between 8-14 hours, food is infected by the spores
o Toxin itself is pore-forming that pokes holes in enterocytes
o Causes pigbell in the germans (bloody diarrhea) associated with pok
- B. cereus is in fried rice. Pretty rapid, vomiting within 2 hours. Forms spores
o Toxin results in fluid accumulation
- Infections
- Salmonella (invasive) – bacterial mediated endocytosis
- Campylobacter jejuni – undercooked chicken. Associated with Guillan-Barre
syndrome
- Vibrio parhaemoylyticus – brackish waters in coastal regions (scratch from
rocks/shells) or ingestions of shellfish
- Yerinia enterocolitica: gram neg rod, raw milk and farm foods, diarrhea, can also
invade mesenteric lymph nodes to cause pseudoappendicits
- E. coli: ETEC (heat labile enterotoxin -ADP ribosylator, watery diarrhea), EHEC
(bloody diarrhea – HUS, shiga toxin)
- Look at handout on Listeria monocytogenes
o Gram + rod
o Grow in many environments (usually cold cuts- can survive high salt), can
grow in refrigerators
 o Immunocompromised (and pregnant women) are susceptible
o Cuase meningitis becasuse they invade cells, they don’t have capsule
- Nonbacterial: know the food poising on cruise ships (norovirus)

▪ Don’t need to know specific little details, know only about the ones talked
about in the case
▪ Know how organisms get in and compete
▪ Know for organisms the adhesisns and recepteors (like fibronectin binding
protein)
● Bacteria that produce fimbriae that help stick to the walls to
overcome the inherent negative charges between the cells that will
usually repulse
▪ Know tropism, why certain organisms like certain places
▪ –chelin or –bactin are always iron binding molecules produced from the
bacteria to try and grab the free Fe
▪ Figure 8-1 is important (breaking down C3b…) Which is a mechanism to
avoid complement deposition? - example questions
● Don’t need to know the speicif cthing about strep that’s mentioned
here…peptidase?
▪ Subverting phagocytosis: production of –lysin (like streptolycin) pore
forming toxin produced by that bacteria
▪ Inhibition of phagosome lysosome fusion. Don’t worry about the specific
examples. Won’t ask speicifc organism unless it was in the case.
▪ Refresh yourself with table 8-3 but don’t get too crazy with it
▪ Know shigella: changes intracellular environment without change in
extracellular?
▪ Superantigens: staph, strep – bind T cells and MhC independent of
antigen to set off a cytokine storm and end with system problems
▪ Antigenic variation, might need to know surface protein antigen that is
variable in a certain type of bacteria (gram + or -)
▪ Proteolysis and antibodies, know IgA proteases clip at hinge region of IgA.
▪ Latency is mentioned…not too important

Other Non-book Organisms

Haemophilus Influenzae
● Why H.flu grows on chocolate agar
○ Can grow it with staph or strep on blood agar
● Gram neg coccobacilli
● Terminology: typable (B would be B type capsule) & non typable (no capsule)
● No capsule→ can’t infect epiglotis & below
● Kid with trouble swallowing, “thumb print” on lateral x-ray=epiglottis
 ● Cellulitis, conjunctivitis, sinusitis, ot media, Epiglottis, lungs-pneumonia, sepsis→
meningitis (need capsule)
● Evidence of non-vaccination (homeschool, immigrant)
Klebsiella pneumoniae
● Urease producer
● Gram neg rod, closely related to e. Coli (does everything it does)
● Highly encapsulated
● Normal oral flora→ aspiration pneumonia (lobar & localized, severe, high fever, currant-
jelly sputum)
○ Alcoholics: low immune system with aspiration of normal oral flora
● UTIs
Actinomyces
● Look like fungi bc long branches
● Actinomyces israelii is anaerobic, not acid fast, sulfur granuels
● most common of actinomyces spp, although there are others that are clsely
related:
○ Streptomyces: aerobic, not acid fast, had sulfur granules
○ Nocardia: aerobic, weakly acid fast
○ Mycobacterium: is aerobic, acid fast
● Facultative anaerobic Gram +rod
● Low grade pneumonia, granulomas (like mycobacterium)
● Major: after tooth extraction→ granuloma→ proceeds like a cellulitis
○ Pus filled lesion that releases sulfur granules
● Treat with debriedment and sustained penicillin
Corynebacterium Diphtherium
● Diptheroids- normal flora bc usually don’t cause disease bc dont have toxin
● Diptheria Toxin: inhibits cellular protein synthesis by ADP-ribosylation of Elongation Factor
2, a ribosomal protein→ tissue destruction in the immediate area of the infection leading to the
pseudomembrane formation (same as pseudomonas toxin A)
● Diptheroid: gram (+) that look like clubs
● Colonize throat, toxin→ kills cells immediately attached→ pseudomembrane (can
obstruct) → toxin becomes systemic→ heart (die HF)
○ Kids die asphyxiation & adults form HF
● Vaccine: inactivated, Td vaccine