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Bacteria - organisms Flashcards

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1
Q

S. aureus - morphology

A 
*Coagulase +
Catalase +
Gram+
cocci - clusters
Yellow cultures
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2
Q

S. aureus - Source, Spread

A

Common commensal: mucosa , skin (*nares)

Contact - thru epithel damage -> lymph, blood

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3
Q

S. aureus - escape defenses

A

*protein A - binds Fc of IgG inhib opsonization

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4
Q

S. aureus - damage to host
3 common
3 specific (only some isolates)

A

1) hemolysins/leukocidins - attack host cell memb, kills leuk
2) fibrinolysin lipases DNAse, hyaluronidase - destroy host structures
3) coagulase - fibrinogen->fibrin = clot, abcess formation, immune escape
4) enterotoxins - *food poisoning, superAg
5) exfoliative toxin 1+2 - break desmoglein -> SSSS/bullous impitigo
6) Tox shock synd toxin(TSST) - superAg -> toxic shock

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5
Q

S. aureus - treatment

A

1st - cell wall synth inhib
90% resist penicillin
MRSA occurring more
vancomycin works most

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6
Q

Coagulase-negative Staphylococci

S. epidermidis - morphology

A 
Most common of coagulase-negative staph
*coagulase -
Catalase +
Gram+
cocci - clusters
representative of all staph (-aureus/saprophyticus)
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7
Q

1) S. epidermidis - Source

2) S. saprophyticus - Source, identification

A

1) commensal on mucosa, skin

2) commensal in *rectum, novobiocin resistant, found in *urine sample

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8
Q

Coagulase-negative Staphylococci

  • Diseases
  • Treatment
A

low virulence organisms- common infection of *foreign object in body
some soft tissue infect
saprocphyticus - UTI (rank#2)

resist penicillin, methicillin
vancomycin works most

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9
Q

Streptococci - morphology

general classification methods:

A

*catalase -
gram +
cocci - chains
classified by: hemolysis patter on blood agar, carbs on cell wall

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10
Q

Beta-hemolytic Strep - classifications A & B

A

beta = full hemolysis, blood plate -> clear
Lancefield A - S. pyogenes
Lancefield B - S. agalactiae

remember B is A and A is P

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11
Q

Alpha-hemolytic Strep

A

alpha = poor hemolysis, blood plate -> ~green
S. pneumoniae (no Lancefield)
viridans-group - all others

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12
Q

Strep Viridans-group - ID

A

all non-hemolytic strep + all a-hemo (-pneumoniae)
Lancefield D (usually)
Commensal in mouth, GI, vagina - contact
with enterococci are only gram + cocci in GI

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13
Q

S. pyogenes - source spread

A

commensal mucosa of upper resp.
spread by droplet, contact
invade through dmgd epithel -> lymph -> blood

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14
Q

S. pyogenes - escape

A

*M-protein - inhib phagocytosis by blocking Cmplmt actn, binds fibrinogen
(Ab can target M-prot, but it varies)
hyaluronic acid “self” structure capsule

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15
Q

S. pyogenes - damage (3 ways)

A

1) *streptolysin O/S - host cell memb attack -> leuk death (S = Oxygen “S”table)
2) streptokinase, DNAse, hyaluronidase - break host structures -> spread
3) S. pyrogenic exotoxins (Spe) - superAg: TSS, scarlet fever

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16
Q

S. pyrogenes - 1) diseases and 2) sequelae

A

1) #1 cause bacterial pharyngitis
2) Suppurative sequelae, Scarlet fever, Acute rheumatic fever, Poststreptococcal acute glomerulonephritis, Skin and soft tissue infections, TSS

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17
Q

S. pyrogenes - Treatment

A

Penecillin

Macrolides for pcn allergies

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18
Q

Strep Viridans-group - Diseases, Treatment

A

*Usually only cause disease in compromised host
Endocarditis, (meningitis, pneumonia)
often resistant to pcn and cephalosporins, all sensitive to vancomycin

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19
Q

Enterococci - morphology

A

same cell wall Ag as grp D Strep
*BUT: grow in *salt, hydrolyze *esculin in *bile
BUT: produce pyrrolidonyl arylamidase (PYR test) and are a- or non-hemolytic
catalase - | gram + | cocci - pairs, short chains

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20
Q

Enterococci - Source, Spread

A

commensal of large intestine

contact

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21
Q

H. influenzae - morphology

A

Gram-negative bacillus
Typable capsule (a,b,c…) or no capsule
Historically, 90% Hib (prior to vaccine)
Now, 80% non-typable

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22
Q

H. influenzae - Diseases

A 
Mucosal (usually not typable) - otidis media, sinusitis, pneumonia, epiglottitis
Metastatic foci (usually type b) - septic arthritis, meningitis
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23
Q

H. influenzae - Source & spread

A

Humans (other children); nasal secretions

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24
Q

H. influenzae - Adhesion

A

Pili, other

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25
Q

H. influenzae - Invasion

A

NP colonization > local infection or bloodstream

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26
Q

H. influenzae - Escape from defense

A

Mostly via capsule

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27
Q

Rickettsia rickettsii - disease

A

Rocky Mountain spotted fever

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28
Q

*R. rickettsii - morph

A
  • gram-neg coccobacillary
  • obligate intracellular
  • hard to see, need special stains
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29
Q

*R. rickettsii - source & spread

A

tick bite (spring & summer)

  • American dog tick (E & S central US)
  • Rocky Mountain wood tick (mt states)
  • host = most mammals
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30
Q

*R. rickettsii - invasion

A
  • tropism for endothelial cells via binding of cell membrane protein & then engulfment
  • spread via bloodstream or lymphatics
  • polymerize & use host cellular actin to propel itself through tissue
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31
Q
  • R. rickettsii - damage
A
  • endothelial cells –> lymphohistiocytic vasculitis (host immune response)
  • increased permeability of vessels –> edema
  • activation of coagulation cascade
  • vascular thrombosis & hemorrhage
  • multi-organ dysfunction, hypovolemia, shock
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32
Q

R. rickettsii - tx

A
  • early tx, rarely can diagnosis be confirmed early since no rash
  • doxycycline, chloramphenicol for pregnant
  • no prophylaxis following tick bite
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33
Q

R. rickettsii - differential

A

invasive meningococcal disease, monocytic or granulocytic ehrlichiosis, viral syndrome

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34
Q

Rickettsia akari - disease

A

Rickettsialpox

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35
Q

*R. akari - Sx

A
  • single painless red papule at site of mite bite –> vesicular –> eschar
  • fever, chills, myalgias, headache, diffuse rash (maculopapular, some vesicular)
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36
Q

*R. akari - morphology

A
  • gram neg
  • coccobacillary
  • intracellular
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37
Q

*R. akari - source & spread

A
  • house mouse mite

- normally mouse reservoir, but will resort to humans when mice exterminated

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38
Q

R. akari - differential

A

chickenpox (no eschar, lesions in crops rather than all at once, more lesions, vesicular)

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39
Q

R. akari - damage

A

proliferates at mite bite –> tissue necrosis –> eschar

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40
Q

R. akari - tx

A

doxycycline

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41
Q

E. chaffeensis - disease

A

human monocytic ehrlichiosis

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42
Q

Anaplasma phagocytophilum - disease

A

human granulocytic anaplasmosis (erlichiosis)

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43
Q

*A. phagocytophilum - source & spread

A
  • *Ioxodes scapularis (black-legged tick)

- white-footed mouse = animal reservoir

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44
Q

*E. chaffeensis - source & spread

A
  • lone star tick

- deer = reservoir

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45
Q

*A. phagocytophilum - invasion

A
  • bind to host P-selectin receptor on PMN for uptake into vacuole via caveolae-mediated uptake
  • blocks NADPH oxidase association & blocks phagolysosomal fusion
  • replicates in vacuole of PMN & then form morula
  • traffic to bone marrow –> thrombocytopenia and to a lesser extent suppress RBC & WBC production
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46
Q

A. phagocytophilum - differential

A

Rocky mountain spotted fever; can co-infect w/Lyme disease

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47
Q

*E. chaffeensis - invasion

A
  • bind to host P-selectin receptor on monocyte for uptake into vacuole via caveolae-mediated uptake
  • blocks NADPH oxidase association & blocks phagolysosomal fusion
  • replicates in vacuole of monocytes & then form morula
  • traffic to bone marrow –> thrombocytopenia
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48
Q

E. chaffeensis - differential

A

Rocky mountain spotted fever

*NOT same vector as Lyme

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49
Q

E. chaffeensis - tx

A
  • doxycylcine, rifampin for pregnant

- no prophylaxis

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50
Q

A. phagocytophilum - tx

A
  • doxycylcine, rifampin for pregnant

- no prophylaxis

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51
Q

N. meningitidis - epidemiology

A

Leading cause of meningitis in children/young adults

Epidemic - college, military, sub-Saharan Africa

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52
Q

N. meningitidis - causes of mortality

A

CNS - herniation

Shock

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53
Q

N. meningitidis - tx

A

Penicillin - some resistance

Speed important

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54
Q

N. meningitidis - prevention

A

Vaccine - Polysacharride-conjugate, quadrivalent (YWCA serotypes, working on B)

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55
Q

N. meningitidis - source and spread

A

Humans

Nasal secretions

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56
Q

N. meningitidis - adhesion

A

Pilli, other

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57
Q

N. meningitidis - invasion

A

NP colonization > mucosal, blood

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58
Q

N. meningitidis - diseases

A

Conjunctivitis, pneumonia, bacteremia, meningitis, PF, Waterhouse-Fredrickson syndrome (bilateral adrenal hemmorhage)

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59
Q

S. agalactiae - morphology

A

Gram positive diplococci, encapsulated

Lancefield typing system, group B

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60
Q

N. meningitis - morphology

A

Gram negative diplococci

Polysaccharide capsule - >13 serotypes

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61
Q

enteric

A

facultative gram-negative rods that can be cultured (though true fecal floral are obligate anaerobes); grow on minimal media

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62
Q

MacConkey agar selects for

A

gram negative bacteria (bile salts in agar)

lactose fermenting stain red

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63
Q

interpretation on Hektoen agar plate

A 
gram neg selective
Salmonella and Shigella surrounded by blue
Salmonella - black colonies
Shigella - green colonies
Other bacteria - yellow/red
  • bile salts to inhibit gram pos
  • lactose w/pH indicator (Salmonella & Shigella don’t ferment)
  • sodium thiosulfate & ferric ammonium citrate for sulfur source (Salmonella use to produce H2S) & precipitate H2S to black precip
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64
Q

Bacteria transmitted primarily by sex (4(+1))

A 
Neisseria gonorrhoeae
Chlamydia trachomatis
Treponema pallidum
Haemophilus ducreyi
(Ureaplasma urealyticum)
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65
Q

Bacteria transmitted SECONDARY by sex (3)

A

Shigella
Salmonella
Campylobacter spp.

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66
Q

STI transmission mechanisms (3)

A

1) Horizontal transmission usually occurs by *mucosal or *dermal contact
2) Vertical transmission usually occurs in the *prenatal or *perinatal periods
3) Pathogens that cause STI are *not hardy and die quickly in the environment

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67
Q

Major Patterns of Bacterial STI - (2)

which bact cause each?

A
  1. Genital Mucosal Inflammation without Ulceration
    ♀ Asymptomatic mucopurulent cervicitis and ♂ asymptomatic or urethritis
    caused by: N. gonorrhoeae, C trachomatis
  2. Ulcerative - ♀ & ♂ Genital or perianal ulcers +/- lymphadenopathy
    Caused by: Treponema pallidum
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68
Q

Chlamydia trachomatis - morphology

A 
Small: 0.25 μm, not seen by light microscopy
gram -
coccoid or bacillus
Obligate intracellular
Little or no peptidoglycan
Cytoplasmic and outer membranes
*dual stage life cycle EB/RB
Multiple serovars (A to L) defined by surface antigen
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69
Q

C. trachomatis - replication

A

– EB: infectious form. Small, dense, does not divide.
– RB: replicating form. Larger, dividing form.

(elementary and reticulate body = EB, RB)
(E = Enters, R = Replicates)

70
Q

C. trachomatis - Host Damage

A

Epithelial cells are killed by replicating organisms
Host response is the primary mechanism of damage
- PMN -> Plasma cells, TH, CTL -> necrosis, epithel prolif -> scar

71
Q

C. trachomatis - escape

A

Little or no immune protection from reinfection

IFN-γ (from Th1, CTL) inhibits RB replication by breakdown of tryptophan (starves bact)

72
Q

Trachoma

A

C. trachomatis Serovars A-C

Person to person transmission by fomites or insects
Repeated infection over life scars inner eyelid → lid scarring → inversion of lid → lashes rub cornea → corneal scarring → visual impairment

73
Q

Chlamydia Genital Infections

A

C. trachomatis Serovars D-K

Genital: ♀: Mild or asymptomatic mucopurulent cervicitis
– Ascending infection → pelvic inflammatory disease (risk of subsequent infertility)
♂: Asymptomatic or urethritis: urethral discharge and dysuria
– Epididymitis, prostatitis

74
Q

Chlamydia - Reactive Arthritis

A

Serovars D-K

warm, swollen joints; the joint is *sterile

75
Q

Reiter’s syndrome

A

C. trachomatis associated urethritis, arthritis, conjunctivitis +/- skin lesions
~80% of patients have HLA-B27

76
Q

Chlamydia Neonatal Infections

A

Serovars D-K

Inclusion conjunctivitis, pneumonia (less)

77
Q

C. trachomatis - tx

A

azithromycin, week of BID doxycycline

78
Q

Neisseria gonorrhoeae - morphology

A

gram -
diplococcus (coffee bean shape)
primarily extracellular

79
Q

Neisseria gonorrhoeae - invasion

A

Attach to non-ciliated epithelial cells → pass through in endocytic vacuole → enter sub-epithelial space

80
Q

N. gonorrhoeae - damage

A

Lipooligosaccharide (LOS) - potent endotoxin causes:

  • cytotoxic to epithel as crosses
  • stims PMN resp to subepithel bact -> epithel dmg and pus
81
Q

N. gonorrhoeae - escape

A

IgA protease

*many pili genes + homolog recomb → changing Ag

82
Q

N. gonorrhoeae - primary genital manifestations

A

♀: Asymptomatic or mild mucopurulent cervicitis

♂: Asymptomatic or urethritis: urethral discharge and dysuria

83
Q

N. gonorrhoeae - secondary sequellae (genital)

A

♀: Ascending infection → pelvic inflammatory disease

♂: Epididymitis and prostatitis

84
Q

N. gonorrhoeae - Localized Extra-Genital

A
  • Anorectal: usually asymptomatic, can have proctitis (pain/pruritus, tenesmus, discharge)
  • Pharyngeal: usually asymptomatic or mild pharyngitis
  • Ocular: variable manifestations, from mild to severe w/ conjunctival inflammation and hyperemia

…AEI - Anus, Eat, I/eye

85
Q

Disseminated Gonococcal Infection
Progression
Risk Factors

A

<1%, Genital infection → bacteremia → suppurative arthritis and or skin lesions
(papule → pustule → bulla)
Risk factors: menstruation, complement deficiency

86
Q

Neonatal N. gonorrhoeae Infection

1) when acquired
2) onset
3) manifestation

A

1) during birth
2) 2-5 days after birth
3) Conjunctivitis → ulcers, pus

87
Q

N gonorrhoeae - treatment

A

Single dose of a third-generation cephalosporin
Azithromycin or doxycycline
Disseminated or extragenital infections require longer treatment`

88
Q

Treponema pallidum - disease

A

syphilis

89
Q

T. pallidum - morphology

A 
gram -
lipid-rich outer memb
flagella w/in outer memb
too skinny to see in light microscope
*use *dark field or immunological stain
90
Q

Clostridium difficile - morph

A
  • gram + baccilus
  • obligate anaerobe
  • forms spores
91
Q

C. difficile - transmission

A
  • hospital wards, nurseries, nursing home, bathrooms

- fecal-oral route

92
Q

C. difficile - vulnerable pop

A

on multiple antibiotics, elderly age, debilitated state, proton pump inhibitors, GI surgery
- new emergence in community among healthy individs

93
Q

C. difficile - key findings

A 
1wk post antibiotics
diarrhea +/- blood
abd cramps
high fever
leukocytosis
94
Q

C. difficile - invasion

A

Toxin A & B bind to cell surface receptors, endocytosis into vacuoles, acidic pH triggers translocation of toxin into cell cytosol, glucosyltransferase on Rho GTPases (inactivate), which normally regulate dynamics of cellular actin cytoskeleton
- pseudomembranes = accumulation of necrotic tissue caused by toxin-induced necrosis of mucosal cells, which may involve entire thickness of mucosa

95
Q

C. difficile - tx

A
  • metronidazole (Flagyl) = good for anaerobes

- vancomycin = good for gram +

96
Q

Enterohemorrhagic E coli - most common serotype

A

O157:H7 (O Ag for LPS, H Ag for flagellum)

97
Q

EHEC - key findings

A

*NO FEVER (~bacteria blocks)
watery bloody diarrhea
intense abd pain

98
Q

EHEC - invasion

A
  • distal ileum & large intestine
  • type III secretion system (injectosome) = delivery of bacterial proteins into host cytosol, machinery attached to both inner & outer membrane
  • Stx1 & Stx2 toxin - modifies ribosomal RNA & blocks protein synthesis –> capillary thrombosis & associated inflammation = hemorrhagic colitis & renal endothelial damage = renal failure
99
Q

EHEC - tx

A

not antibiotics (worsen & increase risk of hemolytic-uremic syndrome probably bc antibiotics stress bacter & increase phage genes, which include Stx toxin)

100
Q

cholera toxin

A
  • Vibrio cholerae
  • ADP-ribosylating toxin
  • activates host cell adenylate cyclase, increase cAMP, increase cAMP-elicited fluid secretion
101
Q

heat-labile toxin

A
  • enterotoxigenic E coli
  • ADP-ribosylating toxin
  • activates host cell adenylate cyclase, increase cAMP, increase cAMP-elicited fluid secretion
102
Q

heat-stable toxin

A
  • enterotoxigenic E coli
  • guanylate cyclase activating toxin
  • activates membrane-bound guanylate cyclse, increase cGMP –> cGMP-elicited fluid secretion
103
Q

Stx

A
  • Shigella dysenteriae
  • RNA glycosidase toxin
  • single-site depurination of ribosomal RNA, inhibits protein synthesis –> cell death
104
Q

Stx1 & Stx2

A
  • enterohemorrhagic E coli
  • RNA glycosidase toxin
  • single-site depurination of ribosomal RNA, inhibits protein synthesis –> cell death
105
Q

Salmonella - source

A

contamination of food, often poorly refrigerated prepared foods

106
Q

Salmonella typhi (+ paratyphi)

A

typhoid fever (systemic Salmonella)

107
Q

Salmonellae - morph

A
  • gram neg rods
  • closely related to E coli & Shigella
  • lactose negative
108
Q

Salmonellae - invasion

A
  • intracellular
  • type III secretion to induce bacteria uptake –> able to enter normally non-phagocytic cells
  • initially through M cells, then inflammatory cells & enterocytes
  • live w/in phagocytic vacuole, but doesn’t exit into cytoplasm
109
Q

Salmonellae - tx

A
  • gastroenteritis = self-limited, NO anitbiotics

- typhoid fever: antibiotics

110
Q

Helicobacter pylori - transmission

A

fecal-oral or oral-oral

- mother-child most impt route of transmission & then reside for decades

111
Q

H pylori - pop

A

US: 2-3x higher in African Americans & Hispanics than non-Hispanic white, prob bc reflection of socioeconomic status & living conditions
- children w/iron deficiency anemia (not sure if linked w/socioeconomic)

112
Q

H pylori - morpho

A
  • curved microaerophilic gram neg rod

- highly motile w/polar flagellum

113
Q

H pylori - detection

A
  • IgG to H pylori Ag
  • breath test for high urease activity of org
  • stool Ag test
  • culture from biopsy material from endoscopy
114
Q

H pylori - invasion

A
  • stomach & proximal SI
  • type IV secretion system to deliver effector protein CagA into cytosol of gastic & duodenal epithlial –> immune response (stomach usually devoid of immune cells)
  • superficial gastritis –> chronic atrophic gastritis –> intestinal metaplasmia –> dysplasia –> gastric adenocarcinoma
  • urease: cleaves ammonia from urea to create relatively alkaline microenviron so can survive in stomach –> progressive loss of ability of gastric epithel to produce acid
115
Q

H pylori - tx

A

proton pump inhibitor & 2 anitbiotics

- though controversial bc may have protective effect against esophageal reflux & cancer

116
Q

*R. akari - lab findings

A
  • transient leukopenia

- transient thrombocytopenia

117
Q
  • Ehrlichia detection
A
  • blood smear with grape-shape in PMN or monocytes
118
Q

acute meningitis - lab findings

A

CSF elevated: opening P, WBC#, %PMN, prot,

Decreased: glucose, CSF:serum ratio

119
Q

Listeria monocytogenes - morph

A

gram +
bacillus
grows in cold (4-10C)
intracellular - *actin based motility and invasion

120
Q

L. monocytogenes - disease

A

Meningoencephalitis
Cerebritis and abscesses common (not true of other organism discussed)
Altered consciousness, seizures, movement disorder

121
Q

L monocytogenes - damage

A

GI disease, sepsis, bacteremia, meningitis, chorioamnionitis

122
Q

L monocytogenes - source spread

A

Zoonosis, present in food as contaminant

spread - GI for most, vertical for newborns

123
Q

S. pneumoniae - morphology

A

Gram positive diplococci

Encapsulated

124
Q

S. pneumoniae - Damage

A

Pneumonia
Meningitis - most common cause
Otitis, sinusitis
Pneumolysin - toxin; binds to cholesterol > pores in membrane

125
Q

S. pneumoniae - Pneumonia clinical symptoms

A

Abrupt onset; pleuritic chest pain; thick “rusty” sputum;

X-Ray: dense consolidation of one lobe

126
Q

S. pneumoniae - detection

A

Sputum gram stain; sputum culture
Catalase negative, optochin sensitive
Urinary antigen test

127
Q

S. pneumoniae - source & transmission

A

Human-Human

Droplet

128
Q

S. pneumoniae - adherance

A

Binds to receptor for platelet activating factor (PAF)

129
Q

S. pneumoniae - damage

A

Pneumlysin

130
Q

S. pneumoniae - escape from defense

A

Capsule

131
Q

S. pneumoniae - treatment

A

Penicillins (resistance increasing)

132
Q

S. pneumoniae - prevention

A

Vaccines:
Children <5 - protein conjugate (13 serotypes)
Adults - polysaccharide (23 serotypes)

133
Q

P. aeruginosa - morphology

A

Gram negative bacillus
Non-enteric
Green pigment, characteristic sweet grape-like odor

134
Q

P. aeruginosa - symptoms

A

Productive cough, dyspnea, fever, chills, confusion, systemic toicity, multifocal infiltrates on x-ray

135
Q

P. aeruginosa - risk factors

A

Noscomial (hospital aquired)
Cystic fibrosis
COPD
Immunocomprimised (HIV)

136
Q

P. aeruginosa - transmission

A

biofilms

137
Q

C. diptheriae - morphology

A

Gram positive bacillus

138
Q

C. diptheriae - damage

A

exotoxin (A/B) inhibits EF-2 > inhibits protein synthesis > cell death

139
Q

C. diptheriae - clinical symptoms

A

Fever, malaise, sore throat, thick membrane on tonsils & adjacent structures

140
Q

C. diptheriae - transmission

A

Droplet, contact

141
Q

C. diptheriae - treatment

A

Antitoxin
Antibiotics
Supportive care (e.g. respiratory)

142
Q

C. diptheriae - prevention

A

vaccine

143
Q

M. tuberculosis - morphology

A

Doesn’t gram stain; acid-fast stain

144
Q

M. tuberculosis - symptoms

A

Fever, night sweats, weight loss, non-productive cough, pleuritic chest pain, atypical pneumonia (granulomas)
Extrapulmonary - other organ systems
Latency, reactivation

145
Q

M. tuberculosis - transmission

A

Aerosol

146
Q

M. tuberculosis - escape defense

A

intracellular - lives within macrophages
Prevents phagocome , prevents phagosome-lysosome fusion
Inhibit IL-12 secretion
Degrades NO

147
Q

L. pneumophila - morphology

A

Gram negative bacillus

148
Q

L. pneumophila - transmission

A

Natural reservoir - amoebae

Environmental exposure: A/C, ventilation, water distribution system

149
Q

L. pneumophila - escape defense

A

Survives within macrophages > replication > host cell lysis

Uses Type IV secretion system

150
Q

B. anthracis - morphology

A

Gram positive rod - sporulating

151
Q

B. antrhacis - reservoir/transmission

A

reservoir: soil (spores)
Also: Animals, humans

152
Q

B. anthracis - clinical symptoms

A

Cutaneous (95%) - papule > eschar; painless; edema
Inhalational - Mediastinitis, necrotizing pneumonia, high fatality
GI - edema, necrosis of affected intestinal segment

153
Q

B. anthracis - damage

A

Antrhax toxin (A/B)
Edema factor > increased cAMP
Lethal factor > blocks MAPKKs

154
Q

Yersinia pestis - morphology

A

Small gram negative coccobacillus

Enterobateriaciae family

155
Q

Y. pestis - reservoir/transmission

A

Primary reservoir: rodents
Blocks flea intestine w/ biofilm > regurgitation into host
Transmission: bite by rodent flea, exposure to human with pneumonic plague

156
Q

Y. pestis - epidemiology (w/in US)

A

Southwest

157
Q

Y. pestis - symptoms

A

Bubonic - sudden onset fever, chills, intensely painful lymph swelling (ubo)
Septicemic (can be secondary to bubonic) - Shock, DIC, purpura, acral gangrene (black death)
Pneumonic - severe pneumonia, no distinguishing features

158
Q

Y. pestis - damage

A

Type III secretion system
Biofilm
Aquisition of foreign genetic material

159
Q

F. tularensis - morphology

A

Gram negative coccobacillus

160
Q

F. tularensis - reservoir/transmission

A

Terrestrial: rabbit reservoir, spread to human via tick, deerfly
Aquatic: muskrats, beavers, voles shed organism into environment

161
Q

F. tularensis - Clinical symptoms

A

Ulceroglandular tularemia: painful maculopapular lesion, lymphadenopathy, fever/myalgia, pneumonia
Typhoidal tularemia: fever, hepatosplenomegaly, pneumonia
Pneumonic: pulmonary infection, granulomas

162
Q

F. tularensis - defense escape

A

Intracellular growth - macrophages, hepatocytes, endothelial cells

163
Q

B. henselae - Clinical symptoms

A

Cat scratch disease
Cutaneous papule/pustule, lymphadenopathy
Bacillary angiomatosis - neovascular proliferation

164
Q

B. henselae - transmission

A

Bite or scratch of cat

Flea bite

165
Q

B. henselae - morphology

A

Intracellular, gram negative pleomorphic

166
Q

T. pallidum - primary infection

A

primary syphilus

hard chancre at infection site - painless lesion with central ulceration and a firm rim

167
Q

T. pallidum - secondary infection

A

2-24wks post primary
lymphadenopathy, fever, rash
rash includes *palms and *soles

168
Q

T. pallidum - tertiary infection

A

years post primary
neurosyphilus - variable
cadriovascular - *Ascending aortic aneurysm caused by damage to vasa vasorum
gumma - noncancerous growth, anywhere

169
Q

T. pallidum - detection

A

nontreponemal tests - done first only detect primary/secondary, detect Ab vs. cardiolipin, can test for successful treatment
treponemal tests - sensitive for syphilus, stay positive even after cure

170
Q

T. pallidum - Tx, side effects

A

penecillin

Jarisch-Herxheimer rxn - fever, hypotension

171
Q

Causes of Genital Lesions
painless
single
chancre

A

painless: T pallidum, C trachomatis
single les: T pallidum, C trachomatis
chancre: T pallidum (hard), chancroid (soft, pustules)

Microbiology (8 decks)

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