Bacteria - organisms Flashcards
1
Q
S. aureus - morphology
A
*Coagulase + Catalase + Gram+ cocci - clusters Yellow cultures
2
Q
S. aureus - Source, Spread
A
Common commensal: mucosa , skin (*nares)
Contact - thru epithel damage -> lymph, blood
3
Q
S. aureus - escape defenses
A
*protein A - binds Fc of IgG inhib opsonization
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
5
Q
S. aureus - treatment
A
1st - cell wall synth inhib
90% resist penicillin
MRSA occurring more
vancomycin works most
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)
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
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
9
Q
Streptococci - morphology
general classification methods:
A
*catalase -
gram +
cocci - chains
classified by: hemolysis patter on blood agar, carbs on cell wall
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
11
Q
Alpha-hemolytic Strep
A
alpha = poor hemolysis, blood plate -> ~green
S. pneumoniae (no Lancefield)
viridans-group - all others
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
13
Q
S. pyogenes - source spread
A
commensal mucosa of upper resp.
spread by droplet, contact
invade through dmgd epithel -> lymph -> blood
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
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
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
17
Q
S. pyrogenes - Treatment
A
Penecillin
Macrolides for pcn allergies
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
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
20
Q
Enterococci - Source, Spread
A
commensal of large intestine
contact
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
22
Q
H. influenzae - Diseases
A
Mucosal (usually not typable) - otidis media, sinusitis, pneumonia, epiglottitis Metastatic foci (usually type b) - septic arthritis, meningitis
23
Q
H. influenzae - Source & spread
A
Humans (other children); nasal secretions
24
Q
H. influenzae - Adhesion
A
Pili, other
25
H. influenzae - Invasion
NP colonization > local infection or bloodstream
26
H. influenzae - Escape from defense
Mostly via capsule
27
Rickettsia rickettsii - disease
Rocky Mountain spotted fever
28
*R. rickettsii - morph
- gram-neg coccobacillary
- obligate intracellular
- hard to see, need special stains
29
*R. rickettsii - source & spread
tick bite (spring & summer)
- American dog tick (E & S central US)
- Rocky Mountain wood tick (mt states)
- host = most mammals
30
*R. rickettsii - invasion
- 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
31
* R. rickettsii - damage
- endothelial cells --> lymphohistiocytic vasculitis (host immune response)
- increased permeability of vessels --> edema
- activation of coagulation cascade
- vascular thrombosis & hemorrhage
- multi-organ dysfunction, hypovolemia, shock
32
R. rickettsii - tx
- early tx, rarely can diagnosis be confirmed early since no rash
- doxycycline, chloramphenicol for pregnant
- no prophylaxis following tick bite
33
R. rickettsii - differential
invasive meningococcal disease, monocytic or granulocytic ehrlichiosis, viral syndrome
34
Rickettsia akari - disease
Rickettsialpox
35
*R. akari - Sx
- single painless red papule at site of mite bite --> vesicular --> eschar
- fever, chills, myalgias, headache, diffuse rash (maculopapular, some vesicular)
36
*R. akari - morphology
- gram neg
- coccobacillary
- intracellular
37
*R. akari - source & spread
- house mouse mite
| - normally mouse reservoir, but will resort to humans when mice exterminated
38
R. akari - differential
chickenpox (no eschar, lesions in crops rather than all at once, more lesions, vesicular)
39
R. akari - damage
proliferates at mite bite --> tissue necrosis --> eschar
40
R. akari - tx
doxycycline
41
E. chaffeensis - disease
human monocytic ehrlichiosis
42
Anaplasma phagocytophilum - disease
human granulocytic anaplasmosis (erlichiosis)
43
*A. phagocytophilum - source & spread
- *Ioxodes scapularis (black-legged tick)
| - white-footed mouse = animal reservoir
44
*E. chaffeensis - source & spread
- lone star tick
| - deer = reservoir
45
*A. phagocytophilum - invasion
- 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
46
A. phagocytophilum - differential
Rocky mountain spotted fever; can co-infect w/Lyme disease
47
*E. chaffeensis - invasion
- 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
48
E. chaffeensis - differential
Rocky mountain spotted fever
| *NOT same vector as Lyme
49
E. chaffeensis - tx
- doxycylcine, rifampin for pregnant
| - no prophylaxis
50
A. phagocytophilum - tx
- doxycylcine, rifampin for pregnant
| - no prophylaxis
51
N. meningitidis - epidemiology
Leading cause of meningitis in children/young adults
| Epidemic - college, military, sub-Saharan Africa
52
N. meningitidis - causes of mortality
CNS - herniation
| Shock
53
N. meningitidis - tx
Penicillin - some resistance
| Speed important
54
N. meningitidis - prevention
Vaccine - Polysacharride-conjugate, quadrivalent (YWCA serotypes, working on B)
55
N. meningitidis - source and spread
Humans
| Nasal secretions
56
N. meningitidis - adhesion
Pilli, other
57
N. meningitidis - invasion
NP colonization > mucosal, blood
58
N. meningitidis - diseases
Conjunctivitis, pneumonia, bacteremia, meningitis, PF, Waterhouse-Fredrickson syndrome (bilateral adrenal hemmorhage)
59
S. agalactiae - morphology
Gram positive diplococci, encapsulated
| Lancefield typing system, group B
60
N. meningitis - morphology
Gram negative diplococci
| Polysaccharide capsule - >13 serotypes
61
enteric
facultative gram-negative rods that can be cultured (though true fecal floral are obligate anaerobes); grow on minimal media
62
MacConkey agar selects for
gram negative bacteria (bile salts in agar)
| lactose fermenting stain red
63
interpretation on Hektoen agar plate
```
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
64
Bacteria transmitted primarily by sex (4(+1))
```
Neisseria gonorrhoeae
Chlamydia trachomatis
Treponema pallidum
Haemophilus ducreyi
(Ureaplasma urealyticum)
```
65
Bacteria transmitted SECONDARY by sex (3)
Shigella
Salmonella
Campylobacter spp.
66
STI transmission mechanisms (3)
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
67
Major Patterns of Bacterial STI - (2)
| which bact cause each?
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
68
Chlamydia trachomatis - morphology
```
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
```
69
C. trachomatis - replication
– 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
C. trachomatis - Host Damage
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
C. trachomatis - escape
Little or no immune protection from reinfection
| IFN-γ (from Th1, CTL) inhibits RB replication by breakdown of tryptophan (starves bact)
72
Trachoma
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
Chlamydia Genital Infections
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
Chlamydia - Reactive Arthritis
Serovars D-K
| warm, swollen joints; the joint is *sterile
75
Reiter’s syndrome
C. trachomatis associated urethritis, arthritis, conjunctivitis +/- skin lesions
~80% of patients have HLA-B27
76
Chlamydia Neonatal Infections
Serovars D-K
| Inclusion conjunctivitis, pneumonia (less)
77
C. trachomatis - tx
azithromycin, week of BID doxycycline
78
Neisseria gonorrhoeae - morphology
gram -
diplococcus (coffee bean shape)
primarily extracellular
79
Neisseria gonorrhoeae - invasion
Attach to non-ciliated epithelial cells → pass through in endocytic vacuole → enter sub-epithelial space
80
N. gonorrhoeae - damage
Lipooligosaccharide (LOS) - potent endotoxin causes:
- cytotoxic to epithel as crosses
- stims PMN resp to subepithel bact -> epithel dmg and pus
81
N. gonorrhoeae - escape
IgA protease
| *many pili genes + homolog recomb → changing Ag
82
N. gonorrhoeae - primary genital manifestations
♀: Asymptomatic or mild mucopurulent cervicitis
| ♂: Asymptomatic or urethritis: urethral discharge and dysuria
83
N. gonorrhoeae - secondary sequellae (genital)
♀: Ascending infection → pelvic inflammatory disease
| ♂: Epididymitis and prostatitis
84
N. gonorrhoeae - Localized Extra-Genital
- 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
Disseminated Gonococcal Infection
Progression
Risk Factors
<1%, Genital infection → bacteremia → suppurative arthritis and or skin lesions
(papule → pustule → bulla)
Risk factors: menstruation, complement deficiency
86
Neonatal N. gonorrhoeae Infection
1) when acquired
2) onset
3) manifestation
1) during birth
2) 2-5 days after birth
3) Conjunctivitis → ulcers, pus
87
N gonorrhoeae - treatment
Single dose of a third-generation cephalosporin
Azithromycin or doxycycline
Disseminated or extragenital infections require longer treatment`
88
Treponema pallidum - disease
syphilis
89
T. pallidum - morphology
```
gram -
lipid-rich outer memb
flagella w/in outer memb
too skinny to see in light microscope
*use *dark field or immunological stain
```
90
Clostridium difficile - morph
- gram + baccilus
- obligate anaerobe
- forms spores
91
C. difficile - transmission
- hospital wards, nurseries, nursing home, bathrooms
| - fecal-oral route
92
C. difficile - vulnerable pop
on multiple antibiotics, elderly age, debilitated state, proton pump inhibitors, GI surgery
- new emergence in community among healthy individs
93
C. difficile - key findings
```
1wk post antibiotics
diarrhea +/- blood
abd cramps
high fever
leukocytosis
```
94
C. difficile - invasion
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
C. difficile - tx
- metronidazole (Flagyl) = good for anaerobes
| - vancomycin = good for gram +
96
Enterohemorrhagic E coli - most common serotype
O157:H7 (O Ag for LPS, H Ag for flagellum)
97
EHEC - key findings
*NO FEVER (~bacteria blocks)
watery bloody diarrhea
intense abd pain
98
EHEC - invasion
- 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
EHEC - tx
not antibiotics (worsen & increase risk of hemolytic-uremic syndrome probably bc antibiotics stress bacter & increase phage genes, which include Stx toxin)
100
cholera toxin
- Vibrio cholerae
- ADP-ribosylating toxin
- activates host cell adenylate cyclase, increase cAMP, increase cAMP-elicited fluid secretion
101
heat-labile toxin
- enterotoxigenic E coli
- ADP-ribosylating toxin
- activates host cell adenylate cyclase, increase cAMP, increase cAMP-elicited fluid secretion
102
heat-stable toxin
- enterotoxigenic E coli
- guanylate cyclase activating toxin
- activates membrane-bound guanylate cyclse, increase cGMP --> cGMP-elicited fluid secretion
103
Stx
- Shigella dysenteriae
- RNA glycosidase toxin
- single-site depurination of ribosomal RNA, inhibits protein synthesis --> cell death
104
Stx1 & Stx2
- enterohemorrhagic E coli
- RNA glycosidase toxin
- single-site depurination of ribosomal RNA, inhibits protein synthesis --> cell death
105
Salmonella - source
contamination of food, often poorly refrigerated prepared foods
106
Salmonella typhi (+ paratyphi)
typhoid fever (systemic Salmonella)
107
Salmonellae - morph
- gram neg rods
- closely related to E coli & Shigella
- lactose negative
108
Salmonellae - invasion
- 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
Salmonellae - tx
- gastroenteritis = self-limited, NO anitbiotics
| - typhoid fever: antibiotics
110
Helicobacter pylori - transmission
fecal-oral or oral-oral
| - mother-child most impt route of transmission & then reside for decades
111
H pylori - pop
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
H pylori - morpho
- curved microaerophilic gram neg rod
| - highly motile w/polar flagellum
113
H pylori - detection
- IgG to H pylori Ag
- breath test for high urease activity of org
- stool Ag test
- culture from biopsy material from endoscopy
114
H pylori - invasion
- 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
H pylori - tx
proton pump inhibitor & 2 anitbiotics
| - though controversial bc may have protective effect against esophageal reflux & cancer
116
*R. akari - lab findings
- transient leukopenia
| - transient thrombocytopenia
117
* Ehrlichia detection
- blood smear with grape-shape in PMN or monocytes
118
acute meningitis - lab findings
CSF elevated: opening P, WBC#, %PMN, prot,
Decreased: glucose, CSF:serum ratio
119
Listeria monocytogenes - morph
gram +
bacillus
grows in cold (4-10C)
intracellular - *actin based motility and invasion
120
L. monocytogenes - disease
Meningoencephalitis
Cerebritis and abscesses common (not true of other organism discussed)
Altered consciousness, seizures, movement disorder
121
L monocytogenes - damage
GI disease, sepsis, bacteremia, meningitis, chorioamnionitis
122
L monocytogenes - source spread
Zoonosis, present in food as contaminant
| spread - GI for most, vertical for newborns
123
S. pneumoniae - morphology
Gram positive diplococci
| Encapsulated
124
S. pneumoniae - Damage
Pneumonia
Meningitis - most common cause
Otitis, sinusitis
Pneumolysin - toxin; binds to cholesterol > pores in membrane
125
S. pneumoniae - Pneumonia clinical symptoms
Abrupt onset; pleuritic chest pain; thick "rusty" sputum;
| X-Ray: dense consolidation of one lobe
126
S. pneumoniae - detection
Sputum gram stain; sputum culture
Catalase negative, optochin sensitive
Urinary antigen test
127
S. pneumoniae - source & transmission
Human-Human
| Droplet
128
S. pneumoniae - adherance
Binds to receptor for platelet activating factor (PAF)
129
S. pneumoniae - damage
Pneumlysin
130
S. pneumoniae - escape from defense
Capsule
131
S. pneumoniae - treatment
Penicillins (resistance increasing)
132
S. pneumoniae - prevention
Vaccines:
Children <5 - protein conjugate (13 serotypes)
Adults - polysaccharide (23 serotypes)
133
P. aeruginosa - morphology
Gram negative bacillus
Non-enteric
Green pigment, characteristic sweet grape-like odor
134
P. aeruginosa - symptoms
Productive cough, dyspnea, fever, chills, confusion, systemic toicity, multifocal infiltrates on x-ray
135
P. aeruginosa - risk factors
Noscomial (hospital aquired)
Cystic fibrosis
COPD
Immunocomprimised (HIV)
136
P. aeruginosa - transmission
biofilms
137
C. diptheriae - morphology
Gram positive bacillus
138
C. diptheriae - damage
exotoxin (A/B) inhibits EF-2 > inhibits protein synthesis > cell death
139
C. diptheriae - clinical symptoms
Fever, malaise, sore throat, thick membrane on tonsils & adjacent structures
140
C. diptheriae - transmission
Droplet, contact
141
C. diptheriae - treatment
Antitoxin
Antibiotics
Supportive care (e.g. respiratory)
142
C. diptheriae - prevention
vaccine
143
M. tuberculosis - morphology
Doesn't gram stain; acid-fast stain
144
M. tuberculosis - symptoms
Fever, night sweats, weight loss, non-productive cough, pleuritic chest pain, atypical pneumonia (granulomas)
Extrapulmonary - other organ systems
Latency, reactivation
145
M. tuberculosis - transmission
Aerosol
146
M. tuberculosis - escape defense
intracellular - lives within macrophages
Prevents phagocome , prevents phagosome-lysosome fusion
Inhibit IL-12 secretion
Degrades NO
147
L. pneumophila - morphology
Gram negative bacillus
148
L. pneumophila - transmission
Natural reservoir - amoebae
| Environmental exposure: A/C, ventilation, water distribution system
149
L. pneumophila - escape defense
Survives within macrophages > replication > host cell lysis
| Uses Type IV secretion system
150
B. anthracis - morphology
Gram positive rod - sporulating
151
B. antrhacis - reservoir/transmission
reservoir: soil (spores)
Also: Animals, humans
152
B. anthracis - clinical symptoms
Cutaneous (95%) - papule > eschar; painless; edema
Inhalational - Mediastinitis, necrotizing pneumonia, high fatality
GI - edema, necrosis of affected intestinal segment
153
B. anthracis - damage
Antrhax toxin (A/B)
Edema factor > increased cAMP
Lethal factor > blocks MAPKKs
154
Yersinia pestis - morphology
Small gram negative coccobacillus
| Enterobateriaciae family
155
Y. pestis - reservoir/transmission
Primary reservoir: rodents
Blocks flea intestine w/ biofilm > regurgitation into host
Transmission: bite by rodent flea, exposure to human with pneumonic plague
156
Y. pestis - epidemiology (w/in US)
Southwest
157
Y. pestis - symptoms
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
Y. pestis - damage
Type III secretion system
Biofilm
Aquisition of foreign genetic material
159
F. tularensis - morphology
Gram negative coccobacillus
160
F. tularensis - reservoir/transmission
Terrestrial: rabbit reservoir, spread to human via tick, deerfly
Aquatic: muskrats, beavers, voles shed organism into environment
161
F. tularensis - Clinical symptoms
Ulceroglandular tularemia: painful maculopapular lesion, lymphadenopathy, fever/myalgia, pneumonia
Typhoidal tularemia: fever, hepatosplenomegaly, pneumonia
Pneumonic: pulmonary infection, granulomas
162
F. tularensis - defense escape
Intracellular growth - macrophages, hepatocytes, endothelial cells
163
B. henselae - Clinical symptoms
Cat scratch disease
Cutaneous papule/pustule, lymphadenopathy
Bacillary angiomatosis - neovascular proliferation
164
B. henselae - transmission
Bite or scratch of cat
| Flea bite
165
B. henselae - morphology
Intracellular, gram negative pleomorphic
166
T. pallidum - primary infection
primary syphilus
| hard chancre at infection site - painless lesion with central ulceration and a firm rim
167
T. pallidum - secondary infection
2-24wks post primary
lymphadenopathy, fever, rash
rash includes *palms and *soles
168
T. pallidum - tertiary infection
years post primary
neurosyphilus - variable
cadriovascular - *Ascending aortic aneurysm caused by damage to vasa vasorum
gumma - noncancerous growth, anywhere
169
T. pallidum - detection
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
T. pallidum - Tx, side effects
penecillin
| Jarisch-Herxheimer rxn - fever, hypotension
171
Causes of Genital Lesions
painless
single
chancre
painless: T pallidum, C trachomatis
single les: T pallidum, C trachomatis
chancre: T pallidum (hard), chancroid (soft, pustules)
