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35 Cards in this Set

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chlamydiae
1. morphology
2. tissue infected
3. body response
1. obligate intracelluar parasite G- bacT; Chlamys - cloak (under membrane)
2. mucosal infections (difficult to grow in cultures)
3. humoral (Abs) & cellular
chlamydiae:
--diagnostics
-- abx sensitivity
type specific chlamydial Abs in serum & secretions - immunofluorescence

***cytoplasmic inclusions***

-- large spectrum; NOT PCN
chlamydiae
-- pathophy (3 steps)
1. elementary body - 0.3 micron: infxous form released from infected host cell (protective envelop), enters cells via endocytosis
2. reticulate [initial] body - 1 micron: replicates w/in host cell vacuoles
3. intra-cytoplasmic inclusions in epithelial cells
3 species of chlamydiae
1. C. pneumoniae - infxs only humans; atypical pneumonia - transmitted by aerosols
2. C. psittaci - avian reservoir; atyp. PNA - aerosols (parakeets/parrots)
3. C. trachomatis
3 categories of C. trachomatis
1. Type A, B, C trachoma - follicular kerato-conjunctivitis
2. Type D-K - urethritis, neonatal PNA, inclusion conjunctivitis
3. Type L1, L2, L3 - lymphogranuloma venereum
C. psittaci
1. aka
2. transmission
3. incubation period
1. ornithosis aka psittacosis
2. aerosols (dust-borne) through inhalation of dried excreta (parakeets, parrots, other birds); BITE of BIRD & DIRECT contact w/ pt
3. 1-3 wks
C. psittaci
1. clinical forms
1. asymptomatic infxn
2. transient flu-like illness - ie viral pneumonitis: fever, malaise, sore throat, cough, dyspnea
3. fatal PNA
C. psittaci
1. gross
2. microscopy
3. lethal disease
4. dx
1. pneumonitis, lung abscesses
2. alveolar damage, consolidations, pulm. edema, pneumocytes may contain INTRA-CYTOPLASMATIC bodies
3. **focal necroses, mononuclear infiltrates in liver,spleen,kidneys,heart
4. rise in specific Abs; culture difficult
Chlamydial urethritis & cervicitis
1. up to 10 % of ppl carry bacT where?
2. 70% of women have...?
3. what is increased by 8-10%/year
4. rank in list of STDs in US
5. What serotypes are 50% of the cases of C. trachomatis due to?
1. repro tract (higher in promiscuous)
2. asymptomatic carriage on cervix
3. prevalence among young, sexually active teens
4. MC STD in US
5. serotyes D-K
Chlamydial urethritis & cervicitis
1. what is seen in infants born by infx'd mothers
2. clinical findings in females
3. in males
4. complications of ds
1. inclusion conjunctivitis & neonatal PNA
2. cervicitis, salpingitis, PID - pelvic inflamm. ds, proctitis
3. prostatitis, epididymitis
4. long term repro damage; ectopic pregnancy, sterility
Chlamydial inclusion conujunctivitis
1. general classification
2. how are newborns infx'd
3. adults?
4. histology
1. suppurative, beningn, self-limiting
2. from mothers
3. directly, or from swimming pools
4. chlamydial inclusions in exudate & lymphcytic infiltration in tissue
C. trachomatis serotypes A, B, C
1. define trachoma
2. significant in global manifestions
3. mostly occurs to whom/where
4. transmission
1. follicular kerato-conjunctivitis
2. leading global cuase of blindness through scarring
3. poor ppl in dry/sandy regions
4. direct contact, flies, fomites (objects)
C. trachomatis serotypes A, B, C
- morphology
- suppuration - deeper tissue inflitration w/ lymphocytes & plasma cells
- formation of lymphoid cell follicles = follicular conjunctivitis
- ulceration of conjuncvtiva, vascular invasion [pannus formation], fibroblast ingrowths
- eventually scarring -> blindness
Chlamydia trachomatis serotypes L1,2,3
1. causes
2. incubation
3. primary lesion
1. lymphogranuloma venereum - STD aka Nicolas Favre disease
2. 4-21 days
3. at site of infxn: penis, labia, vag, cervis, lips, tongue, fingers, anorectal
Chlamydia trachomatis serotypes L1,2,3
3 stages of progression
1. stage I
- small ulcer, at inoculation site, w/ neutrophil infil. & granuloma at base
- chlamydial inclusions in cells
2. Stage II
- suppurative granulomatous lympadenitis
- matted nodes
- stellate abscesses
- fistulae discharging pus
3. Stage III
- chronic inflamm infiltrate
- dense fibrosis
- late stage: rectal stenosis & chronic genital lymphedema [vulvular elephantiasis]
Rickettsiae
1. micro - morphology
2. natural vectors
3. transmission
1. small pleomorphic [rod shape to coccoid] obligate intracellular G- bacT
2. ticks, mites, fleas, lice
3. arthropod bite/contact w/ aerosols from animal excreta
Rickettsiae
1. pathogenesis
2. host defense
1. enters host cells by induced endocytosis -> multiply in several cells types [endothelial]; do NOT generate toxins
2. immune response: cytolytic T lympocyte dependent; gamma-interferon
--Abs can convey passive protection
Rickettsiae
- various vectors & target cells (8!)
1. R. prowazeki - endothelial cells (epidemic typhus - human body lice)
2. R. rickettsii - endothelial cells (RMSF - ticks)
3. R. mooseri - endothelial cells of rodents & humans (Murine typhus - fleas [mus,muris - mouse])
4. E. chaffensis - monocytes & granulocytes (non-specific febrile illness - ticks)
5. Coxiella burnetti - macrophages (Q fever [Queensland] - inhaled aerosols)
6. Bartonella [Rochalimaea] - peri-cellular infxn - lice
7. B. quintana - trench fever
8. B. henselae - endocarditis in homeless, septicemia; in immunocompetent - cat scratch fever - inoculated benign lympho-reticulosis
Rickettsiae
1. dx
2. morphology
a. macroscopic
b. microscopy
1. skin biopsy & immunoflorescent staining; specific serum Ab titers; direct culture
2.
a. skin rash, skin eschar [in spotted fever group]
b. mononuclear inflamm infiltrate, focal vas inflammation, micro-thrombi, ischemia or hemorrhage [rash-associated]
What is an eschar
well circumscribed nodular [swollen], dark encrusted lesion
Louse-borne epidemic typhus
1. cause (R. ______)
2. cycle
3. epidemics
1. R. prowazeki
2. man-louse-man
3. poor sanitation, crowding, famine, war
Louse-borne epidemic typhus
1. transmission/pathology
1. contaminated louse feces penetrates skin abrasions [SCRATCH!!]
2. inhalation of air-borne Rickettsia
3. multiplication in human endothelial cells
4. rupture of endothelial cells releases R. p. in circulation
5. rickettsemia
6. louse taking blood meal from infected human becomes infected w/ rickettsiae
7. obligate intra-cellular G- bacT enters epithelial cells of louse's midgut
8. rickettsia released in lumen of louse intestine contaminating the feces
9. feces deposited on non-infected human skin
what is rickettsemia
human blood circulating rickettsiae
Louse-borne epidemic typhus
1. incubation
2. clinical aspects (triad/severe cases)
1. 8-15 d
2.
triad: fever, h/a, maculopapular rash, apathy, stupor, coma (CNS involved)
severe cases: interstitial PNA, nephritis, myocarditis, encephalitis, shock, gangrene [arteritis]
Louse-borne epidemic typhus
1. microscopy
2. sporadic thyphus- Brill-Zinsser disease
3. dx
1. typhus nodule
2. actual encountered clinical form of typhus: reinfection typhus w/ rickettsiae dormant in spleen
3. detection of rickettsiae - immunofluorescence, abs & Weil-Felix reaction (cross reaction w/ proteus Ags)
What is a typhus nodule
small vessel lesion in brain & other organs, focal infiltration w/ leukocytes, microglial proliferation
R. rickettsii
1. causes
2. transmission
3. incidence in US
1. RMSF - prototype of spotted fever group
2. bite of blood sucking ticks; the salivary glands of the tick, Dermacentor, contain Ricketttsiae. Ticks are both the vectors & the reservoir
3. 200-1100 cases/year
R. rickettsii
1. incubation2. clinical aspect
1. 2-12 d
2. fever, h/a, mm pain
**rash including palms & soles** - beings maculopapular & becomes petechial & purpuric [hemorrhagic], spreads centripetally, from distal extremities to trunk; **eschar at bite site**, absent in mild infections
- necrotic skin foci - fingers, toes, elbows, ears, scrotum
R. rickettsii
1. severe cases
2. microscopy
3. dx
1. micro-infarcts in brain; pneumonitis & secondary bacterial infection
death - shock, renal failure, CNS damage
2. endothelial lesions underlying rash cause arteritis & thrombosis, generatin necrosis
3. urgernt - immunofluorescence demonstrating R. rickettsii in skin biopsy
Mycoplasma
1. aka
2. micro - morphology
3. infects what tissue
1. eaton agent
2. tiny, pleomorphic bacT that lack cell wall, called PPLOs (PNA, pleuritis like organisms]; commonly causes ds of fowl & cattle
3. parasitize membrane cells, binding to epithelial linings of RT & GU tract
Mycoplasma
1. mycoplasma urethritis
2. effects on pregos
1. acute purulent "non-gonococcal" urethritis --> chronic PID
2. may produce chorio-amnionitis which means infxn of placenta, dreadful conditions for pregnancy & life of pregos
M. pneumoniae PNA
1. transmission
2. pathogenesis
1. by aerosol & droplets; only 1-3% exposed become infected; most in close living quarters [barracks, dorms, boarding schools, huge ships]
2. M. pneumoniae bacT disrupt cilia & damages resp epithelium; produces cold agglutinins & complement fixing Abs; these Abs may cause false-positive serologic tests for syphilis
M. pneumoniae PNA
1. microscopy
1. interstitial PNA, alveolar air spaces empty [no inflamm cells], thickened alveolar walls = intra-septal inflamm w/ mononuclear [lymphocytes & plasma cells] infilitrate
M. pneumoniae PNA
1. clinical
- similar to viral PNA;
- 10-30% of comm. acquired atypical PNAs
- low mortality
- walking PNA
- fever, h/a, malaise, sore throat & unprod cough, nasal sxs, chest pain & earache
M. pneumoniae PNA
1. complications
2. Stevens Johnson syndrome
3. DONEZO
1. myocarditis, miringitis [eardrum infxn], transverse myelitis [spine inflamm w/ tetraplegia]
2. peri-orificial [perioral, perianal, periorbital] ecto-dermitis, formed by uncerated papule which can be bacterial super-infected
3. if you're going in order...otherwise, keep on trucking!