bacteria4 Flashcards
RPR and VDRL are nonspecific tests for Ab to this; what give false positives?
cardiolipin; mono and lupus
stain used in dark field microscopy to find syphilis organism
silver
stage of syphilis…most likely no Ab (although maybe some IgM), organism present
primary
stage of syphilis…Ab and organism present
secondary
stage of syphilis…Ab present, but no organisms (no infectious)
tertiary
specific test for fluorescent treponemal Ab absorption test
FTA-Abs
central to pathology of all syphilis lesions…endothelial injury
endarteritis
this develops at site of spirochete entry in primary syphilis infection
hard chancre (fibrotic, collagen)
describes secondary syphilis macular plaques (painless, reddish, raised)
condylomata lata
length of time it takes for secondary syphilis to develop after primary chancre
2-10 weeks
latent period of syphilis
5 years
neurological signs of tertiary syphilis
neurosyphilis, tabes dorsalis (foot drop), Charcot’s joints (can’t feel joints)
virulence factors for mycobacterium tuberculosis
facultative intracellular pathogen, glycolipids (promote resistant to intracellular killing), inhibit MP activation (via IFN) and phagolysosome-fusion, CMI injury
TB infection associated with these things
poverty, malnourishment, immunosuppression (AIDS), elderly, alcoholism
these are developed as result of MP presenting TB antigens in persistent infection (inability of MP to kill bacteria); what is secreted as a result?
Th1; IFN-g
IFN-g (from TH1 cells) causes this in persistent TB infection
aggregation epithelioid MP
direct progression from primary stage of TB will cause this (seen in young, old, and immunocompromised)
disseminated/miliary lesions and meningitis
methods of previously sensitized individual getting secondary TB
re-activation or re-infection
will see these associated symptoms with what stage of TB? weight loss, weakness, anorexia, night sweats, productive cough, blood-streaked sputum
secondary
progressive secondary TB infections can lead to these (*tertiary TB*)
empyema, extension within lung, miliary TB other organs
will see this kind of TB once the infection is drained via thoracic duct/SVC into R heart (hemtagoenous dissemination)
miliary TB
gold standard for diagnosis of TB
positive culture (NOT AFB stain)
most common presentation of tertiary TB
miliary TB
nerves most commonly affected by Leprosy
ulnar and peroneal
form of leprosy that causes granulomas (good CMI)…limited to skin
tuberculoid
these are deficient in patients with lepromatous leprosy; what does this lead to the formation of?
Th1; foam cells (organisms in MP)
stain for syphilis organism (treponema pallidum)
Warthin-Starry
chancres infiltrated with these cells
TH1
vessel wall infiltrates in primary syphilis …endothelial injury (central to syphilis pathology of lesions) –>compromised vessels, ischemia, necrosis, chancre
obliterative endarteritis
characteristics of secondary syphilis infection rash
red, raised, soles and palms (painless, macular plaques)
this is caused by obliterative endarteritis in aorta/aortic root in tertiary syphilis…vaso vasorum affected –> endothelium damaged –> regeneration/fibrosis…middle of aorta becomes ischemic –> can lead to dissection/aneurysm
tree barking
possible cardio complications of tertiary syphilis
aneurysm/dissection of aorta, coronary insufficiency
CSF findings in tertiary syphilis
pleocytosis, increased protein, decreased glucose
formation of these in benign tertiary syphilis (in skin, subcu tissue, bone, joints)
gummas
infiltrate in pathology of tertiary syphilis
lymphoplasmocytic
describes MP and fibroblasts in tertiary syphilis…surrounds central necrosis
palisading
congenital syphilis can be contracted up to this time period after mother has chancre
5 years
signs/symptoms of congenital syphilis
diffuse rash, saddle nose, Hutchinson’s teeth, saber shin, CN 8 deafness
this causes Scrub typhus (transmitted by mites…in far east, china, india) –> rash transitory or absent, possible prominent lymphadenopathy
Orientia tsutsugamushi
what does Ehrlichiosis infect?
PMNs or monocytes
organisms that cause Ehrlichiosis (symptoms similar to RMSF, but rash less prominent)
E. chaffeensis or Anaplasma phagocytophilum
characteristic cytoplasmic inclusions in Ehrlichiosis…shaped like mulberries (actually masses of bacteria)
morulae
transmission of Ehrlichiosis
ticks
transmission of Lyme disease (Borrelia burgorferi)
white-tailed deer tick
causes Lyme disease
Borrelia burgdorferi
Borrelia does this to avoid host production of Ab
shift antigenic markers
primarily responsible for immune reaction that causes most pathology associated with Lyme disease
LPS binding to TLR2 of MP
responsible for perivascular inflammatory infiltrates in Lyme disease –> rash resembles RMSF
mononuclear leukocytes (Lymphoplasmacytic infiltrate)
secondary and tertiary manifestation of lyme disease
chronic arthritis, polyneuropathy, encephalitis
describes Lyme disease rash…bulls-eye appearance with spreading erythematous margins and blanching center
erythema chronicum migrans
symptoms of secondary lyme disease infection (weeks to months after inoculation)
joint disease, muscle pain, cardiac arrhytmias, meningitis w/ CN involvement
seen in arthritis caused by lyme disease (similar to early RA)
synovial hyperplasia, lymphocytes and plasma cells, proliferative arteritis
transmission of relapsing fever (Borrelia recurrentis and hermsii)
lice (hermsii) or rodent ticks (recurrentis)
time for latent period of relapsing fever
1-2 weeks
why Borrelia recurrentis and hermsii can cause successive attacks
new surface antigens
stain/shape for Yersinia pestis (plague)
gram negative bacillus
method of transmission for the plague (Y pestis)
arthropod bite (sylvatic cycle)
where does Yersinia pestis rapidly proliferate
lymphoid tissues
responsible for fever and constitutional symptoms associated with lyme disease
mononuclear lymphocytes
inactivating molecules that regulate actin polymerization…inhibits secretion of inflammatory cytokines
yersinia outer proteins
yersinia outer proteins inhibit this
secretion inflammatory CK
these are seen in plague due to swelling of lymphoid tissue
buboes
more serious complications of plague
leukocytosis, septicemia/DIC, necrosis tissue and blood vessels
symptoms of minor plague
lymphadenopathy and constitutional symptoms
most common form of plague…prominent lymphadenopathy
bubonic
symptoms of pneumonic plague
hemorrhagic, necrotizing pneumonia (primary or secondary to bubonic infection)
stain/shape of Pasteurella multocida
gram negative coccobacillus
Pasteurella multocida causes these rapidly developing symptoms
cellulitis, abscesses, sepsis
treatment for all cat bites/scratches (and dog bites if near joints/tendons)
Augmentin
gives rise to localized lymphadenopathy (cat scrach diseaes)
Bartonella henselae
disease caused by Bartonella henselae in AIDS patients
bacillary angiomatosis
describes Toxoplasma gondii organism
obligate intracellular protozoan
syndrome caused by in utero exposure to Toxoplama gondii
TORCH
may be result of toxoplasma gondii infection in congenital or 3rd trimester
chorioretinitis and blindness
Toxoplasma gondii causes this in AIDS/immunosuppressed
encephalitis
length of time it takes for oocytes of Toxoplasma gondii to mature after being shed in cat feces
24 hours
receptors for Toxoplasma gondii on host cells
laminin
Toxoplasma gondii causes this in normal persons
lymphoid hyperplasia
inhalation of dust-borne contaminated excretia form birds…pneumonia (severe dyspnea) –>interstitial inflammation (edema, hyperemia, mononuclear infiltrate) –>lethal focal necrosis in liver and spleen
Ornithosis
