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Path: Infectious Disease > bacteria4 > Flashcards

bacteria4 Flashcards

1
Q

RPR and VDRL are nonspecific tests for Ab to this; what give false positives?

A

cardiolipin; mono and lupus

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2
Q

stain used in dark field microscopy to find syphilis organism

A

silver

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3
Q

stage of syphilis…most likely no Ab (although maybe some IgM), organism present

A

primary

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4
Q

stage of syphilis…Ab and organism present

A

secondary

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5
Q

stage of syphilis…Ab present, but no organisms (no infectious)

A

tertiary

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6
Q

specific test for fluorescent treponemal Ab absorption test

A

FTA-Abs

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7
Q

central to pathology of all syphilis lesions…endothelial injury

A

endarteritis

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8
Q

this develops at site of spirochete entry in primary syphilis infection

A

hard chancre (fibrotic, collagen)

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9
Q

describes secondary syphilis macular plaques (painless, reddish, raised)

A

condylomata lata

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10
Q

length of time it takes for secondary syphilis to develop after primary chancre

A

2-10 weeks

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11
Q

latent period of syphilis

A

5 years

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12
Q

neurological signs of tertiary syphilis

A

neurosyphilis, tabes dorsalis (foot drop), Charcot’s joints (can’t feel joints)

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13
Q

virulence factors for mycobacterium tuberculosis

A

facultative intracellular pathogen, glycolipids (promote resistant to intracellular killing), inhibit MP activation (via IFN) and phagolysosome-fusion, CMI injury

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14
Q

TB infection associated with these things

A

poverty, malnourishment, immunosuppression (AIDS), elderly, alcoholism

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15
Q

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?

A

Th1; IFN-g

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16
Q

IFN-g (from TH1 cells) causes this in persistent TB infection

A

aggregation epithelioid MP

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17
Q

direct progression from primary stage of TB will cause this (seen in young, old, and immunocompromised)

A

disseminated/miliary lesions and meningitis

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18
Q

methods of previously sensitized individual getting secondary TB

A

re-activation or re-infection

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19
Q

will see these associated symptoms with what stage of TB? weight loss, weakness, anorexia, night sweats, productive cough, blood-streaked sputum

A

secondary

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20
Q

progressive secondary TB infections can lead to these (*tertiary TB*)

A

empyema, extension within lung, miliary TB other organs

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21
Q

will see this kind of TB once the infection is drained via thoracic duct/SVC into R heart (hemtagoenous dissemination)

A

miliary TB

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22
Q

gold standard for diagnosis of TB

A

positive culture (NOT AFB stain)

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23
Q

most common presentation of tertiary TB

A

miliary TB

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24
Q

nerves most commonly affected by Leprosy

A

ulnar and peroneal

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25
Q

form of leprosy that causes granulomas (good CMI)…limited to skin

A

tuberculoid

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26
Q

these are deficient in patients with lepromatous leprosy; what does this lead to the formation of?

A

Th1; foam cells (organisms in MP)

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27
Q

stain for syphilis organism (treponema pallidum)

A

Warthin-Starry

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28
Q

chancres infiltrated with these cells

A

TH1

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29
Q

vessel wall infiltrates in primary syphilis …endothelial injury (central to syphilis pathology of lesions) –>compromised vessels, ischemia, necrosis, chancre

A

obliterative endarteritis

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30
Q

characteristics of secondary syphilis infection rash

A

red, raised, soles and palms (painless, macular plaques)

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31
Q

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

A

tree barking

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32
Q

possible cardio complications of tertiary syphilis

A

aneurysm/dissection of aorta, coronary insufficiency

33
Q

CSF findings in tertiary syphilis

A

pleocytosis, increased protein, decreased glucose

34
Q

formation of these in benign tertiary syphilis (in skin, subcu tissue, bone, joints)

A

gummas

35
Q

infiltrate in pathology of tertiary syphilis

A

lymphoplasmocytic

36
Q

describes MP and fibroblasts in tertiary syphilis…surrounds central necrosis

A

palisading

37
Q

congenital syphilis can be contracted up to this time period after mother has chancre

A

5 years

38
Q

signs/symptoms of congenital syphilis

A

diffuse rash, saddle nose, Hutchinson’s teeth, saber shin, CN 8 deafness

39
Q

this causes Scrub typhus (transmitted by mites…in far east, china, india) –> rash transitory or absent, possible prominent lymphadenopathy

A

Orientia tsutsugamushi

40
Q

what does Ehrlichiosis infect?

A

PMNs or monocytes

41
Q

organisms that cause Ehrlichiosis (symptoms similar to RMSF, but rash less prominent)

A

E. chaffeensis or Anaplasma phagocytophilum

42
Q

characteristic cytoplasmic inclusions in Ehrlichiosis…shaped like mulberries (actually masses of bacteria)

A

morulae

43
Q

transmission of Ehrlichiosis

A

ticks

44
Q

transmission of Lyme disease (Borrelia burgorferi)

A

white-tailed deer tick

45
Q

causes Lyme disease

A

Borrelia burgdorferi

46
Q

Borrelia does this to avoid host production of Ab

A

shift antigenic markers

47
Q

primarily responsible for immune reaction that causes most pathology associated with Lyme disease

A

LPS binding to TLR2 of MP

48
Q

responsible for perivascular inflammatory infiltrates in Lyme disease –> rash resembles RMSF

A

mononuclear leukocytes (Lymphoplasmacytic infiltrate)

49
Q

secondary and tertiary manifestation of lyme disease

A

chronic arthritis, polyneuropathy, encephalitis

50
Q

describes Lyme disease rash…bulls-eye appearance with spreading erythematous margins and blanching center

A

erythema chronicum migrans

51
Q

symptoms of secondary lyme disease infection (weeks to months after inoculation)

A

joint disease, muscle pain, cardiac arrhytmias, meningitis w/ CN involvement

52
Q

seen in arthritis caused by lyme disease (similar to early RA)

A

synovial hyperplasia, lymphocytes and plasma cells, proliferative arteritis

53
Q

transmission of relapsing fever (Borrelia recurrentis and hermsii)

A

lice (hermsii) or rodent ticks (recurrentis)

54
Q

time for latent period of relapsing fever

A

1-2 weeks

55
Q

why Borrelia recurrentis and hermsii can cause successive attacks

A

new surface antigens

56
Q

stain/shape for Yersinia pestis (plague)

A

gram negative bacillus

57
Q

method of transmission for the plague (Y pestis)

A

arthropod bite (sylvatic cycle)

58
Q

where does Yersinia pestis rapidly proliferate

A

lymphoid tissues

59
Q

responsible for fever and constitutional symptoms associated with lyme disease

A

mononuclear lymphocytes

60
Q

inactivating molecules that regulate actin polymerization…inhibits secretion of inflammatory cytokines

A

yersinia outer proteins

61
Q

yersinia outer proteins inhibit this

A

secretion inflammatory CK

62
Q

these are seen in plague due to swelling of lymphoid tissue

A

buboes

63
Q

more serious complications of plague

A

leukocytosis, septicemia/DIC, necrosis tissue and blood vessels

64
Q

symptoms of minor plague

A

lymphadenopathy and constitutional symptoms

65
Q

most common form of plague…prominent lymphadenopathy

A

bubonic

66
Q

symptoms of pneumonic plague

A

hemorrhagic, necrotizing pneumonia (primary or secondary to bubonic infection)

67
Q

stain/shape of Pasteurella multocida

A

gram negative coccobacillus

68
Q

Pasteurella multocida causes these rapidly developing symptoms

A

cellulitis, abscesses, sepsis

69
Q

treatment for all cat bites/scratches (and dog bites if near joints/tendons)

A

Augmentin

70
Q

gives rise to localized lymphadenopathy (cat scrach diseaes)

A

Bartonella henselae

71
Q

disease caused by Bartonella henselae in AIDS patients

A

bacillary angiomatosis

72
Q

describes Toxoplasma gondii organism

A

obligate intracellular protozoan

73
Q

syndrome caused by in utero exposure to Toxoplama gondii

A

TORCH

74
Q

may be result of toxoplasma gondii infection in congenital or 3rd trimester

A

chorioretinitis and blindness

75
Q

Toxoplasma gondii causes this in AIDS/immunosuppressed

A

encephalitis

76
Q

length of time it takes for oocytes of Toxoplasma gondii to mature after being shed in cat feces

A

24 hours

77
Q

receptors for Toxoplasma gondii on host cells

A

laminin

78
Q

Toxoplasma gondii causes this in normal persons

A

lymphoid hyperplasia

79
Q

inhalation of dust-borne contaminated excretia form birds…pneumonia (severe dyspnea) –>interstitial inflammation (edema, hyperemia, mononuclear infiltrate) –>lethal focal necrosis in liver and spleen

A

Ornithosis

Path: Infectious Disease (10 decks)

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