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Path > 2: Anthrax, Syphilis, Mycobacteria > Flashcards

2: Anthrax, Syphilis, Mycobacteria Flashcards

1
Q

organism that causes anthrax

A

bacillus anthracis

  • highly pathogenic
  • encapsulated
  • G(+)
  • spores
  • rod
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2
Q

transmission of anthrax

A
  • contact w/ animals, animal hides, or animal products (bone meal fertilizer)
  • particularly sheep and goats
  • inhaled as a powder (weaponized)
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3
Q

describe cutaneous anthrax

A
  • small hemorrhagic pustule that develops into a black eschar
  • very painful lymphadenitis
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4
Q

describe pulmonary anthrax

A
  • woolsorter’s disease
  • extensive pneumonia with serofibrinous exudation
  • develop septicemia
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5
Q

pathologic mechanisms of anthrax

A
  • antiphagocytic activity
  • edema factor (Ca-dependent, increases cAMP, water out)
  • cytotoxic factor (kills macrophages- evade immunity)
  • leukopenia w/ infections
  • bacteremia may cause meningitis
  • electrolyte imbalance, hemoconcentration and DIC
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6
Q

what leads to death in anthrax?

A

electrolyte imbalance, hemoconcentration and DIC

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7
Q

what bugs are included in group A: highest risk to national security?

A
  • anthrax
  • botulism
  • plague
  • small pox
  • tularemia
  • viral hemorrhagic fevers (ebola)
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8
Q

what bugs are included in group B: second highest risk to national security?

A
  • West Nile virus
  • caliciviruses
  • Hep A
  • Ricin
  • Salmonella
  • E. coli
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9
Q

what bugs are included in group C: emerging pathogens that could be engineer for mass dissemination?

A
  • influenza
  • SARS
  • Rabies
  • MDR TB
  • Yellow fever
  • tick-borne hemorrhagic fevers
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10
Q

why could anthrax be used as a biological weapon?

A
  • environmentally stable
  • high virulence
  • ease of respiratory transmission

inhalation anthrax: low LD50, high fatality rate, basis for anthrax bomb

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11
Q

control of anthrax

A
  • vaccine (limited use in US)
  • penicillin
  • doxycycline
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12
Q

organism of TB

A

mycobacterium tuberculosis

  • acid fast (waxes in cell walls, retain red dye carbolfuchsin)
  • slow growing
  • mostly facultative intracellular
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13
Q

virulence factors of TB

A
  • glycolipids (promote resistance to intracell killing)
  • inhibit IFN-activaiton of macrophages
  • prevent phago-lysosomal fusion
  • stimulate destructive cell-mediated inflammatory injury
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14
Q

histologic hallmarks of TB

A

caseating granulomas (distinctive, but not unique)

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15
Q

characteristic need for transmission

A

requires sustained contact

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16
Q

what is TB associated with?

A
  • poverty
  • malnourishment
  • immunosuppression
  • elderly (reactivation)
  • AIDS
  • alcoholism
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17
Q

TB pathogenesis

A
  • no known endotoxins, exotoxins, or histiolytic enzymes
  • T4HS rxn - destructive lesions
  • tubercle (granuloma) consists of:
    • plump, round histiocytes
    • Langhans’ multinucleate giant cells
    • peripheral collar of fibroblasts
    • with lymphocytes
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18
Q

what results in persistent infection of TB?

A

inability of macrophages to kill bacteria

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19
Q

describe granuloma formation

A

presentation of TB Ag’s by infected macrophages to lymphocytes -> development of TH1 cells -> secretion of IFN-gamma -> TNF induces chemotaxis, collection of more monocytes; IFN-gamma results in aggregation of epithelioid macrophages

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20
Q

picture a granuloma! describe it

A
  • central necrosis (caseating - no nuclei) or not (non-caseating - nuclei still there)
  • surrounded by epithelioid histiocytes, Langhan’s giant cells
  • outer ring of lymphocytes surrounding that
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21
Q

describe primary or latent TB

A
  • no previous TB contact
  • most asymptomatic
  • formation of Ghon focus in lower part of upper lobes or upper part of lower lobes (unilateral)
  • fibrosis, calcification, but rarely progressive disease
22
Q

who might get direct progression of primary/latent TB and what does it cause?

A

kids -> disseminated (miliary) lesions and meningitis

23
Q

describe Ghon foci

A

primary lung lesion with caseating granulomas in draining lymph nodes

24
Q

describe secondary TB

A
  • previously sensitized (reactivation or reinfection)
  • cavitary lesions in apical lobes (higher O2 tension)
  • characteristic sx: fever, night sweats, weakness, loss of appetite, weight loss, productive cough, blood-streaked sputum

rarely see satellite lesions in nodes

25
Q

describe tertiary TB

A
  • progression of secondary lesion
  • extension to other parts of lung, empyema
  • miliary TB in other organs (bacteremia)
  • isolated organ TB (cervical nodes, meninges, kidney, adrenals, bones)
  • drainage of dudes into lymphatics -> dumping into bloodstream via thoracic duct -> redistributed to other lung fields via pulmonary circulation as miliary TB
26
Q

diagnosis of TB

A
  • AFB in sputum
  • gold standard = positive culture***
  • XR findings (cavitary lesions, node calcification)
  • Quanti-feron test (in vitro, measure IFN production in response to TB exposure)
27
Q

what do most individuals who are exposed get?

A

no infection or latent infection

28
Q

when do you start seeing symptoms in TB?

A

when it progresses to secondary disease:

  • pulmonary sx
  • AFB in sputum
  • XR changes
29
Q

what is the most common TB presentation of tertiary TB?

A

miliary TB in lung

30
Q

pathogenesis of leprosy (mycobacterium leprae)

A

infection affecting skin and nerves (cool parts of body)

  • skin: macular, papular, or nodular lesions
  • nerves: ulnar, peroneal
31
Q

leprosy forms of disease: TT vs. LL

A

TT = tuberculoid leprosy: granulomas
-if strong immunity, get T4HS w/ non-caseating granuloma

LL = lepromatous form: NO granulomas

  • lack TH1 immunity
  • proliferation of organisms in macrophages (foam cells)***
  • widespread disease
32
Q

which form of leprosy is contagious?

A

lepromatous form

33
Q

describe organism for syphilis

A

treponema pallidum:

  • microaerophilic spirochete
  • outer sheath that masks bacterial antigens
34
Q

transmission of syphilis

A

sexual

transplacental

35
Q

what stain allows you to see syphilis?

A

Warthin-Starry stain (silver stain on dark field microscopy)

36
Q

diagnosis and serology of syphilis

A
  • RPR, VDRL (screening) - nonspecific for Ab to cardiolipin
  • silver stain on dark field microscopy
  • FTA-Abs test (diagnostic)
37
Q

when can you get false positives for RPR/ VDRL?

A

with mono or lupus

38
Q

Abs vs. presence of organism: primary, secondary, and tertiary disease

A

1: no abs/ organisms present (can get Abs depends on timing)
2: Abs/ organism present
3*: Abs/ no organisms

39
Q

pathogenesis of syphilis

A
  • scarcity of bugs and intense inflam infiltrate - central role for immune response in lesions
  • chancres filled with TH1 cells
  • Ab repsonse does not eliminate infection
  • LYMPHOPLASMACYTIC INFILTRATE
  • endarteritis central to pathology of all lesions
40
Q

what is endarteritis?

A

vasculitis of arterioles that causes ischemia -> tissues supplied by these vessels becomes necrotic

41
Q

describe primary syphilis

A
  • hard chancre at site of invasion
  • intense mononuclear infiltrate w/ plasma cells
  • obliterative endarteritis
  • vessel wall infiltrates

VDRL and FTA-Abs negative**
organisms can be taken from lesions**

42
Q

describe secondary syphilis

A
  • 2-10w after primary chancre
  • related to immune response -> dissemination
  • painless red-brown, macular plaques of skin, mucous membranes (especially PALMS AND SOLES)
  • condylomata lata (elevated broad plaques in region of penis/vulva)
  • infectious - contain dudes**
  • histology similar to chancre (mononuclear infiltrate w/ plasmas)

VDRL and FTA-Abs positive**
organisms can be taken from lesions**

43
Q

describe tertiary syphilis

A
  • latent period of 5y or more
  • CV system most often affected:
    • damage to aorta, aortic root
    • obliterative endarteritis (tree barking of endothelium)
    • aneurysms and dissections, coronary insufficiency
  • neurosyphilis/tabes dorsalis/ Charcot’s joint
  • syphilitic gumma

VRDL and FTA-Abs positive**
canNOT take organisms from lesions**

44
Q

describe Charcot’s joint

A

sensory loss, can’t feel feet -> knock them into ground -> damage ankles/knees

45
Q

describe neurosyphilis

A
  • chronic meningoencephalitis
  • tabes dorsalis
  • charcot joints
46
Q

CSF findings in neurosyphilis

A
  • pleiocytosis
  • increased protein
  • decreased glucose
47
Q

describe benign tertiary syphilis

A
  • formation of gummas

- skin, subQ, bone, joints

48
Q

pathology of tertiary syphilis

A
  • lymphoplasmacytic infiltrates
  • obliterative endarteritis (endothelial proliferation and intimal fibrosis)
  • focal epithelioid granulomas
  • delayed type T4HS
49
Q

when can a fetus get congenital syphilis

A

when it is born up to 5y after the mother first became infected
-may cause late abortion

50
Q

describe symptoms of congenital syphilis

A
  • diffuse rash
  • disseminated lesions - saddle nose
  • infects bones/teeth - saber shin, Hutchinson teeth
  • liver and lung involvement
  • late occurring form: interstitial keratitis, CN8 deafness

Path (10 decks)

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