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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
describe tertiary TB
- 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
diagnosis of TB
- 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
what do most individuals who are exposed get?
no infection or latent infection
28
when do you start seeing symptoms in TB?
when it progresses to secondary disease: - pulmonary sx - AFB in sputum - XR changes
29
what is the most common TB presentation of tertiary TB?
miliary TB in lung
30
pathogenesis of leprosy (mycobacterium leprae)
infection affecting skin and nerves (cool parts of body) - skin: macular, papular, or nodular lesions - nerves: ulnar, peroneal
31
leprosy forms of disease: TT vs. LL
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
which form of leprosy is contagious?
lepromatous form
33
describe organism for syphilis
treponema pallidum: - microaerophilic spirochete - outer sheath that masks bacterial antigens
34
transmission of syphilis
sexual | transplacental
35
what stain allows you to see syphilis?
Warthin-Starry stain (silver stain on dark field microscopy)
36
diagnosis and serology of syphilis
- RPR, VDRL (screening) - nonspecific for Ab to cardiolipin - silver stain on dark field microscopy - FTA-Abs test (diagnostic)
37
when can you get false positives for RPR/ VDRL?
with mono or lupus
38
Abs vs. presence of organism: primary, secondary, and tertiary disease
1*: no abs/ organisms present (can get Abs depends on timing) 2*: Abs/ organism present 3*: Abs/ no organisms
39
pathogenesis of syphilis
- 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
what is endarteritis?
vasculitis of arterioles that causes ischemia -> tissues supplied by these vessels becomes necrotic
41
describe primary syphilis
- 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
describe secondary syphilis
- 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
describe tertiary syphilis
- 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
describe Charcot's joint
sensory loss, can't feel feet -> knock them into ground -> damage ankles/knees
45
describe neurosyphilis
- chronic meningoencephalitis - tabes dorsalis - charcot joints
46
CSF findings in neurosyphilis
- pleiocytosis - increased protein - decreased glucose
47
describe benign tertiary syphilis
- formation of gummas | - skin, subQ, bone, joints
48
pathology of tertiary syphilis
- lymphoplasmacytic infiltrates - obliterative endarteritis (endothelial proliferation and intimal fibrosis) - focal epithelioid granulomas - delayed type T4HS
49
when can a fetus get congenital syphilis
when it is born up to 5y after the mother first became infected -may cause late abortion
50
describe symptoms of congenital syphilis
- diffuse rash - disseminated lesions - saddle nose - infects bones/teeth - saber shin, Hutchinson teeth - liver and lung involvement - late occurring form: interstitial keratitis, CN8 deafness

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