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Micro Post Quiz 3 JXC > 2. Plague, Tularemia & Brucellosis > Flashcards

2. Plague, Tularemia & Brucellosis Flashcards

1
Q

What microbe causes plague?

A

Yersinia pestis

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2
Q

What are the physical and biochemical characteristics of Y. pestis?

A
  • Enterobacteriaceae family
  • Large, bipolar (safety pin) staining, Gm(-), pleomorphic rod
  • Facultative aerobe (notes say “aerobic or facultative aerobic” slides just say “facultative”)
  • Glucose fermenter
  • Non-Lactose fermenting
  • non-motile
  • Catalase +
  • Oxidase -
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3
Q

What do you stain with do see bipolar staining?

A

Giemsa or Wayson stain

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4
Q

What is the epidemiology of plague?

A 
zoonotic transmission
--humans accidental hosts
can be either:
-arthropod --> mammal (bubonic)
-mammal --> mammal (pneumonic)
*pneumonic can be 1° from inhalation or 2° to bubonic plague that causes bacteremia
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5
Q

What is the geographic distribution of plague in the U.S.?

A

mostly southwestern U.S.

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6
Q

Animal resevoirs of Y. pestis?

A

mostly rodents; In U.S. prairie dogs, squirrels, weasels, skunks, woodrat, cats

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7
Q

Arthropod vectors of Y. pestis?

A

rat flea

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8
Q

What is the epidem. of urban plague?

A

epizootic (animal epidem) in urban black rats; as they die off their fleas –> humans; first bubonic then pneumonic

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9
Q

What is the epidem. of rural plague?

A

incidental contact with wild rodents or their fleas;

  • -SW u.s. (10 cases/yr), indian, s. amer, s. afr, s. russia
  • -flea bite, hand contact w/ wild animal, pet
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10
Q

Is Y. pestis and extra- or intra-cellular pathogen?

A

Can be both. Intracellular in monocytes

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11
Q

What virulence factors does Y. pestis employ?

A
  1. F1 antigen = anti-phag capsule (only active at human body temp)
  2. Endotoxin (from LPS)
  3. V & W antigens –> allow intracellular growth in monocytes
  4. exotoxin
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12
Q

What is the role of toxins in plague pathogenesis?

A

Both endotoxin and exotoxins

–endotoxin leads to DIC which causes the cutaneous hemorrhages and necrosis = “black” death

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13
Q

How do you dx plague?

A
  1. smear (and culture per Levinson) from blood, bubo pus or sputum
  2. 4X rise in Ab titer for F1 (caps. Ag)
  3. fluorescent Ab staining against F1
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14
Q

How is plague prevented?

A
  • -72 quarantine for Positive Pts.
  • -flea control
  • -rodent control (esp at ports)
  • -inactivated vaccine (used in Vietnam; no longer available in U.S.)
  • -chemoprophylaxis for exposed w/ tetracycline
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15
Q

How is plague tx’ed?

A

10 days of tetracycline and/or streptomycin (Levinson says combo is tx of choice); chloramphenicol works, too

  • -no significant resistance
  • -surgical drainage not needed
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16
Q

What is the difference between bubonic and pneumonic plague?

A

bubonic:

–bite skin –> local lymph nodes

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17
Q

What are the different clinical presentations of plague?

A
  1. bubonic: fever, malaise & painful lymphadenopathy
  2. pneumonic: fever, cough & SOB
  3. septicemic: DIC, skin hemorrhages, plague meningitis
18
Q

If a pt survives plague, will pt have immunity?

A

yes

19
Q

What is the causative agent of tularemia?

A

Francisella tularensis

20
Q

What is the epidemiology of tularemia?

A

transmitted from infected animals or arthropods to humans; ~200 cases/yr in the 90s; e.g. muskrat trappers in VT

21
Q

What are the animal resevoirs of tularemia?

A

rabbits (handling furs or eating under-cooked), deer

  • -other rodents
  • -cat bites
  • -dog aerosolized when shaking off water in Martha’s Vineyard
    • > 100 different species of wild animals
22
Q

Which are the arthropod vectors of tularemia?

A

ticks (DERMAcentor variabilis) and deer flies

23
Q

Which individuals are at high risk for contracting tularemia?

A

–lab workers, trappers, vets

24
Q

Describe the pathogenesis of tularemia.

A
  1. infection via: handling, tick bite, ingestion or inhalation
  2. skin lesions –> local lymphatics
  3. lymphadenopathy
  4. bacteremia
  5. granuloma formation in reticuloendothelium (spleen, liver)
    * *Survives intracellularly in Monocytes/Macrophages
    * *Endotoxin –> systemic symptoms
25
Q

What is the clinical presentation of tularemia? How does it compare to plague?

A

similar to plague but less severe:

  • -abrupt onset of f/c, malaise
    1. ulceroglandular = 75% of case –> skin ulcer + painful inguinal or axial adenopathy
  1. could also be: typhoidal = bacteremia; pneumonia in 10-15%; GI. oculoglandular

<1% fatality w/ tx

26
Q

How is tularemia dx?

A

tricky and dangerous to culture so send to state lab or CDC

  • -Fluoro Ab of node biopsy
  • -4X rise in titer, but cross reacts w/ brucella
27
Q

How is tularemia tx?

A

7-10 days of streptomycin or 14 days w/ tetracycline

–can relapse from intracellular ones

28
Q

How is tularemia prevented?

A
  • -tick checks/control
  • -where gloves when handling rabbits, muskrats, etc.
  • -vaccine for trappers, lab workers, etc.
29
Q

What are the physical and biochemical properties of Francisella tularensis?

A
  • *not a member of Enterobacteriaceae family
  • small, Gm(-), pleomorphic rod
  • fastidious, slow-growing; requires cytosine and glucose on blood agar
  • cold tolerant
30
Q

What is the ID50 for Francisella tularensis?

A

very low! only 5-10 organisms therefore NIH Category A pathogen

31
Q

How is Brucellosis transmitted?

A
  • -unpasturized milk and milk products (particularly in developing world and hipster enclaves)
  • -abattoirs
32
Q

What animal vectors are assoc’d with which strains of Brucella spp.?

A

B. abortus = cattle (dairy or contact)
B. suis = swine (abattoir or skin contact)
B. melitensis = goats/sheep (goat’s milk)

33
Q

Where does the organism localize in farm animals?

A

the placenta; causes spontaneous abortion; puts vets and farmers at risk during birthing

34
Q

What are the physical and biochemical properties of Brucella spp.?

A

pleomorphic, fastidious, Gm- rods

  • grows slowly
  • requires 10% CO2
35
Q

What are other names for infection w/ Brucella spp?

A

Malta Fever; Mediterranean fever

36
Q

What are the clinical features of brucellosis? Why?

A

systemic, non-focal sx b/c attacks the widespread reticuloendothelial system

  • -FUO
  • -f/c myalgias, h/a, arthralgias
  • -severe complications: osteomyelitis in the vertebrae and endocarditis; can be due to persistance of intracellular state
37
Q

What is the pathogenesis of Brucellosis?

A

ingestion by PMNs/multiply in monocytes –. granulomas in kidney, liver, spleen and bone marrow

38
Q

How do we control Brucellosis in u.s.?

A
  1. Pasteurize milk!
  2. occupational protection (mesh gloves, eye protection)
  3. vaccinate young female calves w/ B. abortus vaccine
  4. test milk, then individuals, “destroy infected animals”
39
Q

How do you tx brucellosis?

A

rifampin + doxycycline for 6 weeks

  • -25% relapse rate
  • -1-2% mortality
40
Q

What causes relapsing fever?

A

.

Micro Post Quiz 3 JXC (6 decks)

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