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M1 S3 > Micro Post Q3 > Flashcards

Micro Post Q3 Flashcards

1
Q

Describe the bacteriology & morphology of Yersinia pestis

A

–Pleomorphic: large rod-shaped or coccobacillary gram-negative bacterium

–Grayish-white, non-hemolytic colonies

–facultative intracellular organism, prefers to inhabit monocytes

A member of Enterobactericeae

  • -> facultative aerobic
  • -> non-lactose fermenter
  • -> glucose fermenter
  • -> oxidase negative

–non-motile

–catalase +

–Safety pin, bipolar staining using Wright, Wayson, Wright, or Giemsa stain

–> Giemsa: Methylene blue stains the DNA at each end, the middle is clear

–Plague is normally a zoonotic disease

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2
Q

What is the ICD of Yersinia pestis?

A

1-10 organisms

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3
Q

What are the characteristics of member of Enterobactericeae?

A
  • facultative bacteria
  • gram-negative rod
  • oxidase negative
  • ->oxidase is part of cytochrome C
  • can be glucose or lactose fermenting
  • Some members of family Enterobactericeae: E. coli, Klebsiella, Shigella, Serratia marcesens, and Enterobacter
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4
Q

Describe the transmission of bubonic plague.

A

Bubonic plague: rat flea to mammals
– Flea acquires Y. pests after blood meal

– Y. pestis multiplies, obstructs foregut

– Obstructed flea attempts to feed, regurgitates 24,000 organisms on bite site –SLOPPY FLEA!

    • Organisms enter lymphatics, causes regional adenitis (“bubo”) in the mammal
  • -> Bubo= infected lymph node

– Transmission can also be via direct contact with infected tissues (i.e. a dead squirrel)

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5
Q

Describe the transmission of primary pneumonic plague.

A

Primary Pneumonic Plague: mammal to mammal
– Mammal to mammal transmission, usually rodents with incidental involvement of humans

– Bubonic plague leads to secondary pneumonia in index case

– Spread via respiratory droplets to cause primary pneumonia in a contact

– Cats are known to have pneumonic plague

–>Respiratory droplets from infected cats or humans with pneumonic plague → primary pneumonic plague

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6
Q

Describe the urban plague.

A

URBAN PLAGUE (domestic, murine– or affecting mice or related rodents)

– Epizootics (animal epidemics) among urban black rats and their fleas (Xenopsylla cheopis)

– Humans involved as rats die and their fleas seek new hosts

    • Initial case bubonic, then pneumonic
  • ->3 major epidemic (CE/ AD 546, 1346, 1894)
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7
Q

Describe the rural plague.

A

– Sporadic human cases related to travel or residence in rural areas

– Enzootic and epizootic pattern among wild rodents and their fleas

    • Distribution:
  • -> US cases- 10 cases/ year in southwestern US

–> India, South America, South Africa, Southern Russia

– Mode of acquisition worldwide: rats

– Mode of acquisition in US
1. FLEA BITE
2. HAND CONTACT with infected mammal
—->Infected squirrel, weasel, skunk, woodrat, cats
• Infected by fleas or
• Consume infected rodents

  1. Contact with DOMESTIC PETS
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8
Q

How do you prevent Y. pests spread?

A

Prevention
– Flea control programs in enzootic areas frequented by humans

– Avoid ill rodents

– Inactivated vaccine

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9
Q

What is the pathogenesis/ virulence factors of Y. pests?

A

Extracellular pathogen

    • F1 antigen: antiphagocytic capsule required for virulence
  • -> Anti-phagocytic properties present at 37 degrees Celsius (mammalian temperature) but not at 28 degrees Celsius (flea temperature)

– V and W antigens: needed for survival within macrophages

Intracellular pathogen
– Persistence within mammalian monocyte

Toxins

    • Classical LPS endotoxin
    • Exotoxin
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10
Q

What are the clinical features of bubonic plague?

A

Bubonic plague (flea bite): chills, fever, malaise, and painful lymphadenopathy

– 2-6 day incubation period

– Progression: Lymph node (bubonic plague) –> large regional lymph node ulcerates –> bacteria can invade the bloodstream (septicemic plague – bacteremia) –> lung (secondary pneumonic plague)

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11
Q

What are the clinical features of pneumonic plague?

A

Pneumonic plague (primary and secondary): fever, cough, SOB

– Hallmark: copious amounts of bloody sputum

– Fatal- eventually progressing for 2-4 days into respiratory failure and shock

– Rapidly developing pneumonia

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12
Q

What are the clinical features of septicemic plague?

A

Septicemic plague (flea bite): non bubo, widespread dissemination via blood → DIC

DIC
– Abdominal pain, shock, and bleeding into skin and other organs

– Tissue necrosis due to DIC

– Septicemic plague is a progression from untreated bubonic or rarely primary pneumonic plague

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13
Q

What are the potential complications of a Y. pestis infection?

A

– Disseminated intravascular coagulation (DIC): skin hemorrhages (“black death”)

– Plague meningitis

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14
Q

What are the diagnostic tests for Y. pests?

A
  1. Confirmed by fluorescent antibody (FA microscopy) test against the F1 antigen (capsule)

–> from buboes, sputum, or blood sample

  1. Serology: 4x rise in antibody (passive hemagglutination) to F1 capsule is diagnostic
  2. Blood culture:
    - -> Usually positive
    - -> Many have a very high number of organisms (>10^6 and visible on peripheral smear)
    - -> Safety pin appearance with bipolar Wayson, Giemsa, or Wright stain.
  3. Isolation of Yersinia pests
    - ->dangerous
    - -> pleomorphic gram negative rod
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15
Q

What is the treatment for Yersinia pestis?

A

– 10 days of tetracycline, streptomycin, chloramphenicol, or sulfa drugs

    • Chemoprophylaxis of persons with close contact
  • -> due to high level of mortality
  • -> due to ease of transmission
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16
Q

How does one gain immunity to Yersinia pests?

A

– Antibody that develops is protective

    • Inactivated vaccine that protects against bubonic plague; used by US troops in Vietnam
  • -> Plague vaccine is no longer available in the US
17
Q

What is the mortality rate for Yersinia pests?

A

Mortality
– 60-90% untreated

– 15% with treatment

– 5% with early antibiotics

– US mortality 15% overall

18
Q

Name the members of Enterobactericeae that are glucose fermenters, non-lactose fermenters.

A
  • -Salmonella
  • -Proteus species
  • -Shigella
  • -Yersinia pestis

E. coli is a glucose fermenter and a lactose fermenter

19
Q

What is the ICD of Franciscella tularensis?

A

ICD 5-10 organisms

20
Q

Describe the bacteriology of Franciscella tularensis.

A

– Small unencpasulated pleomorphic gram negative

    • Fastidious aerobic slow grower
  • -> Requires cysteine and glucose on blood agar for growth (or thioglycollate)

–>Also grows on chocolate agar

    • LOVES TO GROW IN LOW TEMPERATURES
  • -> Cold tolerant- survives in water for up to 90 days

–> Survives for weeks at low temperatures in the environment (water soil, or animal carcasses)

– A category A priority agent (NIH)

– Zoonotic disease among rodents and rabbits

21
Q

Describe the general epidemiology of Franciscella tularensis.

A

– Zoonotic disease transmitted from infected animals or arthropods to humans

–> Usually not spread from person to person

– Narrow geographical distribution 30-70 degrees North

–>Widespread distribution in northern hemisphere in 100 wild mammals, 9 domestic animals, birds, insects, and water

22
Q

What are the routes of human infection for Franciscella tularensis?

A

Rabbit: hand contact or ingestion partly cooked meat
–Winter disease in eastern US

Arthopod-borne: ticks (Dermacentor variabilis), deer flies (Chrysops discalis), and others
–Summer disease in the western US

Other:
– handling infected tissues (muskrat trappers in Vermont)

–animal bite (cat)

–Ingestion of contaminated food, water, or soil

–Inhalation of infective aerosols from animals with tularemia pneumonia

  • -laboratory aerosol (dangerous to handle in regular lab)
  • ->Shaking dog aerosol (infected wet dog aerosolized Tularemia by shaking itself dry inside a cottage in Martha’s Vineyard in 1978)
23
Q

How do you prevent the spread of Franciscella tularensis?

A

– Ticks: check ticks frequently in endemic areas, remove by mouth parts

– Rabbits, muskrats: protective gloves when dressing animals

– Vaccine (live attenuated): for lab workers, trappers at risk—research in progress, NOT YET LISCENCED

24
Q

What is the pathogenesis of Franciscella tularensis?

A
    • Inoculation (skin or lung)
  • ->Tick bite: organisms injected directly while feeding or bite wound contaminated by feces

– Organisms cause skin lesions,

– Enter lymphatics

– Produce local lymphadenopathy

– Then bacteremia with granuloma formation in the reticuloendothelial system (spleen, liver)

– Intracellular survival in monocytes

– Endotoxin plays role in initial systemic symptoms

25
Q

What are the clinical features of Franciscella tularensis?

A

– 3-5 day incubation period

– Abrupt onset of fever, chills, malaise

– Specific syndromes:

  1. Ulceroglandular
    - Most common
    - Skin ulcer and painful adenopathy (inguinal, axillary)
    - -> similar to bubonic plague clinical presentation

-Can progress to typhoidal pneumonia if untreated

  1. Typhoidal pneumonia (bacteremia)
    - can progress to Tularemia pneumonia if untreated
  2. Tularemia pneumonia (secondary) – primary pneumonia uncommon (from aerosols of animal with tularemia pneumonia)
26
Q

What are the possible complications of Franciscella tularensis?

A

Pneumonia in 10-15%

27
Q

What is the mortality of Franciscella tularensis infection with treatment?

A

Mortality

28
Q

How do you diagnose Fransciscella tularensis?

A
  • Difficult and dangerous to culture; laboratory accidents
  • ->Dangerous (aerosol)

-Fluorescent antibody staining of node biopsy

  • Serologic: 4x titer rose or single titer greater than/ equal to 1:160 in 50-70% at two weeks
  • ->BUT cross-reacts with brucella
29
Q

What is the treatment for Franciscella tularensis?

A
  • Streptomycin [bacteriocidal] for 7-10 days
  • Alternative: tetracycine 14 days
  • Chloramphenicol also used
  • Ciprofloxacin may be effective
30
Q

What is the post exposure prophylaxis for Franciscella tularensis infection?

A

Doxycycline and ciprofloxacin

31
Q

What causes relapse of Franciscella tularensis infections?

A

Relapses occur from intracellular persistence

M1 S3 (6 decks)

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