Micro Post Q3 Flashcards
(31 cards)
Describe the bacteriology & morphology of Yersinia pestis
–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
What is the ICD of Yersinia pestis?
1-10 organisms
What are the characteristics of member of Enterobactericeae?
- 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
Describe the transmission of bubonic plague.
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)
Describe the transmission of primary pneumonic plague.
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
Describe the urban plague.
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)
Describe the rural plague.
– 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
- Contact with DOMESTIC PETS
How do you prevent Y. pests spread?
Prevention
– Flea control programs in enzootic areas frequented by humans
– Avoid ill rodents
– Inactivated vaccine
What is the pathogenesis/ virulence factors of Y. pests?
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
What are the clinical features of bubonic plague?
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)
What are the clinical features of pneumonic plague?
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
What are the clinical features of septicemic plague?
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
What are the potential complications of a Y. pestis infection?
– Disseminated intravascular coagulation (DIC): skin hemorrhages (“black death”)
– Plague meningitis
What are the diagnostic tests for Y. pests?
- Confirmed by fluorescent antibody (FA microscopy) test against the F1 antigen (capsule)
–> from buboes, sputum, or blood sample
- Serology: 4x rise in antibody (passive hemagglutination) to F1 capsule is diagnostic
- 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. - Isolation of Yersinia pests
- ->dangerous
- -> pleomorphic gram negative rod
What is the treatment for Yersinia pestis?
– 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
How does one gain immunity to Yersinia pests?
– 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
What is the mortality rate for Yersinia pests?
Mortality
– 60-90% untreated
– 15% with treatment
– 5% with early antibiotics
– US mortality 15% overall
Name the members of Enterobactericeae that are glucose fermenters, non-lactose fermenters.
- -Salmonella
- -Proteus species
- -Shigella
- -Yersinia pestis
E. coli is a glucose fermenter and a lactose fermenter
What is the ICD of Franciscella tularensis?
ICD 5-10 organisms
Describe the bacteriology of Franciscella tularensis.
– 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
Describe the general epidemiology of Franciscella tularensis.
– 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
What are the routes of human infection for Franciscella tularensis?
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)
How do you prevent the spread of Franciscella tularensis?
– 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
What is the pathogenesis of Franciscella tularensis?
- 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
