Zoonoses I Flashcards
pathogens shared with animals count for what percentage of infections in human
greater than 60%
zoonoses pathogen classes
helminths: taenia solium
protozoa: toxoplasma gondii
bacterial: campylobacter jejuni
virus: influenza
prions: BSE and v CJD
how does a zoonosis become an epidemic
interaction between pathogen, vector, host
the worst route of transmission of zoonoses and why it is such a problem
inhalation because pulmonary symptoms tend to be the deadliest
causative agent of anthrax and characteristics of this agent
bacillus anthracis
large, box-car, gram negative rod, aerobic and spore forming
is person to person transmission common in anthrax
no
virulence factor of anthrax
toxins and its polypeptide capsule (poly-D-glutamic acid)
toxins in anthrax
three proteins on large plasmid pXO1: lethal factor (LF), edema factor (EF), and protective antigen (PA) make up the toxins
PA + EF = edema toxin
PA + LF = lethal toxin
what is so significant about the capsule of anthrax
it is an amino acid capsule made from three genes (CapA, CapB, CapC) from plasmid pXO2 - only one serotype
function of the virulence factors of anthrax
- capsule - inhibits phagocytosis of replicating cells
- edema toxin - cAMP allows accumulation of fluid in tissue
- lethal toxin - stimulates macs to release TNFalpha, IL-1B and other inflammatory toxins
- both toxins inhibit host innate immunity
what is the pathogenesis of cutaneous anthrax
begins at primary site of infection as papule then progresses through vesicular stage to a depressed black necrotic ulcer called eschar
without antibiotics there is an increased chance from 1% to 20% chance of death
clinical manifestation of anthrax
cutaneous - least life threatening
septicemic - higher mortality
pulmonary - highest mortality –> “wool sorter disease”
clinical manifestation of inhalation anthrax
flu like symptoms so myalgia, fatigue, fever but then they get dyspnea and hypoxia
half of people get meningitis
diagnosis of anthrax
culture or biopsy then do PCR
agent that causes brucellosis and its characteristics
brucella
gram neg non motile short rod that is facultatively intracellular hence requires complex artificial media in vitro
4 types of brucella found in human and animals they are found in
b. melitensis - goats, sheep, camel
b. abortus - cattle
b. suis - pig
b. canis - dog
reservoir of brucella and its transmission to humans
animals make milk, their urine, feces
drinking the milk, access through skin breaks, mucosal membrane, aerosols, splashes
organism is killed by pasteurization
pathogenesis of brucella
- once skin or mucosal membrane is penetrated it is carried to lymphatics by PMNs
- cells multiply within mac by inhibiting phagosome lysosome fusion
- humoral response ineffective since hidden inside macs
- T cell response required but if it fails it multiplies within RES
- waves of bacteria from these sites are released –> recurrent infections
symptoms in acute infection with brucellosis
- brucella melitensis is most severe
- brucella suis causes abscess formation
- sweating, high fever, swinging fever, headaches, scrotal pain
- lymphadenopathy and splenomegaly
symptoms in chronic infection with brucellosis
night fever, sacro ileitis, weight loss, depression
how do you diagnose brucellosis
blood culture which show brucella melitensis most of the time
epidemiology of leptospirosis
- leptospira interrogans is most common
- shed in rat urine/rodent urine
characteristics of leptospira interrogans
tight spiral
sensitive to heat, drying, and most chemicals
enters host by penetrating skin or mucous membrane
disease that one can acquire from leptospira interrogans and its description
weils disease and it is leptospira multiplying and damaging endothelium of small blood vessels
where can leptospira be isolated
blood and CSF then later on in disease it can be isolated in urine
clinical feature of leptospirosis
conjunctival congestion, viral like meningitis, icteric symptoms, and pulmonary ARDS
how is leptospirosis diagnosed
increased PMNs, liver enzymes rise, viral pattern of meningitis, decreased platelets,
serology and PCR
pathogen in tularemia aka rabbit fever and its characteristics
francisella tularensis
gram neg short rods that is nutritionally fastidious because it is facultative
agar used for tularemia
cysteine glucose blood agar
pathogens that use thayer martin
both tularemia and neisseria gonorrhea
animals and vectors associated with tularemia
rabbits and ticks
clinical manifestations of tularemia
ulcero-glandular (from injection - lowest mortality)
typhoidal (from ingestion - higher mortality)
pneumonia (from inhalation - highest mortality)
what should be seen on serodiagnosis of tularemia
1:40 to 1:320 in 1 to 2 weeks
treatment of tularemia
aminoglycoside
