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micro 8 > Zoonoses -Bac Inf 1 > Flashcards

Zoonoses -Bac Inf 1 Flashcards

1
Q

Zoonotic Diseases definition

A

diseases spread to man through contact with animals or which have animal reservoirs.

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2
Q

anthrax -organism, vector, reservoir?

A
  • bacillus anthracis
  • no vector
  • cattle sheep goats
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3
Q

brucellosis-organism, vector, reservoir?

A
  • brucella abortus; B melitensis; B suis
  • no vector
  • cattle sheep goats
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4
Q

pasteurellosis- organism, vector, reservoir?

A
  • pasteurella multocida
  • no vector
  • cats dogs
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5
Q

melioidosis- organism, vector, reservoir?

A
  • burkholderia pseudomallei
  • no vector
  • probably has reservoir but dont know which animal
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6
Q

leptospirosis- organism, vector, reservoir?

A
  • leptospira interrogans
  • no vector
  • rodents, small mammals
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7
Q

tularemia- organism, vector, reservoir?

A
  • francisella tularensis
  • vectors: ticks, deerflies
  • rabbits, hares
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8
Q

plague- organism, vector, reservoir?

A
  • yersinia pestis
  • vector: fleas
  • rodents, prarie dogs
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9
Q

lyme disease- organism, vector, reservoir?

A
  • borrelia burgdorferi
  • vector: ticks
  • mice, deer
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10
Q

relapsing fever-organism, vector, reservoir?

A
  • borrelia recurrentis
  • lice
  • no reservoir animal
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11
Q

Bacillus anthracis - causes and organism info

A
  • anthrax durp
  • large, aerobic, spore forming, gram positive rod, long chains, pairs or as single cells
  • Gram-stained organisms (from culture media) have squared ends, = “boxcar” appearance
  • spores can be observed in culture and in soil, and can remain viable for decades: not generally observed in clinical samples
  • non-motile
  • grow quite readily on conventional laboratory culture media (blood agar plates)
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12
Q

Bacillus anthracis - pathogeneisis

A
  • protein capsule: poly-D-glutamic acid; not produced in culture; antiphagocytic (NOT PEPTIDOGLYCAN)
  • toxin (s): three protein subunits which combine to form two different toxins ; responsible for much of the pathology associated with disease
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13
Q

Anthrax toxins:

A
  • Lethal factor (LF)
  • Protective antigen (PA)
  • edema factor (EF)
  • lethal toxin = Lethal factor + Protective antigen===> tissue damage and shock
  • edema toxin = Protective antigen + Edema factor===> edema
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14
Q

Bacillus anthracis - how do you get infected?

A
  • spores can be inoculation, ingestion, or inhalation
  • contact with infected animals or animal products
  • spores may be present in contaminated soil, or animal furs, hides, wool or skin
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15
Q

Bacillus anthracis - disease process

A
  • spores germinate, producing vegetative cells which produce toxin
  • PA binds to cellular receptors on numerous tissues and cell types
  • PA is cleaved by cellular enzymes to an active form and forms a multimeric complex on the cell surface
  • LF and / or EF bind to this complex and are internalized by the cell
  • LF disrupts normal cellular signaling events leading to cell death, inflammation, and tissue damage.
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16
Q

What is edema factor?

A
  • Bacillus anthracis toxin
  • adenylate cyclase that increases intracellular cAMP levels, disrupting cellular ion/H2O transport, thereby causing edema.
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17
Q

Bacillus anthracis - vectors?

A

cattle, sheep, goats, horses –> animals become infected while grazing in contaminated pastures

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18
Q

Bacillus anthracis - most commonly aqcuired…

A
  • most human cases acquired through the inoculation of spores: direct inoculation or contamination of existing open wounds
  • inhalation is the principal route of transmission favored for the use of anthrax as a biological weapon
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19
Q

Bacillus anthracis - rare to acquire via…

A

infection by ingestion of contaminated meat is a rare route of acquisition

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20
Q

Bacillus anthracis - inoculation with spores=

A

cutaneous anthrax

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21
Q

Bacillus anthracis - ingestion of spores =

A

gastrointestinal anthrax

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22
Q

Bacillus anthracis - inhalation of spores =

A

inhalation anthrax

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23
Q

Cutaneous Anthrax - presentation:

A
  • Small red papule, then vesicle, then necrotic ulcer (eschar) with black center
  • Described as painless
  • May be accompanied by lymph node swelling
  • Lesions may resolve over a period of several weeks
  • MOST CASES HERE
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24
Q

Gastrointestinal Anthrax - presentation:

A
  • Upper GI involvement includes oropharyngeal ulcerations (tongue, tonsils, esophageus) with cervical adenopathy and fever
  • Intestinal involvement includes abdominal pain, nausea, fever, bloody vomit, bloody diarrhea
  • May progress to sepsis
  • Case-fatality rates as high as 100 %
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25
Q

Inhalation Anthrax

A
  • Initially presents as non-productive cough, shortness or breath, myalgia, fatigue, and fever
  • Followed by increasing fever, drenching sweats, extreme dyspnea, cyanosis, lymphadenopathy, shock, and in most cases death.
  • Mortality rate is 45 to 75% even with treatment
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26
Q

Anthrax Diagnosis

A
  • Clinical signs
  • History of exposure
  • Gram-stain of clinical samples (wound exudate, lymph node material, pleural fluid, blood)
  • Large numbers of organisms typically present
  • Culture
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27
Q

Anthrax - treatment/prevention

A
  • antibiotic treatment: Penicillin & Ciprofloxacin (start cipro until youre sure its not a penicillin resistant strain)
  • vaccination: Effective in animals; Limited use in humans (military, lab workers, veterinarians)
  • dispose of infected animals
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28
Q

Brucella sp - disease name and orgnaism details:

A
  • brucellosis
  • small, slow-growing, aerobic, gram-negative coccobacillus.
  • difficult to grow in culture–require specialized media –> INTRACELLULAR PATHOGEN (inside monocytes and macrophages)
  • organism is hidden from humoral ijmmune system
  • spreads throughout bod via monoytes/macrophages
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29
Q

B. abortus vector?

A

cattle

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30
Q

B. melitensis vector?

A

goats and sheep

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31
Q

B. suis vector?

A

pigs

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32
Q

CMI (IFN-gamma) essential to resolution of which disease?

A

Brucellosis – Brucella sp. - these suckers live inside monocytes and macrophages— need inf gamma to piss off the macrophages to activate them

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33
Q

Brucella sp. -brucella abortus; B melitensis; B suis- endotoxin

A

the composition of the O-antigen (polysaccharides) of Brucella LPS can vary greatly, and appears to affect virulence.

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34
Q

Brucella sp - brucella abortus; B melitensis; B suis.- human infection how?

A

-initiated through direct contact with animal secretions
-through the conjunctiva or small skin lesions
consumption of contaminated foods – unpasteurized milk / dairy
-inhalation of infectious aerosols
-typically an occupational disease in slaughter house workers, butchers, veterinarians, farmers and ranchers

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35
Q

Brucella sp - brucella abortus; B melitensis; B suis- where in the world most common?

A

Mediterranean, Latin America, Middle East

ESP UNPASTURIZED DAIRY PRODUCTS

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36
Q

Brucella sp.- brucella abortus; B melitensis; B suis- disease progression

A
  • Initially non-specific symptoms
  • Fever, chills, night sweats, myalgia, arthralgia, cough
  • Fever may be intermittent – “undulant fever”
  • Advanced disease
  • GI symptoms (nausea, vomiting, diarrhea)
  • Bone and joint infections
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37
Q

Brucella sp - brucella abortus; B melitensis; B suis - dianosis

A
  • Culture blood, bone-marrow, and organ biopsy samples
  • Growth may take several days or several weeks to appear
  • Serological and molecular techniques
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38
Q

Brucella sp - brucella abortus; B melitensis; B suis- treatment/prevention

A

-Treatment: Doxycycline
-Prevention:
limit occupational exposure
pasteurization of dairy products
vaccination of animals

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39
Q

Pasteurella multocida causes waht disease and organism details

A

-Pasteurellosis
-gram-negative, facultatively anaerobic coccobacilli
-related to the genus Haemophilus
-commensals or normal flora in the nasopharynx of many animals (including dogs and cats)
grows well on the both blood and chocolate agar
-possess LPS and is encapsulated

40
Q

most common agent of human disease?

A

p multocida

41
Q

Pasteurella multocida - human infection?

A

bite/scratch of cat or dog

42
Q

Pasteurella multocida - disease progression

A
  • wound begins to redden and swell
  • becomes painful
  • cellulitis and abscess formation may occur
  • may be accompanied lymphadenopathy
  • possible spread to tendons, joints, and bones if untreated
43
Q

Pasteurella multocida - diagnosis/treatment

A 
-Diagnosis:
clinical signs
history of exposure
cultivation and biochemical testing
-Treatment: Penicillin
44
Q

Burkholderia pseudomallei - causes waht disease and organism details

A

-meliodosis
-motile, gram-negative rod –> has LPS
(related to Pseudomonas )
-normally found as a saprophyte in surface waters and soil
-polysaccharide capsule
-lethal toxin and degradative enzymes
-type III secretion system
-intracellular pathogen(?)

45
Q

Burkholderia pseudomallei - msot common where in the world?

A

southeast asia and australia

46
Q

Burkholderia pseudomallei - human infection

A
  • small wounds or abrasions are contaminated with soil or water containing the organisms
  • zoonotic nature of infection has been brought into question due to the lack of evidence supporting direct transmission from animals to humans
  • need to be in regular contact with soil and water
47
Q

Burkholderia pseudomallei - disease progression

A

-most exposed individuals are thought to remain asymptomatic
-may develop following several days incubation, or may remain latent for months / years
-initial cutaneous disease =single or multiple tender nodules or abscess accompanied by lymphadenopathy, fever and malaise
may resolve spontaneously or the infection may become systemic
-pulmonary disease may vary in severity from bronchitis to necrotizing pneumonia accompanied with high fever, dyspnea, and cough with sputum.

48
Q

Burkholderia pseudomallei - diagnosis/treatment/prevention

A
  • Laboratory identification is dangerous - call someone who knows what theyre doing
  • Clinical signs, history of travel to endemic areas
  • Treatment and Prevention: long term treatment with high doses of antibiotics
49
Q

Leptospira interrogans - causes waht disease and organism details

A
  • leptospirosis
  • thin, motile, gram-negative, spiral shaped bacteria with terminal “hooks”
  • grow slowly in culture with optimal growth occurring between 28O-30O C.
  • poorly staining, require specialized techniques of microscopy to view (dark-field microscopy)
50
Q

Leptospira interrogans - disease progression

A
  • can invade abraded skin as well as intact mucus membranes - contact with water that has animal urine
  • enter the bloodstream and disseminate
  • mechanism of bacterial virulence are poorly understood
  • most infections thought to present as self-limited, nonspecific febrile illnesses
51
Q

Leptospira interrogans - is found where in the world most often?

A

hawaiian isalnds - exposure to water with animal urine!

52
Q

Leptospira interrogans - human infection

A
  • develops following the aquisition of bacteria from water contaminated by animal urine
  • most infections result from recreational (swimmers) or occupational exposure (veterinarians)
53
Q

Leptospira interrogans - first stage of disease progression

A
  • febrile influenza-like illness
  • organism may be detected in blood, urine, and CSF
  • symptoms last for ~1 week
  • followed by resolution or progression to second phase
54
Q

Leptospira interrogans - secondstage of disease progression

A
  • patient may present with meningitis, inflammation of the eye, jaundice, renal failure, and petechial rash
  • may progressive to respiratory, hepatic, and / or circulatory failure
  • mortality of 5 to 40% have been reported
55
Q

Leptospira interrogans - diagnosis/treatment/prevention

A

-Diagnosis
thorough history including occupational and recreational activities and potential animal contacts
cultivation and biochemical testing is difficult
serology is generally employed to confirm infection
-Treatment: Penicillin and Ampicillin
-Prevention: Limiting exposure to animal urine

56
Q

Francisella tularensis- causes waht disease and organism details

A
  • tularemia
  • is a small, slow-growing, aerobic, Gram-negative coccobacillus
  • difficult to grown in culture.–> intracellular pathogen of monocytes and macrophages
  • intracellular pathogen
  • ->prevents phagosome-lysosome fusion and acidification
  • -> CMI: macrophage activation is crucial to the resolution of infection
  • Encapsulated
  • ->pathogenicity is strongly associated with capsule production: antiphagocytic properties; protects the bacteria from lysis by the complement system
  • possess LPS
57
Q

Francisella tularensis-human infection

A
  • Acquired through contact with infected blood or tissue
  • Inhalation of infected blood aerosol (skinning of animals)
  • Ingestion of contaminated meat
58
Q

Francisella tularensis- disease progression

A
  • initial symptoms of fever, chills, headache arthralgias, and lassitude
  • Ulceroglandular tularemia
  • Oculoglandular tularemia
  • Pneumonic tularemia
59
Q

Francisella tularensis-is found where in the world most often? time of year? reservoir?

A
  • Primarily a disease of the Northern Hemisphere
  • United States: Oklahoma, Missouri, Arkansas
  • Summer infection=tick season
  • Fall / Winter=small game season
  • hares and rabbits
60
Q

Francisella tularensis-vector?

A

hard shelled ticks - less likely for humans to get this way… usually need to be directly in contact with animal - skinning rabbits… etc

61
Q

Francisella tularensis-Diagnosis

A
  • History or exposure and clinical suspicion
  • Serology and molecular techniques
  • Cultivation is slow and difficult
62
Q

Francisella tularensis-treatment/prevention

A

-Treatment: Gentamicin
-Prevention:
prevent tick bites
hunter education
take precautions when skinning animals

63
Q

Ulceroglandular tularemia

A
  • caused by Francisella tularensis
  • Develops following direct inoculation or tick bite
  • red, painful swollen papule
  • becomes purulent and ulcerates
  • regional lymph nodes swelling
  • Lymph nodes may suppurate (fill with pus) and may even ulcerate.
  • Patient may become bacteremic
64
Q

Oculoglandular tularemia

A

-caused by Francisella tularensis
-Develops following ocular inoculation
painful conjunctivitis with swollen cervical lymph nodes develops

65
Q

Pneumonic tularemia

A
  • caused by Francisella tularensis
  • develops following the inhalation of an infectious aerosol
  • pneumonitis (lung inflammation) and eventually sepsis
  • high rate of morbidity and mortality unless promptly recognized and treated
66
Q

Yersinia pestis- causes what disease and organism details?

A
  • plague (same frmo back in the days = black death in europe)
  • a non-motile, gram-negative rod (Enterobacteriaceae)
  • proteinaceous capsule
  • grows well on most conventional laboratory media
  • histological stains (Giemsa) reveal a rod shaped organism with a characteristic bipolar staining, giving the appearance of a “closed safety pin”
67
Q

Yersinia pestis- pathogenesis

A
  • Capsule
  • LPS
  • Three plasmids associated with virulence
    1) encode proteins which facilitate the regurgitation of bacteria by fleas
    2) enhance bacterial survival in macrophages
    3) allow the organism to resist complement mediated lysis
68
Q

Yersinia pestis- most common part of the world?

A

Africa

-more cases reported now in: New Mexico, Arizona, California, Colorado, Nevada, and Wyoming

69
Q

Yersinia pestis- transmission

A

-the natural cycle of disease is in rodent and fleas
-human infection is accidental / incidental
the bite of infected fleas
-bites and scratches of cats that have killed infected rodents
-inhalation of aerosol during the skinning and cleaning of infected rodents
-human to human transmission (pneumonic plague) is possible

70
Q

Bubonic plague - presentation

A
  • Yersinia pestis
  • initial symptoms of fever, chills, headache, myalgias
  • painful lymphadenopathy develops proximal to the portal of entry – “buboes”
  • surrounding area become swollen and inflamed
  • overlying skin may become stretched and desquamate.
  • if untreated, buboes may perforate leading to bacteremia and septic shock
  • 50% mortality
71
Q

Pneumonic plague -presentation

A
  • Yersinia pestis
  • inhalation of respiratory droplets from a person or animal
  • may develop in individuals secondary to bubonic plague
  • primary pneumonic plaque
  • initial signs include fever, headache, myalgias, and respiratory signs (cough, sputum production, chest pains, labored breathing)
  • progresses rapidly (2-3 days) to symptoms of hemoptysis, increasing respiratory distress, cardiopulmonary insufficiency, cyanosis, and circulatory collapse
  • secondary pneumonic plague develops somewhat more slowly
  • bacteria can be readily observed in sputum samples
  • 100% mortality
72
Q

Yersinia pestis- diagnosis/treatment

A 
-Diagnosis:
Call the CDC ! Typically requires the intervention of state or federal labs due to infectivity
-travel history!
Symptoms and exposure history
-Treatment: Streptomycin
73
Q

“closed safety pin appearnace?

A

Yersinia pestis- plague

74
Q

Borrelia burgdorferi - causes what disease and organism details

A
  • Lyme Disease
  • gram neg spirochete
  • microaetophilic
  • difficult to culture
75
Q

Borrelia burgdorferi- Major reservoir, vectors and peak months?

A
  • white-footed mouse and white-tailed deer
  • TICK VECTOR
  • early stage seen msot often in summer motnhs
76
Q

Borrelia burgdorferi- disease progression

A

-Early stage 1 (localized infection) – one or more skin lesions at the site of bite
Lesion starts as small macule or papule, then enlarges (bull’s eye rash; erythema migrans)
-Early stage 2 (disseminated infection) – ~3-5 weeks after the tick bite, the bacteria disseminate via the bloodstream
Systemic symptoms – including arthralgia, myalgia, cardiac dysfunction and neurologic signs
-Late infection, stage 3 (persistent infection) – develops months to years after the initial infection –> Arthritis (one or more joints with knee most often affected), skin discoloration and swelling, neurologic complaints (numbness, memory loss)

77
Q

Borrelia burgdorferi- diagnosis

A
  • Symptoms, physical findings and history of exposure

- Serology of limited use in endemic areas

78
Q

Borrelia burgdorferi- treatment/prevention

A
  • For early symptoms – doxycycline, amoxicillin or cefuroxime
  • For lyme arthritis – ceftriaxone, doxycycline or amoxicillin
  • Prevention by limiting exposure to ticks
79
Q

Leading vector-borne disease in the US ? second most?

A

Borrelia burgdorferi- - lyme disease

rocky mountain fever

80
Q

major vector in northeast and midwest for lyme disease

A

Ixodes scapularis

81
Q

major vector on west coast for lyme disease

A

Ixodes pacificus

82
Q

bulls eye rash - organism is?

A

borrelia burgdorferi- lyme disease - bitten by an infected tick!

83
Q

bluish-red skin lesions associated with

A

late, disseminated lyme disease - borellia burgdorferi

84
Q

Borrelia recurrentis- causes what? organism info?

A

-relapsing fever
-poorly staining gram-negative spirochetes
difficult to grow in culture
-Borrelia recurrentis is the agent responsible for louse borne (epidemic) relapsing fever
-many other species can cause tick borne (endemic) relapsing fever

85
Q

Borrelia recurrentis- how to get infection? pathogenesis?

A
  • acquired through the bite of an arthropod vector
  • enters the circulation and disseminates to multiple organs
  • evades immunological defenses through antigenic variation: single bacterium can express ~ 3 dozen unique variable major proteins on its surface; humoral immune system always trying to catch up
  • results in a succession of febrile and afebrile cycles (relapsing fever)
  • probably a response to the changing amount of organisms( and LPS) in the blood stream
86
Q

Borrelia recurrentis- disease presentation

A
  • symptoms of chills, fever, headache, muscle aches
  • splenomegaly and hepatomegaly may develop
  • symptoms last from 3 to 7 days, then resolve and return after another week
  • several episodes of relapse may occur before resolution
  • mortality rates of 5 to 40% have been reported
87
Q

Borrelia recurrentis- Diagnosis

A
  • organism may be observed in Giemsa stained blood smear
  • cultivation requires specialized media
  • serological and molecular techniques are frequently used to confirm diagnosis
88
Q

Borrelia recurrentis- treatment & prevention

A
  • treated is with tetracycline or erythromycin.

- Prevent disease by limiting exposure to the arthropod vectors

89
Q

epidemic relapsing fever caused by? vecotr? reservoir? where is this prevalent

A
  • Borrelia recurrentis - BODY LOUSE VECTOR - HUMAN RESERVOIR AND HUMAN TO HUMAN TRANSFER (NOT A ZOONOTIC DISEASE)
  • issue in north africa
90
Q

Endemic relapsing fever - caused by? vector? reservoir? where is this prevalent?

A

many other species of borellia sp. - SOFT SHELLED TICK VECOTR - rodent, and soft shell tick reservoir
-worldwide issue
endemic = always maintained at low level in geographical area

91
Q

box car appearance

A

bacillus anthracis

92
Q

scratched by a cat or bitten by some animal - organism is?

A

pasterurella multocida or highly uncommon but possible yersenia pestis

93
Q

contact with water - potential organisms?

A

leptospira interrogans and Burkholderia pseudomallei

94
Q

spiral shaped bacteria with terminal hooks - organism?

A

leptospira interrogans

95
Q

antigenic variance to avoid immune detection?

A

borellia recurrentis!

micro 8 (6 decks)

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