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MSII Microbiology > Unit 2 - Zoonoses > Flashcards

Unit 2 - Zoonoses Flashcards

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1
Q

what is the definition of a zoonotic disease?

A

contagious disease passed from an animal to a human

-human population is not part of life cycle (accidental insertion that is often dead end host)

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2
Q

what is the etiologic classification of zoonoses?

A
  1. viral
  2. bacterial
  3. parasitic
  4. mycotic
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3
Q

what are the routes of transmission of zoonotic diseases?

A

vary

  • contact with saliva, blood, urine, or feces of infected animal
  • bite by a tick, mosquito, or fly (vector)
  • eating or drinking something unsafe
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4
Q

what are the vectors for:

  • Bacillus antrhacis
  • Francisella tularensis
  • Brucella species
  • Yersinia pestis
  • Bartonella henselae
A 
Bacillus anthracis - no vector (usually)
Francisella tularensis - ticks, mosquitos, deer flies
Brucella species - no vector
Yersinia pestis - fleas
Bartonella henselae - fleas, ticks
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5
Q

what is “anthrax”?

A

Bacillus anthracis (relatively large spore-forming G+ rod)

  • highly infectious and fatal disease of mammals and humans
  • occurs where animals have previously died of anthrax (spores remain viable for decades)
  • -any grazing animal progress from normal appearance to dead within hours (most are just found dead)
  • no vector
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6
Q

what are the types of anthrax one can get?

A
  1. cutaneous
  2. inhalational
  3. gastrointestinal
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7
Q

describe cutaneous bacillus anthracis?

A

small sore that develops into a blister

  • blister then develops into skin ulcer with black area in the center
  • usually significant edema (may go away, but eschar remains)
  • blister and ulcer don’t hurt
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8
Q

describe gastrointestinal anthrax?

A

nausa, loss of appetite, bloody diarrhea, fever + bad stomach pain

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9
Q

describe inhalation anthrax?

A
  • cold or flu symptoms
  • can include a sore throat, mild fever, and muscle aches
  • later, symptoms include cough, chest discomfort, SOB, tiredness, and muscle aches
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10
Q

what is treatment for anthrax?

A

Ciprofloxacin and doxycycline

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11
Q

explain what Francisella Tularemia is? the types?

A

aerobic G- rod transmitted by rabbits via ticks, horseflies, or mosquitoes

  • type A: more virulent (US and Canada)
  • type B: less virulent (Europe and Asia)
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12
Q

what are the organs you can get Francisella Tularemia?

A
  1. ulceroglandular
  2. glandular
  3. oculoglandular
  4. oropharyngeal
  5. pneumonic
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13
Q

what is ulceroglandular Grancisella Tularemia?

A

most common form

  • usually occurs following tick or deer fly bite, or after handling infected animal
  • skin ulcer appears at site where organism entered body
  • ulcer is accompanied by swelling of regional lymph glands, usually in armpit or groin
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14
Q

what is glandular Grancisella Tularemia?

A

similar to ulceroglandular tularemia, but without an ulcer

  • also generally acquired through bite of infected tick or deer fly, or by handling sick or dead animals
  • swelling of regional lymph glands, usually in armpit or groin
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15
Q

what is oculoglandular Grancisella Tularemia?

A

occurs when bacteria enter through eye

  • usually when a person is butchering an infected animal and touches his eyes
  • symptoms are irritation/inflammation of eye and swelling of lymph glands in front of the ear
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16
Q

what is oropharyngeal Grancisella Tularemia?

A

results from eating or drinking contaminated food or water

-may have sore throat, mouth ulcers, tonsilitis, swelling of lymph glands in neck

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17
Q

what is pneumonic Grancisella Tularemia?

A

breathing dust or aerosols containing organism

  • most serious form of tularemia
  • cough, chest pain, difficulty breathing
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18
Q

what is general information about Brucella?

A

usually transmitted to humans by contact with infected farm animals

  • no vector
  • many different species, and each one infects different hosts and has different serovars
  • not all are human pathogens
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19
Q

what is the biovar/serovar, natural host, and human pathogenicity of:

  • Brucella abortus
  • B. melitensis
  • B. suis
  • B. canis
  • B. ovis
  • B. neotomae
  • B. maris
A 
B. abortus - 1-6, 9; cattle; yes
B. melitensis - 1-3; goats, sheep; yes
B. suis:
-1,3; swine; yes
-2; hares; yes
-4; reindeer, caribou; yes
-5; rodents; yes
B. canis - none - dogs, other canines; yes
B. ovis - none; sheep; no
B. neotomae - none; desert wood rat; no
B. maris - unknown; marine mammals; unknown
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20
Q

what are signs of Brucella infection in cattle?

A
  • third trimester abortions (with B. abortus)
  • retained placenta (once expelled, will have leathery appearance)
  • endometritis
  • birth of dead or weak calves (respiratory distress and lung infections)
  • low milk yield
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21
Q

how is Brucella transmitted to humans?

A
  1. contact of conjunctiva or broken skin with infected tissues
    - blood, urine, vaginal discharge, aborted fetuses, placentas
  2. ingestion
    - raw milk and unpasteurized dairy products
    - rarely through undercooked meat
  3. inhalation of infections aerosols
    - pens, stables, slaughter houses
  4. person-to-person transmission is very rare

incubation varies from 5 days to 3 months

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22
Q

human Brucella disease

A
  • can affect any organ or organ system
  • cyclical fever in acute disease
  • variability in acute clinical signs
  • -headache, weakness, arthralgia, depression, weight loss, fatigue, liver dysfunction
  • chronic brucellosis is hard to define
  • -length, type of response to treatment variable
  • -localized infection
  • blood donations of infected persons shouldn’t be accepted
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23
Q

what are the organs that can be affected in human Brucella infection?

A
  1. osteoarticular complications (20-60%)
    - arthritis, spondylitis, osteomyelitis)
  2. hepatosplenomegaly (33%)
  3. GI complications (2-20%)
  4. GU involvement (6-8%)
    - orchitis and epididymitis most common
  5. neurological (3-5%)
    - depression, mental fatigue
  6. cardiovascular (1-3%)
    - endocarditis (most common cause of death)
24
Q

how do we diagnose humans with Brucella?

A
  • isolation of organism in culture (G- rod)
  • -blood, BM (highest yield), other tissues
  • serum agglutination test
  • -titer >1:160
  • -4x or greater rise in titer
  • immunofluorescence
  • -organism in clinical specimens
  • PCR
25
Q

treatment of human Brucella?

A
  1. doxycycline for 6 weeks (or longer) + Streptomycin for first 14-21 days
  2. doxycycline/gentamycin appears just as effective
26
Q

what is the prognosis for Brucella?

A
  • recovery is common
  • may last days, months, years
  • disability is often pronounced
  • about 5-8% of treated cases relapse
  • -failure to complete treatment regimen
  • -sequestered infection requiring surgical drainage
  • case-fatality rate <2% (untreated)
  • -endocarditis caused by B. melitensis
27
Q

explain what Yersinia pestis

A

G- rod that causes plague

-isolated from bubo aspirates, blood cultures, or sputum if pneumonic

28
Q

what is the clinical presentation of plague?

A
  • incubation period is 1-6 days
  • history is suggestive of exposure to rodents, rodent fleas, wild rabbits, sick/dead carnivores, or patients with pneumonic plague
  • can be bubonic, pneumonic, or septicemic
29
Q

explain what bubonic plague is

A

> 80% of patients

  • rapid onset of fever and painful, swollen, tender lymph nodes
  • usually inguinal, axillary, or cervical
30
Q

explain what pneumonic plague is

A

high fever, overwhelming pneumonia, cough, bloody sputum, chills
-easy to spread this

31
Q

explain what septicemic plague is

A

most dramatic presentation

-fever, prostation, hemorrhagic or thrombotic phenomena, progresses to acral gangrene

32
Q

what is treatment for plague?

A

parenteral antibiotic therapy with streptomycin is first-line therapy
-alternatively gentamycin or doxycycline (if limited to oral therapy)

33
Q

explain plague transmission

A

two types

  • sylvatic cycle: wild rodent or infective flea has direct contact with human to cause bubonic plague
  • urgan cycle: domestic rodent or infective flea have direct contact with human to cause bubonic plague
34
Q

explain Carrion’s disease transmission

A

Bartonella bacilliformis transmitted by sandfly vector, although reservoir is not fully known

35
Q

what does Carrion’s disease look like?

A
  1. primary infection: acute form (Oroya fever) or asymptomatic
  2. asymptomatic chronic bacteremia
  3. chronic form (verruga peruana)
36
Q

how does one get cat-scratch disease?

A

Bartonella henselae infect larvae, which lay eggs, which grow and infect kittens

  • kittens then bite or scratch humans <21 yo
  • kittens can also transmit to each other
  • -remains in kitten bloodstream for up to 1 year
37
Q

what are clinical manifestations of a normal immune system infected with cat scratch disease?

A
  1. fever; enlarged, tender lymph nodes that develop 1-2 weeks after exposure
  2. papule or pustule forms at inoculation site
  3. unusual manifestations such as granulomatous conjunctivitis, neuroretinitis, atypical pneumonia, or endocarditis may occur in small percentage of patients
38
Q

what are clinical manifestations of an immunocompromised person infected with cat scratch disease?

A 
Bacillary angiomatosis (caused by B. henselae or B. quintana) and peliosis hepatitis occur in people with HIV
-presents as skin, subcutaneous, or bone lesions (bacillary angiomatosis
39
Q

treatments for cat scratch disease if:

  • extensive adenopathy
  • bacillary angiomatosis)
  • endocarditis
A

extensive adenopathy: single dose of azithromycin

bacillary angiomatosis: erythromycin and doxycyclin

endocarditis: gentomycin and/or doxycycline

40
Q

what are pathogens associated with cat bites?

A
  1. Pasteurella multocida
  2. Bartonella henselae
  3. Fracisella tularensis
  4. Capnocytophaga canimorsus (main one in dogs)
41
Q

what are pathogens associated with dog bites?

A
  1. Capnocytophaga canimorsus

2. Pasteurella multocida (main one in cats)

42
Q

what is Pasteurella multocida?

A
  • commonly associated with cat bite infection (75%)
  • -25% dog bite
  • often clinical evidence of wound infection w/in a few hours of bite injury, scratch, or lick
43
Q

what is the clinical presentation of Pasteurella multocida?

A
  1. cellulitis or abscesses +/- bacteremia
  2. occasional cause of pneumonia and endocarditis
  3. metastatic seeding of internal organs from bacteremia
  4. meningitis (rare), most often in young children or elderly
44
Q

what can infection with Pasteurella multocida induce?

A

rapidly progressive infections similar to Group A Streptococcus or Vibrio
-patient may rpesent within a few hours of a cat bite with established severe infection

45
Q

how is diagnosis of Pasteurella multocida made? treatment?

A

diagnosis based on culture (wound swab, blood, body fluid)

treatment with amoxicillin/clavulanate, ampicillin/sulbactam, penicillin, ciprofloxacin, levofloxacin, doxycycline
-1st generation cephalosporins, cloxacillin, erythromycin, and clindamycin NOT effective

46
Q

what is Capnocytophaga canimorsus?

A

faculatively anaerobic G- rod part of normal oral flora of dogs and cats
-many patients have history of dog bite or scratch, less commonly in cats

47
Q

what is the clinical presentation of Capnocytophaga canimorsus?

A
  1. cellulitis
  2. bacteremia/sepsis
  3. meningitis and endocarditis (rare)
  4. if severe: shock, DIC, acral gangrene, disseminated purpura, renal failure, meningitis, pulmonary infiltrates
  5. fulminant sepsis following dog > cat bites, particularly in asplenic, alcoholic, or immunosuppressed
48
Q

treatment of capnocytophaga canimorsus if mild VS severe?

A

mild (dog or cat bites)

  • prefer Amoxicillin or clavulanate
  • alt Clindamycin, doxycycline

severe cellulitis/sepsis

  • prefer: Penicillin G or Clindamycin
  • alt: Ceftriaxone, ciprofloxacin, or meropenem
49
Q

how to prevent Capnocytophaga canimorsus in asplenic patients?

A

amoxicillin or clavulanate for 7-10 days

50
Q

explain the bacteriology of leptospira

A

L. interrogans is small, 0.25 uM diameter

  • invisible to light microscope
  • motile: paired axial flagella, corkscrew motion
  • reasonably sturdy to live outside host for weeks
  • pet and lifestock reservoirs, shed in urine
  • passed to humans by contact with contaminated water (world’s most common zoonosis)
  • endemic canine leptospirosis is becoming more common in US
51
Q

explain leptospirosis pathogenesis

A

bilious typhoid

  • from contaminated water (swimming) or food
  • enter abraded skin, mucous membranes, cross into lymphatics –> leptospirema
  • acute febrile illness followed by more mild, self-limiting symptoms or severe multiorgan involvement
  • normal incubation 5-14 days, but variable
52
Q

what is the normal course of leptospirosis?

A

anicteric

  • phase 1 (acute): leptospira circulate in blood and multiply in blood vessel endothelium
  • -vasculitis from leptospiral toxins releases blood into tissues and deprives target tissues of O2
  • -initial sepsis can kill susceptible hosts, but most clear it with opsonizing Ig
  • -spirochetes persist in privileged sites for weeks to months afterward
  • phase 2 (delayed, immune): new or continued growth of leptospira in organs cause more severe symptoms
  • -liver: jaundice
  • -kidneys: renal failure
  • -lungs: hemorrhage
  • -CNS: aseptic meningitis
  • -vascular system overall: HUS, DIC, thrombotic, TTP
53
Q

what is icteric leptospirosis

A

Weil disease

  • phase 2 follows 1 with little delay and greater severity
  • 5-40% mortality
54
Q

exam diagnosis for leptospirosis

A
  1. acute: 5-7 days of high fever, rigor, sudden headache, nausa, anorexia, diarrhea, cough, rash, muscle pain, calf/lumbar
  2. delayed/immune phase: 1-3 afebrile days, 4-30 days resumed illness w/ organ-specific symptoms (renal failure, jaundice, HUS, meningitis, DIC, lung hemorrhage, myocarditis, delirium)
  3. eye exam: conjunctivial suffusion (redness w/o exudate), uveitis
  4. chest X-ray for cardiac or lung involvement
  5. biliary tract US for liver involvement
  6. history (eating/swimming in endemic areas
55
Q

what do leptospirosis labs look like?

A
  • leptospires can sometimes be cultured from patient urine
  • can sometimes be seen by darkfield from centrifuged urine or CSF
  • confirmation of diagnosis requires serology of paired acute and convalescent sera by CDC
  • PanBio dipstick is FDA approved
  • histology: silver or IF staining of bipsies may reveal leptospires
  • routine bloodwork:
  • -anemia from DIC
  • -elevated urea nitrogen and serum creatinine from renal infection
  • -elevated bilirubin and alkaline phosphatase from liver infection
  • -elevated serumc CK levels from muscle infection
56
Q

what is treatment of leptospirosis?

A

infection itself: Penicillin G (alt. doxycycline, 3rd gen cephalosporins
-maintain hydration

organ damage: admission for supportive care, restricted diet
-kidneys usually heal after recovery

Jarisch-Herxheimer reaction

57
Q

leptospirosis prevention?

A

sanitation: rodent control, use of protective clothing when working with livestock
vaccination: none useful in US, some foreign countries vaccinate against their local serovars
prophylaxis: oral doxycycline for anticipated short-term exposures (military deployments, adventure travel)

MSII Microbiology (23 decks)

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