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Bacteriology (mine) > Zoonoses > Flashcards

Zoonoses Flashcards

1
Q

What are the virulence factors for Borrelia Burgdorferi?

A
  1. Outer surface lipoprotein A (OspA): primes PMN into releasing lysosomal granules and superoxides which contribute to joint pain (infectious arthritis); spreading factor by converting plasminogen into plasmin to digest ECM and aid in spread; primary immunoprotective antigen (serodiagnosis with western blot; Anti-OspA Abs are borrelia-cidal)
  2. OspB: (not as impt) 2o protective antigen; mutants lacking this factor are less invasive; used for serodiagnosis by Western blot
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2
Q

What’s the relation between OspA and B cell response?

A

tha antigen is not sufficiently expressed in mammalian host to induce a B cell response

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3
Q

Why was the OspA vaccine (LYMErix) withdrawn?

A

bc the antibody generated was cross-reactive with proteins foudn in joints (bc of molecular mimicry) -> autoimmune arthritis

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4
Q

What stage of ixodes tick has infectious Borrelia Burgdorferi?

A

ALL stages but nymph stage is most impt in transmitting disease

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5
Q

How do ticks transmit the bacteria Borrelia Burgdorferi to hosts?

A

vomitting into wound (usu. infected within 24hrs of tick feeding)

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6
Q

What causes the symptoms seen during the first stage of Borrelia Burgdorferi infection?

A

bacteria itself

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7
Q

What causes the symptoms seen in the second stage of Borrelia Burgdorferi infection?

A

inflammatory response

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8
Q

What causes the symptoms seen in the third stage of Borrelia Burgdorferi infection?

A

autoimmune response

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9
Q

Is antibiotics effective in first stage of Borrelia Burgdorferi infection?

A

yes

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10
Q

When does stage one of Borrelia appear?

A

1 week after bite

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11
Q

When does stage two of Borrelia appear?

A

weeks to months after tick bite

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12
Q

When does stage three of Borrelia appear?

A

months to years after tick bite

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13
Q

What are some other symptoms during the second stage of Borrelia infection not covered by sketchy?

A

acute arthritis and meningitis

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14
Q

Is antibiotics helpful during the second stage of Borrelia infection?

A

may or may not be bc bacteria may be gone

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15
Q

What symptoms are found in the 3rd stage of Borrelia infection that was not on sketchy?

A

chronic skin lesions, chronic fatigue syndrome

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16
Q

Will antibiotics work in the 3rd stage of Borrelia infection?

A

no, bacteria is already eradicated

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17
Q

What is particularly diagnostic for Borrelia?

A

erythema chronicum migrans (ECM)

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18
Q

What specimen can be collected to test serology for Borrelia infection?

A

blood, CSF, synovial fluid

(the earlier, the better bc bacteria still there)

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19
Q

What lab diagnostic tools can be used to diagnose Lyme disease?

A
  1. check for Borrelial Ag or anti-Borrelial Ab by ELISA or Western Blot

2, use PCR to look for Borrelial DNA in tick or tissue

  1. immunostain biopsy sample for bacteria (look for spirochete)
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20
Q

What’s the treatment for Lyme disease?

A

doxycycline (1st choice, also has anti-inflammatory mechanisms), amoxicillin (beta lactams), cefuroxime, or erythromycin (macrolide) taken 2-4 times a day for 2-4weeks

no vaccine!

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21
Q

What does borrelia recurrentis cause?

A

high, recurrent and relapsing fever

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22
Q

What is the virulence factor for Borrelia recurrentis?

A

variable major protein (VMP): surface protein that varies antigenic epitopes in response to immune clearance (immune response is cyclic until body creates enough Abs to eliminate Ags)-> cause recurrent fevers (less severe with each recurrence)

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23
Q

What is this?

A

Borrelia Burgdorferi (note the spirals)

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24
Q

How are VMP genes activated?

A

gene conversion: 1 clone can give rise to 20 serotypes

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25
Q

What vector is used for epidemic spread of Borrelia recurrentis?

A

human body louse (no animal reservoir)

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26
Q

Describe the method of Borrelia recurrentis spread epidemically.

A

bacteria multiples in lice blood (hemolymph)-> lice bites host-> host crushes lice through scratching-> bacteria enters bite wound-> bacteria multiply locally and then spread into bloodstream (systemic)

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27
Q

What are the clinical presentations of Borrelia recurrentis epidemic infection?

A

high fever and chills that remits and reoccurs (as VMP changes), sometimes delirium, arthacalgia and myalgia

disease rarely fatal

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28
Q

How is borrelia hermsii transmitted?

A

soft tick-borne endemic

animal reservoir = rodent

progresses through humans same way BUT remains in bloodstream!

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29
Q

What are the clinical presentations of Borrelia Hermsii?

A

same as B. recurrentis

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30
Q

How is Borrelia species ID’ed?

A

blood smears prepared from febrile episodes when bacteria in bloodstream (looks like a spiral thread)

giemsa and wright stain

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31
Q

What is the recommended treatment for Borrelia infection?

A

low dose antibiotics to avoid Jarisch-Herxheimer reaction (high dose beta lactams would release mini-cytokine storms)

antibiotics: penicillin, tetracyclines (tetracycline, doxycycline) or macrolide (erthromycin) for few days

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32
Q

What are the virulence factors for leptospirosis?

A

unknown for most part bc hard to grow

  1. HlyX hemolysin
  2. possibly invasins
  3. very motile (only thing we’re certain of)
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33
Q

What fluid is Leptospirosis transmitted in?

A

urine (rat or dog) and amniotic fluid

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34
Q

How does the Leptospirosis bacteria enter human host?

A

enters mucous membranes or damaged skin

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35
Q

What is the spectrum of illnesses of leptospirosis?

A

uveitis, meningitis, pulmonary hemorrhage syndrome, Weil’s disease (hepatic and renal dysfunction)

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36
Q

Describe the biphasic cycle of Leptospirosis infection.

A

incubation period of 2-20 days

  1. acute stage (leptospiremia / anicteric): spiking fever and lasts ~1 week; septicemia (gets into bloodstream to spread to CSF and kidneys)
  2. convalescent stage (leptospiruria & immunity / icteric - Weil’s Syndrome): spreads to liver and kidneys (jaundice and renal failure); most lethal is spread to heart (myocarditis); autoimmune uveitis and interstitial nephritis (from Abs responding to bacteria months to years after)
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37
Q

How do we ID the leptospirosis is in the acute phase?

A

serology for IgM in CSF or blood sample

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38
Q

What lab diagnostic tools are used to ID leptospirosis?

A
  1. Microscopic Agglutination Test (MAT): serodiagnosis
  2. culture in vitro: see motile, gram - spiral with hooked ends
  3. immunostaining tissues
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39
Q

What’s the form of treatment for Leptospirosis?

A

doxycycline, penicillin, or fluoroquinolones

dog and other animals vaccination

40
Q

What are the virulence factors for Rickettsia rickettsii?

A
  1. rOmpA: immunodominant surface-exposed Ags (immunoprotective); serves in adhesion and helps bacteria get inside body (bc obligate intracellular pathogen)
  2. phospholipase: mediates internalization
41
Q

How is Rickettsia rickettsii introduced into human body?

A

Dermancentor tick saliva

42
Q

Explain the pathogenesis of Rickettsia rickettsii.

A

bacteria multiply in skin -> spread to bloodstream -> infect vascular endothelial cells of lungs, spleen, brain, and skin (result in vasculitis)

43
Q

Can rickettsia rickettsii be grown in vitro on agar plate?

A

no (must be grown on cell lines)

44
Q

What is clinically seen in rickettsia rickettsii?

A

fever, headache, myalgia, nausea, petechial rash (occuring from microclots), splenomegaly and neuro symptoms

mortality of 10% - shock from multiple organ-system failure

45
Q

Explain the Weil-Felix test.

A

cross reaction with O antigens of 3 proteus vulgaris strains causing agglutination of rickettsia

not very specific or sensitive

46
Q

What other tests are used to diagnose Rickettsia rickettsi?

A
  1. complement fixation test: look for 4-fold increase in titer
  2. indirect immunofluoresnce test: detect IgG, IgM

both are looking for bacteria antigens

47
Q

What is the treatment plan for Rickettsia?

A

tetracycline, chlorophenicol, fluoroquinolone (drugs that can go intracellular!)

48
Q

What disease does rickettsia rickettsii cause?

A

rocky mountain spotted fever

49
Q

What disease does rickettsia prowazekii cause?

A

epidemic typhus

50
Q

What are the vectors for rickettsia prowazekii?

A

head (Pediculus humanus capitis) and body (P. humanus corporis) lice

*infection actually KILLS the lice (so vector merely form of transport; not serving as reservoir)

51
Q

What is the reservoir for Rickettsia prowazekii?

A

flying squirrels

52
Q

What clinical symptoms are seen in Rickettsia prowazekii?

A

disease and symptoms like RMSF but mortality up to 40%

Brill-Zinsser disease: recrudescence of old typhus infections; bacteria lays dormant for 50 years with host not showing any symptoms of typhus

53
Q

What’s the treatment for Rickettsia prowazekii?

A

tetracycline and chloramphenicol orally for 3-4 days

used DDT to de-louse

54
Q

What are the virulence factors for Q fever?

A
  1. phase I antigens: (complex carbs on LPS) block Abs to bacterial surface proteins; Abs to these antigens are found in chronically ill
  2. phase II antigens: derived from phase I when it undergoes deletion mutation (proteins on bacterial cell wall are now exposed); Abs to these antigens are found in acutely ill
55
Q

What is the vector for animal-animal transmission of Coxiella?

A

tick

56
Q

Where does the Coxiella bacteria replicates?

A

within phagocytosis

57
Q

How does Q fever present?

A

most infections are sub-acute and unapparent

  1. acute disease = atypical pneumonia (after 20days incubation; nonproductive and diffuse) that can spread to liver and cause diffuse granulomas
  2. chronic disease = chronic endocarditis on artificial/previously damaged valves (only seen in 5% of infection)
58
Q

How do we clinically ID Q fever?

A

PCR or serology to look for phase Ag

(Giemsa stain)

59
Q

What’s the form of treatment for Q fever?

A

acute: tetracycline
chronic: tetracycline with rifampin or trimethoprim-sulfa

(bactrim works too)

vaccines for uninfected troops in high risk areas

60
Q

What’s the virulence factor for Bartonella henselae?

A

unknown but probably endotoxin

61
Q

Besides cats, how else can cat scratch fever be spread?

A

flea bites

62
Q

What’s the presentation of cat scratch disease?

A

papules (3-10 days after and persists for 2-3 weeks)

LN are NOT hemorrhagic

regional lymphadenopathy (2-3weeks after and lasts few months)- may see splenomegaly if spread to spleen

NO constitutive symptoms (fever, chills, etc)

63
Q

Bacillary Angiomatosis looks like ____?

A

Kaposi’s Sarcoma: differentiates with biopsy

64
Q

What else can Bartonella henselae lead to that was not covered by sketcy?

A

hepatic or spenic peliosis (seen in immunocompromised): cystic blood-filled lesions; have hepatosplenomegaliy, weight loss, nausea, fever, elevated liver enzymes and alkaline phosphate levels

65
Q

How do we ID Bartonella?

A

(hard to gram stain the small, slightly curved gram - rods)

do serology and physical findings

66
Q

What’s the mode of treatment for Bartonella?

A
  1. immunocompetent: supportive therapy (warm compress on enlarged LN, analgesics, aspiration of inflammed nodes)
  2. immunocompromised: (bacillary angiomatosis and peliosis) erythromycin/doxycycline (macrolide/tetracycline)
67
Q

What are the virulence factors for Ehrlichia chaffeensis, Ehrlichia ewingii, Anaplasma phagocytophilum?

A

unknown

68
Q

What’s the vectors for Ehrlichia chaffeensis, Ehrlichia ewingii, Anaplasma phagocytophilum?

A

ixodes ticks

69
Q

What do Ehrlichia chaffeensis, Ehrlichia ewingii, Anaplasma phagocytophilum infect?

A

monocytes or granulocytes (bc they’re obligate intracellular pathogens)

70
Q

What is clinically seen from infection by Ehrlichia chaffeensis, Ehrlichia ewingii, Anaplasma phagocytophilum?

A
  1. symptoms similar to RMSF but no rash
  2. Human monocytic ehrlichiosis (HME) - E. chaffeensis ; human granulocytic ehrlichiosis (HE)- E. wingii/ A. phagocytophilum
  3. leukopenia and thrombocytopenia bc blooc cell death
  4. can be fatal depending on severity of infection
71
Q

How do we ID Ehrlichia chaffeensis, Ehrlichia ewingii, Anaplasma phagocytophilum?

A

immunofluoresence and serology (ELISA to look for 4-fold increase in titer)

72
Q

What’s the treatment plan for Ehrlichia chaffeensis, Ehrlichia ewingii, Anaplasma phagocytophilum?

A

tetracycline or chloramphenicol or rifampicin (bc they’re intracellular pathogens)

73
Q

What are the virulence factors of Pasteurella multocida?

A

anti-phagocytic capsule and endotoxin

74
Q

Where do we normally see Pasteurella multocida?

A

normal flora of animals like cats and dogs (oral cavity and nasopharynx)

75
Q

What are the clinical presentations of Pasteurella multocida?

A
  1. cellulitis (1-2 days after bite) with no clear pus
  2. chronic lung infection in people with pre-existing chronic pulmonary disease or those with heavy exposure to animals
76
Q

How do we ID Pasteurella?

A

culture on blood or chocolate agar (small gram - rods)

77
Q

How do we treat Pasteurella?

A

beta-lactams also fluoroquinolones (levo or moxifloxacin)

78
Q

What are the virulence factors for Bacillus Anthracis?

A
  1. polypeptide capsule: made of D-glutamic acid and is anti-phagocytic; genes found on plasmid pX02
  2. protective antigen: common binding subuit for other 2 toxins; immunoprotective (used as vaccine component)
  3. edema toxin: an adenylate cyclase causes cells to swell and burst through dysregulation of cAMP
  4. lethal toxin: metalloprotease cleaves MAP kinase and induces apoptosis in (macrophages) cells; acts on monocytes which secrete mediators -> cause T cell proliferation
79
Q

Where do we have the genes for edema an lethal toxin?

A
  1. protective antigen on their binding subunit
  2. both are encoded on giant plasmids within the organism
80
Q

How does bacillus antracis enter host?

A

spores (viable for at least 50years) primary mode of infection through skin (cutaneous form) or inhalation and mucous membranes (respiratory form)

81
Q

How does the cutaneous form of bacillus antracis develop?

A

papules-> black eschar (painless ulcer with coal-black necrotic center)

if don’t heal -> spread to lymphatics and bloodstream -> septicemia and death

82
Q

What’s the inhalation anthrax called?

A

Woolsorter’s disease (have to inhale 10-20K spores for it to germinate in alveolar macrophages): first nonspecific (low grade fever, dry cough, malaise due to dying macrophages releasing proinflammatory cytokines) then pulmonary edema, mediastinal hemorrhage, widened mediastium due to massive toxemia (respiratory distress and shock)

100% fatal

83
Q

How do we ID bacillus antracis?

A
  1. gram stain fluid and pus (from local lesion, blood sputum, and CSF [since can cause meningitis]): look for gram + rods
  2. grow on blood agar plate to look for non-motile and non-hemolysis
  3. chest xray (widened mediastinum)
84
Q

How do we treat Bacillus anthracis?

A
  1. ciprofloxacin (cipro: fluroquinolone) or doxycycline
  2. vaccines for at risk groups
  3. Raxibacumab (monoclonal Ab): blocks binding of protective Ag to cells to prevent/reduce toxemia; often used WITH cipro

*antibiotics NOT effective for pulmonary anthrax bc bacteria gone

85
Q

What are the virulence factors for Yersinia Pestis?

A
  1. pH 6 adhesin: pilus adhesin that’s maximally expressed at ph6 (the pH of encapsulated phagolysosome)
  2. yersinia adherence (YadA): another adhein protein; host receptors (beta-1 integrins, laminin, and fibronectin)

*both these adhesins are chromosomely encoded and expressed only at 37oC

  1. yersinia outer membrane proteins (Yops): introduced via type III secretion; yopH (tyrosine phosphate activity- interferes with intercellular signalling), yopM (indirectly affects signalling by preventing platelets from releasing cytokines), yopE (destroys actin monofilaments - cytoskeletal elements)
  2. YpkA (Ypkinase): serine/threonine kinase activity-> also interferes with host cell signal transduction
  3. LcrV** **(V antigen): master switch for controlling all of Yops
  4. Fraction 1 (Fra 1): protein capsule with anti-phagocytic property that activates complement (plasmd encoded)
  5. plasminogen activator: degrades C3b and C5a; paradoxically degrades Yops; dissolves fibrin clots (spreading factor: MAIN function)
86
Q

What are the two cycles of Yersinia Pestis infection?

A
  1. Sylvatic cycle: fleas -> varmints/vermins (prairie dogs and other rodents) -> humans
  2. urban cycle: rats -> fleas -> humans

*bubonic plague: person-to-person; survivable

*pneumonic plague: person-to-person via respiratory route; almost 100% fatal; primed to kill (no lag time)

87
Q

What is clinically seen in plague from Yersinia pestis?

A
  1. since spread to lymphatics, see bubo (inflamed hemorrhagic LN) and black nodule (can spontaneously ulcerate and drain sometimes leading to recovery)
  2. spread to lungs (pneumonia), liver, heart
  3. ischemic gangrene in distal extremities
88
Q

How do we ID Yestinia Pestis?

A
  1. stain blood, sputum, aspirates from buboes for Gram - rods: see bipolar staining; can also use giemsa stain and immunofluorescence sain)
  2. on BAP, see colonies that look like beaten copper
89
Q

What is the mode of treatment for Yestinia Pestis?

A

streptomycin (aminoglycosides) and tetracycline

also need to treat contacts of pneumonia plague with prophylactics

90
Q

What are the virulence factors for Francisella tularensis?

A

antiphagocytic capsule and endotoxin

91
Q

What are reservoirs for Francisella tularnesis (Rabbit fever / tularemia)?

A

rodents, rabbits, beavers, carnivores

92
Q

How do humans get infected with rabbit fever?

A
  1. handling skin or carcass
  2. insect vectors (deer flies and ticks)
  3. animal bites (carnivores)
  4. inhalation (pneumonia!)

*very very invasive - only need a small amount for disease

93
Q

What infections can arise from Francisella infection?

A

*pretty much anything with mucous membrane

  1. ulcerglandular, glandular (lymphadenopathy), oculoglandular (conjuctivitis, and lymphadenopathy), oropharungeal (ulcers), ulcerglandular (cutaneous ulcers and lymphadenopathy)
  2. systemic: 30-60% mortality; acute illness with septicemia
  3. pneumonic
94
Q

How do we ID rabbit fever?

A
  • *do not culture!** (bc highly virulent)
    1. serology: look for rise in titer in convalescent serum
  1. fluorescent assay for antigens
95
Q

How do we treat Rabbit Fever?

A

streptomycin or gentamycin (aminoglycoside)

doxycycline, ciprofloxacin

no effective vaccine

Bacteriology (mine) (6 decks)

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