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Y2S1 - SAM I > Exam 2 - more infectious diseases > Flashcards

Exam 2 - more infectious diseases Flashcards

1
Q

What is the etiology of plague?

A

Yersinia pestis

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2
Q

What is the reservoir and transmission for plague?

A

Flea-rodent-flea reservoir
Transmission by ingestion of infected prey / flea bites
Cats highly susceptible

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3
Q

What clinical signs are consistent with plague?

A
  1. Bubonic (rodent ingestion)
    pyrexia, dehydration, lymphadenopathy, hyperesthesia
  2. Septicemic
    hematogenous spread to organs (esp lungs)
    fatal within 1-2 days
  3. Pneumonic
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4
Q

How is plague diagnosed?

A

Sample: Needle aspirates from affected tissues
Gram stain - monomorphic population of gram neg organisms (safety pin morphology)
Serology - 4x increase to confirm

REPORTABLE: submit culture samples and fixed slides

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5
Q

How is plague treated?

A

Isolate 48-72 hours and handle carefully (zoonotic)
Aminoglycosides (eg. amikacin) DOA
-chloramphenicol if CNS affected
-doxy/fluoroquinolones if aminoglycosides contraindicated

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6
Q

What is the etiology for leptospirosis?

A

Leptospira interogans sensu lato

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7
Q

What is the reservoir for leptospirosis? How is it transmitted?

A

Rats/other rodents/water sources
Viable for months in soil saturated by urine
Seen in late summer/early fall
Transmission by urine (and others)

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8
Q

What is the pathogenesis for leptospirosis?

A

Leptospires penetrate intact mms / abraded, scratched, water-softened skin.
7 day incubation and spread
*Renal colonization (renal tubular epithelial cells) - shedding in urine by 2 weeks post-infection
*Hepatic injury

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9
Q

What clinical signs are associated with leptospirosis infection?

A

Acute kidney disease
Hematemesis, hematochezia, epistaxis, petechial hemorrhages
Lung injury (‘lepto lungs’) - vasculitis with fluid exudate/pulmonary hemorrhage

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10
Q

How is leptospirosis diagnosed?

A

*Microscopic agglutination test (MAT)
Lab findings - leukocytosis, thrombocytopenia, azotemia, liver elevation
Imagine - renomegaly, interstitial to nodular alveolar densities

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11
Q

How is leptospirosis treated?

A

Parenteral ampicillin/amoxicillin (1-2 weeks)

+Doxycycline (PO for 2-3 weeks) to eliminate carrier state

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12
Q

What is the etiology for lyme disease?

A

Borrelia burgdorferi sensu stricto

Motile spirochete

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13
Q

How is lyme disease transmitted? What time of year does it occur?

A

Ixodes scapularis

Late spring/early summer infection of new hosts

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14
Q

What is the pathogenesis of lyme disease?

A

Lives in tick midgut - during blood meal OspC upregulated - movement to salivary glands - skin injection (~48 hours of attachment
Infects synovial tissue - joint fluid inflammation

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15
Q

What is lyme nephritis? What signs are seen? How is it treated?

A

Glomerulonephritis with immune complex deposition
Leads to protein loss in urine (UPC >5)
Most common in young labs and goldens
Tx as other kidney dz + immune suppression
(methylpred, ACE inhibitors, low dose aspirin, renal diet)

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16
Q

What clinical signs are associated with lyme disease?

A

Develop 2-5 months after tick bite

Fever, inappetance, polyarthritis (shifting leg lameness), generalized lymphadenopathy

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17
Q

How is lyme disease diagnosed?

A

4DX or QuantC6 (detects C6 Ab production)

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18
Q

How is lyme disease treated?

A

Doxycycline for 1 month (should respond in 1-2 days)

amoxicillin alternatively

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19
Q

What abnormality is found in ALL rickettsial diseases?

A

Thrombocytopenia

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20
Q

How are ALL rickettsial diseases treated?

A

Doxycycline

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21
Q

How are rickettsial diseases diagnosed? Which is the exception?

A

4DX

Except R. ricketsii (no in house test)

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22
Q

What is the etiology of CME? Which cells does it infect? What is its vector?

A

Ehrlichia canis
Monocytes/macros
Rhipicephalus sanguineous

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23
Q

What is the pathogenesis of CME?

A

Incubation 8-20 days
Acute phase: replication within reticuloendothelial tissues, vasculitis, PLT dysfunction, thrombocytopenia
Subclinical phase: sequestration of E. canis in spleen
Chronic phase (not all dogs): pancytopenia, death d/t hemorrhage and SBIs

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24
Q

What clinical signs are consistent with CME?

A

Acute: bleeding, neuro signs, hyphema, dyspnea, lameness
Chronic: +edema, PU/PD, SBIs

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25
Q

In which rickettsial diseases can morulae be seen?

A

CGE (E. ewingii) and CGA (A. phago)

Cannot be distinguished!

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26
Q

What are the negative prognostic indicators of CME?

A

severe leukopenia
severe anemia
increased aPTT

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27
Q

What are the gold standard screening test and confirmatory tests for CME?

A

IFA (rarely done, 4DX easier)

Confirmation by immunoblot (at least 21 days post-infection) or PCR (4-10 days post-infection)

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28
Q

What is the etiology of CGE? Which cells does it infect? What is its vector?

A

Ehrlichia ewingii
Neutrophils
Amblyomma americanum

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29
Q

What is the pathogenesis and CS of CGE?

A

3-4 week incubation

Acute disease only - fever, polyarthritis, thrombocytopenia

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30
Q

What is the etiology of CGA? Which cells does it infect? What is its vector?

A

Anaplasma phagocytophilum
Neutrophils
Ixodes

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31
Q

What is the pathogenesis and CS of CGA?

A

Incubation 1-2 weeks
Most dogs not clinical!
Self-limiting febrile illness

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32
Q

What is the etiology of canine cyclic thrombocytopenia? Which cells does it infect? What is its vector?

A

Anaplasma platys
Platelets
Rhipicephalus sanguineous

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33
Q

When is canine cyclic thrombocytopenia suspected?

A

Thrombocytopenia with NO other signs

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34
Q

What is the etiology of RMSF? Which cells does it infect? What is its vector?

A

Rickettsia rickettsii
Endothelial cells
Rhipicephalus / Amblyomma / Dermacenter

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35
Q

Which rickettsial disease is reportable in humans, and in some places dogs?

A

RMSF

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36
Q

What is the pathogenesis of RMSF?

A

Transfer of organism in HOURS

Epithelial cell infection - vasculitis - clotting/thrombosis - DIC

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37
Q

What CS are consistent with RMSF?

A 
Fever
Retinal hemorrhages
Neutrophilic polyarthritis
Respiratory / GI signs
Edema, petechiation
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38
Q

Describe the life cycle of toxoplasma.

A
  • Infection by ingestion of sporozoites/bradyzoites or transplacental/translactational of tachyzoites
  • Rapidly dividing tachyzoites disseminate throughout host (intracellular)
  • Bradyzoites encyst in tissues (chronic infection)
  • Cat excretes oocysts with sporozoites (2 weeks)
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39
Q

What clinical signs are associated with toxoplasmosis?

A

Adult cats - self-limiting diarrhea
Kittens/immunosuppressed - disseminated disease
Dogs - neuromuscular dz or disseminated dz (puppies, rapidly fatal)

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40
Q

How is toxoplasma diagnosed?

A

Serology + CS (many animals are seropositive)

41
Q

How is toxoplasma treated?

A

Clindamycin x4 weeks
TMS if CNS infection
Topical steroids for uveitis

42
Q

Describe the life cycle/pathogenesis of neospora.

A

Canine ingests feces/undercooked meat (transplacental also)
Acute infection (tachyzoites)
Encysted bradyzoites in muscle and neuro tissue
Sporulated oocysts excreted

43
Q

What clinical signs are associated with neospora infection?

A

Puppies (<6 months)
-Ascending paralysis, typically alert/mentally appropriate
Adult dogs
-multifocal CNS involvement

44
Q

How is neospora diagnosed?

A

Serology

45
Q

How is neospora treated?

A

Clindamycin x4-8 weeks

Treat ALL pups in a litter

46
Q

What are the etiologies of babesia?

A

B. canis - dogs, large piroplasm
B. gibsoni - dogs, small piroplasm
B. felis - cats, Africa only

47
Q

Describe the transmission and pathogenesis of babesia.

A

Ixodes tick feeds 1-3 days
Sporozoites in tick saliva injected
Attach to RBC and endocytosed
Intracellular replication and RBC rupture

48
Q

What clinical signs are associated with babesia infection?

A 
Hemolytic anemia (many dogs subclinical)
-lethargy, depression, pallor, icterus, hemoglobinuria
49
Q

DDx for babesia infection?

A

IMHA
Zinc toxicity
PK/PFK deficiencies

50
Q

How is babesiosis diagnosed?

A

PCR

51
Q

How is babesiosis treated?

A

B. canis - Imidocarb (SLUD side effects)

B. gibsoni - Azithromycin

52
Q

Describe the transmission and pathogenesis of cytauxzoon.

A

Felid host
Transmitted by Amblyomma ticks
Phase 1: tissue phase
-Merozoites inoculated via ticks, invade mononuclear cells, infected macros occlude vessels, multi-organ failure

Phase 2: erythrocytic phase
-Merozoites infect RBCs (piroplasm), destruction and phagocytosis of RBCs

53
Q

What clinical signs are associated with cytauxzoon?

A

Weakness, anorexia, fever
Icterus, pallor
Dyspnea
CNS signs

RAPID course (<7 days) and high fatality

54
Q

How is cytauxzoon diagnosed?

A

PCR

55
Q

How is cytauxzoon treated? What is the survival rate?

A

Atovaquone + azithromycin

60% survival

56
Q

Which species of hepatozoon is found in America? How is it transmitted?

A

H. americanum

Amblyomma maculatum - ticks ingested by dogs

57
Q

Describe the transmission and pathogenesis of hepatozoon.

A

Dog ingests tick
Sporozoites released and penetrate gut
Invade mononuclear cells - organ dissemination
Infection of skeletal and cardiac muscle
Pyogranulomatous myositis +/- periosteal reaction (puppies)

58
Q

What clinical signs are associated with hepatozoon infection?

A

Fever, progressive weight loss with good appetite
Hyperesthesia and pain, rear limb ataxia
Ocular discharge
PU/PD

59
Q

How is hepatozoon diagnosed?

A

Histo, PCR, serology

Marked leukocytosis and neutrophilia

60
Q

What ddx should be considered for hepatozoon-associated periosteal bony changes in puppies?

A

Hypertrophic osteodystrophy

61
Q

How is hepatozoon treated?

A

TMS + clindamycin + pyrimethane (x2 weeks)
Docoquinate (x2 years) to decrease relapses
*NO tx eliminates tissue phase

62
Q

Describe the life cycle and pathogenesis of leishmaniasis

A

Promastigotes in female sandfly gut injected into host
Amastigotes infect macrophages
Dissemination to hemolymphatics
Sandfly ingests amastigotes in blood

63
Q

What clinical presentations are associated with leishmaniasis?

A
  1. May clear organisms and become resistant
  2. Asymptomatic carriers
  3. Progressive immunosuppression (T-lymphoid) and immune-complex deposition
    lymphadenopathy, splenomegaly
    generalized skin lesions, NON pruritic
    polyarthritis, GN, vasculitis, uveitis
64
Q

How is leishmania diagnosed?

A

PCR

65
Q

How is leishmania treated and prevented?

A 
Pentavalent antimonials (eg. allopurinol)
*relapse very common, often tx lifelong
K9 advantix repels sandflies
66
Q

What is the etiology of Chagas disease?

A

Trypanosoma cruzi

67
Q

Describe the pathogenesis of Chagas/trypanosoma

A

Kissing bug defecates into bite wound
Trypomastigote (blood form) enters host and disseminates hematogenously
Infects macrophages (amastigote)
Migration to cardiac and skeletal muscle
2-3 weeks, trypomastigotes rupture from host cells
Progressive myocardial degeneration (DCM)

68
Q

What clinical signs are associated with Chagas/trypanosoma?

A

Acute disease: myocarditis (R sided failure with ascites/pleural effusion)
Chronic disease: DCM

69
Q

How is trypanosoma infection diagnosed?

A

Cytology, serology, PCR

70
Q

How is Chagas/trypanosoma treated?

A

Anti-parasitics (eg nifurtimox / benzinidazole)
*Does not stop DCM!
Poor prognosis, 1-5 years

71
Q

Which systemic mycosis is reportable in Minnesota?

A

Blastomycosis

72
Q

Which species does blastomyces infect?

A

Dogs and humans

73
Q

Describe the pathogenesis of blastomyces

A

Saprophytic mycelial form in environment - makes spores
Inhalation of spores
Body temp triggers transformation into yeast
Incubation 1-3 months
Asexual repro in body and dissemination via vessels and lymphatics

74
Q

What are the common sites of infection for blastomyces, and which CS are expected?

A

Lungs (primary), eyes, skin, bone
Pyrexia, anorexia, weight loss, lymphadenopathy
Mycotic pneumonia

75
Q

How is blastomycosis diagnosed?

A 
Rads are variable
-Diffuse interstitial miliary (classic)
-Alveolar (ddx aspiration pneumonia)
-Mass pattern (ddx neoplasia)
Cytology: broad-based budding
Antigen testing (urine sample)
76
Q

How is blastomycosis treated?

A

Itraconazole (microencapsulated) for 6 months

NSAIDS and gluocorticoids for first few days

77
Q

What is the prognosis for blastomycosis and what are the poor prognostic indicators?

A 
25% mortality, 20% relapse within first year
PPI:
-severe pulmonary involvement
-CNS involvement
-more than 3 body systems involved
78
Q

Where is histoplasma found? What species does it infect?

A

Warm, humid environments (SE)

Humans, dogs, cats

79
Q

Describe the pathogenesis of histoplasma

A 
Saprophytic mycelial form
Spore formed - ingested or inhaled
Incubation ~2 weeks
Yeast conversion in body
Phagocytized by mononuclear cells
Disseminates via vessels and lymphatics
80
Q

What are the common sites of infection for histoplasma, and which CS are expected?

A 
Lungs or intestine (primary), spleen, liver, LNs, eyes, BM, adrenals
Subclinical infection common
Pyrexia, anorexia, weight loss
Mycotic pneumonia
Diarrhea (rare in cats)
81
Q

How is histoplasma diagnosed?

A

Diffuse interstitial miliary lung pattern
Intestines may be thickened, friable, hemorrhagic
Cytology - small, round yeast found intracellular (macros and neutrophils)

82
Q

How is histoplasma treated?

A

Itraconazole +/- amphotericin B 4-6 months

Steroids NOT recommended

83
Q

What is the prognosis for histoplasma and what are the poor prognostic indicators?

A

Good for localized respiratory
Poor to fair for disseminated
PPI: BNS, ocular, or bone involvement

84
Q

Where is coccidioidomycosis found? Which species does it infect?

A 
SW states (valley fever), rainfall followed by draught
Dogs more often than cats
85
Q

Describe the pathogenesis of coccidioidomycosis.

A

Saprophytic mycelial form
Infective spores (arthoconidia) inhaled)
Incubation 1-3 weeks
Conversion to spherule, releases endospores

86
Q

What clinical signs are consistent with coccidioidomycosis?

A

Most cases subclinical or mild respiratory
Pregnancy/immunosuppression/massive exposure leads to severe pulmonary infection
-pulmonary abscesses, fibrosis, bronchiectasis
-hilar lymphadenopathy
-osteomyelitis (ddx osteosarcoma)

Skin lesions common in cats (relatively immune)

87
Q

How is coccidioidomycosis diagnosed?

A

Tube precipitation test (IgM) - 2-3 weeks post-exp

Complement fixation Abs (IgG) - 4-6 weeks post-exp

88
Q

How is coccidioidomycosis treated?

A

Any azole for 12 months (frequent relapses off therapy, may need lifelong tx)

89
Q

What is the prognosis for coccidioidomycosis?

A

Good for local respiratory

Poor to fair for disseminated

90
Q

Where is cryptococcus found? What species does it infect?

A

Ubiquitous and worldwide, common in bird droppings

Cats more than dogs

91
Q

What clinical signs are consistent with cryptococcosis?

A

Nasal/facial deformities in cats (ddx neoplasia)

CNS signs most common in dogs

92
Q

How is cryptococcus diagnosed?

A

Cytology - thick capsule

93
Q

How is cryptococcus treated? How is tx monitored?

A

Itraconazole

  • fluconazole for CNS dz
  • amphotericin B if unresponsive

Ag agglutination test (serum or CSF) for monitoring
-tx until titer negative (6-18 months) or forever if FeLV+

94
Q

What is the prognosis for cryptococcus? What is a favorable indicator?

A

Good to excellent, except if CNS dz

Decrease in titer 10x over 2 months = favorable

95
Q

What breed develops SYSTEMIC aspergillosis?

A

German Shepherds

96
Q

What is the pathogenesis for systemic aspergillosis?

A

Inhaled then hematogenously spread
Branching fungal hyphae
Multiorgan infiltrate

97
Q

How is systemic aspergillosis diagnosed?

A

Cytology

Serum and urine Ag test

98
Q

How is systemic aspergillosis treated? What is the prognosis?

A

Azoles, amphotericin B

Grave prognosis - no cure, 0-25 months

Y2S1 - SAM I (3 decks)

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