Vector borne disease Flashcards

1
Q

What tick transmits Anaplasma phagocytophilum?

A

Ixodes scapularies and Ixodes pacificus

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2
Q

Anaplasma phagocytophilum causes what disease?

A

Canine granulocytic anaplasmosis - infects granulocytes (primarily neutrophils)

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3
Q

What tick transmits Anaplasma platys?

A

Rhipicephalus sanguineus

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4
Q

Anaplasma platys causes what disease?

A

Canine cyclic thrombocytopenia - infects platelets

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5
Q

How is Hepatozoon transmitted?

A

Ingestion of Rhipicephalus sanguineus (H. canis) or Amblyomma maculate (H. americanum) ticks

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6
Q

What are the clinical signs of Hepatozoon americanum infection?

A

Lethargy, fever, locomotory abnormalities, hyperesthesia, PLN

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7
Q

What organism transmits Leishmania?

A

Infected female sandflies

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8
Q

Leishmania is endemic in what breed in North America?

A

Foxhounds

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9
Q

What organism transmits Trypanosoma cruzi?

A

Feces contaminated bite from or ingestion of triatomine bug vectors (kissing bugs)

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10
Q

Infection with Trypanosoma results in what?

A

Acute or chronic myocarditis

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11
Q

What ticks transmit Borrelia burgdorferi?

A

Ixodes scapularis (black legged tick) and Ixodes pacificus (Western Black legged tick)

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12
Q

What tick is this?

A

Ixodes scapularis

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13
Q

Describe the life cycle of Ixodes ticks

A

Larva or nymphs feed on infected rodents and become infected; adults feed on deer or dogs and transmit the infection

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14
Q

What outer surface protein does the Borrelia express in the tick midgut?

A

Osp A

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15
Q

When the tick ingests a blood meal, the Borrelia move to the tick salivary glands and begin to express what outer surface protein?

A

Osp C

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16
Q

How long must a tick be attached to transmit Borrelia?

A

~48 hours

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17
Q

When do dogs develop clinical signs of Lyme disease (fever, lameness) after a tick bite?

A

2-5 months - chronic disease

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18
Q

What is the synovial fluid cytology of a dog with Lyme disease?

A

Can be normal or have marked numbers of non-degenerate neutrophils (>5000)

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19
Q

What Borrelia antigen does the 4Dx test for?

A

C6 protein

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20
Q

What characteristics define the order Rickettsiales?

A

Obligate intracellular bacteria, form morulae within host cells

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21
Q

What cell type is infected by Ehrlichia canis?

A

Monocytes

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22
Q

What cell type is infected by Rickettsia rickettsii?

A

Endothelial cells

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23
Q

What tick transmits Ehrlichia canis?

A

Rhipicephalus sanguineus (brown dog tick)

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24
Q

What tick transmits Ehrlichia ewingii?

A

Amblyomma americanum (Lone star tick)

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25
Q

What three ticks are capable of transmitting Rickettsia rickettsii?

A

Amblyomma americanum (Lone star tick), Dermacenter (American Dog tick), and Rhipicephalus sanguineus

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26
Q

What is the cell tropism for Ehrlichia ewingii?

A

Neutrophils

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27
Q

In the acute phase of canine monocytic erhlichiosis, where are the organisms replicating? How long does this phase last?

A
  • 1-4 weeks
  • Replicate in the reticuloendothelial tissues (spleen, LNs)
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28
Q

What are the clinical signs of the acute phase of canine monocytic erhlichiosis?

A
  • Vasculitis, platelet dysfunction and thrombocytopenia lead to bleeding
  • Lethargy, inappetence
  • Fever
  • Lameness (polyarthritis)
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29
Q

What is the outcome of the acute phase of canine monocytic erhlichiosis?

A

Recover in 2-4 weeks or become a carrier

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30
Q

In the subclinical phase of canine monocytic erhlichiosis, where is the organism sequestered?

A

In the spleen

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31
Q

What are the clinical signs/pathologic abnormalities in chronic canine monocytic erhlichiosis?

A
  • Pancytopenia (or thrombocytopenia, anemia with marked granular lymphocytosis), bone marrow hypoplasia, marked monoclonal gammopathy
  • Fever, weight loss
  • Bleeding
  • Edema
  • Death due to hemorrhage or secondary infections
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32
Q

What clinicopathologic abnormality is seen in all three phases of canine monocytic erhlichiosis?

A

Thrombocytopenia

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33
Q

What disease is caused by Ehrlichia ewingii?

A

Canine granulocytic ehrlichiosis

34
Q

What are the clinical signs of canine granulocytic ehrlichiosis?

A

Only acute disease
Fever, lethargy, anorexia
Neutrophilic polyarthritis

35
Q

Morulae are observed within neutrophils. What are the two differentials?

A

Ehrlichia ewingii
Anaplasma phagocytophilum
Cannot differentiate on a blood smear

36
Q

What are the clinical signs of canine or feline granulocytic anaplasmosis?

A

Many dogs are not clinical
Fever, lethargy, lymphadenopathy, splenomegaly, lameness
Very rarely, epistaxis or petechial hemorrhages

37
Q

How long do antibodies take to form against Ehrlichia ewingii?

A

One month - may be negative when the dog is clinical

38
Q

How often do dogs become thrombocytopenic with canine cyclic thrombocytopenia?

A

Cycles of bacteremia and thrombocytopenia every 1-2 weeks

39
Q

Unlike Lyme and Anaplasma, how long must a tick be attached to transmit Rocky Mountain Spotted fever?

A

Hours - much shorter transmission

40
Q

How does Rickettsia ricketsii spread between adjacent endothelial cells?

A

Actin polymerization

41
Q

What are the clinical signs/clinicopathologic changes with Rocky Mountain Spotted fever?

A
  • Fever, weight loss, anorexia
  • Abnormal hemostasis, petechia, microthrombosis, retinal hemorrhage
  • Edema
  • Neutrophilic polyarthritis
  • Hypoalbuminemia
  • Thrombosis/necrosis
  • Shock => oliguria, anuria
42
Q

What tick is this?

A

Amblyomma americanum

43
Q

What tick is this?

A

Dermacentor

44
Q

According to the meta analysis on Lyme vaccination, what adverse events occurred with vaccination?

A

Mild swelling and reddening at the injection site in 2% of dogs, resolved by 72 hours

45
Q

What organism causes tick borne relapsing fever?

A

Borrelia turicatae and Borrelia hermsii

46
Q

What are the clinical signs and lab work abnormalities with tick borne relapsing fever?

A

Pyrexia, lethargy, signs of neurologic disease, severe thrombocytopenia, large numbers of spirochetes on blood smear

47
Q

Resistance to atovaquone is caused by what mutation in Babesia gibsoni? What percent of infections have this mutation?

A
  • Cytochrome B mutations
  • Only 3.5% pretreatment - no need to test unless the dog demonstrates resistance
48
Q

What two small Babesia species, other than Babesia gibsoni, may be transmitted by dog fighting?

A

Conradae and vulpes

49
Q

What negative prognostic indicators were found in acute Babesia canis infections?

A

Nonsurvivors had:
- Higher lactate, triglycerides, phosphate
- Lower hematocrit, leukocyte count, platelet count

50
Q

In dogs with Chagas disease, what ECG abnormalities were most common?

A

Ventricular arrhythmia, AV block

51
Q

In dogs with Chagas disease, what cardiac abnormalities were associated with decreased survival?

A

Ventricular arrhythmias, AV block, right ventricular enlargement

52
Q

In five cats with Cytauxzoon, all five had evidence of DIC. However, what coagulation abnormality was not present?

A

No cats had low antithrombin activity

53
Q

What tick species transmits Cytauxzoon?

A

Primarily Amblyomma americanium. Experimentally, Dermacentor can but less effectively

54
Q

Describe the pathogenesis of Cytauxzoon in the cat

A
  1. Sporozoites from the tick infect macrophages and undergo asexual reproduction (schizogony) to form schizonts
  2. Schizonts spread and can be found in LNs, spleen, liver, lung, bone marrow, etc
  3. Schizonts for parasitic thrombi => blood vessel occlusion, ischemia, tissue necrosis and death
  4. When schizonts rupture, they release piroplasms, which infect RBCs
55
Q

What are the clinical signs of Cytauxzoon in cats?

A
  • Lethargy, anorexia, fever (up to 106)
  • Icterus, lymphadenopathy, hepatosplenomegaly
56
Q

Without treatment, how rapidly do cats with Cytauxzoon die?

A

2-3 days after peak in temperature

57
Q

What are the common clinicopathologic findings with Cytauxzoon?

A

Leukopenia with toxic neutrophils
Thrombocytopenia
Hyperbilirubinemia
Hypoalbuminemia

58
Q

What is the prognosis of cats with Cytauxzoon treated with atovaquone and azithromycin?

A

64% survival

59
Q

What is tick paralysis and what is it caused by?

A
  • Caused by neurotoxins in the saliva of Ixodes holocyclus ticks
  • Acute, progressive, ascending lower motor neuron paralysis
60
Q

How is tick paralysis treated?

A
  • Clip the coat - remove all ticks
  • Administer tick antitoxin serum
  • Quiet environment, monitor for respiratory failure => ventilate
61
Q

What samples are most likely to be positive for schizont-laden macrophages?

A

Spleen aspirates (77%) > LN aspirates (56%) > blood smear (33%)

62
Q

Describe Hepatozoon canis infection in dogs

A
  • Immunocompetent dogs are typically subclinical or have mild clinical signs (fever, lethargy, depression)
  • H. canis resides in the bone marrow, LNs, and spleen
63
Q

Describe Hepatozoon americanum infection in dogs

A
  • Much more severe than H. canis
  • Induces pyogranulomatous inflammation in tissues => fever, weight loss, poor BCS, muscle atrophy and intense pain, weakness
  • Mucopurulent ocular discharge common, bloody diarrhea can occur
64
Q

What are the clinicopathologic findings in dogs infected with H. americanum?

A

Marked neutrophilic leukocytosis - 20K to 200K cell/uL
Mild to moderate anemia
Elevated CK

65
Q

How is H. americanum diagnosed?

A
  • Identification of gamonts in peripheral leukocytes
  • PCR
  • Pathognomonic “onion skin” cysts or pyogranulomatous inflammation on muscle biopsy = gold standard
66
Q

How is H. canis treated?

A
  • Lifelong infection that cannot be completely cleared
  • H canis: imidocarb twice monthly until the parasite is no longer evidence on blood smears for 2-3 months
67
Q

How is H. americanum treated?

A
  • 14 day course of TMS, clindamycin, and pyrimethamine or ponazuril will usually induce remission of clinical signs but many will relapse in 2-6 months
  • Decoquinate can be used for at least 2 years to prevent relapse
68
Q

Name 4 potential cutaneous signs of Leishmaniasis in dogs

A
  • Non pruritic exfoliative dermatitis
  • Periorbital alopecia
  • Nodular dermatitis +/- ulceration
  • Pustular dermatitis
  • Mucocutaneous ulcerative lesions
  • Vasculitis

Skin lesions are the most frequent clinical sign!

69
Q

Name 5 systemic signs of Leishmaniasis in dogs

A
  • Lymphadenopathy
  • Weight loss/poor BCS
  • Splenomegaly
  • Uveitis or keratoconjunctivitis
  • Epistaxis
  • Lameness
  • Systemic vasculitis
  • Glomerulonephritis

Renal disease is the most common cause of mortality

70
Q

What is the treatment for Leishmania in dogs?

A

Meglumine antimoniate (4 weeks) + allopurinol
or Miltefosine (28 days) + allopurinol

71
Q

What immune response predominates in dogs with subclinical infections of Leismania? In dogs with severe clinical disease?

A

Subclinical: Th1 responses dominate
Clinical: Th2 responses dominate

72
Q

When can allopurinol be discontinued in Leishmania cases?

A

When complete physical and clinicopathologic recovery has occurred WITH a marked decrease in antibody levels (negative or borderline)

73
Q

What samples should be used for Leishmania PCR?

A

Bone marrow, LN, spleen, skin, conjunctiva
Blood is not sensitive

74
Q

The presence of what Lyme antibodies are indicative of natural exposure as these antigens are not present in any vaccine?

A

C6, VlsE, and OspF

75
Q

What Lyme antibody increases first and how long is it elevated?

A

OspC antibodies increase by 2-3 weeks, then wanes in 3-5 months

76
Q

How long does it take for OspF antibodies to form?

A

6-8 weeks, remain increased in untreated dogs

77
Q

When should quantitative C6 titers be checked in dogs with Lyme disease?

A

Pretreatment, then at 3 and 6 months to monitor for decrease. Increased result may indicate re-exposure or relapse

78
Q

What is the clinical presentation of dogs with Lyme arthritis?

A

Acute monoarticular or polyarticular lameness with joint swelling, fever, lethargy, and mild local lymphadenopathy

79
Q

How rapidly do dogs with Lyme arthritis respond to antibiotics?

A

1-2 days

80
Q

Dogs that test positive for Lyme should be screened for proteinuria how frequently?

A

2-3 times per year, even if treated with antibiotics