Infectious Dz - Blood Borne 2 Flashcards

1
Q

What are hemotropic mycoplasmas also known as?

A

Haemobartonellosis

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2
Q

Where do hemotropic mycoplasmas reside?

A

on the RBC surface

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3
Q

What causes haemobartonellosis in cats?

A

Mycoplasma haemofelis, Candidatus mycoplasma haemominutum, and Candidatus mycoplasma turicensus

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4
Q

What is the most pathogenic cause of haemobartonellosis in cats?

A

Mycoplasma haemofelis

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5
Q

What does Mycoplasma haemofelis cause in immunocompetent cats?

A

moderate to severe hemolytic anemia

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6
Q

What causes feline infectious anemia?

A

Mycoplasma haemofelis

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7
Q

What is infection with hemoplasmas associated with in cats (risk factors)?

A

the male sex, nonpedigree status, and outdoor access

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8
Q

What causes haemobartonellosis in dogs?

A

Mycoplasma haemocanis and Candidatus mycoplasma haematoparvum

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9
Q

True or False: Clinical disease of Haemobartonellosis is more common in dogs.

A

False - it is more common in cats

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10
Q

How are hemotropic Mycoplasmas transmitted?

A

Not entirely known - fleas and other arthropod vectors, biting (blood exchange not just saliva), and blood transfusions

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11
Q

When does anemia occur post infection of Mycoplasma haemofelis?

A

2-34 days after infection

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12
Q

What occurs in the acute phase of M. haemofelis infection?

A

Extravascular hemolysis

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13
Q

What causes the anemia in the acute phase of M. haemofelis infection?

A

It is caused by erythrocyte bound antibodies leading to extravascular hemolysis

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14
Q

If the acute phase of M. haemofelis infection is not treated, what is the mortality rate?

A

1/3 of cats will die

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15
Q

True or False: Cats can be chronically infected with M. haemofelis even though they have recovered from their illness.

A

True

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16
Q

What are the clinical signs of M. haemofelis infection?

A

Lethargy, inappetence, pallor, weakness, weight loss, and dehydration

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17
Q

If anemia develops rapidly in patients with infection of M. haemofelis, what clinical signs will be present?

A

Vocalize, collapse, neurologic signs, and death

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18
Q

What will a patient show in physical examination when infected with M. haemofelis?

A

Fever, weakness, pallor, tachypnea, and tachycardia

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19
Q

What will a CBC show in actively infected M. haemofelis patients?

A

regenerative anemia (reticulocytosis, macrocytosis, nucleated RBCs, polychromasia, hypochromasia) and the blood may autoagglutinate

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20
Q

What will a chemistry show in actively infected M. haemofelis patients?

A

Increased ALT from hypoxia, mild to moderate hyperbilirubinemia, prerenal azotemia, and hyperproteinemia

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21
Q

What will a UA show in patients with M. haemofelis?

A

+/- bilirubinuria

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22
Q

How can Haemobartonellosis be diagnosed?

A

Cytology and PCR

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23
Q

What is the test of choice for diagnosing Haemobartonellosis?

A

PCR

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24
Q

If a cat tests positive for M. haemominutum or M. turicensus on PCR and has anemia, what should be done next?

A

You should look for alternate causes of anemia because these agents are unlikely to cause anemia

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25
Q

When should Haemobartonellosis be treated?

A

When clinical signs and lab abnormalities are consistent with hemoplasmosis

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26
Q

What can be used to treat Haemobartonellosis?

A

Doxycycline (tx of choice). Marbofloxacin, and Pradofloxacin as well as supportive care

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27
Q

What supportive care should be given to patients with Haemobartonellosis?

A

IV fluids, blood transfusions, +/- glucocorticoid to suppress associated immune-mediated hemolytic process

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28
Q

How is Haemobartonellosis prevented?

A

Keep cats indoors, flea and tick control, and screen blood donors

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29
Q

Which of the following should make you question your diagnosis of anemia due to hemotropic Mycoplasma in a 2 YO MC DSH cat?

a. The cats anemia resolved with doxycycline therapy
b. The cat is FeLV/FIV negative
c. The cat lives in a multicat household and none of the other cats are sick
d. The cat’s blood is autoagglutinating
e. Your PCR comes back as positive for M. haemominutum, but negative for M. haemofelis and M. turicensis

A

e. Your PCR comes back as positive for M. haemominutum, but negative for M. haemofelis and M. turicensis

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30
Q

What structures do Erlichia species create in their infected hosts?

A

morulae (bacterial cluster) within phagosomes of circulating leukocytes

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31
Q

What does Ehrlichia canis infect and what does it cause?

A

monocytes causing canine monocytic ehrlichiosis

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32
Q

What does Ehrlichia ewingii infect and what does it cause?

A

Infects granulocytes causing canine granulocytic ehrlichiosis

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33
Q

What does Ehrlichia chaffeensis infect and what does it cause?

A

It causes human monocytic ehrlichiosis, dogs are the reservoir for this organism

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34
Q

What transmits E. canis?

A

Rhipicephalus sanguineus Just know ticks

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35
Q

What transmits E. ewingii and E. chaffeensis?

A

Ambylomma americanum Just know ticks

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36
Q

How do ticks pick up E. canis?

A

Tick larvae or nymphs acquire infection when they feed on infected dogs and it is transmitted transstadially within the tick

37
Q

What classifications of disease does Canine Monocytic Ehrlichiosis present as?

A

Acute, subclinical, and chronic

38
Q

When does acute Canine Monocytic Ehrlichiosis present?

A

Within 1-4 weeks post infection

39
Q

What mechanisms are important in disease pathogenesis of acute Canine Monocytic Ehrlichiosis?

A

immune-mediated mechanisms

40
Q

What clinical signs are associated with acute Canine Monocytic Ehrlichiosis (CME)?

A

Lethargy, inappetence, fever, weight loss, lymphadenopathy, splenomegaly, petechial/ecchymotic hemorrhages, neurologic signs

41
Q

What causes the lymphadenopathy and splenomegaly in acute CME cases?

A

The replication of E. canis in reticuloendothelial tissues

42
Q

What causes the petechial ecchymotic hemorrhages in acute CME cases?

A

thrombocytopenia and platelet dysfunction from immune-mediated platelet attack

43
Q

What happens in subclinical cases of CME?

A

The organism is sequestered in the spleen allowing it to avoid host immune system via antigenic variation

44
Q

What CBC changes are associated with subclinical CME?

A

Only platelet counts may be subnormal

45
Q

What disease process is associated with chronic CME?

A

pancytopenia

46
Q

What clinical signs are associated with chronic CME?

A

Fever, lethargy, inappetance, bleeding tendencies, weight loss, and vision change

47
Q

What will you find on a PE of a patient with ehrlichiosis?

A

lethargy, fever, peripheral lymphadenopathy, splenomegaly, mucosal petechial hemorrhages, epistaxis, neurological signs, ocular abnormalities, and thin and muscle atrophy in chronic ehrlichiosis

48
Q

What will you find on CBC in acute cases of CME?

A

thrombocytopenia and non regenerative anemia (Reticulocytosis, microcytosis, normocytic, normochromia)

49
Q

What will you find on CBC in chronic cases of CME?

A

Pancytopenia with nonregenerative anemia and thrombocytopenia

50
Q

What will you find on a chemistry in patients with CME?

A

hypoalbuminemia, hyperglobulinemia (usually polyclonal), +/- elevated ALT and ALP

51
Q

What irregularity may you seen on a UA in patients with CME?

A

+/- proteinuria

52
Q

How is CME diagnosed?

A

Serology (IFA or ELISA snap test) and PCR

53
Q

True or False: Positive initial serum antibody titer reflects active ehrlichial disease.

A

False - it may reflect previous exposure and not ehrlichial disease so it is important to retest 3-4 weeks later to demonstrate seroconversion

54
Q

What do you do if you find incidental Ehrlichia positive in a dog you were just testing for heartworm?

A

Thorough PE and lab testing to look for signs of CME Only a positive SNAP plus clinical signs supports an ehrlichia diagnosis

55
Q

What if a sick dog tests positive for Ehrlichia on a SNAP 4Dx test?

A

Perform quantitative serologic testing so a titer can be obtained as a baseline for acute and convalescent serologic testing

56
Q

What stage of disease is PCR better than serology in diagnosing Ehrlichia?

A

It is more sensitive for early diagnosis of CME than serology in acute disease cases because there is not enough time for antibody production for serology to detect

57
Q

When is serology better than PCR in diagnosing Ehrlichia?

A

In chronic CME because there are low circulating organism numbers

58
Q

What ‘test’ is very important in diagnosing Ehrlichia?

A

Resolution of clinical signs in response to therapy

59
Q

What is the treatment of choice for CME?

A

Doxycycline and supportive cares as needed

60
Q

How quick does improvement occur once treatment has started in patients with acute CME?

A

in 24-48 hours

61
Q

Do dogs with chronic CME always respond to treatment?

A

Dogs with severe chronic CME may not respond to treatment or cytopenias may resolve over several months

62
Q

How is CME prevented?

A

avoid tick infested areas, remove ticks early if infected with ticks, ectoparasiticides, and screen blood donors

63
Q

Bear is a 4 YO MC Flatcoat retriever that has presented for acute epistaxis. He recently moved to Iowa from Puerto Rico. On PE you discovered epistaxis and a mild fever of 103.0 F. He has thrombocytopenia, a PCV of 27%, and he has 20,000 reticulocytes (low). He is 4Dx Ehrlichia SNAP positive. What do you want to do next for Bear?

a. Start treating with doxycycline
b. Euthanize because Ehrlichia has a terrible prognosis
c. Send of a tick panel for Ehrlichia PCR and serology, and to look for other co-infections
d. Transfuse with pRBCs because he is anemic

A

a and c

64
Q

What is the reservoir for E. ewingii?

A

White-tailed deer

65
Q

What form of disease does E. ewingii cause?

A

acute only

66
Q

Where does E. ewingii replicate?

A

in the neutrophil delaying neutrophil apoptosis

67
Q

What clinical signs do patients with E. ewingii infections have?

A

No signs to fever, lethargy, anorexia, and neutrophilic polyarthritis

68
Q

How is E. ewingii diagnosed?

A

4Dx SNAP test or PCR

69
Q

How is E. ewingii infection treated?

A

Doxycycline

70
Q

What causes canine granulocytic anaplasmosis?

A

Anaplasma phagocytophilum - infects neutrophils

71
Q

What causes canine thrombocytic anaplasmosis?

A

Anaplasma platys

72
Q

What is the pathogenesis of Canine granulocytic anaplasmosis (CGA) infection?

A

Once transmitted by a tick, it enters the blood stream, attaches to ligands on the surface of neutrophils. It then enters the neutrophils via endocytosis. The organism survives the harsh neutrophil environment by bypassing phagolysosome pathways and dysregulating neutrophil function.

73
Q

What clinical signs are associated with CGA?

A

A vast majority have no clinical signs! But some can be a self-limiting febrile illness, lethargy, fever, inappetence, lameness, and sometimes GI signs (vomiting +/- diarrhea)

74
Q

What will you find on a PE in a patient with CGA?

A

Fever of up to 106.7 F, lymphadenopathy, splenomegaly, +/- lameness

75
Q

What will you find on a CBC in patients with CGA?

A

Thrombocytopenia, mild nonregenerative anemia, and morulae within granulocytes

76
Q

What will you find on Chemistry in patients with CGA? UA? Synovial fluid analysis?

A

Chemistry - mild to moderate hypoalbuminemia Urinalysis - proteinuria Synovial fluid analysis - Neutrophilic polyarthritis +/- morulae

77
Q

How is CGA diagnosed?

A

Serology (IFA and SNAP 4Dx) and PCR

78
Q

What test do you want to do when diagnosing CGA early on?

A

PCR

79
Q

Do positive results imply CGA is the cause of illness? Negative results?

A

No Negative results also don’t imply anything because it can be negative in early stages of disease

80
Q

Since a positive IFA titer can reflect exposure of A. phagocytophilum, what must the results be to indicate Anaplasma is the cause of the disease?

A

fourfold rise in titer

81
Q

What is the treatment of choice for CGA?

A

Doxycycline

82
Q

What is the prognosis for CGA?

A

Excellent - in 24-48 hours most dogs clinically improve and platelet counts normalize in 2-14 days

83
Q

What does A. platys cause?

A

canine cyclic thrombocytopenia

84
Q

Are there clinical signs associated with A. platys infections?

A

No, it causes thrombocytopenia without other clinical signs

85
Q

How is A. platys infection diagnosed? Treatment?

A

Diagnosed by seeing morulae in platelets or via PCR Treated with Doxycycline

86
Q

Do cats get anaplasmosis?

A

Yes, clinical signs appear similar to those in dogs. It should be considered when more common causes of disease are not apparent

87
Q

Moses is an 8 YO MC mixed breed dog presented for a sudden onset of lethargy, anorexia, and vomiting. On physical examination you noted he had a fever of 105.8 with prominent mandibular lymph nodes. He is thrombocytopenic and has a morulae located in a granulocyte. The chemistry and UA were WNL. You note that he has splenomegaly on rads. His 4Dx snap test was negative across the board. What are your top differentials based on the morulae in a granulocyte?

A

E. ewingii and A. phagocytophilum

88
Q

Moses is an 8 YO MC mixed breed dog presented for a sudden onset of lethargy, anorexia, and vomiting. On physical examination you noted he had a fever of 105.8 with prominent mandibular lymph nodes. He is thrombocytopenic and has a morulae located in a granulocyte. The chemistry and UA were WNL. You note that he has splenomegaly on rads. His 4Dx snap test was negative across the board. Why do you think the snap test was negative?

A

Too acute an infection to have performed antibodies

89
Q

Moses is an 8 YO MC mixed breed dog presented for a sudden onset of lethargy, anorexia, and vomiting. On physical examination you noted he had a fever of 105.8 with prominent mandibular lymph nodes. He is thrombocytopenic and has a morulae located in a granulocyte. The chemistry and UA were WNL. You note that he has splenomegaly on rads. His 4Dx snap test was negative across the board. What are your next diagnostic and therapeutic tests?

A

Baseline and convalescent serology, PCR, and treat with Doxycycline