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ACVIM GENERAL MY OWN > Infectious > Flashcards

Infectious Flashcards

1
Q

what are morulae ?

A

clusters of bacterium, often within phagosomes, which hide within the phagosome to evade the immune system

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2
Q

what tick born diseases cause morulae

A

ricketsial diseases Anaplasma, (phagocytophilum and plays) and ehrlichia (canis and erwingii), anaplasma

Protozoal tick spread disease (babesia toxoplasma)

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3
Q

Erlichia’s preferential host is exclusively in the?

A

Dogs, all parts of the life cycle are on dogs

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4
Q

What is transdadial vs transoverial

A

Transstadial transmission occurs when a pathogen remains with the vector from one life stage (“stadium”) to the next.

transovarian transmission (transmission from parent to offspring via the ovaries) occurs in certain arthropod vectors as they transmit pathogens from parent to offspring

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5
Q

All tick disease cause what change on CBC?

A

Thrombocytopaenia

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6
Q

which tick born disease can cause a monoclonal gammopathy with CD8 granular lymphocytosis

A

Erlichia

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7
Q

What are the most commonly affected breeds

A

German shepherds, doberman and spaniels (black and tan)

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8
Q

what are the difference between monoclonal and polyclonal lymphocytosis

A
  1. Polyclonal Lymphocytosis:Definition: In polyclonal lymphocytosis, lymphocytes (a type of white blood cell) are derived from multiple clones of immune cells. This means that a diverse range of lymphocytes is involved, indicating a general immune response.

Cause: It typically occurs in response to infections, autoimmune diseases, or other inflammatory processes. Because it involves many clones of lymphocytes, it’s usually a normal or reactive process.

  1. Monoclonal Lymphocytosis:Definition: Monoclonal lymphocytosis refers to the proliferation of lymphocytes from a single clone. All the lymphocytes in this case are genetically identical, arising from a single abnormal cell.

Cause: This type of lymphocytosis is more concerning because it can indicate a lymphoproliferative disorder or malignancy, such as chronic lymphocytic leukemia (CLL) or lymphoma. In monoclonal lymphocytosis, the cells are often abnormal or cancerous.

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9
Q

Is canine herpesvirus enveloped or non enveloped?

A

Enveloped

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10
Q

How is canine herpesvirus transmitted?

A

Direct oronasl contact, and transplacental

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11
Q

What cells does canine herpesvirus affect?

A

Respiratory and urogenital

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12
Q

Describe the lifespan of the canine herpesvirus

A

IP 6-10 days: lifelong latent infection of neural ganglia with periodic reactivation of shedding

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13
Q

A neonate presents to you with incessant vocalization, anorexia, dyspnea, and abdominal pain. Which microorganism do you suspect?

A

Canine herpesvirus

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14
Q

What, if any, effects does canine herpesvirus have if a naive bitch is infected during the last 3 weeks of gestation?

A

Late term abortion or neonatal death within the first few weeks

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15
Q

What is the gold standard method of diagnosis?

A

Virus isolation or PCR

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16
Q

What is the prognosis for canine herpesvirus?

A

Poor for infected puppies

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17
Q

Is there a vaccine available against canine herpesvirus? If so, what kind?

A

No vaccine is available

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18
Q

Name a differential diagnosis for canine herpesvirus

A

Bacterial sepsis

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19
Q

Describe the feline panleukopenia virus

A

SS non-enveloped DNA virus

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20
Q

Which species are affected by feline panleukopenia?

A

Domestic and wild cats, foxes, mink, and racoons

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21
Q

What is a predisposing factor for feline panleukopenia?

A

Being a cat <1 yr of age

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22
Q

What is the mode of transmission/infection for feline panleukopenia?

A

Fecal-oral, contaminated fomites, in utero

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23
Q

Describe the life cycle of feline panleukopenia

A
  • Replicates in oropharlymphoid tissue, after that disseminates in blood to all tissues
  • Replicates in dividing cells like parvo
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24
Q

Describe the clinical signs of feline panleukopenia

A
  • GI
  • CNS
  • Hydrocephaly
  • Cerebellar hypoplasia
  • Retinal degeneration
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25
Q

What labwork findings do you usually see with feline panleukopenia?

A
  • Leukopenia (65%)
  • Thrombocytopenia (54%)
  • Anemia 48%
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26
Q

What is the gold standard method for diagnosing feline panleukopenia?

A

Canine parvovirus antigen

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27
Q

What is the prognosis for cats with feline panleukopenia?

A

Cats that survive the first 5 days of treatment usually recover

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28
Q

FIP is a mutation of what virus?

A

Feline coronavirus

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29
Q

Is the FIP virus enveloped or nonenveloped?

A

Enveloped

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30
Q

List 3 predisposing factors for FIP

A
  • Multicat environments
  • Purebreeds (Abyssinian, Bengals, Birmans)
  • Bimodal distribution
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31
Q

Are neuro signs more common with wet or dry FIP?

A

Dry

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32
Q

What is the mode of transmission for FIP?

A

Fecal to oral

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33
Q

How long can FIP survive in the environment?

A

< 1-2 days; readily inactivated by disinfectants

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34
Q

How many day after infection does FIP begin to shed?

A

2 days

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35
Q

Why does non effusive FIP occur?

A

Due to partial CMI response

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36
Q

Why does effusive FIP occur?

A

Occurs in cats unable to mount an immune response

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37
Q

FIP affects (monocytes/macrophages/lymphocytes) (choose 2)

A

FIP affects monocytes and macrophages. It does NOT affect lymphocytes

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38
Q

What percentage of FIP cases have neurological signs?

A

10%

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39
Q

After cardiomyopathy and neoplasia, what is the next most common cause of pericardial effusion in cats?

A

FIP

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40
Q

What is a common labwork finding in an FIP cat?

A
  • Hyperglobulinemia
  • A:G ratio is usually <0.8
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41
Q

Is distemper an enveloped or unenveloped virus?

A

Enveloped

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42
Q

Aside from dogs, what species are susceptible to distemper?

A

Raccoons, ferrets, mink, and large wild felidae

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43
Q

What is the mode of transmission of distemper?

A

Oronasal, all secretions

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44
Q

When does distemper shedding usually resolve?

A

Shedding usually resolves after 1-2 weeks, but up to 3-4 months

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45
Q

Is distemper hardy in the environment?

A

No, it dies after a day at room temp and is inactivated by heat, drying, and disinfectants

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46
Q

What are some clinical signs/pathophysiology of distemper?

A
  • Respiratory, GI
  • CNS signs (demyelinating leukoencephalomyelitis weeks to years after infection), myoclonus
  • Myocarditis, fever, anorexia, diarrhea
  • Hyperkeratosis of foot pads, enamel hypoplasia
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47
Q

What labwork findings will you see with distemper virus?

A

CDV inclusions in RBC/WBCs

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48
Q

What type of vaccine is available for distemper virus?

A

Modified live vaccine

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49
Q

Is canine parvovirus an enveloped or non enveloped virus?

A

Non enveloped

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50
Q

What is the mode of transmission of parvo?

A

Fecal to oral - affects oropharyngeal tissue

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51
Q

What are some clinical signs of parvo?

A

Enteritis, bone marrow suppression, and myocarditis (if infected in utero)

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52
Q

When we think of the parvovirus we see clinically, is that CPV 1 or CPV 2?

A

CPV 2. CPV 1 has less to no pathogenesis

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53
Q

Name 3 breeds that are especially susceptible to parvo

A

Rottweilers, Dobermans, Pitt Bulls

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54
Q

Is rabies an enveloped or non enveloped virus?

A

Enveloped

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55
Q

What species can be affected by rabies?

A

All warm blooded animals. Endemic in fox, raccoon, skunk, bat

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56
Q

What is the mode of transmission of rabies after inoculation?

A

It enters the myocytes then spreads to NMJ, travels to CNS within intraxonal fluid from peripheral nerves

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57
Q

What are the 3 stages of rabies?

A
  • Prodromal (change in behaviour)
  • Ferocious
  • Paralytic
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58
Q

In rabies patients, death is expected in how many days?

A

7-10

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59
Q

What is the gold standard diagnosis for rabies?

A

Direct fluoroscent antibody of nervous tissue

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60
Q

Describe FIV

A

It is a retrovirus; enveloped RNA virus

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61
Q

What species does FIV affect?

A

Cats and wild cats

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62
Q

What are some predisposing factors of FIV?

A
  • History of bite wounds
  • Older age
  • Male
  • Outdoor access
  • FeLV infection
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63
Q

What are the modes of transmission of FIV?

A
  • Bites
  • Transplacental through milk
  • Venous blood transfusion
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64
Q

Is FIV hardy in the environment?

A

No, it is very susceptible to disinfection

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65
Q

Describe the life cycle of FIV

A
  • FIV invades cells via CD134, which is expressed on feline CD4+ T cells, B cells, activated macrophages, and CXCR4 (chemokine)
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66
Q

In FIV, RT enzyme is prone to_____? What does this do to retroviral DNA?

A

Prone to error; mutation rate of retroviral DNA is high, which causes disruption of proto-oncogenes

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67
Q

What are the 3 phases of FIV?

A
  • Acute
  • Subclinical
  • Terminal
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68
Q

What clinical signs will you see with FIV?

A
  • Transient neutropenia due to decreased CD4
  • Gingivostomatitis
  • Diarrhea
  • Fever
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69
Q

What is the most common labwork finding with FIV?

A

Hyperproteinemia (94.5-11g/dL)

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70
Q

What is the gold standard diagnosis for FIV?

A
  • The ELISA FIV antibody against P24 core protein
  • Western Blot
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71
Q

What is the treatment for FIV?

A

Zidovuldin: blocks reverse transcription of retrovirus and inhibit infection of new cells - best in acute infection

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72
Q

What does the chance of lymphoma increase to if the patient has FIV?

A

5x higher chance

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73
Q

Describe the FELV virus

A

Retrovirus; enveloped RNA virus

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74
Q

What is the mode of transmission of FELV?

A
  • Prolonged close contact with salivary secretions
  • Biting (to a lesser extent)
  • Transplacental transmission
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75
Q

Describe the life cycle of FELV

A
  • Progresses more rapidly than FIV and is more pathogenic
  • Many cats in early stage of FeLV infection regress to Permanent viral latency
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76
Q

What are some clinical signs of FeLV?

A
  • Fever
  • Lethargy
  • Peripheral lymphadenopathy
  • Neoplasia
  • Opportunistic infections
  • PRCA
  • Immune mediated disease
  • Neuro
  • Repro
  • GI
  • Spastic pupil syndrome
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77
Q

What will you see on labwork in FeLV infection?

A

Macrocytic anemia

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78
Q

What is the gold standard diagnosis for FeLV?

A
  • p27 ELISA antigen testing
  • Culture or PCR of bone marrow
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79
Q

What is a treatment for FeLV?

A
  • Zidovudine
  • Feline recombinant interferon omega
  • Human recombinant interferon alpha
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80
Q

What does the chance of developing lymphoma increase to in an FeLV patient?

A

60x higher chance of developing lymphoma

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81
Q

What is the most common type of lymphoma seen in FeLV patients?

A

Thynic/mediastinal

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82
Q

Ehrlichia canis is an _____ gram ____ bacteria

A

Intracellular gram negative

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83
Q

What is the distribution of ehrllichia canis?

A

Worldwide, but usually tropical/subtropical

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84
Q

What species are affected by e.canis?

A

Dogs, cats (reported, but clinical ehrlichiosis rarely reported)

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85
Q

What is a predisposing factor for e.canis?

A

GSD are more susceptible
A 1998 paper showed non-spenectomized dogs have worse disease

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86
Q

What is the mode of transmission of e.canis?

A

Transmitted via Rhipicephalus sanguineus (Brown Dog Tick) and Derm. variabilis

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87
Q

What cells does e.canis affect?

A

Infects monocytes

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88
Q

What is the life cycle of e.canis?

A

Transmitted only transstadially (from larva to nymph to adult) within tick, but not transovarially. Organism transmits to dog via tick bite, where it infects monocytes. Tick larvae or nymphs acquire infections when they feed on infected dogs

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89
Q

E.canis infection has what phases?

A

Acute, Subclinical, and Chronic

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90
Q

What are some clinical signs of e.canis?

A
  • Vasculitis
  • Fever
  • Lethargy
  • Inappetence
  • Weight loss
  • Lymphadenomegaly
  • Splenomegaly
  • Mucosal hemorrhage
  • Uveitis
  • Pallor edema
  • Sometimes neuro
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91
Q

What labwork findings do you see with e.canis?

A
  • Thrombocytopenia
  • Non-regenerative anemia
  • Hyperglobulinemia
  • Morulae may be visible in circulating monocytes
  • Pancytopenia is seen with chronic disease (hypoplasia of all bone marrow cells)
  • Marked granular lymphocytosis and bone marrow plasmacytosis may occur
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92
Q

What is the gold standard diagnosis for e.canis?

A

IFA (indirect immunofluorescent antibody)
Serologic cross reactivity to other Ehrlichia species occurs
PCR is helpful in the acute ehrlichiosis

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93
Q

How many days post infection can IFA be detected?

A

7-28 days

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94
Q

What is the treatment for e.canis?

A

Doxycycline x 28 days. Most dogs with acute disease show clinical improvement within 1-2 days

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95
Q

What are some mortality risk factors for e.canis?

A
  • Severe leukopenia
  • Severe anemia
  • Hypokalemia
  • Prolonged aPTT
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96
Q

Describe ehrlichia chaffensis

A

Human monocytic ehrlichiosis

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97
Q

E.chaffensis is an _____, _____ bacteria

A

Intracellular, Gram negative

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98
Q

What is the distribution of e.chaffensis?

A

Southern and south central US

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99
Q

What species does e.chaffensis affect?

A

Dogs as possible reservoir, but a disease of humans

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100
Q

What is the mode of transmission of e.chaffensis?

A

Transmitted via Amblyomma Americanum; infects monocytes

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101
Q

What are some clinical signs of e.chaffensis?

A
  • Vasculitis
  • Vomiting
  • Epistaxis
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102
Q

What is the gold standard diagnosis for e.chaffensis?

A

PCR

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103
Q

What is the treatment for e.chaffensis?

A

Tetracycline

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104
Q

Describe ehrlichia ewingii

A

Canine granulocytic ehrlichiosis; intracellular gram negative bacteria

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105
Q

Can you culture e.ewingii?

A

No

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106
Q

What is the distribution of e.ewingii?

A

South central, SE US

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107
Q

What species is affected by e.ewingii?

A

Dogs

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108
Q

How is e.ewingii transmitted?

A

Transmitted via Ambylomma Americanum

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109
Q

What cells does e.ewingii infect?

A

Granulocytes - neutrophils, eosinophils, basophils

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110
Q

How is e.ewingii transmitted?

A

Only transsladially (from larva to nymph to adult) within tick, but not transovarially

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111
Q

What are some clinical signs of e.ewingii?

A
  • Fever
  • Lethargy
  • Inappetence
  • Lameness/reluctance to move
  • Stiff gait
  • Joint effusion
  • Poss neuro signs
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112
Q

What are some labwork findings with e.ewingii?

A
  • Non regenerative anemia
  • Thrombocytopenia
  • Reactive lymphocytosis
  • Morulae may be visible, but indistinguishable from A. phagocytophilum
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113
Q

What is the gold standard diagnosis for e.ewingii?

A

Can use Idexx 4DX (serology) but not specific to e.ewingii; PCR only means to confirm active infection

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114
Q

What is the treatment for e.ewingii?

A

Doxycycline x 14-28 days

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115
Q

Describe anaplasma phagocytophilum

A

Canine granulocytic anaplasmosis; gram negative obligate intracellular bacteria

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116
Q

What is the distribution of anaplasma phagocytophilum?

A

Upper midwest, NE, and western states in US, most of the world

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117
Q

What species are affected by anaplasma phagocytophilum?

A

Dogs, cats, humans

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118
Q

What are some predisposing factors for infection with anasplasma phagocytophilum?

A
  • Infection with other tick borne pathogens is a risk factor
  • In upper Midwest US, a bimodal age distribution exists, with 25% of dogs 1 year or less, and 50% of at least 8 years
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119
Q

What is the mode of transmission of anasplasma phagocytophilum?

A

Transmitted by Ixodes scapularis/pacificus; ticks must attach for 1.5-2 days for transmission to occur

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120
Q

What is the life cycle of anasplasma phagocytophilum?

A
  • Infects neutrophils, but also eos, where it forms host membrane-enclosed morulae
  • Enters neutrophil through caveolae-medendocytosis, reduces neutrophil motility and phagocytosis; delays neutrophil apoptosis
  • Can also infect bone marrow cells, endothelial cells, megakaryocytes
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121
Q

What are some clinical signs of Anaplasma phagocytophilum?

A
  • Majority of dogs show no clinical signs
  • Fever, lethargy, inappetence, sameness (polyarthritis)
  • Less commonly V/D, cough, epistaxis and neck pain
  • Mild Peripheral lymphadenopathy Splenomegaly, petechiae
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122
Q

What are some labwork findings in Anaplasma phagocytophilum?

A
  • Mild to moderate thrombocytopenia (90% of dogs) +/- other cytopenias (dogs have anti-platelet antibodies)
  • Hypoalbuminemia, hyperglobulinemia, proteinuria
  • Cats rarely are thrombocytopenic, they are most commonly lymphopenic
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123
Q

What is the gold standard diagnosis for Anaplasma phagocytophilum?

A
  • Acute and convalescent serology
  • PCR may be more useful for acute infection
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124
Q

What is the treatment and prognosis for Anaplasma phagocytophilum?

A

Doxycycline x 14-28 days with good prognosis

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125
Q
A
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126
Q

What species does Anaplasma platys affect?

A

Dogs

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127
Q
A
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128
Q

How is Anaplasma platys transmitted?

A

Suspected to be transmitted by Rhipicephalus sanguineus

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129
Q

What is the life cycle of Anaplasma platys?

A

Infects platelets, where it forms morulae

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130
Q

What are the clinical signs of Anaplasma platys?

A

Usually shows no signs, however fever, lethargy, lymphadenopathy, uveitis, pallor, and mucosal hemorrhages can occur

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131
Q

What labwork findings can you see with Anaplasma platys?

A

Thrombocytopenia (can be <20,000), +/- Mild non regenerative anemia

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132
Q

What is the gold standard diagnosis for Anaplasma platys?

A
  • Can use acute and convalescent serology with IFA but cross-reacts with A. phagocytophilum
  • ELISA assays only indicate previous exposure to Anaplasma species
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133
Q

What is the recommended treatment for Anaplasma platys?

A

Doxycycline x 7-28 days

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134
Q

Co-infection of dogs with A.platys and E.canis may lead to more severe_________

A

Anemia

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135
Q

Describe Rickettsia rickettsii

A
  • Rocky Mountain Spotted Fever (RMSF)
  • A gram negative, obligately intracellular bacteria
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136
Q

What is the distribution of RMSF?

A
  • Americas (North, Central, and South)
  • Most cases in the US occur in SE and south central states
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137
Q

What species does RMSF affect?

A

Dogs and humans

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138
Q

What are some predisposing factors for RMSF?

A
  • Dogs that live outdoors
  • Severe disease reported in English springer spaniels with phosphofructokinase deficiency and GSDs (RBC fragility)
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139
Q

What is the life cycle of RMSF?

A
  • It infects endothelial cells thus causing vasculitis, then spreads through lymphatics or directly into bloodstream to small capillaries
  • Bacterial outer membrane protein (OmpA) and outer membraine protein B (OmpB) are important for attachment, adhesion, and virulence
  • It is an acute disease. Chronic infection has not been documented in dogs or people
  • Transstadial and transovarial
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139
Q

How is RMSF transmitted?

A

via Dermacentor, Rhipicephalus sanguineus, Ambyloma

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140
Q

What are some PE findings with RMSF?

A
  • Vasculitis (causes rash in people that look like spots)
  • Acute fever (80% of dogs)
  • Vomitting, ocular signs, lymphadenomegaly, Splenomegaly, Peripheral edema, cutaneous hyperemia and necrosis, polyarthritis, Neuro signs, epistaxis, tachypnea, petechia, ecchymosis
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141
Q

What labwork findings will you see with RMSF?

A
  • Thrombocytopenia (Vasculitis, IM destruction)
  • Non regenerative anemia
  • Hypoalbuminemia
  • Hyponatremia
  • Mild hyperbilirubinemia
  • Proteinuria
  • Prolonged aPTT
  • Increased serum fibrinogen
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142
Q

What is the gold standard diagnosis for RMSF?

A
  • Acute and convalescent serology via indirect micro immunofluorescence (MIF) that detect IgM and IgG antibodies
  • There may be cross reactivity with Bartonela henselae
  • PCR confirms active infection, but not very sensitive
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143
Q

What is the recommended treatment for RMSF?

A

Doxycycline x 7-14 days

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144
Q

What is the prognosis for RMSF?

A

Good

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145
Q

What is Neorickettsia helminthoeca?

A
  • Salmon Poisoning Disease (SPD)
  • A gram negative, obligately IC bacteria
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146
Q

What is the distribution of Neorickettsia helminthoeca?

A

West coast US, British Columbia

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147
Q

What species are affected by Neorickettsia helminthoeca?

A

Dogs, foxes, coyotes, raccoons, captive bears

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148
Q

What are some predisposing factors for Neorickettsia helminthoeca?

A

Intact male dogs and Labradors are overrepresented

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149
Q

What is the mode of transmission of Neorickettsia helminthoeca?

A

Ingestion of infected trematode vector Nanophyetus salmincola, usually from uncooked or undercooked freshwater fish

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150
Q

What is the life cycle of Neorickettsia helminthoeca?

A
  • IP 2-14 d
  • Ingestion of encysted metacercariae is followed by mat of the trematode, which feeds on intestinal mucosa and inoculates the rickettsia into host
  • Infected trematode ova are shed in stool for 60-250 days. After several months, miracidia develop develop within the eggs, hatch, and penetrate the snail where they develop into rediae which gives rise to cercariae, which penetrate skin of fish and encyst as metacercariae
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151
Q

What are some PE findings with Neorickettsia helminthoeca?

A
  • Granulomatous inflammation in the stomach, intestines, LN, and spleen
  • Fever (70%), lethargy, inappetence to anorexia (100%), V/D (70%), Neuro signs (<20%), lymphadenomegaly, epistaxis, melena
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152
Q

What are some labwork findings with Neorickettsia helminthoeca?

A
  • Thrombocytopenia (70%)
  • Anemia (40%)
  • Hypoalbuminemia (>80%)
  • Hypoglobulinemia
  • Hypocholesteralemia
  • Elevated liver enzymes
  • Hyperbilirubinemia
  • Proteinuria
  • LN aspiration cyt with histiocytic hyperplasia should make you think of SPD
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153
Q

What is the gold standard diagnosis for Neorickettsia helminthoeca?

A
  • Combo zinc sulfate fecal float/fecal sedimentation (sensitivity likely >90%, specificity near 100%) + consistent clinical signs
  • LN or splenic aspirate cytology for detection of N.helminthoeca within macrophages (sens >70%)
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154
Q

What is the recommended treatment for Neorickettsia helminthoeca?

A

Tetracycline x 7 days; treat fluke infection with praziquantel

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155
Q

What is the prognosis for Neorickettsia helminthoeca?

A

Early treatment has excellent prognosis; without treatment will die within 5-10 days

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156
Q

What antimicrobials are NOT effective against Neorickettsia helminthoeca?

A
  • 1st generation cephalosporins
  • Penicillins
  • Aminoglycosides
  • Metronidazole
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157
Q

Describe mycoplasma haemofelis/haemocanis

A
  • A small unculturable mycoplasma that reside on the surface of RBCs
  • Cocci that sometimes form short chains of 3-6 organisms
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158
Q

What is the distribution of mycoplasma haemofelis/haemocanis?

A

Worldwide

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159
Q

What are some predisposing factors for M.haemofelis?

A
  • Younger age
  • Male
  • FeLV/FIV+
  • Splenectomy?
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160
Q

What are some predisposing factors for M.haemominutum?

A
  • Older
  • Male
  • FIV+
  • Nonpedigree
  • Outdoor
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161
Q

What are some predisposing factors for M.haemocanis?

A
  • Splenectomized dogs
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162
Q

What is the mode of transmission of M.haemocanis/haemofelis?

A
  • Biting or aggressive interactions are suspected
  • Ticks are suspected to transmit M.haemocanis
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163
Q

What tick transmits M.haemocanis?

A

Rhipicephalus sanguineus

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164
Q

What is the life cycle of M.haemocanis/haemofelis?

A
  • Organisms attaches to the surface of RBCs and cause extravascular hemolytic anemia with a strong regenerative response
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165
Q

What are some clinical signs of M.haemocanis/haemofelis?

A
  • Fever, lethargy, inappetence, weakness, pallor, pica, sudden death
  • Splenomegaly, mild icterus
  • Dogs with hemoplasmosis usually have no fever
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166
Q

What are some labwork findings with M.haemocanis/haemofelis?

A
  • Macrocytic, regenerative anemia
  • Howell-jolly bodies +/- agglutination +/- thrombocytopenia
  • Elevated ALT/AST due to hypoxia, hyperbilirubinemia
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167
Q

What is the gold standard diagnosis for M.haemocanis/haemofelis?

A
  • PCR
  • If using cytology, organisms need to be distinguished from basophilic stippling and Howell-Jolly bodies
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168
Q

What is the recommended treatment for M.haemocanis/haemofelis?

A

Doxycycline x 14 days in cats, suggested longer course for dogs (4 weeks - 12 weeks)

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169
Q

What is the prognosis for M.haemocanis/haemofelis?

A

Good with treatment

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170
Q

Describe Mycobacterium (M.tuberculosis complex, M. avium complex, lepromatous mycobacteria, nontuberculous mycobacterium)

A

Aerobic, nonmotile, non spore forming, gram positive, acid-fast pleomorphic bacilli

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171
Q

What is the distribution of mycobacterium?

A

Worldwide

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172
Q

What species are affected by mycobacterium?

A
  • Animals and humans
  • Cats are resistant to infection with M.tuberculosis
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173
Q

What are some predisposing factors for M.avium complex?

A
  • Being a basset hound, mini schnauzer
  • Possibly Yorkies, possibly due to an inherited CMI deficiency
  • Siamese, Abyssinians, and Somalis may be predisposed
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174
Q

What is the mode of transmission for M.tuberculosis complex?

A
  • Dogs are usually infected by aerosol exposure from humans (reverse zoonosis)
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175
Q

What is the mode of transmission for M.microti?

A
  • Cats are often infected with M.microti/M.bovis via rodents
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176
Q

What is the mode of transmission of M.avium complex?

A
  • Environ saprophytes (soil, dust, aquatic environment)
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177
Q

What is the mode of transmission of lepromatous mycobacteria?

A

Innoculation of the organism into skin through rodent or cat bites

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178
Q

What is the life cycle of mycobacterium?

A
  • Organism is ingested by macrophages but survive and replicate in them
  • Destruction of macrophages recruits lymphos/monos, which initiates tubercle form
  • MAC: cause opportunistic infection in immunocompromised individuals
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179
Q

What are some clinical signs of mycobacterium infection?

A
  • Cutaneous nodular, ulcerated, or draining skin lesions
  • Peripheral or intern lymphadenopathy
  • Penumonia
  • Osteomyelitis
  • Granulo infiltrates of lungs, liver, kidneys, LNs
  • 75% of cats with M.bovis/Microti have cutaneous nodular lesions +/- mandibular lphadenopathy
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180
Q

What are some labwork findings with mycobacterium?

A
  • Hypoalbuminemia
  • Hy[erglobulinemia
  • +/- hypercalcemia
  • Acid-fast staining insens
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181
Q

What is the gold standard diagnosis for mycobacterium?

A

Mycobacterial culture for MTBC infection

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182
Q

What is the recommended treatment for mycobacterium?

A
  • Isolation
  • Treatment is controversial due to possible zoonosis
  • Cats MTBC: fluoro/azithromycin/rifamycin; surgical excision of skin lesions if no dissemination
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183
Q

Describe leptospirosis

A
  • Zoonotic spirochete
  • Disease in dogs is primary by L. interrogans and L. kirschneri
  • Within the genus Leptospira there are more than 250 different serovars
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184
Q

What is the distribution of lepto?

A

Worldwide

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185
Q

What species are affected by lepto?

A

Dogs, rarely cats, humans

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186
Q

What are some predisposing factors for lepto?

A
  • Exposure to wildlife or farm animals
  • Exposure to water: outbreaks in dogs have occurred with periods of high annual rainfall
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187
Q

What is the mode of transmission of lepto?

A
  • Ingestion or contamination of a wound with urine/contaminated water
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188
Q

Is lepto hardy in the environment, or easily killed?

A

It is readily inactivated in the environment with excessive heat, UV radiation, disinfection, and freezing, but when conditions are optimal, it can survive in water/wet soil for weeks to months

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189
Q

What is the life cycle of lepto?

A

Penetrates intact MM or abraded skin, multiplies rapidly in the bloodstream leading to vaculitis and multiorgan failure; IP 7 days

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190
Q

What is the pathophys of lepto?

A
  • Kidney and hepatic injury, less commonly myocardial damage, repro compromise, severe pulmonary hemorrhage syndrome (SPHS)
191
Q

What are some clinical signs of lepto?

A
  • Fever, lethargy, reulctance to move, anorexia, PU/PD (2nd NDI), v/d, icterus, respiratory difficulty, uveitis, mild general periph lymph, muscle pain, epistaxis
192
Q

What are some labwork changes seen with lepto?

A
  • 80-90% of dogs have azotemia
  • 53% of dogs have thrombocytopenia
  • 77% have glucosuria, proteinuria
  • 15% have elevated PT/PTT
193
Q

What is the gold standard diagnosis for lepto?

A

Paired titers using microscopic agglutination test (MAT) - affected by previous vaccine, usually not more than 1:1600

194
Q

What is the recommended treatment for lepto?

A

Doxy x 14 days

195
Q

What is the prognosis for lepto?

A

Excellent with early treatment

196
Q

Describe borrelial burgdorferi

A
  • Lyme Borelliosis
  • Vector borne spirochetosis caused by motile, corckscrew shaped bacteria
197
Q

What is the distribution of borrelial burgdorferi?

A

North America, Europe, Asia

198
Q

What species are affected by borrelial burgdorferi?

A

Humans, dogs

199
Q

What are some predisposing factors for borrelial burgdorferi?

A

Goldens and labs are overrepresented with Lyme nephritis

200
Q

Which tick transmits borrelial burgdorferi?

A

Ixodes ticks

201
Q

What is the life cycle of borrelial burgdorferi?

A
  • Infection is passed transstadially within the tick (larvae to nymph to adult) and not transovarially (from adult to egg)
  • Spirochete replicates at site of tick attachment, then replicates and spreads through connective tissue
  • Initial signs occur 2-5 months after tick bite
202
Q

What are some clinical signs of borrelial burgdorferi?

A
  • Most dogs (90%) have no signs
  • Can develop fever, non-erosive arthritis, lyme nephritis (membranoprolifglomeruloneph, many dogs with lyme neph are thrombocytopenic and have polyarthritis)
  • Lethargy, fever, lameness, swollen, painful joints, mild peripheral lymphadenopathy
203
Q

What are some labwork findings with borrelial burgdorferi?

A
  • Thrombocytopenia +/- anemia
  • Lyme nephritis
  • Isosthenuria, proteinuria (UPC 5 to >15)
  • Low AT act
  • Renal biopsy: subendothel dep of IgM, IgG, and C3 detected within glomeruli
  • Joint fluid: nondegn neut >5000 to >10,000 cells/ul)
204
Q

What is the gold standard diagnosis for borrelial burgdorferi?

A
  • Western blot
  • C6 ELISA detects antibodies against a portion of the VlsE lipoprotein (det IgG antibodies 3-5 weeks after infection, not affected by Lyme vax
  • Available in 4DX and quant C6 send out test
205
Q

What is the recommended treatment for borrelial burgdorferi?

A
  • Doxy x 4 weeks
  • Clinical response usually within 2 days
  • Amoxicillin can be used if doxy not tolerated
  • Lyme nephritis: clinical improvement doesn’t generally occur with doxy lone, need to tx PLN (ARB or ACEi, nutritional support, antithromb +/- immunosuppressants)
206
Q

What is the prognosis for borrelial burgdorferi?

A

Prognosis for Lyme arthitis is good, prognosis guarded to poor with Lyme nephritis

207
Q

What is the most common vector borne infection in humans in the US?

A

borrelial burgdorferi

208
Q

What is the primary mode of transmission of borrelial burgdorferi to humans?

A

Nymphal ticks because they’re small and go unnoticed

209
Q

What is the first sign of borrelial burgdorferi infection in humans?

A

A ‘bulls-eye’ rash that doesn’t occur in dogs

210
Q

Describe Bartonella henselae and carrridgeiae and Bartonella vinsonii susp berkhoffii

A
  • Bartonellosis
  • Fastidious
  • Intraerythrocytic gram negative bacteria
211
Q

What is the distribution of Bartonella?

A
  • Worldwide
  • Highest prevalence in subtropical/tropical regions
212
Q

What species are affected by Bartonella?

A
  • Cats (main reservoir for B. henselae)
  • Dogs
  • Humans
213
Q

What are some predisposing factors for Bartonella?

A
  • <1 year old cats and stray cats more likely to be bacteremic
  • Older cats are more likely to be seroive
  • Prevalence of bacteremic cats highest in warm, humid climates
214
Q

What is the mode of transmission of Bartonella?

A
  • Fleas (Ctenocephalides felis)
  • Poss other flea species (Pulex) and vectors like ticks, lice, biting flies
215
Q

What is the life cycle of Bartonella?

A
  • After infection, replicates in RBCs and can also infect endothelial cells and bone marrow progenitor cells, then establishes chronic, often subclinical bacteremia
216
Q

What are some clinical signs of Bartonella?

A
  • Most infections in dogs and cats are subclinical
  • Cats: endocarditis, myocarditis, diaphragm myositis (B. henselae), probable assoc with osteomyelitis, sys reactive angioendotheliomatosis (B. v. berkhoffii)
  • Dogs: endocarditis (usually affects mitral valve), sys pyogran dz/lymphadenitis, hepatitis, erosive polyarthritis. Susp to cause polyarth, epistax, thrombocyto, splenomeg
217
Q

What labwork findings would you see with Bartonella?

A

Mild, nonregen anemia, var leukocyt, mild thrombocytopen, hypoalbumin, +/- hyperglob, proteinuria, ALT/ALP elev

218
Q

What is the gold standard diagnosis for Bartonella?

A
  • Culture THEN PCR using Bartonella Alpha Proteobacteria Growth Medium (BAPGM): risk of false positive since healthy dogs/cats can have Bart in their blood
  • Do NOT use serology (fewer than half of antibody-pos cats are bacteremic, and 3-15% of antibody-neg cats are bacteremic
219
Q

What is the recommended treatment for Bartonella?

A
  • Efficacy hasn’t been established for any antimicrobial to eliminate Bartnella bacteremia in cats/dogs
  • Doxy + fluoroquinolone
220
Q

What is the prognosis for Bartonella?

A
  • Prognosis of Bart endocarditis in dogs/cats is generally poor
  • Dogs: complications of endocarditis include TE dz, neutrophilic polyarthritis
221
Q

What effects can Bartonella have on immunocompromised humans?

A
  • Causes cat scratch disease in immunocompetent humans as well as vasculoprolif disorders in immunocomp humans
222
Q

Describe Brucella canis

A

Small, gram negative, non spore form aerobic coccobacillus

223
Q

What is the distribution of Brucella canis?

224
Q

What species are affected by Brucella canis?

A

Humans, dogs

225
Q

What is the mode of transmission of Brucella canis?

A
  • Direct exposure to contaminated body fluids (oral, nasal, conj, venereal), Transplacental, direct cut innoc, aerosol route
226
Q

Is Brucella canis hardy in the environment?

A

No, it is readily inactivated by disinfectants such as quaternary amm compounds, bleach)

227
Q

What is the life cycle of Brucella canis?

A

Reproduce in regional LN, bacteremia —> reticuloendothelial cells, prostate, uterus, and placenta (B. canis has predilection for steroid-dep (reproductive) tissues)

228
Q

What are the clinical signs of Brucella canis?

A
  • No signs or infert, abort, discospondylitis
  • Uveitis
  • Rarely osteomy/meningoenceph
  • Clinical signs usually subtle
  • Rarely fever, lumbar pain, lameness, weight loss, leth, preg loss
  • Scrotal enlarge/dermatitis, test atrophy, lymphadenopathy, splenomegaly
229
Q

What screening test is used for Brucella canis?

A

Rapid slide agglut test (RSAT/ME-RSAT)

230
Q

What is the gold standard diagnosis for Brucella canis?

A

Usu based on clin signs, serology, culture, history, and/or PCR assays, B. canis culture

231
Q

What is the treatment for Brucella canis?

A
  • Report
  • Removal from breeding
  • Prog/quarantined, euthanasia, neutering
  • AB tx has been unrewarding, likely because it is IC and bacteremia is periodic
  • Combo tetracycline and aminoglycosides
232
Q

What is the prognosis for Brucella canis?

A

Relapses are common

233
Q

What should increase your suspicion for B.canis?

A
  • A lack of abnormalities on labwork
  • NY state DL at Cornell, Tifton Vet Dx/Invest lab in Georgia, and UF = reliable for def testing
234
Q

Describe Clostridium botulinum

A
  • Botulism
  • Gram positive, anaerobic spore forming bacilli
  • Extremely resistant in the environment
235
Q

What is the distribution of Clostridium botulinum?

236
Q

What species are affected by Clostridium botulinum?

A

Rarely in dogs, esp rare in cats

237
Q

What are some predisposing factors for Clostridium botulinum?

A

Most afflicted dogs are medium to large breed and intact

238
Q

What is the mode of transmission of Clostridium botulinum?

A

Ingestion of preformed toxin within carrion; resists boiling and disinfection with alcohol or formalin

239
Q

What is the life cycle of Clostridium botulinum?

A
  • Botulism in dogs/cats almost alway results from ingestion of toxin C (A-G exist)
  • Absorbed into blood stream –> travels to NMJ of peripheral cholingergic synapses and inhibits release of ACh
240
Q

What are the clinical signs of Clostridium botulinum?

A
  • Ascending symmetrical flaccid paralysis
  • ME
  • Signs of autonomic dysfunction
  • Clinical signs occur within 12-72 hours after ingestion
  • Death can occur due to resp muscle paralysis
  • Fever usually absent, ataxia, pelvic limb paresis
  • Quadriplegic but can still wag tail
  • Tachypnea (from diaphraghm muscle weakness)
  • Aspiration pneumonia
241
Q

What is the gold standard diagnosis for Clostridium botulinum?

A

Mouse inoculation bioassay

242
Q

What is the treatment for Clostridium botulinum?

A
  • No specific treatment
  • Equine antitoxin available for humans
243
Q

What is the prognosis for Clostridium botulinum?

A

Good without complications

244
Q

What is a differential diagnosis for Clostridium botulinum?

A
  • Polyradiculoneuritis, paralytic rabies, tick paralysis, MG
245
Q

Describe Clostridium tetani

A
  • Tetanus
  • A gram positive anaerobic spore forming bacilli
246
Q

What is the distribution of Clostridium tetani

247
Q

What species are affected by Clostridium tetani?

A

Occasionally dogs, rare in cats

248
Q

What are some predisposing factors for Clostridium tetani?

A
  • Occurs most often in young, large breed, active, intact male dogs
  • Cats are often young with outdoor access
249
Q

What is the mode of transmission of Clostridium tetani?

A
  • Cutaneous inoculation of spore into a wound
  • Resists boiling and disinfecting with alcohol or formalin
250
Q

What is the life cycle of Clostridium tetani?

A
  • Replicates locally in wound, binds to presyn terminals of LMNs
  • Travels via retrograde axonal flow
  • Interferes with release of GABA and glycine
251
Q

What are some clinical signs of Clostridium tetani?

A
  • Unhindered excit of motor neurons
  • Spastic paralysis and dysfunction of SNS and PSNS
  • Clinical signs occur 3d to 3 weeks
  • Dysphagia, regurg, voice change, death due to resp muscle paralysis
  • Disease in cats usually localized to limb
  • In dogs, wrinkled forehead, erect ears, retracted lips (risus sardonicus), prolonged 3rd eyelid, muscle stiffness, hyperthermic, difficult to exprss bladder, hypoventilation, bradycardia
252
Q

What are some labwork findings with Clostridium tetani?

A
  • Mild increase AST
  • Myoglobinuria
  • Severe hyperthermia in dogs may lead to lab evidence of MODS
  • Rarely dogs have evidence of hiatal hernia
253
Q

What is the treatment for Clostridium tetani?

A
  • Antitoxin + antibiotics against C.tetani (metro or pen G)
  • Tetanus antitoxin is more widely available, single IV dose (equine antitoxin), or IM (Human)
  • Antitoxin admin doesn’t reverse exisitng paralysis, but may neutralize free toxin
254
Q

What is the prognosis for Clostridium tetani?

A

Good without complications

255
Q

What are some differential diagnoses for Clostridium tetani?

A
  • Strychnine toxin
  • Hypocalcemia
  • Metaldehydetox
  • Extraocmyositis
256
Q

Describe Yersinia pestis

A
  • Plague
  • Non motile, gram negative coccobacilli
  • Belongs to Enterobacteriaceae
257
Q

What is the distribution of Yersinia pestis?

A

Southwest US

258
Q

What species are affected by Yersinia pestis?

A

Cats are considerably more susceptible than dogs

259
Q

What is the mode of transmission of Yersinia pestis?

A

Flea borne via a variety of rodent flea species, ingestion of infected rodents/rabbits

260
Q

What is the life cycle of Yersinia pestis?

A
  • IP 1-6 days
  • Yp is maintained in wild burrowing rodents; after inoculation by fleas, Y pestis is taken up by mononuclear cells where it survives and replicates, then is carried by lymphatics to regional LNs
261
Q

What are some clinical signs of Yersinia pestis?

A
  • Fever (71%)
  • Lethargy, inappetence, lymphadenopathy (up to 8cm abscesssated)
  • SC abscess, bubo (enlarged and tender LN)
  • In some cats, bubo form is accompanied by bacteremia, with associated endotoxemia and sepsis, and DIC/MODS can occur
  • Death can occur in as few as 2-3 days without treatment
262
Q

What is the gold standard diagnosis for Yersinia pestis?

A

Acute and convalescent serology
- Also can use culture, direct fluorescent antibody testing (IFA) on LN aspirates, tissues

263
Q

What is the treatment for Yersinia pestis?

A
  • Isolation, contact public health authorities, abscess drainage, PPE worn, AB (doxycycline x 10d or gentamicin x 10d), treatment for fleas
264
Q

What is the prognosis for Yersinia pestis?

A

Good with prompt treatment

265
Q

How zoonotic is Yersinia pestis?

A

10% of human plague cases result from exposure to infected cats (bites,scratches, resp droplets, infected fleas)

266
Q

What are some differential diagnoses for Yersinia pestis?

A
  • Tulaermia
  • Cat bite abscesses
  • Strep
  • FIP
267
Q

Describe Francisella tularensis

A
  • Tularemia
  • Aerobic, gram negative coccobacillus
  • Extremely infectious but uncommon
268
Q

What is the distribution of Francisella tularensis?

A

Most disease reported in US, Northern Hemisphere

268
Q

What species are affected by Francisella tularensis?

A

Dogs, cats, humans

269
Q

What are some predisposing factors for Francisella tularensis?

A
  • Cats are more susceptible than dogs
  • Hx of rabbit ingestion most often described
270
Q

What is the mode of transmission of Francisella tularensis?

A

Transmitted via tickets (Dermacentor andersoni/variabili and A.americanum), biting flies, inhalation or ingestion of organism, direct skin contact

271
Q

What is the life cycle of Francisella tularensis?

A
  • IP 1-5 days
  • Survives in macrophages through evasion of cell dest by phagosomes and inhibition of resp burst, disseminated to local LN –> bacteremia and sepsis
  • Can infect hepatocytes and alv epith cells
272
Q

What are some clinical signs of Francisella tularensis?

A
  • Fever, lethargy, inappetence, lymphadenopathy, SC abscesses, draining skin lesions, splenomegaly, hepatomegaly, icterus, vomiting, oral/lingual ulcers
273
Q

What are some labwork findings with Francisella tularensis?

A
  • Thrombocytopenia common in cats
  • Hypoglycemia, azotemia, liver enzyme elevation, hyperbilirubinemia
  • Many cats are diagnosed on necropsy
274
Q

What is the gold standard diagnosis for Francisella tularensis?

A

Acute and convalescent serology

275
Q

What is the treatment for Francisella tularensis?

A
  • Isolation
  • Contact public health authorities
  • Parenteral aminoglycosides such as gentamicin, doxycycline is associated with higher relapse rate in humans x 2-3 weeks
276
Q

How zoonotic is Francisella tularensis?

A

Cats and less commonly dogs can transmit tularemia to humans (usually cat bites)

277
Q

What are some differential diagnoses for Francisella tularensis?

A
  • Plague
  • Cat bite abscess
  • Strep infection
  • FIP
  • Mycobacterial infection
278
Q

Describe Blastomyces dermatitidis

A
  • Blastomycosis
  • Dimorphic fungus with thick, refractile cell wall
  • Broad-based budding
279
Q

What is the distribution of Blastomycosis?

A
  • Primarily North America, Great Lakes area, Ohio and Miss river valleys
280
Q

What species is affected by Blastomycosis?

A
  • Dogs, humans, cats (rarely rep), sea lions
281
Q

What are some predisposing factors for Blastomycosis?

A
  • Young, adult, large breed
  • Slight male predisposition
  • Coonhounds, pointers, Weimers, labs, goldens, and dobies are overrepresented
  • Living near water, exposure to soil disturbance
282
Q

What is the mode of transmission of Blastomycosis?

A
  • Inhalation of conidia from environment; rarely cutaneous inoculation: extrapulmonary sites of predilection: skin, eye, bone, repro, CNS
283
Q

What is the life cycle of Blastomycosis?

A
  • IP est 5-12 weeks
  • Grows as a mycelial form in environ and as a thick walled budding yeast in tissues
  • Hyphae within soil produce conidia, which become aerosolized and inhaled by host, where they transform into yeast that can resist dest by neutrophils
284
Q

What are some clinical signs of Blastomycosis?

A
  • Yeasts trigger pyogran inflammation
  • Fever (50%), inappetence, weight loss, cough, tachypnea, resp diff, nod/ulcerative cutan lesions, ocular lesions, lameness, GI signs, PU/PD, neuro (<5%), nasal signs, TE
285
Q

What are some labwork findings with Blastomycosis?

A
  • Mild, non-regen anemia
  • Hyperglob (60%)
  • Hypoalbuminemia (77%)
  • Mild hypercalcemia
  • Proteinuria
  • Lung rad patterns variable
  • 25% have tracheobronchial lymphadenopathy
286
Q

What is the gold standard diagnosis for Blastomycosis?

A
  • Urine Blastomyces cell wall galactomannan antigen (94% sensitivity, cross react may occur)
  • Cytologic exam (insens, ~70% on TTL)
287
Q

What is the treatment for Blastomycosis?

A
  • Itraconazole !3-6 months +/- amphotericin B
288
Q

What is the prognosis for Blastomycosis?

A
  • Cure rates 50-75%, relapse can occur
  • Negative prognostic indicators: CNS, severe lung disease, high band neutrophil count
289
Q

Describe the zoonosis of Blastomycosis

A
  • Virul factor BAD-1 (cell surface glycoprot) is an adhesin that binds to host cell receptors on macrophages
  • Genotypes A-E
  • Dogs are sentinels for human exposure
290
Q

What are some differential diagnoses for Blastomycosis?

A
  • Neoplasia
  • Other deep mycoses
  • Protothecosis
  • Mycobacteria
291
Q

Describe Hisoplasma capsulatum

A
  • Histoplasmosis
  • Dimorphic, soil-borne fungus
  • Non-encapsulated
  • 2-4 micron in dm, oval, surrounded by clear halo (similar in size to Sporothrix)
292
Q

What is the distribution of Hisoplasma capsulatum?

A
  • Worldwide, esp Ohio/Miss/Tenn/Miss river valleys
293
Q

What species are affected by Hisoplasma capsulatum?

A

Dogs, cats, and humans

294
Q

What are some predisposing factors for Hisoplasma capsulatum?

A
  • Sporting or workingdogs
  • Pointers overrepresented
  • Weim and Brittany Spaniels are at increased risk
  • Cats are more susceptible than dogs
  • Persians slightly over represented
  • Soil disturbance
  • Exploration of bat caves
295
Q

What is the mode of transmission of Histoplasmosis?

A
  • Inhalation of microconidia from environment
  • Bats are the primary reserv and dissem it; H cap is found in high concentrations in avian guano
296
Q

What is the life cycle of Histoplasmosis?

A
  • IP 2-3 weeks to several years
  • In soil, mycelial phase forms macroconidia and microconidia
  • Microcon are inhaled by mamm hosts
  • Within lungs, the microcon transition to unicellular yeast and enters and replicates inside alveolar macrophages
  • yeast migrate to local LNs, liver, spleen
297
Q

What are some clinical signs of Histoplasmosis?

A
  • Gran response in lungs, fibrosis, scarring
  • Predil for bone marrow
  • SI, LI, panc, skin, bones, CNS, eyes
  • Dissem dz occurs in dogs with def CMI
  • Fever, cough, tachypnea, organomeg, diarrhea/GI signs (can occur w/o resp signs)
  • Weight loss,m pallor, icterus, hepatosplenomeg, lymphadenomeg
  • Nasal discharge
  • Non-spec in cats
  • 20% of cats have skeletal involvement
298
Q

What are some labwork findings in Histoplasmosis?

A
  • Mild to severe no-reg anemia, var WBC count, +/- thrombocytopenia
  • Mild to severe hypoalbumin (>75% dogs/cats)
  • Dogs: hyperglob, inc LEs, hyperbilirubin, inc PT/PTT (poss from DIC)
  • Cats: inc ALT/AST, rarely hyperbilirubin and ALP
  • Hypercalc and hyperglob poss
299
Q

What is the gold standard diagnosis for Histoplasmosis?

A
  • Urine Histo antigen test (cross-react may occur)
  • Antigen levels become undetectable with successful tx
  • Cytologic exam
300
Q

What is the recommended treatment for Histoplasmosis?

A
  • Itraconazole or fluconazole ~6-12 months +/- amphotericin B (for severe pulmonary, diss, ro CNS disease)
301
Q

Where else can you find Histo organisms?

A
  • Bone marrow is a common site to yield organisms in cats, even with minimal hematologic abnormalities
302
Q

Describe Coccidiodes immitis

A
  • Coccidioidomycosis
  • C. immitis lim to central valley of CA
  • C. posadasii is found elsewhere; dimorphic, soil-borne fungi
  • On cyto, spherules are round, deeply basophilic, double walled, slightly crinkle struct, occ endospores are seen (thin, nonstain halo)
302
Q

What are some differential diagnoses for Histoplasmosis?

A
  • Other deep mycoses, protothecosis, mycobacteria
303
Q

What is the distribution of Coccidiodes immitis?

A
  • SW US (Bakersfield endemic “Valley Fever” and AZ)
  • Mexico, Central/South America
304
Q

What species are affected by Coccidiodes immitis?

A
  • Humans and dogs, less commonly cats
305
Q

What are some predisposing factors for Coccidiodes immitis?

A
  • Large-breed, young adult dogs
  • Housed outside during the day, roaming areas >1 acre, walking in the desert
306
Q

What is the mode of transmission of Coccidiodes immitis?

A
  • Inhalation of arthroconidia
  • Rarely cut inoculation
307
Q

What is the life cycle of Coccidiodes immitis?

A
  • Mycelium are chains of haploid, multinuc, barrelshaped arthroconidia (or arthrospores) in environ
  • The arthroconidia fragment and are aerosolized and inhaled by animal host and phagocytosed by alveolar macrophages, where they enlarge into a spherule
  • 100s of endospores develop within the spherule, which are released when spherule ruptures
  • Each endospore that escapes immune dest enlarges into a new spherule
308
Q

What are some clinical signs of Coccidiodes immitis?

A
  • Diss to lymphatics or hematogenously
  • Usually affects lungs/chest LNs, but can go to osteoart sites, CNS, skin, LNs, eyes, testes, prostate, pericardium
  • Cough, fever (67% of dogs), inapp, weight loss, tachypnea, lameness, SC masses or drain skin lesions, lymphadenopath, neuro
309
Q

What are some labwork findings with Coccidiodes immitis?

A
  • Mild, non-reg anemia, almost all dogs have hypoalbum, 50% dogs/cats have hyperglob, uncomm hypercalc, proteinuria
310
Q

What is the gold standard diagnosis for Coccidiodes immitis?

A
  • Qualitative gel immunodiffusion (ID) assay for IgG or ImG antibodies, IgM is det within 2-5 weeks, and IgG appears after 8-12 weeks
  • Cyto for spherules or endospores but insens
311
Q

What is the treatment for Coccidiodes immitis?

A
  • Fluconazole or itraconazole for 6 mo-years
  • Amphotericin B reccomended for dogs with refractory or severe disease
  • IgG antibody titers decrease with successful tx, should be continued until lesions resolve and titer is 1:2 or lower
312
Q

What is the prognosis for Coccidiodes immitis?

A

Dogs with just pulmonary inf have best prognosis; prognosis poor for dogs with CNS involvement

313
Q

When is Valley Fever most likely to cause infection?

A
  • Infection usually follows cycle of moist condition, dry period, then soil distruption
314
Q

What are some differential diagnoses for Valley Fever?

A
  • Neoplasia, other deep mycoses, mycobacteriosis
315
Q

Describe Cryptococcus (gatii, neoformans)

A
  • Cryptococcosis
  • Dimorphic, basidiomycetous
  • In host tissue yeast form, round to oval with var sized capsule
  • Narrow based budding of 1-2 daughter cells
316
Q

What is the distribution of Cryptococcus (gatii, neoformans)?

317
Q

What species are affected by Cryptococcus (gatii, neoformans)?

A
  • Cats (most common syst mycosis in cats)
  • 8x higher incidident in cats vs dogs, get C.gatii)
  • Dogs (Get C. neoformans)
  • Humans
318
Q

What are some predisposing factors for Cryptococcus (gatii, neoformans)?

A
  • Young adult cats and dogs
  • American cocker spaniel dogs strongly predisposed
  • Prox to soil disturbance
  • 25% of infected cats are housed excl indoors
319
Q

What is the mode of transmission of Cryptococcus (gatii, neoformans)?

A

Inhalation of basidiospores (or poss desiccated yeasts) from environ, weathered bird (esp pigeon) guano, decaying plant mat, can stay viable for 2 years in pigeon lofts

320
Q

What is the life cycle of Cryptococcus (gatii, neoformans)?

A
  • IP 2-13 months
  • In enviornment, filamentous form (or teleomorph) bearing basidiospores that convert to yeast form in host tissues
  • 2 mating types, a (alpha) and a alpha is more prev in environ/clin samples
  • In lab conditions, the 2 mating types fuse and adopt dikaryotic filamentous state called perfect state, which produces basidia, small club shaped structures on which basidiospores form
  • Cells of alpha mating type can also undergo asexual reproduction via monokaryotic fruiting
  • Within tissues, reproduces by forming 1-2 daughter cells (buds) conn to parent cell by narrow base
321
Q

What are some clinical signs of Cryptococcus?

A
  • Nasal cavity is the primary site of infection
    =- Polysacc capsule is continuously shed into host’s EC fluid and inhibits phagocyt, depletes complement, and inhibits eff T cell response
  • Can spread to LN, eye, skin, and CNS (strong tend to invade meaning), bone
  • Fever rare, in contrast to cats, dogs freq develop severe dissem disease (80% have involvement of mult anat sites)
  • PE: nasal signs, stritor, stertor, otitis media, lymphadenomegaly, skin nodules, CNS signs
322
Q

What are some labwork findings with Crytpococcous?

A
  • Non-regen anemia, occ yeast on urine sed
  • Yeast are visible in most crypto meningitis using India ink
  • Occ marked deterioration in Neuro status after CSF collection
  • 80% of cats have normal AUS
  • Dogs can have changes to SI, panc, intraabdomin lymphadenomeg, ascites
323
Q

What is the gold standard diagnosis for Cryptococcus?

A
  • Latex agglutination assay for detection of cryptococcal polysacchardie capsular antigen
  • False negatives are more common in dogs that cats
  • Can use cytology
  • Crypto grows as a yeast rather than a mold so is less likely to represent a lab hazard
324
Q

What is the recommended treatment for Cryptococcus?

A
  • Amph B is the most effective anticryptococcal agent, and a combo of ampho B and 5-flucytosine is considered optimal therapy for cats (and humans, but NOT dogs), with CNS
  • Dogs with disseminated disease or CNS disease should be treated with ampho B and fluconazole (DO NOT use flucytosine in dogs, causes toxic epidermal neurolysis)
325
Q

What is the prognosis for Cryptococcus?

A
  • 60% of cats may be cured after initial course of therapy but prognosis is more guarded for dogs
  • MST for CNS crypto is 13d in cats and 7 days in dogs
  • Reduction in titer typically lag behind clinical improvement
326
Q

What are some other facts about Cryptococcus?

A
  • Sign pulmonary involve is rare
  • Yeast capsule composed of Polysacc called glucuronoxylomannan (GXM); this capsule protects the fungus from phagocytosis as well as from environment insults (dessic)
327
Q

What are some differential diagnoses for Cryptococcus?

A
  • Cats: other deep mycoses (sporothrix), mycobact, nocardiosis, neop, EGC
  • For crypto rhin: nasal lymphoma, FB, asperg
328
Q

Describe Sporothrix schenckii

A
  • Sporotrichosis
  • Dimorphic, saprophytic fungi
  • On cyto: Round to cigar shaped yeasts inside neutrophils, macrophages, or EC
329
Q

What is the distribution of Sporothrix schenckii?

A
  • Tropical and temp zones worldwide
330
Q

What species does Sporothrix schenckii affect?

A
  • Cats (more susceptible than dogs)
  • Dogs (rare)
  • Humans
331
Q

What are some predisposing factors for Sporothrix schenckii?

A

Male cats are overrepresented

332
Q

What is the mode of transmission of Sporothrix schenckii?

A
  • Cutaneous innoculation or inhalation of conidia, cont claw or bite wounds, autoinoculation during groom, even direct contact with inf cats without a break in skin
333
Q

What is the life cycle of Sporothrix schenckii?

A
  • Converts to yeast form in tissues
  • Yeasts have adhesions on surface that binds fibronectin, imp for virulence
334
Q

What are some clinical signs of Sporothrix schenckii?

A
  • Cutaneous, mucosal, or extracutaneous forms
  • Cutaneous lesions are crusted, plaque-like, or nodule w draining skin lesions (80% of cats have multiple cutaneous lesions)
  • Can disseminate
  • Cutaneous lesions (usually on head)
  • Fever, lymphadenopathy
  • Vomiting, weight loss, sneezing, coughing, tachypnea, stertor, nasal discharge
335
Q

What are some labwork findings with Sporothrix schenckii?

A
  • Mild anemia, neutrophilia, hyperglobulinemia, Hypoalbuminemia
  • Chest rads usually normal
336
Q

What is the gold standard diagnosis for Sporothrix schenckii?

A
  • Cytology (high sensitivity, ~ 80% in cats, lower in dogs)
337
Q

What is the recommended treatment for Sporothrix schenckii?

A
  • Itraconazole 4-6 months
  • Alternative therapies for refractory disease include supersat potassium or sodium iodide, terbinafine, or ampho B
338
Q

What is the prognosis for Sporothrix schenckii?

A
  • Good with treatment
  • 40-70% cure rate rep in cats
  • Relapse may occur 3-18 months after d/c antifungal therapy
339
Q

What are some other facts about Sporothrix schenckii?

A
  • Direct transmission can follow contact between inf cats and humans, esp cat bites/scratches
  • Spont reg of cutaneous lesions has been described in dogs
340
Q

What are some differential diagnoses for Sporothrix schenckii?

A
  • Other deep mycoses , mycobacterial infections, nocard, actinomyc, leishmaniasis, SCC, EGO
341
Q

Describe Aspergillus fumigatus (SNA/bronchpulm in dogs/ats; dissem in cats), Asperigillus terreus/deflectus (dissem in dogs), Aspergillus felis (SOA in cats)

A
  • Aspergillosis; Sinonasal (SA)sino-orbital (SOA - only cats), disseminated; Saprophytic, hyaline mold; cyto: Septate, branch at 45 degree angles
342
Q

What is the distribution of Aspergillus fumigatus, terreus/deflectus, felis?

343
Q

What species are affected by Aspergillus fumigatus, terreus/deflectus, felis?

A

Dogs, cats, humans

344
Q

What are some predisposing factors for Aspergillus fumigatus, terreus/deflectus, felis?

A
  • SNA (dogs): large, non-brachycephalic, esp GSDs
  • Bronchopulm/Dissem (dogs): GSDs are predisposed (43x more likely to develop dissem dz), females 3x to dev diss
  • SNA/SOA (cats): brachycephalics; cats with diss/bronchopulm asper often have underlying immunosupp cond (DM, cancer)
345
Q

What is the mode of transmission of Aspergillus fumigatus, terreus/deflectus, felis?

A
  • Inhalation of conidia from environment
  • Dissemination may be from ingestion (case report)
346
Q

What is the life cycle of Aspergillus fumigatus, terreus/deflectus, felis?

A
  • Conidia (or spores) inhaled, enlarge, and germinate to form hyphae in nasal cav/sinuses
  • SNA is a noninvasive disease (doesn’t extend beyond mucosal epith)
  • Pulm/dissem: hyphae get into bloodstream
347
Q

What are the clinical signs of Aspergillus fumigatus, terreus/deflectus, felis?

A
  • Sinonasal: nasal disease/sneezing/epistaxis , normal to increased airflow, nare depigment can invade brain
  • Sino-orb (only in cats): invades submuc nasal tissue/sinus, ext thru orbital bone. Exophthal, mass, ulcers
  • Disseminated: vertebral endplates/discs, renal pelvis, spleen long bones, LNs, but any organ can be affected
  • Inappetence, weight loss, spinal pain, lameness, Neuro, pelvic limb paresis/paralysis, cough, Vomiting, fever (25% of dogs), periph lymphaden, vis impair
348
Q

What are some labwork findings with Aspergillus fumigatus, terreus/deflectus, felis?

A
  • Mild nonregen anemia, neutrophil, hypoalbum, hyperglob, azotemia, hypercalcemia, proteinuria, fungal hyphae in urine
  • Rhino/sinoscopy: plaques white, gray, yellow, black, green; serum galactomannan antigen ELISA assays sucks in dogs/cats
349
Q

What is the gold standard diagnosis for Aspergillus fumigatus, terreus/deflectus, felis?

A
  • SNA: cyto (high sens); inter fungal culture with caution, as can be found in URT of healthy animals
  • ELISA for IgG antibodies in cats to Dx SNA (95% sens, spec 93% Vet Clin N 2020, Barrs)
  • SOA: culture of asp or biopsy from retrobulbar mass vry sgg
  • Dissem: Galactomann antigen (ELISA) VERY sensitive (cross-react do occur), can do cyto/cult (urine, blood, LN etc)
350
Q

What is the recommended treatment for Aspergillus fumigatus, terreus/deflectus, felis?

A
  • SNA: mech debridement of plaques with sinus treph PRN: as long as cribriform plate is intact, debridement is followed by clotrimazole or enilconazole top therapy
  • Unclear whether add os sys antifungal helps, can use voricon
  • Cats with SOA: itra or posaconazole and/or ampho B
  • Dissem: NO FLUC, asper is intrinsically resistant to fluconazole, most widely used is itra, vori, posaconazole +/- ampho B
  • Bronchopulm: best prognosis
351
Q

What is the prognosis for Aspergillus fumigatus, terreus/deflectus, felis?

A
  • SNA: variable (30-100%), serology monitor not useful
  • SOA in cats: guarded to poor >50% tx cats failed tx in 1 study
  • Dissem: poor Prog for adv dx. May use posaconazole + terbinafine. May need lifelong therapy, not sure if monitor Galactomann will help
352
Q

What are some other facts about Aspergillus fumigatus, terreus/deflectus, felis?

A
  • SNA: if crib plate dest present, topc tx can lead to dev of life-threat Neuro signs or failure to recover from anes
  • SNA/SOA uncommon and dissem/Bronchopulm are rare in cats
  • Loc Bronchopulm asper is rare in dogs/cats
  • False pos can occur on ELISA Galactomannan antigen if received Plasmalyte IVF
353
Q

What are some differential diagnoses for Aspergillus fumigatus, terreus/deflectus, felis?

A
  • Sinonasal: Neoplasia (can cause false pos on Galactomannan antigen test)
  • Rhinitis
  • Oronasal fist
  • Crypto
354
Q

Describe pythium insidiosum

A
  • Pythiosis (often grouped with lagenidiosis and zygomycosis);
  • Water mold
355
Q

What is the distribution of pythium insidiosum?

A
  • Tropical/sub tropical worldwide, esp Gulf Coast of US
356
Q

What species are affected by pythium insidiosum?

A

Dogs, less commonly cats and humans

357
Q

What is the mode of transmission of pythium insidiosum?

A
  • Likely penetration of damaged skin or mucosa by motile zoospores (attach to damaged tissues), usually after exposure to standing freshwater sources
358
Q

What is the life cycle of pythium insidiosum?

A
  • Prod of motile, flagellate zoospores that act as infective eleme in wet environ
359
Q

What are the clinical signs of pythium insidiosum?

A
  • GI: severe, seg, transmur thick of GIT (predil gastric outflow area), mes lymphadeno
  • Chronic, Prog wt loss, v/d, anorexia
  • Cut form: usually at base of tail, ventral neck, extrem, perineum, nonhealing wounds and invasive mass that contain ulc nodules and draining tract
360
Q

What are some labwork findings with pythium insidiosum?

A
  • Eos, anemia, hyperglob, hypoalb
361
Q

What is the gold standard diagnosis for pythium insidiosum?

A
  • ELISA antibody test @ LSU, highly sens and spec
  • Cyto: hyphae (broad, rarely septate with tapered rounded ends), but can’t diff from lagen/zygomyc
362
Q

What is the prognosis for pythium insidiosum?

A

Usually fatal. After comp sx res of inf tissues, a dram dec in antibody levels is det within 2-3 mo

362
Q

What is the treatment for pythium insidiosum?

A
  • Aggressive sx resection with wide margins + removal/biopsy of reg LNs, followed by med therapy if not conf of margins of at least 5cm (itraconazole and terbinafine)
363
Q

What are some differential diagnoses for pythium insidiosum?

A
  • GI form: neop, zygoycosis, histo, eosinohilic gastroent, chronic FB
  • Cut form: lagenidiosis, zygomycosis, mycobac, actino
364
Q

Describe Rhinosporidium seeberi

A
  • Rhinosporidiosis
  • Aquatic protistan parasite (orig thought to be fungal)
365
Q

What species are affected by Rhinosporidium seeberi?

A

Dogs, less commonly cats and humans

366
Q

What is the distribution of Rhinosporidium seeberi?

A

Worldwide, esp warm/wet regions (US: south central, SE)

367
Q

What are some predisposing factors for Rhinosporidium seeberi?

A

Young adult large breed dogs

368
Q

What is the mode of transmission of Rhinosporidium seeberi?

A

Unknown - susp acquired from contact with wet environment +/- w mucosal trauma

369
Q

What are the clinical signs of Rhinosporidium seeberi?

A
  • ZSlow-growing polypoid nasal masses, can protrude from nares; sneezing, stertor, d/c epistaxis
370
Q

What are some labwork findings with Rhinosporidium seeberi?

A

Contrast enhancing nasal mass on CT

371
Q

What is the gold standard diagnosis for Rhinosporidium seeberi?

A

Cyto or histo nasal mass

372
Q

What is the recommended treatment for Rhinosporidium seeberi?

A

Surgical excision (can be cur, but recurrence can occur), Dapson (not in cats) and keto have been used for refract disease

373
Q

What is the prognosis for Rhinosporidium seeberi?

A

Relapses can occur

374
Q

Is Rhinosporidium seeberi zoonotic?

A

Humans acquire this from environment, no zoonosis rep

375
Q

What are the differential diagnoses for Rhinosporidium seeberi?

A
  • Distemper, bact pneumonia, mycobacter, fungal pneumonia, pulm neop
376
Q

Describe Toxoplasma gondii

A
  • Toxoplasmosis
  • Coccidian, one of most prev parasites inf warm blooded vert
377
Q

What is the distribution of Toxoplasma gondii?

378
Q

What species are affected by Toxoplasma gondii?

A
  • Casts (def host, only cats complete sex phase, many other intrmed hosts
  • Dogs with gen toxo usually immunosupp
379
Q

What is the mode of transmission of Toxoplasma gondii?

A
  • Ingestion of any of 3 life stage (sporozoite contained in oocyst, tachyzoite, bradyzoite), or transplac, or transmamm (only cats)
  • After sporulation (form of sporozoites within oocyst), oocysts can survive in the environ for months to years and resist to most disinfectants
  • Cats usually inf via carnivorous feeding
380
Q

What is the life cycle of Toxoplasma gondii?

A
  • Def host (cats): cats ingest bradyzoites in tiss, bradyzoite transf into merozoites, which rep in epthl cells of GIT, then trans into micro- & macrogametes, which fuse to make a zygote. Zygote transf into unsporulated oocyst, which is shed in feces for 3-21d. Sporozoites dev within shed oocysts after 1-5d, called sporulation
  • Intermed host: after oocyst ing, released sporozoites can penetrate intest tract and diss in blood/lymph as tachyzoites. Tachyzoites penet most mamm cells, rep asex within infect cells until cell is destroyed. If approp immune resp occurs, rep of tachyzoites is atten, and slowly dividi bradyazoites dev that persist within cysts in extraintest tiss
381
Q

What are the clinical signs of Toxoplasma gondii?

A
  • Intermed host: slowly div bradyzoite contain cysts form in CNS, muscles, visceral org
  • Cats (def/inter): usually no clin dsigns, SI diarrhea: fatal extraintest toxo can dev from overwhelm IC rep of tachyzoites (hepatic, pulm, CNS, panc tissues), kittens inf via transp/transmm most severe signs
  • Chronic tox: uveitis, chorioret, cut les, fever, muscle hyperesth, myocard, wt loss, anorexia, sz, atax, icterus, diarr, resp dist, panc
  • Dogs: resp, GI, neuromusc, fever, v/d, resp dist, ataxia, sz, icterus, myocard, ocular signs, cut lesions
382
Q

What are some labwork findings with Toxoplasma gondii?

A

Nonregen anem, hyperbili, elev ALT/ALP, proteinuria
- Chest rads diffuse interstit to alv patt
- Cyto of brady/tachyzoites (sens low), also in dogs, N.caninum tachyzoites can’t be disting: fecal float (cats)

383
Q

What is the gold standard diagnosis for Toxoplasma gondii?

A
  • Combo of antibod + IgM titer >11:64 or 4x increase in IgG, consist clin signs, + response to ther
  • IgM titer: 2-4 wk post inoc, neg within 16 wks, have higher PPV than IgG
  • IgG titer: 3-4 wk post inco-life. By time IgG antibod detect, oocyst shedd pd usu been completed
  • Heal cats can have IgG tit >1:10,000 as long as 6yr after exper inoc: Rising T.gondii IgG antibody tit occur in healthy infec cats as well as cats with clin tox
384
Q

What is the treatment for Toxoplasma gondii?

A
  • Clindamycin or TMS - if see improvement after 1 wk, continue for 4 weeks
  • If poor response to therapy after 7d, consider alternative drug
385
Q

What is the prognosis for Toxoplasma gondii?

A
  • Prog poor with hepatic, CNS, or pulm dz: chronic (latent) infection can become activated via immunosuppressive drugs or conditions: T.gondii inf can’t be elimn, most will be antibody + for life
386
Q

Is Toxoplasma gondii zoonotic?

A

There is a significant risk to the fetus after transplac infect and to any immunocompromised person: infect of rodents with T.gondii leads to alter behav so that rod is less fearful of cats

387
Q

What are the differential diagnoses for Toxoplasma gondii?

A

In dogs, Neospora, chronic IC bact infect, fungal infection

388
Q

Describe Neospora caninum

A
  • Neosporosis
  • Obligately intracell coccidial protozoan parasite closely res T.gondii; oval to crescent-shaped, can’t be disting from T.gondii
389
Q

What is the distribution of Neospora caninum?

390
Q

What species are affected by Neospora caninum?

A

Dogs (def host, only dogs complete sex phase)

391
Q

What are some predisposing factors for Neospora caninum?

A

Seroprev increases with age, higher in free roaming dogs, dogs on cattle farms/rural areas; commonly affected breeds: boxers, Rohedians, bull mastiffs, greyhounds, bassets, Labs, Rotties, Westies

392
Q

What is the mode of transmission of Neospora caninum?

A

Transplacent, transmamm route, ing infect tissue (muscle, liver, brain, heart muscle) of intermed hosts or bovine fetal mem

393
Q

What are some clinical signs of Neospora caninum?

A
  • Clinical signs uncommon
  • Transplac leads to myosit, polyradiculo of LS spinal nerve roots
  • Exercise intol, ataxia, high-stepp gait, splaying of pelv limb, urinary incont, bunny hop, muscle pain, tetrapleg, inabil to open mouth, dysphag, resp diff, ME, less common hep, pneum, memingoenceph, myocard/adult dogs dev polymyositis and/or meningoenceph, predilec for cerebellum, fever rare
393
Q

What is the life cycle of Neospora caninum?

A
  • Oocysts sporulate and become inf 24-72 hours after shed in canine feces, environ-res
  • Oocysts ing sporozoites are released from oocyst in the GIT and pen intestinal epith cells, then dissem to variety of tissues where they encyst as bradyzoite cysts
394
Q

What are some labwork findings with Neospora caninum?

A
  • Should susp in <1 yr dog with ascend paralysis and m atrophhy; occ mild nonregen anemia, inc CK, ALT, hyperglob
  • PCR : DNA of N.caninum can be detect in tissues from healthy dogs
395
Q

What is the gold standard diagnosis for Neospora caninum?

A
  • ELSIA or indir IFA IgM and IgG, seroconv occurs 2-3 weeks post inf and rising titer can be ID’d in acutely inf dogs
  • Chronic infect dogs won’t have this rise; cyto of tachyzoites of skin/CSF/body fluid
396
Q

What is the recommended treatment for Neospora caninum?

A
  • Clindamycin for >8 wks, tx is usually only temp, parti, or completely ineffective
  • Other drugs tried are TMS, and clinda+pyrimethanine
397
Q

What is the prognosis for Neospora caninum?

A
  • Prognosis for puppies once muscle contract has dev is poor
  • Reactiv of subclin inf can occur after tx with immunosupp drugs or chemo
398
Q

What are some other facts about Neospora caninum?

A
  • In dogs, preg is assoc with reactiv of bradyzoite cysts, with repl of tachyzoites and subseq abortion or transplac trans
399
Q

What are some differential diagnoses for Neospora caninum?

A
  • Toxoplasmosis, sarcocystosis, hepatozoonosis, deep mycosis
400
Q

Describe Leishmania infantum

A
  • Leishmanisosis
  • Visceral leishmanisosi and Americtegumentary leish, al oc cut form that occurs in S. Ameri; Protozoa
401
Q

What is the distribution of Leishmania infantum?

A
  • ZS. Europe, Middle East, Central/South America, some parts of US (usually dogs import from S. Europe)
402
Q

What species are affected by Leishmania infantum?

A
  • Dogs (consid major reservoir for L. infantum inf), less commonly cats; also humans
403
Q

What are some predisposing factors for Leishmania infantum?

A
  • > 2 yr, prol exp to outdoors, lack of top insecticide use +/- short coat
  • Some auth have desc biomodal age dist @ 3 and 8 yr
  • Stray dogs, poor sanitation
404
Q

What is the mode of transmission of Leishmania infantum?

A
  • Phlebotomus and Lutzomyia sandlies, blood transfusion, vertical, venereal
405
Q

What is the life cycle of Leishmania infantum?

A
  • IP: up to 7 years
  • Life cycle altern between 2 major forms: promastigote and amastigote
  • Promastigote resides in gut of sandfly vector, elong flag form
  • Promast are inoc into tissues when sandfly feeds, where they are phagocyt by macrophages in dermis and transform into amastigotes (IC, nonmot, ovoid or round)
  • Amastigotes survive in macrph phagolycososomes, cause inflt macroph rupture and release amastigotes to inf other macroph. then dissem to reg lymph and blood to inf RES
406
Q

What are the clinical signs of Leishmania infantum?

A
  • Cut lesions (50-90%)
  • Alop, scaling, and/or ulc, can be nod or pap, long/brittle claws
  • Sys signs: fever, wt loss, m atrophy, inapp, leth, oral ulc, hepatosplenomeg, lymphadenomeg (65-90%), ITP, IMPA, myositis, ocular dz, vasc, glomerulonephr, can culm in nephrotic syn or renal failure
  • Anemia may be due to combo of bld loss, inflamm, renal failure, IMHA, marrow aplasia
  • Almost any org can be aff
  • Am tegum L: nod skin les @ site of sandfly bite +/- ulc
407
Q

What are some labwork findings with Leishmania infantum?

A
  • Non regen anemia, mild thrombocyto in 50% dogs, pancyto may be pres, hyperglob, hypoalbumin (75%), azotemia, proteinuria
  • Amastig may be visible on synovial fluid or bone marr cyto
  • Antinuc antibody tests are + in 50% of dogs, many dogs + Coombs test
408
Q

What is the gold standard diagnosis for Leishmania infantum?

A
  • Cyto of amastigote, but can be confused with T.cruzi, Histoplasma, or Sporothrix
  • Serology (IFA, ELISA) - sens 90-95% spec 80-91% in non-vax) but in endemic areas + sero test don’t imply dz
409
Q

What is the treatment for Leishmania infantum?

A
  • Regard of tx used, compl cure is rare, and relapses frequent
  • Combo meglumine antimoniate (not read avail in US) and allopurinol until clin signs resolv and qunat sero becomes neg
  • Comp or near-comp clin remission rates of 65-100% have been rep,, relapse rates of 10%; alt tx miltefosine, ampho B
410
Q

What is the prognosis for Leishmania infantum?

A
  • PCR may be useful to monitor efficacy of tx
  • Long term allopurinol can lead to xanthine urolith; vaccine available (CaniLeish) lic in Europe
  • Use of ectoparasiticides prevent dz
411
Q

What are some other facts about Leishmania infantum?

A
  • Some dogs comp elim infect, small % of dogs develop severe, life threat dz
  • Lymphadeno can be severe and be sugg of lymphoma
  • Hyperglobulin can rarely be caused by monoclonal gammopathy
  • TOC for human visc leish is lipid-com ampho B
412
Q

What are some differential diagnoses for Leishmania infantum?

A
  • Canine monocytic ehrlichiosis, babesiosis, histoplasm, brucellosishemic neop, SLE
413
Q

Describe babesia canis, B. gibsoni< B. conradae (dogs), B. felis, B. cati (cats)

A
  • Babesiosis
  • Intraerythrocytic protozoan parasite
  • B.canis; large pyriform in single or pairs
  • B.gibsoni/conradae: single IC org
414
Q

What is the distribution of Babesiosis?

A

Worldwide, but different Babesia spec vary in geograph distrib; B.canis more common in Southern US

415
Q

What species are affected by Babesiosis?

A

Domestic dogs and cats

416
Q

What are some predisposing factors for Babesiosis?

A
  • Pitties are more likely to die when dx’d with severe inf with B.canis
  • B. gibsoni: most dogs are American pitties
  • B. conradae: S. Cali, hx of coyote fights
417
Q

What is the mode of transmission of Babesiosis?

A
  • Variety of tick vectors, fight/biting (B.gibsoni), vert transm, bld transfusion
418
Q

What is the life cycle of Babesiosis?

A
  • When ticks invov in transm, sporozoites release as tick feeds, enter bloodstream, then attach to, and are endocyt by RBCs
  • Within RBCs, they undergo asex repro (merogony), and daughter cells infect new RBCs, sex/asex repro happens in tick; parasite antigens are incorp on RBC surface and induce host-opson antibodies—> hemo anemia
419
Q

What are some clinical signs of Babesiosis?

A
  • Anemia more severe in splenect dogs; Virul B.canis, canis, and B. canis rossi strains can induce sepsis-like syndrome with MODS, cause ARF, neuro, DIC, ARDs, hepatopath, “red biliary syndrome” - severe intravasc hemo with hemo conc
  • Fever (waxes/wanes), wt loss, weakness, leth, anorex, weak, jaundice, splenomeg, muc pallor, bound pulse, muc hemorr, pancreatitis
420
Q

What are some labwork findings with Babesiosis?

A
  • Regen anemia (with or without autoagglut + Coombs, spherocytes)
  • Thrombocytopenia, hyperglob, azotemia, proteinuria
  • Cats: elev ALT, hyperbilirubin
421
Q

What is the gold standard diagnostic for Babesiosis?

A
  • PCR - most sens/spec of detect active infection
  • IFA antibody- acute/convasc
  • Blood smear ID (poor sens), for B. canis, periph cap beds at ear tip or nailbed may yield higher numbers
  • Cats: Primaquine phosphate, but eff dose is close to lethal dose
  • Tick control for prevention
422
Q

What is the treatment for Babesiosis?

A
  • B. canis: imidocarb diproprionate 1 inj
  • B. gibsoni/conradae: atovaquone and azithromycin x 10d
  • PCR tes 60 & 90 days after finishing
423
Q

What is the prognosis for Babesiosis?

A
  • Pulmonary, CNS, and renal comp are assoc with a higher rate of mortality, pers lactate conc >40 mg/dL is a poor prog indicator
424
Q

What is another fact about Babesiosis?

A

An unnamed Babesia has been iso from dogs in N. America that had been splenectomized or undergoing chemo; in FL kennel, greyhounds had 50% seroreact

425
Q

What are some differential diagnoses for Babesiosis?

A
  • Mycoplasma (haemocanis/felis), IMNHA, ITP, other causes of hemolysis, Ehrlichia canis, RMSF, bact endocarditis
426
Q

Describe Cytauxzoon felis

A
  • Cytauxzoonosis; hemoprotozoan parasite, intraerythrocytic signet ring inclusion
427
Q

What is the distribution of Cytauxzoon felis?

A

South-Central, South-Eastern, and mid-Atlantic US, S. America

428
Q

What species are affected by Cytauxzoon felis?

A

Any felid; bobcats are major reservoir hosts

429
Q

What are the predisposing factors for Cytauxzoon felis?

A

Typically outdoor cats from wooded suburban or rural areas, coming into contact with tick that rec fed on inf bobcat

430
Q

What is the mode of transmission of Cytauxzoon felis?

A
  • Amblyomma americanum (Lone Star tick), poss. Dermacentor variab (American dog tick)
431
Q

What is the life cycle of Cytauxzoon felis?

A
  • Tick inoculates org into host as sporozoite, and exists within host in both a non-RBC (schizont) and a RBC (piroplasm) form
  • 2 weeks after inoc, schizogony occurs, where mononuclear cells occlude small veins and caps, most not in liver, lung, spleen, and LNs
  • Obstruct fuels hypoxic tissue dam and rel of inflamm cyto —> SIRS, sepsis, DIC, MODS, fever vs hypotherm (preced death), icterus, pallor, nictit mem elev, inc RR, hepatosplenomeg, lymphadeno, sz, obtund
432
Q

What are some labwork findings with Cytauxzoon felis?

A
  • Pan or bicytopenia, signet ring intraerythrocytic inclusion, hyperbilirubin, elev LEs, elev PT/PTT (DIC)
433
Q

What is the gold standard diagnostic test for Cytauxzoon felis?

A
  • Blood smear (most commonly used method)
  • RBC piroplasms or schizont-pregnant mononuclear cells; FNA of spleen, liver, LN, or luns for schizont-laden mononuclear cells (schizogony precedes piroplasm dev)
  • **PCR tests are more sens dx test, although healthy, chronic carr cats can be + **
434
Q

What is the recommended treatment for Cytauxzoon felis?

A
  • TOC is combo of atovaquone susp and azithromycin x 10d
  • Doesn’t consist elimin parasitemia, but path burden drops to levels below PCR det; tick prevention
435
Q

What is the prognosis for Cytauxzoon felis?

A
  • 60% cats survive with atovaquone/azithromycin
436
Q

What are some differential diagnoses for Cytauxzoon felis?

A

Hemotropic mycoplasmosis, tularemia, cholangiohep, sepsis, IMHA

437
Q

Describe Hepatozoon americanum (American canine hepatozoonosis), Hepatozoon canis

A
  • Hepatozoonosis
  • Protozoal parasite
  • Sex stage is the gamont, app as light blue to clear oblong struct with a faintly stain nuc within cyto of neut or monocytes (gamont of H. canis are slightly larger)
438
Q

What is the distribution of Hepatozoonosis?

A
  • H. americanum: Southesastern and south-central US
  • H. canis: Asia, Africa, S. Europe, Middle East, Americas
439
Q

What species are affected by Hepatozoonosis?

A
  • Domestic dogs (serve as intermediate host), possibly some wild carnivores
440
Q

What are some predisposing factors for Hepatozoonosis?

A
  • Hunting and rural dogs, dogs allowed to roam
441
Q

What is the mode of transmission of Hepatozoonosis?

A
  • Primarily ingestion of tick vectors
  • H. americanum: Amblyomma maculatum
  • H. canis: vector is Rhipicephalus sanguineus
442
Q

What is the life cycle of Hepatozoonosis?

A
  • Dog groom itself (not from tick bite), ingests tick, bile in GIT causes rel of sporozoites, which pen the intest epith wall and are transport to target organs/tissues, likely within mononuclear cells
  • H. ameri: inf cells pref travel to skelet m, where each organ dev within its host cell and becomes lodged between myocytes, creating an “onion skin cyst” with conc layers of mucopolysacc
  • Merogony occurs within cyst, and the cyst ruptures, releasing merozoites, which then spread thru blood to other sites or become gamonts in WBCs
  • H. canis: inf cells carried by lymph/blood to spleen, marrow, LN, liver, kidneys where org divide asex thru Merogony. 2 forms of meronts form, either containing many micromerozoites or 4 macromerozoites. Larger macromero cont asex cycle, micromerozoites invade neutrophils and monocytes and become gamonts
443
Q

What are the clinical signs of Hepatozoonosis?

A
  • H. Americanum: severe dz, signs assoc with pyogranulomas that form in muscle when meronts rupture; fever (86%), myositis, can mimic meningitis/disko, bone lesion look like HO - rads demon periosteum new bone form on diaphysis of long bones, mucourulent ocular d/c (77%), weight loss, m atrophy, nephrotic syndrome/TE dz, hyperesthesia, lameness, sifttness, inability to rise, lymphadenomeg
  • H. canis: have no or no mild signs unless immunosupp or conc dz. Leth, fever, weight loss, hepatitis, glomeruloneph, pneumonitis, splenomeg, lymphadenomeg
444
Q

What labwork findings can you see with Hepatozoonosis?

A
  • H. americanum: Often extreme leukocytosis (mean 80,000 cells/uL, 100% charact by neutrophilia, nonregen anemia, plat normal to inc, mild inc ALP, severe artifactual hypoglycemia due to high WBCs, hypoalbum
  • H. canis: anemia, thrombocytopenia (1/3), variable leukocyte count (can be up to 150,000/uL), hyperglob, hypoalbumin, inc ALP/CK
445
Q

What is the gold standard diagnosis for Hepatozoonosis?

A
  • PCR via Auburn; M biopsy should be perf in dogs susp of having H.americanum but have neg PCR; cyto of sexual stage, gamonts, inside neut or monocytes
446
Q

What is the recommended treatment for Hepatozoonosis?

A
  • H. americanum: No tx effect elim tissue stage of H. americanum, remission of clin signs achieved using combo TMS Clindamycin, and pyrimethamine x 14d or ponazuril followed by long-term (2 yr) admin of decoquinate
  • Relapse occurs 2-6 months without decoquinate
  • H. canis: Imidocarbdipropionate until gamonts no longer seen on blood smear, +/- doxycycline; tick prev
447
Q

What is the prognosis for Hepatozoonosis?

A
  • H. americanum: good prognosis with long-term admin of decoquinate with excellent QOL. Dogs with multiple relapses and no decoquinate carry a guarded to poor prognosis
  • H. canis: low parasitemia have good long-term prog, high parasitemia have guarded prognosis
448
Q

Is Hepatozoonosis zoonotic?

A
  • Despite name, no zoonosis and rarely affects liver
  • H. americanum: return of ocular discharge is freq first indic of relapse following tx
449
Q

What are some differential diagnoses for Hepatozoonosis?

A
  • Sterile or infectious meningitis, bacterial disco, Lyme, Ehrlichia canis, toxoplasmosis
450
Q

Describe Trypansoma cruzi

A
  • American trypanosomiasis
  • Chagas disease
  • A flagellated protozoan parasite
451
Q

What is the distribution of Trypansoma cruzi?

A
  • Central and South American; to lesser ext southern US, esp Texas
452
Q

What species is affected by Trypansoma cruzi?

A
  • Dogs, humans, >150 other dom/wild mammalian species
453
Q

What is the mode of transmission of Trypansoma cruzi?

A
  • Bite from, or ingestion of reduviid (kissing bug) vectors, primarily Triatoma species; blood transfusion, vertical transm
454
Q

What is the life cycle of Trypansoma cruzi?

A
  • 3 forms; Trypomastigote circle in host’s blood, amastigote are host IC form, epimastigote found in arthropod vector; in US, princ wildlife reserve are opossums/raccoons
  • **After infection, trypomastigotes enter macroph, transform into amastigotes, and multiply by binary fission. Altern, they spread hematog and inf myocardiocytes, trans into amastigotes, multiply and transf back into trypomastig
    – Host cell then ruptures and trypomastigotes are rel back into circ
  • Vector becomes inf when it ingests circ trypomastigotes
455
Q

What are the clinical signs of Trypansoma cruzi?

A
  • Usually cardiac disease or rarely neuro
  • 3 phases of Chagas; myocardial in dogs: acute, latent, chronic
  • Acute myocardial from rupture of myocardio, leth, fever, inappp, gen lymphadeno, pale mm, arryth, hepatosplenomeg, diarrhea
  • Dogs that survive acute phase enter prolo latest phase and some of these dogs dev chronic myocardial with DCM, heart failure, pulse def, ascites
  • Neuro signs: meningoenceph as a dir result of parasite invas of CNS, weakness, atax, exagg spinal refl
456
Q

What are some labwork findings with Trypansoma cruzi?

A
  • Elev ALT, AST, azotemia, mod to severe hypoalbumin +/- hyperglob in acutely aff dog;
  • Serum trop 1 rise slowly and peak at 10-30mg/dL by 21 DPI
  • ECG: dec R-wave amp, axis shift, T-wave inc, vent arrhythmia, AV blocks
  • **Echo of pup with acute myocardial are usually normal
  • Chronic Chaga’s cause RV dilation, dec FS/EF
457
Q

What is the gold standard diagnosis for Trypansoma cruzi?

A

Pos serology in assoc with consist clin signs is most common means of dx
- Serology cross-reacts with antibodies to Leishmania, healthy animals may test pos; Cyto of thick-film buffy-coat smear is more sens than blood smear
- LN asp, and fluid, but low sens and org often not found with chronic tryp
- PCR limited availability

458
Q

What is the recommended treatment for Trypansoma cruzi?

A
  • Benznidazole (usually w glucocorticoids) x 60 days, severe adverse effect of nifurtimox preclude its use; most dogs are dx’d with Chagas’ during chronic stage and tx direct against T.cruzi at this stage don’t sign alter outcome of disease
  • Tx should be directed toward heart failure and vent arrythmia
459
Q

What is the prognosis for Trypansoma cruzi?

A
  • Poor because lack of eff treatments
  • Dog’s dx’d at older age (mean 9 year) survive longer (30-60 Mon) than dogs dx’d at younger age (mean 4.5 yr, survive 5 months)
460
Q

Is Trypansoma cruzi zoonotic?

A

Transmission to humans can occur after needle stick injury

461
Q

What are some differential diagnoses for Trypansoma cruzi?

A
  • Myocard
  • DCM
  • Parvoviral mycoard
  • E. canis
  • Babesiosis
  • Leushmaniosis
  • MUE: Distemper, neosporosis
462
Q

Describe Tritrichomonas foetus

A
  • Trichomoniasis
  • Flagellate protozoan
463
Q

What is the distribution of Tritrichomonas foetus?

464
Q

What species are affected by Tritrichomonas foetus?

A

Cats, less commonly dogs

465
Q

What are some predisposing factors for Tritrichomonas foetus?

A
  • Clinical signs most common in purebred, young animals housed in crowded environ; uncommon in feral cats
466
Q

What is the mode of transmission of Tritrichomonas foetus?

A
  • Fecal-oral (shared litter boxes, mutual grooming likely contribute)
467
Q

What is the life cycle of Tritrichomonas foetus?

A
  • Ing organisms in environ (cont water, urine, feces, cat litter), adheres to intest epith and incites a LP and neutrophilic inflamm resp
468
Q

What are some clinical signs of Tritrichomonas foetus?

A
  • Clinical signs variable and range from subclin inf to chronic, large bowel intract diarrhea, signs often are intermittent
  • Cont or intermitt large bowel diarrhea most common in kittens, proctitis, fecal incont
469
Q

What is the gold standard diagnosis for Tritrichomonas foetus?

A
  • InPouch Culture of feces - sens 55%
  • Fecal smear *trophozoite sim in size to Giardia, but can be different by pres of undulting memb, rapid forward motion, lack of convae surface and single nucleus
470
Q

What is the recommended treatment for Tritrichomonas foetus?

A
  • Ronidazole x 14 d (higher doses and twice daily rose regi can result in usu reversible Neuro signs, teratogenic)
471
Q

What are some differential diagnoses for Tritrichomonas foetus?

A
  • All causes of large bowel diarrhea (Isospora, C perfringens, dietary intol, IBD)
  • Giardia

ACVIM GENERAL MY OWN (15 decks)

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