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ACVIM GENERAL MY OWN > Infectious COPY > Flashcards

Infectious COPY 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

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
143
Q

What is the recommended treatment for RMSF?

A

Doxycycline x 7-14 days

144
Q

What is the prognosis for RMSF?

145
Q

What is Neorickettsia helminthoeca?

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

What is the distribution of Neorickettsia helminthoeca?

A

West coast US, British Columbia

147
Q

What species are affected by Neorickettsia helminthoeca?

A

Dogs, foxes, coyotes, raccoons, captive bears

148
Q

What are some predisposing factors for Neorickettsia helminthoeca?

A

Intact male dogs and Labradors are overrepresented

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

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
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
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
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%)
154
Q

What is the recommended treatment for Neorickettsia helminthoeca?

A

Tetracycline x 7 days; treat fluke infection with praziquantel

155
Q

What is the prognosis for Neorickettsia helminthoeca?

A

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

156
Q

What antimicrobials are NOT effective against Neorickettsia helminthoeca?

A
  • 1st generation cephalosporins
  • Penicillins
  • Aminoglycosides
  • Metronidazole
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
158
Q

What is the distribution of mycoplasma haemofelis/haemocanis?

159
Q

What are some predisposing factors for M.haemofelis?

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

What are some predisposing factors for M.haemominutum?

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

What are some predisposing factors for M.haemocanis?

A
  • Splenectomized dogs
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
163
Q

What tick transmits M.haemocanis?

A

Rhipicephalus sanguineus

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
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
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
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
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)

169
Q

What is the prognosis for M.haemocanis/haemofelis?

A

Good with treatment

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

171
Q

What is the distribution of mycobacterium?

172
Q

What species are affected by mycobacterium?

A
  • Animals and humans
  • Cats are resistant to infection with M.tuberculosis
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
174
Q

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

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

What is the mode of transmission for M.microti?

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

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

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

What is the mode of transmission of lepromatous mycobacteria?

A

Innoculation of the organism into skin through rodent or cat bites

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
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
180
Q

What are some labwork findings with mycobacterium?

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

What is the gold standard diagnosis for mycobacterium?

A

Mycobacterial culture for MTBC infection

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
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
184
Q

What is the distribution of lepto?

185
Q

What species are affected by lepto?

A

Dogs, rarely cats, humans

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
187
Q

What is the mode of transmission of lepto?

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

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

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 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

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
351
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)
352
Q

What is the distribution of Francisella tularensis?

A

Most disease reported in US, Northern Hemisphere

353
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

ACVIM GENERAL MY OWN (15 decks)

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