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Doctor of Veterinary Medicine (Work in progress) > Veterinary Medicine - Infectious diseases > Flashcards

Veterinary Medicine - Infectious diseases Flashcards

1
Q

What disease is caused by Erlichia Canis?

A

CME - Canine Monocytic Ehrlichiosis

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2
Q

Canine Monocytic Ehrlichiosis (CME) - Blood Smear - Possible findings

A

Activated monocytes

In 5% of cases (Extremely low sensitivity) - Morulas of Ehrlichia can be found in the cytoplasm monocytes at the feathered edge

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3
Q

Canine Monocytic Ehrlichiosis (CME) - Name 3 predisposed breeds and to what particular stage of the disease are they predisposed?

A

German shepherd, Husky, Malamute

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4
Q

Canine Monocytic Ehrlichiosis (CME) - Which lab finding can be found across all disease stages?

A

Thrombocytopenia

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5
Q

Canine Monocytic Ehrlichiosis (CME) - How long after infection are anti-platelets antibodies formed?

A

5 Days

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6
Q

From what platelet count you might start seeing spontaneous bleeding due to thrombocytopenia?

A

<30,000

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7
Q

Canine Monocytic Ehrlichiosis (CME) - Diagnosis - How can serology be useful in determining Ehrlichia Canis is the cause for the dogs current illness?

A

Seroconversion (4x) over a period of 2 weeks

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8
Q

Ehrlichiosis - Diagnosis - In general serology is more useful for Ruling Out Ehrlichiosis (T/F)

A

True

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9
Q

Canine Monocytic Ehrlichiosis (CME) - Treatment - At what stage of the disease Steroids might be useful?

A

Chronic stage

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10
Q

Canine Monocytic Ehrlichiosis (CME) - What is the vector?

A

Tick - Rhipicephalus sanguineous

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11
Q

Canine Monocytic Ehrlichiosis (CME) - Transmitted transovarially/transstadially?

A

Transstadial

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12
Q

Canine Monocytic Ehrlichiosis (CME) - What is the target cell for Ehrlicia Canis

A

Macrophages\Monocytes

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13
Q

Canine Monocytic Ehrlichiosis (CME) - How long does it take for an infected tick to transmit E.Canis to an animal after it started feeding

A

3 Hours

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14
Q

Canine Monocytic Ehrlichiosis (CME) - In what season do you see the most cases of E.Canis (Acute stage)

A

Summer months

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15
Q

Canine Monocytic Ehrlichiosis (CME) - Incubation period

A

1 - 3 Weeks

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16
Q

Canine Monocytic Ehrlichiosis (CME) - Chronic - What are the main 2 causes of death?

A

Sepsis

Anemia

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17
Q

Canine Monocytic Ehrlichiosis (CME) - Acute phase - Clinical signs

A

Lethargy

Anorexia

Fever

Lynphadenomeglay

Splenomegaly

Petechiae, ecchymoses

Melena/hematochezia, Pigmenturia, Epistaxis

Uveitis

Lameness

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18
Q

Canine Monocytic Ehrlichiosis (CME) - Acute phase - Common lab findings

A

Leukocytosis/Leukocytopenia

Monocytosis

Thrombocytopenia (Mild-moderate)

Blood smear - Activated monocytes +- Morulas

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19
Q

Canine Monocytic Ehrlichiosis (CME - Acute phase - Duration

A

1-4 Weeks

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20
Q

Canine Monocytic Ehrlichiosis (CME - Sub-clinical phase - Duration

A

Months-years

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21
Q

Canine Monocytic Ehrlichiosis (CME) - Sub-clinical phase - Common lab findings

A

General progression towards Pancytopenia: Leukopenia
Possible anemia (mild non-regenerative)
Thrombocytopenia

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22
Q

Canine Monocytic Ehrlichiosis (CME) - Sub-clinical phase - Clinical signs

A

None

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23
Q

Canine Monocytic Ehrlichiosis (CME) - Chronic phase - Clinical signs

A

Lethargy

Anorexia

Fever

Pale mucosal membranes

Lymphadenomeagly

Splenomegaly

Petechiae, ecchymoses, Epistaxis

GI Signs

CNS signs

Uveitis

Retinal separation

Lameness

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24
Q

Canine Monocytic Ehrlichiosis (CME) - In what stage of the disease do most owners bring their dog to the vet for the first time (Acute/Sub-clinical/Chronic)

A

Chronic stage

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25
Q

Canine Monocytic Ehrlichiosis (CME) - Chronic phase - Lab findings

A

Pancytopenia (Anemia, Leukopenia, Thrombocytopenia)

Hypoalbuminemia

Hyperglobulinemia (Polyclonal)

Mild elevation of liver enzymes

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26
Q

Canine Monocytic Ehrlichiosis (CME) - Chronic phase - Bone marrow cytological findings

A

Hypocellular bone marrow

Lipid deposition replacing bone marrow

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27
Q

Canine Monocytic Ehrlichiosis (CME) - Chronic phase - What are the Immune-mediated elements of the disease?

A

Immune complex formation

Auto-agglutinin formation (Comb’s Positive)

Anti-platelet antibodies

Anti-nuclear antibodies

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28
Q

Canine Monocytic Ehrlichiosis (CME) - Antibodies are the main defense against CME (True/False)

A

False

They do more harm than good

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29
Q

Canine Monocytic Ehrlichiosis (CME) - How long does it take for thrombocytopenia to resolve after treatment has began? (Acute stage)

A

10-14 Days

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30
Q

Canine Monocytic Ehrlichiosis (CME) - Thrombocytopenia - 4 Mechanisms in which E.Canis can cause thrombocytopenia

A

Increased consumption (e.g. Vasculitis)

Sequestration in the spleen

Destruction (IMT)

Decreased production in the bone marrow (Chronic stage)

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31
Q

Canine Monocytic Ehrlichiosis (CME) - Diagnosis - Blood smear - In what percentage of cases can morulas be seen? In what section of the smear? In what stage of the disease?

A

4%

Feathered edge

Acute

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32
Q

Canine Monocytic Ehrlichiosis (CME) - Can CME be transmissible through blood transfusion?

A

Yes

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33
Q

Canine Monocytic Ehrlichiosis (CME) - Diagnosis - Best diagnostic method

A

Blood PCR

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34
Q

Canine Monocytic Ehrlichiosis (CME) - Treatment - Treatment of choice (Acute stage), Treatment for chronic stages, Monitoring

A

Doxycycline - 3-4 Weeks.

Chronic stage:
Fluids, Anti-pyretics

Anemia - Blood transfusion, Darbepoetin.

Leukpoenia - G-CSF

Broad-spectrum antibiotics (2nd infections due to leukopenia)

Immunosuppression (e.g. GC, +/- 2nd drug such as Cyclosporine).

CBC (Monitor thrombocytopenia) + PCR

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35
Q

Canine Monocytic Ehrlichiosis (CME) - Treatment - Epistaxis

A

Acepromazine (+/- Benzodiazepines)

Adrenaline-soaked gauze

Tranexamic acid

Yunnan Baiyao

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36
Q

Canine Monocytic Ehrlichiosis (CME) - Negative prognostic indicators

A

Severe anemia

Severe thrombocytopenia

Severe leukopenia

Prolonged aPTT

Hypokalemia

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37
Q

Canine Monocytic Ehrlichiosis (CME) - Prevention

A

Anti-tick treatment

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38
Q

Anaplasma Platys - Vector

A

Rhipicephalus sanguineous

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39
Q

Anaplasma Platys - Target cell of the parasite

A

Platelets

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40
Q

Anaplasma Platys - Hallmark clincal-pathological finding

A

Cyclic thrombocytopenia (every 10-14 days)

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41
Q

Anaplasma Platys - Can be transmissible through blood transfusion (T/F)

A

True

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42
Q

Anaplasma Platys - Treatment

A

Doxycycline for 3-4 weeks

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43
Q

Anaplasma Platys - Causes a more severe disease when comes with CME co-infection (T/F)

A

True

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44
Q

Anaplasma Phagocytophilum - Target cell of the parasite

A

Neutrophils

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45
Q

Anaplasma Phagocytophilum - Acute / Chronic Disease Mostly?

A

Acute

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46
Q

Anaplasma Phagocytophilum - Lab findings

A

Anemia

Thrombocytopenia (90% of cases)

Lymphopenia

Hypoalbuminemia

Hyperglobulinemia

ALP Increase

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47
Q

Anaplasma Phagocytophilum - Diagnosis - Is blood smear a sensitive tool to detect the parasite?

A

Yes. Parasite can be detected in majority of cases

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48
Q

Anaplasma Phagocytophilum - Diagnosis

A

Blood smear, PCR

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49
Q

Anaplasma Phagocytophilum - Treatment, Prevention

A

Doxycycline

Tick prevention

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50
Q

Mycoplasma haemofelis - Modes of transmission

A

Bites

Fleas (unproven)

Blood transfusion

Intra-utero

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51
Q

Mycoplasma - Main type seen on blood smears

A

Mycoplasma Haemofelis

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52
Q

Mycoplasma haemofelis - Pathogenesis

A

Extravascular hemolysis => Strong regenerative anemia

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53
Q

Mycoplasma haemofelis - Blood smear findings

A

Anisocytosis

Polychromasia

Spherocytosis

Nucleated RBCs

Howell-jolly bodies.

RBCs infected with Mycoplasma can also be seen occasionally

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54
Q

Mycoplasma haemofelis - Classic signalment and concurrent pathologies to look for in infected cats

A

Male cats coming in contact with other cats

Co-infections causing immunosuppression (e.g. FIV, FeLV).

Abscess - A frequent finding occurring several weeks before acute disease with mycoplasma

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55
Q

Mycoplasma in cats - What types are usually associated with sub-clinical infection?

A

Candidatus M. hemominutum

Candidatus M. turicensis

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56
Q

Mycoplasma haemofelis - Clinical signs in acute episode

A

Fever

Lethargy

Anorexia

Pale mucus membranes

Splenomegaly

Lymphadenomegaly

Occasionally jaundice

Tachycardia

Tachypnea

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57
Q

Mycoplasma haemofelis - Diagnosis - Is blood smear useful for detecting the parasite? Also, in what percentage of clinical cats can Mycoplasma be detected in blood smears?

A

Mycoplasma (Haemofelis) can be detected in blood smears. However, bacteremia is cyclic and can disappear after 2 hours. Also, even if collected in the bacteremic phase - When collected with EDTA, after a while the parasite dissociate from the RBCs and die off - another source for false negative

50% of cases. If suspicion is high - keep taking blood samples every couple of hours

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58
Q

Mycoplasma haemofelis - Diagnosis (Gold standard)

A

PCR

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59
Q

Mycoplasma - Transmissible through blood transfusion?

A

Yes

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60
Q

Mycoplasma - Treatment

A

Doxycycline for 3-4 weeks

Fluoroquinolones also considered effective

GC if IMHA is suspected \ No-response to GC

Blood Transfusion if indicated

Anti-Pyretics, Fluids

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61
Q

Mycoplasma - Prognosis

A

Good. Clinical Improvement can be seen after 2-3 days from start of treatment. May remain a sub clinical carrier for years or for life / may experience repeat episodes.

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62
Q

Babesiosis - Modes of transmission

A

Tick bite

Blood Transfusion

Dog bite (B.Gibsoni)

Intrauterine (Some Spp.)

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63
Q

Babesiosis - Mechanisms of hemolysis (4)

A

RBC Rupture (Intravascular hemolysis)

Complement-mediated

Extravascular hemolysis

IMHA

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64
Q

Babesiosis - Breed predisposition - B.Vogeli

A

Greyhound

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65
Q

Babesiosis - Breed predisposition - B.Gibsoni

A

Pitbull

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66
Q

Babesiosis - Factors that determine severity of disease

A

Age (Young - more severe)

Babesia species ( B.Rossi > B.Canis > B.Vogeli)

Breeds (Greyhound, Pitbull)

Concurrent disease\Immunosuppression\Neoplasia

Splenectomy

Co-infections

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67
Q

Babesiosis - Clinical signs

A

Fever

Tachycardia

Tachypnea

Anorexia

Lethargy

Pale Mucus Membranes

Splenomegaly

Lymphadenomegaly

Pigmenturia

Icterus

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68
Q

Babesiosis - Common CBC findings

A

Regenerative anemia

Thrombocytopenia (mild-moderate)

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69
Q

Main differential for babesiosis

A

Primary \ Secondary IMHA

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70
Q

Babesiosis - B.Rossi - Name of specific pathology only to B.Rossi

A

Cerebral Babesiosis

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71
Q

Babesiosis - B.Vogeli - Mild/Moderate/Severe disease? Detectable in blood smear?

A

Mild-moderate

Parasitemia usually detectable

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72
Q

Babesiosis - B.Canis - Mild/Moderate/Severe disease? Detectable in blood smear?

A

Mild-severe

Parasitemia doesn’t usually correlate with severity

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73
Q

Babesiosis - B.Rossi - Mild/Moderate/Severe disease?

74
Q

Babesiosis - B.Vulpes - Main host

A

Fox (Can be transmitted to dogs)

75
Q

Babesiosis - Diagnosis (Gold standard)

76
Q

Babesiosis - Treatment - Large spp.

A

Imidocarb (Imizol) - 2 treatments14 days apart

77
Q

Babesiosis - Treatment - Small spp. (3 treatment modalities)

A

1) Atovaquone + Azithromycin

2) Clindamycin

3) Clindamycin + Imidocarb + Diminazine Aceturate (for Atovaquone resistant strains)

78
Q

Babesiosis - Supportive Treatment

A

Fluids

Blood Transfusion

Vitamins & Iron

*Steroids (controversial)

79
Q

Hepatozoonosis - Modes of transmission

A

Swallowing an infected tick

Intrauterine

80
Q

Hepatozoonosis - Transmissible In blood transfusion?

81
Q

Hepatozoonosis - Hepatozoon Canis - Vector

A

Rhipicephalus Sanguineous

82
Q

Hepatozoonosis - Hepatozoon Canis - Usually mild disease (True/False)

83
Q

Hepatozoonosis - Hepatozoon Canis - What percentage of cases have a high amount of parasitemia? What cells are Affected?

A

15% (8%-100% of Neutrophils infected)

Neutrophils and monocytes

84
Q

Hepatozoonosis - Hepatozoon Canis - Clinical signs in cases of severe disease

A

Cachexia

Fever

Splenomegaly

Lymphadenomegaly

Pale mucus membrane

85
Q

Hepatozoonosis - Hepatozoon Canis - Treatment? How effective is the treatment

A

Imidocarb (Imizol)

Decrease in parasitic load but will always remain in the bloodstream

86
Q

Hepatozoonosis - Hepatozoon Americanum - Clinical signs

A

Muscle Pain

Muscle Atrophy

Fever

Mucopurulent conjunctivitis

Lameness

Weight Loss

87
Q

Hepatozoonosis - Hepatozoon Americanum - Modes of Transmission

A

Swallowing in infected tick

Perdition of an infected animal

88
Q

Hepatozoonosis - Hepatozoon Americanum - Whats the severity of Parasitemia usually seen

A

Low (present in <1% of neutrophils)

89
Q

Hepatozoonosis - Hepatozoon Americanum - Lab findings / Imaging

A

Severe leukocytosis (20k-200k neutrophils)

Hyperglobulinemia

Increased ALP

X-Ray - Periosteal reactions

90
Q

Hepatozoonosis - Hepatozoon Americanum - Diagnosis

A

PCR

Muscle biopsy

91
Q

Hepatozoonosis - Hepatozoon Americanum - Treatment and Prognosis

A

TMS + Permethrin + Clindamycin (Not really effective)

If remission is achieved - Decoquinqate (Coccidiostat)

Prognosis: Grave

92
Q

Hepatozoonosis - Hepatozoon Felis - Target tissue

93
Q

Hepatozoonosis - Hepatozoon Felis - Common concurrent diseases

94
Q

Hepatozoonosis - Hepatozoon Felis - Mild/Severe disease?

95
Q

Can Babesia be transferred through bites?

A

Yes - B.Gibsoni (Pitbulls)

96
Q

Splenectomy predisposes dogs to what infective disease?

A

Babesiosis

97
Q

What diagnostic tool can differentiate between the different large Babesia species?

98
Q

Leishmaniasis - Name some known species of leishmania

A

L.Infantum

L.Major

L.Tropica

99
Q

Leishmaniasis - Name the specie that commonly causes disease in dogs

A

L.Infantum

100
Q

Leishmaniasis - If owners ask if their pet is posing a threat to other people - What would you tell them?

A

Usually the risk of zoonosis is very low. However, immunosuppressed people and infants are at greater risk

101
Q

Leishmaniasis - What formLife stage can be found in the blood? and in what cell?

A

Amastigote

Macrophages\Monocytes

102
Q

Leishmaniasis - Vector

A

Phlebotomus fly

103
Q

Leishmaniasis - Modes of transmission

A

Fly bite

Syringes

Blood transfusion

Intrauterine

104
Q

Leishmaniasis - Possible clinical signs

A

Splenomegaly

Lymphadenomegaly

Dermal changes

Weight loss

Ocular Disease (e.g. Uveitis, Keratitis, Conjunctivitis, Blepharitis, KCS)

Onychogryposis

Epistaxis

Hyperkeratosis of the nasal planum and foot pads

Signs of kidney failure (e.g. Oliguria, anuria, Vomiting)

105
Q

Leishmaniasis - Possible lab findings

A

Anemia (Usually mild non-regenerative)

Thrombocytopenia (Mild)

Elevation of liver enzymes

Hyperglobulinemia (Polyclonal gammopathy)

Hypoalbuminemia (NaPP, PLN)

Azotemia (CKD)

Proteinuria (PLN)

106
Q

Leishmaniasis - Possible dermal findings

A

Exfoliative dermatitis with alopecia

Ulcerative dermatitis

Nodular dermatitis (Boxers)

Mucocutaneous dermatitis

Papular dermatitis

107
Q

Leishmaniasis - What is the effect on the kidneys? Explain the basic pathophysiology and how to approach it diagnostically?

A

Deposition of immune-mediated complexes causing glomerulonephritis and eventually CKD

Urinalysis - check for proteinuria. If positive => Proceed with checking UPC (Urine protein creatinine ratio)

108
Q

Leishmaniasis - What is the cause of death in the majority of cases?

A

Kidney failure (Glomerulonephritis leading to tubulointerstitial lesions and CKD)

109
Q

Leishmaniasis - Possible & most common ocular findings (5)

A

Anterior uveitis

Conjunctivitis

Keratoconjunctivitis

Periocular alopecia

Blepharitis

110
Q

Leishmaniasis - What percent of cases present with epistaxis? What are the possible mechanisms?

A

<10% of cases of Leishmaniasis

-Ulcerative lesions
-Anti-platelet antibodies
-Thrombocytopathy
-Hyperviscosity syndrome (Hyperglobulinemia)

111
Q

Leishmaniasis - What percentages of cases present with thrombocytopenia

A

30-50% of cases

112
Q

Leishmaniasis - Diagnosis

A

History and clinical signs

CBC (Anemia, Thrombocytopenia)

Panel (Hyperglobulinemia, Azotemia)

UA (Proteinuria, UPC)

1) Serology (88-100% Sensitivity in clinical dogs. Only 30-60% in dogs without clinical signs

2) Cytology - Amastigotes (Skin\Lymph nodes\Spleen\Bone marrow\Conjunctiva)

3) PCR (Not from blood! from Spleen\LN\BM )

113
Q

Leishmaniasis - What tissues to sample for PCR?

A

Lymph nodes

Spleen

Bone marrow

NOT BLOOD URINE!

114
Q

What are “Mott cell”” with “Russel bodies”? In what diseases can you find it?

A

Plasma cell with vacuoles ocontaining Immunoglobulins

Any disease that produces large amount of immunoglobulins, classically infectious diseases such as Leishmaniasis and neoplasia such as Lymphoma

115
Q

Leishmaniosis - Treatment options

A

Allopurinol

Meglumine Antimoniate

Miltefosine

Best - Combination of Allopurinol + Meglumine \ Allopurinol + Miltefosine.

*When treating with Allopurinol - best to switch to a low purine diet to avoid formation of xanthine uroliths (e.g. Hill’s u/d)

116
Q

Leishmaniasis - When is it okay to stop treatment

A

All 3 conditions must be met:

1) Cessation of clinical signs

2) Normalization of CBC\Panel\UA

3) Normalization of Leishmania antibody titer (Monitored with quantitative serology)

117
Q

Leishmaniasis - What is the main side effect of Allopurinol?

A

Xanthinuria (usually after years of therapy)

118
Q

Leishmaniasis - When can you expect to start seeing clinical improvement after starting treatment? And when can you start seeing significant improvement?

A

1 Month

3 Months

119
Q

Leishmaniasis - Prevention

A

Anti-fly collars

Vaccinations if available

120
Q

Leishmaniasis - Recommended monitoring

A

Every month for 6 months - Physical exam

Every 3 months - CBC + Creatinine + UPC

Every 6 months - Serology + Full panel

121
Q

Leishmaniasis - Prognosis - Stage 1 (Clinical findings, Lab findings, Overall prognosis)

A

Solitary lymph node enlargement

Papular dermatitis

No abnormal clinical-pathological findings on blood tests

Prognosis: Good

122
Q

Leishmaniasis - Prognosis - Stage 2 (Clinical findings, Lab findings, Overall prognosis)

A

Generalized lymphadenopathy

Cutaneous disease

Onychogryposis

Epistaxis

Loss of Appetite & Weight loss

Mild non-regenerative anemia

Thrombocytopenia

Hyperglobulinemia

Hypoalbuminemia

Substage-a) Creatinine <1.4 , UPC < 0.5 (Normal )

Substage-b) Creatinine <1.4 (Normal) ,UPC = 0.5-1 (Mild proteinuria)

Prognosis: Good to guarded

123
Q

Leishmaniasis - Prognosis - Stage 3 (Clinical findings, Lab findings, Overall prognosis)

A

Stage 2 signs plus immune-mediated complex pathologies:

Vasculitis

Uveitis

Glomerulonephritis

Stage 2 findings plus CKD: UPC = 1-5 Creatinine 1.4-2 mg\dL (CKD Stage 2)

Prognosis: Guarded to poor

124
Q

Leishmaniasis - Prognosis - Stage 4 (Clinical findings, Lab findings, Overall prognosis)

A

Stage 3 plus:

PTE

Nephrotic syndrome

End stage kidney disease

Stage 3 Plus: Creatinine 2.1-5 (CKD Stage 3) or >5 mg\dL (CKD Stage 4) UPC >5 (Nephrotic syndrome)

Prognosis: Poor

125
Q

Leishmaniasis - What level of Thrombocytopenia do we Expect?

126
Q

Leishmaniasis - What type of dermal changes do Boxers usually have? What other animals tend to get them?

A

Nodular dermatitis

Cats

127
Q

FeLV - Modes of transmission

A

Orally (Saliva)

Intra-uterine

Blood transfusion

128
Q

FeLV - Where does the virus multiply?

A

Bone marrow

Respiratory epithelium

Salivary glands

129
Q

FeLV - What is the sub-type that is passed from cat to cat

130
Q

FeLV - What are the more pathogenic types?

A

FeLV B, FeLV C

131
Q

FeLV - When are cats most susceptible to catching the virus? (Young/Old)

A

Young

Risk of infection goes down as the cat ages

132
Q

FeLV - Pathophysiology

A

Cat eats viral matter => Enters oropharyngeal lymphatic tissues (Tonsils) => Can abort here and be rid of the virus (“Abortive Infection”).

If not: Primary viremia => Reaches bone marrow => Can be suppressed here (“Regressive Infection”) and be eliminated, or go into latency => Stress \ Immunosuppression => Secondary (Persistent) viremia: Virus migrates to: Lymph nodes, Salivary glands and respiratory epithelium => Cat becomes FeLV positive & secretion in saliva & clinical signs begin

133
Q

FeLV - Can a persistently infected queen pass the virus to her litter?

134
Q

FeLV - Clinical signssyndromes

A

Fever

Lethargy

Anorexia

Lymphadenomegaly

Diarrhea, Vomiting

Neoplasia: Lymphoma - Mostly - T-cell (60x higher risk than normal cats)

Leukemia

Bone marrow suppression: Anemia, Granulocytopenia and\or Lymphopenia, Thrombocytopenia (Pancytopenia)

Secondary infections (e.g. Mycoplasma, Toxoplasmosis)

Myoproliferative disorders

Myriad of syndrome: Nephrotic syndrome, Urinary incontinence, Uveitis, CNS signs, infertility and abortions.

135
Q

FeLV - Diagnosis - What type of test is it and what does it search for specifically in the virus?

A

Serology (IFA ELISA)

FeLV antigen - Core antigen p27

136
Q

FeLV - If a cat turns out positive in the Test - what is your next step, when and why?

A

Test again after 2-3 months - to see if the viremia is transient or persistent (Primary vs. secondary). If positive for the second time - persistent viremia and clinical signs are imminent

137
Q

FeLV - Treatment

A

Neoplasia - Chemotherapy

Bone marrow suppression - Darbepoetin \ G-CSF \ Steroids

Treat 2nd infections and keep cat indoors

138
Q

FeLV - Whats the difference between cats with lymphoma who also have FeLV and ones that only have Lymphoma?

A

Lymphoma + FeLV - Very short remission (25 days) &laquo_space;Lymphoma Only (~500 days)

139
Q

FeLV - Prevention and protocol

A

Vaccination: 2 Doses after 2 months old, then another one after a year, then booster every 2 years

140
Q

FeLV - Can serology testing distinguish between the virus and the vaccine?

141
Q

FIV - Classic signalment

A

Male cats older than 5 years

Outside cats > indoor cats

142
Q

FIV - Modes of transmission

A

Biting

Saliva

Milk

143
Q

FIV - Where is the majority of the virus concentrated in the body?

A

Salivary glands

144
Q

FIV - Pathophysiology

A

Primary infection and proliferation in local lymph nodes inside of T-cells

2-4 Weeks later => Primary viremia (antibodies are created). No significant clinical signs at this point.

Asymptomatic period (years) - Virus can be isolated and CBC abnormalities might be detected

Disease eruption - Generalized lymphadenomegaly, Fever, Leukopenia

145
Q

FIV - Cells in which the virus proliferates

A

T-Cells - CD4 (Mainly)

CD8

Megakaryocytes

Bone marrow cells

Macrophages

146
Q

FIV - What is the cause for clinical signs

A

Immuno-compromise and secondary infections

147
Q

FIV - Name the 5 stages of the disease

A

Acute stage

Asymptomatic stage

Persistent generalized lymphadenomegaly

AIDS Related complex

AIDS

148
Q

FIV - Acute stage - Duration

149
Q

FIV - Acute Stage - Clinical signs\Lab findings

A

Fever

Depression

Lymphadenopathy

Diarrhea

Possible leukopenia

150
Q

FIV - Asymptomatic stage - What mainly happens at this stage that progresses the disease towards its next stage?

A

Decrease in CD4 cells

151
Q

FIV - Persistent generalized lymphadenopathy - Clinical signs\Lab findings

A

Weight loss

Lymphadenopathy

Anemia, Leukopenia

152
Q

FIV - AIDS-related complex stage - Clinical signs\pathologies

A

Possible behavioral changes

Neoplasia - mainly Lymphosarcoma

Secondary infections (GI, Dermal, Respiratory, Mouth, Urinary tract, Eye, Kidney)

Anemia, Leukopenia

153
Q

FIV - AIDS Stage - Clinical signs\ Lab findings

A

Severe weight loss

50% of cases - Gingivitis

Secondary infections

CNS Signs

Anemia, Leukopenia

154
Q

FIV - Most common Clinical sign in cats diagnosed with the disease

A

Gingivitis (50% of cases)

155
Q

FIV - When to suspect? (5 Categories/Examples)

A

Chronic recurrent disease - Not responsive to treatment

Appearance of diseases that usually occur due to immunosuppression\In association with FIV - Toxoplasmosis, Mycoplasma, Hepatozoon Felis

Opportunistic infections : Gingivitis, Skin, Ears, Eyes

Neoplasia (B-cell Lymphoma)

Persistent leukopenia / Anemia

156
Q

FIV - When to suspect? (Lab findings)

A

Persistent anemia

Persistent leukopenia

Hyperglobulinemia

157
Q

FIV - When to suspect - Diseases that are associated with FIV

A

Mycoplasma

Toxoplasma

Hepatozoon

158
Q

FIV - What is the neoplasia associated with FIV?

A

B-cell Lymphoma

159
Q

FIV - Lymphoma - How more likely do cats develop Lymphoma when infected with FIV? In younger or older cats?

A

5x More likely

Younger cats with FIV develop Lymphoma more frequently

160
Q

FIV - Diagnosis

A

Serology - detection of antibodies created 4-5 weeks after infection

161
Q

FIV - Diagnosis - How? When? (Why then?)

A

Serology

> 4 Months old (before that - might be false positive because of passive protection from the queen)

In general: If suspicion is high and serology comes back negative - might be false negative - Test again 2-3 months later (might be the acute stage and antibodies have not yet formed).

162
Q

FIV - Diagnosis - End stage disease isn’t always positive on serology (T/F)

A

True

Due to severe immunosuppression and decreased production of antibodies

163
Q

FIV - Treatment

A

Antibiotics\Anti-fungal for secondary infections

Steroids to decrease chronic inflammation effects (bad long-term)

Iron, Vitamins

Blood Transfusion (anemia)

164
Q

FIV - Prognosis

A

In the asymptomatic stage: Great. Cat can remain healthy for many years

When AIDS develops - Poor.

165
Q

Which has the better MST - FIV or FeLV?

A

FIV - Can live a full life if asymptomatic stage persists

FeLV - 50% mortality 2 years after diagnosis. 80% mortality after 3 years

166
Q

FIV - Prevention

A

Mainly keep FIV-positive cats away from uninfected ones

167
Q

FIV - Prevention - FIVFeLV viruses can remain in the environment for weeks/months (T/F)

A

False

Only for a few days and after that its safe to bring in healthy cats.

168
Q

FIV - Prevention - Vaccination is an important part in prevention (T/F)

A

False

Not reliable enough (as opposed to FeLV vaccine)

169
Q

Leptospirosis - Common cause of disease in dogs and cats (T/F)

A

False

Causes disease in dogs but not in cats (But cats can serve as a reservoir)

170
Q

Leptospirosis - Main mode of infection

A

Through wounds in the skin and mucosal surfaces that come into contact with polluted water

171
Q

Leptospirosis - Associated pathologies and organs affected

A

Acute kidney injury (Damage to the tubular epithelium)

Hepatitis (Can be severe and acute)

Uveitis (Caused by immune complexes)

Coagulopathies (Vasculitis and thrombocytopenia)

172
Q

Leptospirosis - L. icterohaemorrhagiae - Main pathologies (2)

A

Icterus

Mild liver lesions

173
Q

Leptospirosis - L. grippothyphosa - Main pathology

A

Chronic active hepatitis

174
Q

Leptospirosis - Clinical signs

A

Fever

Lethargy

Anorexia

Vomiting

Oliguria, Anuria (AKI)

Pu\Pd

Icterus

Abdominal pain

Muscle pain

Uveitis

Less common: Bleeding disorders ,(Melena\Hematochezia\Pigmenturia\Epistaxis\Petechiae & ecchymosis)

Cough, Dyspnea (Pulmonary bleeding)

175
Q

Leptospirosis - Can remain Chronic\Sub-clinical. From what organ does the bacteria keep being spread?

A

Kidney

Spread via the urine.

176
Q

Leptospirosis - When to suspect?

A

AKI

Hepatitis

Uveitis

Fever of unknown origin

177
Q

Leptospirosis - Lab findings

A

CBC:
Leukopenia / Leukocytosis

Anemia (Inflammation/Bleeding)

Thrombocytopenia (Mild-moderate).

Panel:
Elevation of liver enzymes (ALT, ALP)

Hyperbilirubinemia

Hypoalbuminemia (NaPP, Vasculitis, Bleeding)

Azotemia

Hyperphosphatemia

Hypocalcemia

Hyperkalemia (AKI)

Hyponatremia, Hypokalemia, Hypochloridemia (Vomiting)

Urinalysis: Isosthrnuria, Bilirubinuria, Proteinuria, Glucosuria, Hematuria, Cylindruria, Pyuria

PT/aPTT - Prolonged

178
Q

Leptospirosis - Diagnosis (Main methods)

A

Serology - Microscopic agglutination test (MAT) - May yield false negative in the acute phase of the disease. 2nd test for seroconversion 7-14 days later may be necessary

PCR (Blood/Urine) - Must be done before antibiotic treatment or would result in false negative
*In the first week of disease - Blood is the prime choice because of high concentration of the bacteria in the blood. After the first week - Urine should be tested instead.

179
Q

Leptospirosis - Treatment

A

Isolate from other dogs!

Antibiotics: Ampicillin (for acute disease)

Doxycycline for 14 days (to clear the bacteria from the kidneys and prevent carrier-state)

Treat AKI (Fluids, Diuretics, Treat hyperkalemia, hypertension, acidosis, Dialysis if indicated)

Anti-oxidants (Hepatitis)

Plasma (DIC)

Oxygen (if indicated in cases of pulmonary hemorrhage)

180
Q

Leptospirosis - Prevention

A

Vaccine

First - 8 Weeks

Booster 2-4 weeks later

Then yearly shot

181
Q

Leptospirosis - Vaccine - what type is it? Protection period? Protects against all serovar?

A

Bacterin

12-18 Months

No

Doctor of Veterinary Medicine (Work in progress) (17 decks)

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