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Doctor of Veterinary Medicine (Work in progress) > Veterinary Medicine - Infectious diseases Pt.2 > Flashcards

Veterinary Medicine - Infectious diseases Pt.2 Flashcards

1
Q

Borrelia Persica - Name of the disease

A

Relapsing fever

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2
Q

Relapsing fever - Disease in dogs/cats?

A

Both

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3
Q

Relapsing fever - What type of bacteria is it?

A

Spirochete

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4
Q

Relapsing fever - Vector

A

Soft-tick - Ornithodoros tholozani

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5
Q

Relapsing fever - Clinical signs (3), CBC findings

A

Fever (In dogs, not in cats)

Anorexia

Lethargy

Anemia, Thrombocytopenia

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6
Q

Relapsing fever - Difference in clinical signs between cats and dogs

A

Dogs have fever. Cats don’t

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7
Q

Borrelia Vs. Leptospira - Which one can be identified in blood smears

A

Borrelia

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8
Q

Relapsing fever - Prognosis

A

Good (80% survival) - Responds well to antibiotics

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9
Q

Relapsing fever - What concurrent infection is common in dogs? (In some countries)

A

Babesia Negevi

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10
Q

Parvo - How do you get rid of the virus from the environment\surfaces?

A

Chlorine

Glutaraldehyde

Formalin

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11
Q

Parvo - Remains for a very short/long time in the environment? Why?

A

Very long time

Virus lacks an envelope

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12
Q

Parvo - In what tissues does the virus proliferates?

A

Bone marrow (WBC)

GI epithelium

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13
Q

Parvo - Modes of transmission

A

Oro-fecal

Intrauterine

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14
Q

Parvo - What is another pathology exhibited in puppies younger then 4 weeks old?

A

Myocarditis

Heart failure and sudden death (Due to a different CPV strain then the one causing GI disease)

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15
Q

Parvo - In what specific anatomical location in the GI Mucosa does the virus proliferate?

A

Crypts

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16
Q

Parvo - Pathogenesis

A

Viral material is ingested and enters the blood stream through the Peyer’s patches and the lymphatic tissue in the mouth:

1) Oropharyngeal LN

2) GI Mesenteric LN. => Viremia => Bone marrow, Thymus, Lymph nodes (Destruction of lymphocytes and neutrophils)

2 Options from there:

1) Proliferation in the GI mucosa (Severe gastroenteritis - common) with risk of secondary bacterial translocation from the gut to the bloodstream - Sepsis

Proliferation in cardiomyocytes (Sudden death - rare)

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17
Q

Parvo - How long does it take for clinical signs to manifest post-infection? When does the dog begin to secrete to virus?

A

Clinical signs begin 4 days post infection

Secretion of the virus - 3 days post infection

In other words - viral particle shedding begins BEFORE clinical signs!

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18
Q

Parvo - Factors influencing severity of disease (4)

A

Age (Young&raquo_space;> Adult)

Vaccination status

Concurrent GI infection (Opportunistic bacteria, Worms)

Sensitive dog breeds (Rottweiler, Pincher)

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19
Q

Parvo - Clinical signs

A

Lethargy

Anorexia

Fever

Vomiting (+- hematemesis)

Diarrhea (+- Melena \ Hematochezia)

Abdominal pain

Distended bowel loops

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20
Q

Parvo - Possible lab findings

A

CBC:
Leukopenia - Lymphopenia, Neutropenia
*Rebound (Recovery stage) - Leukocytosis - Monocytosis, Neutrophilia.

Panel:
Hypochloridemia, Hypokalemia, Hyponatremia (Diarrhea, Vomiting)

Hypoglycemia (Sepsis)

Hypoglobulinemia

Hypoalbuminemia

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21
Q

Parvo - Bone marrow cytology findings

A

Degeneration and toxicity in myeloid cells and megakaryocytes

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22
Q

Parvo - Radiological finding

A

Ileus and GI filled with gas

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23
Q

Parvo - US Findings

A

Free peritoneal fluid

GI Thickening, Ileus and distension

Mesenteric LN enlargement

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24
Q

Parvo - Diagnosis

A

PCR (Blood Feces)

Antigen-kit (Feces)

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25
Q

Parvo - Diagnosis - What’s the problem with PCR used on feces?

A

False positive

Vaccinated in the weeks prior infection

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26
Q

Parvo - Diagnosis - What’s the problem with the antigen-kit used on feces?

A

False negative: Viral particles may associate with antibodies and not be detected, or the virus isn’t secreted at the time of sampling).

False positive: Vaccinated in the weeks prior to infection

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27
Q

Parvo - Treatment

A

-Intensive fluid therapy (Preferably through a central catheter)

-Correct electrolytes (Mainly potassium), Hypoglycemia

-Colloids if severely hypoproteinemic

-GI support: Anti-emetics (Multiple if necessary), Pro-motiles, GI protectants. -Apatite stimulant (Only after vomiting and severe nausea has subsided

-Analgesia

-Antibiotics for 2nd infections (Combination of Beta-lactam + Aminoglycoside when dehydration is corrected - considered treatment of choice)

-De-worming

-Keep warm & clean

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28
Q

Parvo - Possible complication (3)

A

Sepsis, Intussusception, Peripheral edema / Ascites / Pleural effusion (Hypoalbuminemia)

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29
Q

Parvo - Monitoring - 3 Parameters

A

CBC, Creatinine, Electrolytes

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30
Q

Parvo - Prevention

A

Puppy vaccination

Bitch vaccination (before conception)

Isolate sick from healthy

Clean surfaces

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31
Q

Parvo - Vaccination regiment

A

First shot - 6 weeks

2 More shots every 2-4 weeks

Booster - 6-12 months of age

Booster every 3 years

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32
Q

Feline Panleukopenia - How to get rid of viral particle on surfaces?

A

Chloride

Glutaraldehyde

Formalin

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33
Q

Feline Panleukopenia / Parvovirus - Through what receptor do the viruses invade the cells?

A

Transferrin receptor

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34
Q

Feline Panleukopenia - Where does the Virus replicate?

A

Villi crypts in the small intestine

Lymphocytes

Bone marrow progenitor cells

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35
Q

Feline Panleukopenia - Modes of transmission

A

Oro-fecal

Intra-uterine

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36
Q

Feline Panleukopenia - What is the result of infection in the first trimester of pregnancy?

A

Embryonic death & absorption

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37
Q

Feline Panleukopenia - What is the pathology associated with infection in the second trimester of pregnancy and onward towards neonatality?

A

Cerebellar hypoplasia - “Feline ataxia syndrome”

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38
Q

Feline Panleukopenia - What cells in the cerebellum are affected in cerebellar hypoplasia?

A

Purkinje and granular cells

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39
Q

Feline Panleukopenia - What is the result of infection in cats beyond their neonatality?

A

Replication in the GI epithelium - Enteritis

Replication in lymphatic tissues Bone marrow - Panleukopenia

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40
Q

Feline Panleukopenia - Incubation period

A

As early as 2 days

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41
Q

Feline Panleukopenia - Clinical signs

A

Fever

Lethargy

Anorexia

Vomiting

Hypersalivation

Diarrhea

Abdominal pain

Distended bowel loops

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42
Q

Feline Ataxia Syndrome - Caused by which pathogen? When did the infection occur? Clinical signs?

A

Feline Panleukopenia virus

2nd trimester to neonatality

Hypermetria, Intention tremor, Ataxia

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43
Q

Feline Panleukopenia - Diagnosis

A

CBC - Leukopenia - Neutropenia

Antigen-kit (Feces)

PCR (Feces)

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44
Q

Feline Panleukopenia - Prevention? Regiment?

A

Vaccine

First Shot - 6-8 weeks

2 Booster shots every 2-4 weeks

Another shot at 6-12 months

Shot every 3 years

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45
Q

Feline Panleukopenia - Vaccination of pregnant cats is totally safe (T/F)

A

False

It’s a live attenuated virus that can still cause Abortion\Cerebellar hypoplasia

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46
Q

Feline Panleukopenia - Treatment

A

-Intensive fluid therapy (Preferably through a central catheter)

-Correct electrolytes (Mainly potassium), Hypoglycemia

-Colloids if severely hypoproteinemic

-GI support: Anti-emetics (Multiple if necessary), Pro-motiles, GI protectants. -Apatite stimulant (Only after vomiting and severe nausea has subsided

-Analgesia

-Antibiotics for 2nd infections (Combination of Beta-lactam + Aminoglycoside when dehydration is corrected - considered treatment of choice)

-De-worming

-Keep warm & clean

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47
Q

Infectious Canine Hepatitis - Name the Pathogen

A

Canine Adenovirus - 1

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48
Q

Infectious Canine Hepatitis - Mode of transmission

A

Oronasal coming in contact with urine, feces, saliva

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49
Q

Infectious Canine Hepatitis - Signalment

A

Dogs <1 year of age

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50
Q

Infectious Canine Hepatitis - Main systems affected

A

Liver

Kidney

Eyes

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51
Q

Infectious Canine Hepatitis - Clinical signs - Acute disease

A

Fever

Lethargy

Anorexia

Hematemesis

Diarrhea

Lymphadenopathy

Uveitis \ Corneal edema (Blue Eye) \ Glaucoma

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52
Q

Infectious Canine Hepatitis - Clinical signs - Sub-clinical

A

Pharyngitis

Tonsillitis

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53
Q

Infectious Canine Hepatitis - Clinical signs - Chronic disease)

A

CNS signs due to hepatic encephalopathy

Ascites

Weight Loss

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54
Q

Infectious Canine Hepatitis - Complications? Caused by what mechanism?

A

Glomerulonephritis

Uveitis\Glaucoma

DIC

Immune-mediated complexes

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55
Q

Infectious Canine Hepatitis - Lab findings

A

CBC:
Panleukopenia - Lymphopenia + Neutropenia

AST, ALT, ALP elevation

Hyperbilirubinemia

Hypoglycemia

Proteinuria, Bilirubinuria

Coagulation abnormalities

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56
Q

Infectious Canine Hepatitis - Prevention

A

Vaccine - against CAV-2

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57
Q

Infectious Canine Hepatitis - Diagnosis

A

Serology (Seroconversion)

PCR

Liver biopsy (Post-mortem)

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58
Q

Infectious Canine Hepatitis - Treatment

A

Supportive treatment:
Fluids
GI supportive treatment
Broad-spectrum antibiotics
Treat DIC (Plasma/Whole blood)
Treat uveitis (i.e. Atropine, Local GC/NSAIDs)

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59
Q

Corona virus in cats - Name the 2 pathogens originating from the virus

A

Feline Enteric Corona Virus (FECV)

Feline Infectious Peritonitis (FIP)

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60
Q

Feline Infectious Peritonitis (FIP) - Internal mutation hypothesis - Explain

A

FIP is originally FECV that undergoes mutation internally in individual cats - happens in <5% of FECV-infected cats. While FECV is infectious and is transmitted via an oro-fecal route - FIP is not considered infectious

61
Q

Feline Infectious Peritonitis (FIP) - What strain is infectious - FECV / FIP

62
Q

Feline Infectious Peritonitis (FIP) - Pathogenesis

A

Exposure to viral material - (Oro-nasal exposure) => Replication in tonsils and Small intestine => FECV => Gastroenteritis and mild diarrhea.

At a later stage FECV mutates to FIP:

Option A: Strong immune system destroys the virus => Healthy +- carrier state

Option B: Moderate immune reaction => Dry form (chronic disease): Infiltration of macrophages/monocytes => Formation of granulomas => Clinical signs vary and depend on the affected organs => Death

Option C: Weak immune reaction => Wet form (acute disease): Infiltration of macrophages/monocytes => Ascites/Pleural effusion => Death

63
Q

Feline Infectious Peritonitis (FIP) - Signalment

A

Young cats in multi-cat households - Incidence begins to rise after weaning and reaches peak at 6-18 months. Second peak: >10 years old

64
Q

Feline Infectious Peritonitis (FIP) - Mortality increases\decreases with age

A

Decreases. But another peak after the age of 10

65
Q

Feline Infectious Peritonitis (FIP) - Risk factors for infection

A

Multi-household cats

Stress

Weaning

Co-Infections (e.g. FeLV)

66
Q

Feline Infectious Peritonitis (FIP) - Wet form - Clinical signs

A

Fever

Anorexia\Normal\Increased appetite

Weight loss

Pale mucus membranes \ Cyanosis

Icterus

Dyspnea, Tachypnea

Pleural\Abdominal\Pericardial effusion

Uveitis

67
Q

Feline Infectious Peritonitis (FIP) - Dry form - Clinical signs

A

Varies - Depends on where the granulomas are formed (Kidney \ Liver \ Eye \ CNS \ GI \ Peritoneum)

68
Q

Feline Infectious Peritonitis (FIP) - Properties of the typical effusion collected in the wet form

A

Non-septic exudate

Protein-rich (>3.5 g\dL) with low cellularity

Yellowish-color with fibrin

Cytology - Predominantly activated macrophages and non-degenerate neutrophils.

69
Q

Feline Infectious Peritonitis (FIP) - What’s the name of the test performed on fluids to test if its rich in fibrin? Other DDs if positive results

A

Rivalta

Septic peritonitis

Lymphoma

70
Q

Feline Infectious Peritonitis (FIP) - Lab findings (Including CSF)

A

Leukocytosis: Neutrophilia + Lymphopenia

Mild non-regenerative anemia

Hyperbilirubinemia

Hyperglobulinemia

Hypoalbuminemia

CSF - Protein rich, Pleocytosis predominantly neutrophils

71
Q

Feline Infectious Peritonitis (FIP) - Serological tests are a viable option for diagnosis. Explain

A

No! Can’t differentiate between FIP and FECV based on serology. FIP diagnosis based on serology = Malpractice! Mainly assists in ruling out the disease.

72
Q

Feline Infectious Peritonitis (FIP) - PCR is a viable option for diagnosis. Explain

A

While PCR has increased likelihood for diagnosis (Better specificity than serology), FIP can have a variety of mutations that won’t be detected by PCR. One current diagnostic method is to send a sample of abdominal effusion for PCR that checks for a few of the most common mutations (by IDEXX).

73
Q

Feline Infectious Peritonitis (FIP) - Diagnosis - Gold standard

A

Histopathology \ Immunohistochemistry

PM - Fibrin deposition + granulomas on omentum and serosal surfaces in both wet & dry forms

74
Q

Feline Infectious Peritonitis (FIP) - Prognosis

A

Without specific treatment - Grave

Wet form - 8 Days MST from diagnosis

In recent years - new treatments have improved prognosis significantly

75
Q

Feline Infectious Peritonitis (FIP) - Treatment

A

Supportive:
Fluids
Anti-emetics
Appetite stimulant

Drain abdominal effusion - only if fluid accumulation is contributing to dyspnea - and only drain about 30% - to avoid worsening of hypoalbuminemia, Hypokalemia

Oxygen (in case of dyspnea)

*Several FIP-specific treatments have emerged in past years (e.g. GS-441, Remdesivir) that have shown remarkable results with complete recovery from what was once a fatal disease - including FIP with CNS involvement.

76
Q

Feline Infectious Peritonitis (FIP) - Prevention

A

Reduce crowding & and keep hygiene

77
Q

Feline Infectious Peritonitis (FIP) - Prevention - No vaccine available (T/F)

78
Q

Spirocercosis - Pathogenesis

A

Host beetle\Paratenic host is swallowed => Dissolves in the stomach => Worm migrates through gastric and coeliac artery walls => Travels through the walls of the descending thoracic aorta => Migrates to the esophageal wall and creates granulomas through which it lays its eggs.

79
Q

Spirocercosis - Time from infection to egg shedding

80
Q

Spirocercosis - What season has the highest incidence? Why?

A

Winter months

Host beetles are common in the summer and life-cycle completion from ingestion of an infected beetle takes 6 months.

81
Q

Spirocercosis - X-ray findings and Pathologies associated with S.Lupi infection

A

Chest X-rays:
-Spondylitis (T6-T12)
-Aortic mineralization
-Soft tissue opacity in the caudo-dorsal mediastinum

Aortic dissection and rupture
CNS Lesions - Classically hemiparesis/plegia.
Aortic thromboembolism (Saddle thromboembolism)
Pyothorax (esophageal rupture)
Hypertrophic osteopathy
Sialoadenosis
Neoplastic transformation (Fibrosarcoma / Osteosarcoma)

82
Q

Spirocercosis - Clinical signs

A

Regurgitation

Ptyalism

Sialoadenosis

Weight loss

Hypertrophic osteopathy

Dyspnea, Tachypnea, Cough (Aspiration pneumonia, Pulmonary metastasis)

CNS signs - classically hemiparesis\plegia (Aberrant migration)

Sudden death (Aortic rupture)

83
Q

Spirocercosis - Diagnosis

A

Chest X-rays

Fecal floatation

Endoscopy

84
Q

Spirocercosis - Treatment

A

Ivermectin \ Doramectin \ Milbemycin (Good for MDR1 Positive) \ Advocate

Treat regurgitations:
Feed from a high place (can use a Baileys chair) with high frequency + low quantity meals.

Metoclopramide + PPI when esophagitis is evident

Gastric tube is also an option

85
Q

Canine Distemper Virus - Modes of transmission

A

Aerosol (Main)

Saliva

Urine

Feces

Conjunctival and nasal secretion

86
Q

Canine Distemper Virus - When are dogs most susceptible and why?

A

3-6 months old

When passive protection wears off

87
Q

Canine Distemper Virus - In what tissues does the virus tend to persist?

A

Eyes

Neurons

Foot pads

88
Q

Canine Distemper Virus - Elaborate on the neurological syndromes caused by the virus

A

Acute encephalomyelitis - Direct damage to neurons and myelin

Chronic encephalomyelitis - Immune mediated damage to neurons and myelin

Chronic progressive encephalomyelitis - CNS Disease where the virus is not completely removed from the CNS

Old dog encephalitis - Appears years after the acute portion of the disease

89
Q

Canine Distemper Virus - Clinical Signs

A

Fever

Anorexia, Lethargy

Vomiting, Diarrhea

Cough, Dyspnea

Serous to purulent secretions from nose and eyes

Hyperkeratosis of nasal planum and foot pads

Enamel hypoplasia

Abdominal pustules

Eye - Acute blindness (Optic neuritis), Conjunctivitis, Uveitis, KCS

CNS diseases - Rhythmic myoclonus (Pathognomonic), Signs of central multi-focal disease

90
Q

Canine Distemper Virus - Possible ocular findings

A

Conjunctivitis

Uveitis

KCS

Hyperreflective Retina (Scarring)

Optic neuritis

Blindness

91
Q

Canine Distemper Virus - Respiratory Tract Findings

A

Serous-mucopurulent discharge

Cough

Pneumonia

92
Q

Canine Distemper Virus - Miscellaneous findings (3 Classical distemper-associated findings)

A

Enamel hypoplasia

Hyperkeratosis of nasal planum and foot pads

Rhythmic myoclonus

93
Q

Canine Distemper Virus - CNS disease in adult dogs is usually preceded by a systemic disease right before it (True/False)

A

False

Usually suffered from systemic disease as a young dog. Can remain non-clinical for months-years before developing CNS signs

94
Q

Canine Distemper Virus - CBC finding

A

Lymphopenia

95
Q

Canine Distemper Virus - Blood smear findings

A

Inclusion bodies can be found in RBCs, WBCs and platelets

96
Q

Canine Distemper Virus - CSF findings

A

Increase in Protein (>25 g\dL)

High cell count (lymphocytes Mainly)

97
Q

Canine Distemper Virus - Diagnosis

A

History and clinical signs - Signs of GI, Respiratory, CNS, and more specific signs such as rhythmic myoclonus, Enamel hypoplasia, Hyperkeratosis

Visualization of inclusion bodies (e.g. Blood smear, Conjunctival swab)

Serology - preferably on CSF - compare to blood - Antibody titer should be higher than blood titer

Quantitative RT-PCR on various samples (e.g. Conjunctiva, Nasal secretions, Blood, Urine)

IFA or FISH on Biopsy samples (Can be used on samples from foot pads)

Post-mortem

98
Q

Canine Distemper Virus - Diagnosis - CSF - Possible reasons for false positive in serological testing (Blood\CSF)

A

False positive on blood samples:
Dogs can have antibodies in the blood due to previous exposure and not necessarily due to disease

False positive on CSF samples:
-Contamination of CSF samples with blood during sampling
-Blood-brain barrier breached due to systemic inflammation

99
Q

Canine Distemper Virus - Treatment

A

Supportive

100
Q

Canine Distemper Virus - Prevention and regiment

A

Vaccination (Modified-live)

6-8 Weeks - first shot

2 more shots 2-4 Weeks apart

Booster 6-12 months

Shot every 3 Years

101
Q

Infectious Tracheobronchitis (“Kennel Cough”) - Clinical signs

A

Muco-purulent discharge from nose

Coughing \ retching

Fever

Anorexia (Occasionally)

102
Q

Infectious Tracheobronchitis (“Kennel Cough”) - How long until clinical signs resolve

103
Q

Infectious Tracheobronchitis (“Kennel Cough”) - Causative agents

A

Bordetella Bronchiseptica (Mainly)

Other possible pathogens:
CAV-2
Para-influenza
Influenza
Herpes
Mycoplasma

104
Q

Infectious Tracheobronchitis (“Kennel Cough”) - How long do dogs remain infective/contagious

A

2-3 Months

105
Q

Infectious Tracheobronchitis (“Kennel Cough”) - B.Bronchiseptica - Pathogenesis

A

The Bacteria attaches to the cilia and inhibits the muco-ciliary apparatus - causing local inflammation and increased mucus production

106
Q

Infectious Tracheobronchitis (“Kennel Cough”) - Once the dog recovers - the dog is immune for life (T/F)

A

False

Only for 1 year

107
Q

Infectious Tracheobronchitis (“Kennel Cough”) - Diagnosis

A

History (Vaccination status, Staying in highly populated habitats such as kennels, Exposure to sick dogs)

Clinical signs

108
Q

Infectious Tracheobronchitis (““Kennel Cough””) - Treatment

A

Option 1: Do nothing - Disease usually self-limiting

Option 2: Doxycycline (or Azithromycin), Anti-tussives, Anti-pyretics, Appetite stimulant

109
Q

Infectious Tracheobronchitis (“Kennel Cough”) - Prevention

A

Remove from densely-populated areas

Separate from sick dogs

Vaccines:
1) Bordetella - Intranasal IgA (One dose) \ Parenteral (2 shots 14 days apart)

2) Vaccinations against CAV, PI.

110
Q

Feline Respiratory Disease Complex - Name the main pathogens

A

Herpesvirus

Calicivirus

Chlamydia

Less commonly: Bordetella Bronchiseptica, Mycoplasma

111
Q

Feline Herpes Virus (FHV) - Modes of transmission

A

Oronasal

Conjunctival secretions

112
Q

Feline Herpes Virus (FHV) - Clinical signs

A

Anorexia, Lethargy

Fever

Sneezing

Nasal and ocular secretions (Serous to mucopurulent)

Conjunctival hyperemia (Conjunctivitis)

Keratitis, Corneal ulcers, Sequestrum formation

Ulcers in the oral cavity (Stomatitis)

113
Q

Feline Herpes Virus (FHV) - Severe diseases in young/old cats

A

Young

Acute death in kittens

114
Q

Feline Herpes Virus (FHV) - How does it cause death in young kittens

A

Dehydration

Secondary bacterial infection

115
Q

Feline Herpes Virus (FHV) - Only CBC Finding

A

Neutrophilia

116
Q

Feline Herpes Virus (FHV)) - How many remain latent carriers? of them, how many secrete the virus?

A

80% - latent carriers

50% of them intermittently secrete the virus

117
Q

Feline Calicivirus - Modes of transmission

A

Oronasal secretions

Conjunctival secretions

118
Q

Feline Calicivirus - Clinical signs

A

Anorexia, Lethargy

Fever

Sneezing

Nasal and ocular secretions (Serous to mucopurulent)

Conjunctival hyperemia (Conjunctivitis)

Ulcers in the oral cavity (Stomatitis)

Lingual ulcer (highly characteristic of Calicivirus)

Virulent strains: Icterus, Pneumonia (Tachypnea, Dyspnea), Lameness (Polyarthritis), Edema and ulceration of face and feet)

119
Q

Feline Calicivirus - What is the clinical sign most associated with Calicivirus infection?

A

Lingual ulcers

120
Q

Feline Calicivirus \ FHV - What is the difference in “Carrier State” between the 2 viruses?

A

FHV - Most remain carriers for life and intermittently secrete the virus for a few weeks at a time.

Calicivirus - Cats are only temporarily carriers after recovery from acute disease and eventually overcome the virus and is completely removed. They remain contagious for 2-3 weeks minimum.

121
Q

Feline Calicivirus - Virulent systemic disease (VSD) - Clinical signs

A

Sub-cutaneous edema in the legs and face

Ulceration in legs and face

Dyspnea, Tachypnea (Pneumonia)

Lameness (Polyarthritis)

Icterus

122
Q

Feline Calicivirus / FHV - Diagnosis

A

Mainly history and clinical signs!

PCR from Conjunctiva, Mouth (Lingual ulcer), Skin, Blood

123
Q

Feline Calicivirus \ FHV - Treatment

A

Clean nasal and ocular secretions

Specific anti-viral treatments (Herpes) - Famciclovir, Lysine

Antibiotics (2nd Infections) - Doxycycline \ Azithromycin \ Augmentin

Fluids, Anti-pyretics

Analgesia

Oxygen, Nebulization

Treat corneal ulcers (Herpes)

124
Q

Feline Chlamydia - Main target organ

A

Conjunctiva

125
Q

Feline Chlamydia - Clinical signs

A

Conjunctivitis

Blepharospasm

Eye secretions

Very mild rhinitis with sneezing and secretions

126
Q

Feline Chlamydia - Signalment

A

Young

2-12 Months old

127
Q

Feline Chlamydia - Diagnosis

A

Mainly Hx and clinical signs!

Isolation from conjunctival swabs

IFA

PCR from conjunctiva

128
Q

Feline Chlamydia - Treatment

A

Doxycycline \ Tetracycline

Clean secretions

129
Q

Feline Respiratory Disease Complex - Prevention

A

Vaccination for:

1) FHV

2) Calicivirus

3) Chlamydia

130
Q

Rabies - What is the only animal that can be an asymptomatic carrier?

131
Q

Rabies - Mode of transmission

A

Bites

Contact of infected saliva with lesions

132
Q

Rabies - Pathogenesis

A

Bite => Virus travels to myocyte cytoplasm => NMJ => PNS => Spinal cord => Brain => Salivary glands

133
Q

Rabies - Incubation period and 2 factors affecting it

A

10 Days - 1 Year

1) Location of bite (Further from the brain = Longer incubation period)

2) Amount of virus inserted

134
Q

Rabies - When does a dog become contagious in relation to appearance of clinical signs?

A

2 Weeks before clinical signs appear!

135
Q

Rabies - What are the names of the 4 stages

A

Prodromal phase

Dumb phase \ Furious phase

Paralytic phase

136
Q

Rabies - Prodromal phase - Clinical signs

A

Anorexia

Unease

Vomiting

Salivation

Behavioral changes

137
Q

Rabies - Dumb phase - Clinical signs

A

Depression

Dementia

138
Q

Rabies - Furious phase - Clinical signs

A

Extreme Unease

Increased vocalization

Extreme aggressiveness

Seizures

Extreme salivation

Aimless walking

139
Q

Rabies - Paralytic phase - Clinical signs

A

Paresis \ Paralysis

Hydrophobia

Pharyngeal paralysis - Dysphagia

Salivation

Change in vocals

Mandibular Paralysis, Facial paralysis

Head tilt

140
Q

Rabies - Diagnosis

A

PCR - Saliva \ CSF \ Hair Follicle

Post-mortem: IFA of brain, Identify Negri-bodies in brain, Immunohistochemistry of brain tissue

Biological test - Inject infected material to mice - death after 2 weeks.

141
Q

Rabies - Treatment

A

Do not treat! Keep in quarantine for 10 days!

142
Q

Rabies - Vaccination in humans - Name the 2 vaccines

A

Rabies Immune Globulin (RIG) - Passive

Human Diploid Cell Vaccine (HDCV) - Active.

143
Q

Rabies - Vaccination in dogs - Regiment

A

First shot - 12 Weeks

2nd shot - 1 year of age

In endemic countries - Yearly shots

144
Q

Rabies - Prevention

A

Vaccinate all dogs once a year

Vaccinate wild animals

Deal with roaming dogs

Vaccinate all personal dealing with animals

145
Q

Rabies in cats - Rare\Common?

A

USA - Common (More than in dogs) - transmitted to cats from raccoons

146
Q

Rabies in cats - Prevention

A

Vaccine

12 Weeks - first shot

1 year of Age - 2nd Shot

147
Q

When systemic Aspergillosis infection is suspected - What test has a good Sp and Sn for detection of the organism? in what bodily fluids?

A

Aspergillosis Antigen Test in Serum and Urine

148
Q

In addition to anemia (Regenerative), what other CBC change is common in Babesiosis?

A

Thrombocytopenia

149
Q

FIP - Signalment, Clinical signa and classic labwork findings

A

Young (~1y.o.) or aging (~10-12y.o) cats from multiple cat household. C.S.

Anorexia/Hyporexia

Lethargy

Fever

Weight loss

Jaundice

Dyspnea

Ascites

Could also present with other multiple classical c.s. in the dry form - depending on the location of the lesions (e.g. kidney, liver, CNS, Ocular)

Classical Lab findings:
Neutrophilia
Non-regenerative anemia
Hyperbilirubinemia
Hyperglobulinemia (Polyclonal)
Hypoalbuminemia

Effusion: Non-septic exudate (TS <3 g/dL) consisting mainly of reactive macrophages and neutrophils..

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

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