Canine Viral Diseases Flashcards

1
Q

What are respiratory viruses that affect dogs?

A
  • Canine influenza
  • Canine herpesvirus 1
  • Canine distemper virus
  • Canine adenovirus 2
  • Canine parainfluenza
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2
Q

Describe the taxonomy of canine herpesvirus 1 (family and subfamily)?

A

Family: Herpesviridae
Sub family: Alphaherpesvirinae

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3
Q

What type of genome does canine herpesvirus have?

A

Double stranded DNA virus.

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4
Q

What is the disease associated with canine herpesvirus 1?

A

Hemorrhagic disease in pups

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5
Q

Where does canine herpesvirus relicate?

A

Endothelial cells

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6
Q

How are adults infected with canine herpesvirus?

A

Venereal or respiratory infection

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7
Q

How are neonates infected with canine herpesvirus?

A

Ingestion, inhalation (birth canal, contact, fomites)

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8
Q

Can canine herpesvirus be transmitted in utero?

A

Yes, through the placenta.

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9
Q

How does age of infection with canine herpesvirus affect disease in neonates?

A

Less than 1 week old pups:
- Lymphoid hyperplasia can lead to generalized infection: diffuse necrotizing vasculitis, multifocal hemorrhagic necrosis of many organs (including CNS). May recover with residual CNS signs or can result in illness/death.
OR
- Localized infection and replication can occur with persistence in respiratory or genital tracts, leading to latency.

Over 2 week old pups:
- Localized infection and replication can occur with persistence in respiratory or genital tracts, leading to latency.

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10
Q

Describe the pathogenesis of canine herpesvirus in fetuses.

A
  • Fetuses are infected in utero, leading to leukocyte-associated viremia and lymphoid hyperplasia.
  • Generalized infection occurs leading to diffuse necrotizing vasculitis (widespread inflammation and death of blood vessel tissues) or multifocal hemorrhagic necrosis (multiple areas of bleeding and tissue death occur in various organs, including the central nervous system).

Outcomes:
- Prenatal effects: Abortion, stillbirth, or infertility.
- Neonatal effects: Illness or death in newborn puppies OR recovery with residual CNS signs.

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11
Q

What factors contribute to the latent reactivation of canine herpesvirus in adult dogs?

A
  • Stress
  • Immunosuppression
  • Pregnancy
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12
Q

Describe the pathogenesis of canine herpesvirus in adult dogs.

A
  • The virus infects epithelial cells in the venereal and respiratory tracts, then the virus enters the bloodstream (viremia).
  • Localized infection and replication: The virus establishes a localized infection and replicates in the affected tissues.
  • The virus can persist in the respiratory and genital tracts and can enter a latent state.

From the latent state, the virus can reactivate and lead to:
- Ocular form: Affecting the eyes
- Placentitis: Inflammation of the placenta
- Mild rhinitis
- Vesicular vaginitis
- Posthitis: Inflammation of the prepuce

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13
Q

How does infection with canine herpesvirus differ in adults compared to neonates or fetuses?

A

Typically, adult infections are less severe and more localized than neonate or fetus infections that typically cause generalized infection.

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14
Q

What are the clinical signs of canine herpesvirus in adult dogs?

A
  • Ocular form: Affecting the eyes, corneal edema and cataracts
  • Placentitis: Inflammation of the placenta
  • Mild rhinitis
  • Vesicular vaginitis
  • Posthitis: Inflammation of the prepuce
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15
Q

What is the site of latency of canine herpesvirus?

A

Trigeminal or lumbosacral ganglia

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16
Q

Describe the pathogenesis of canine herpesvirus in neonates.

A

Initial infection occurs through ingestion or inhalation via the birth canal, contact, or fomites.

Age-dependent susceptibility:
- Neonates <1 week old are highly susceptible. The virus replicates in epithelial cells and invades the mucosa. Can either lead to leukocyte associated viremia or localized infection. Can lead to diffuse necrotizing vasculitis or multifocal hemorrhagic necrosis of many organs, including the central nervous system (CNS).
- Puppies >2 weeks old are less susceptible and get localized infection and latency.

Outcomes <1 wk:
- Recovery (possibly with residual CNS signs)
- Neonatal illness or death

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17
Q

What factors influence the infection progression with canine herpesvirus?

A
  • Body temperature (replicates more efficiently at lower body temps)
  • Immunocompetence
  • Maternal antibodies
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18
Q

What lesion is pathognomonic of canine herpesvirus 1?

A

Petechial hemorrhage in the renal cortex.

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19
Q

Where in the CNS can herpesvirus be found?

A

Cerebellum (in glial nodules)

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20
Q

How is canine herpesvirus diagnosed?

A
  • Pathognomonic lesions (petechiae on kidney/liver)
  • Virus isolation from tissues (liver, kidney, spleen, lung)
  • Histologic finding of intranuclear inclusion bodies
  • Viral neutralization assay available at animal health lab in Guelph
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21
Q

How is canine herpesvirus controlled?

A

There is no vaccine available.

Maternal antibody in colostrum protects pups. Removing pups from an infected mother via c-section and keeping them isolated may prevent death if the virus has not yet crossed the placental barrier.

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22
Q

Is canine herpesvirus enveloped or naked?

A

Enveloped

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23
Q

Is canine adenovirus 1 enveloped or naked?

A

Naked

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24
Q

What type of genome does canine infectious hepatitis have?

A

Double stranded DNA virus.

Caused by the virus canine adenovirus 1

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25
Q

Describe the taxonomy of canine infectious hepatitis (family and genus)?

A

Family: Adenoviridae
Genus: Mastadenovirus

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26
Q

What disease does canine adenovirus 1 cause?

A

Canine infectious hepatitis

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27
Q

Describe the structure of canine adenovirus.

A
  • Naked
  • Hexagonal shape
  • Pentons at each corner of hexagons that possess projecting fibers
  • Fibers mediate attachment of virus to cell receptors
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28
Q

Where does canine adenovirus replicate?

A

In nucleus.

Form intranuclear inclusions.

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29
Q

What disease does canine adenovirus 2 cause?

A

Infectious canine tracheobronchitis (kennel cough)

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30
Q

Infectious canine hepatitis is most common in which age group?

A

Within a year of age. However, unvaccinated dogs may get the disease at any time.

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31
Q

Which species are affected by CAV-1?

A

Dogs, coyotes, foxes, other canids and bears.

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32
Q

How can CAV-1 be killed?

A
  • Iodine
  • Phenol
  • Sodium hydroxide
  • Heating for 5 mins between 50-60 degrees
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33
Q

How is CAV-1 spread?

A
  • Oronasal transmission (contact with fomites)
  • Ectoparasite transmission
  • Aerosol transmission (unlikely)
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34
Q

Where is CAV-1 excreted?

A

In saliva, feces and resp mucus during the acute phase (5-10 days).

In urine for 6-9 months during chronic phase (starts at day 10-14).

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35
Q

What are the two ways that CAV-1 can cause damage to tissues?

A
  • Deposition of antibody-antigen complexes in vessels and tissues.
  • Viral replication causing cell damage.
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36
Q

Viral replication of CAV-1 causes damage to what cells/tissues and what is the consequence?

A
  • Hepatocytes (acute hepatitis, intranuclear inclusions, chronic hepatitis)
  • Renal tubule cells (nephritis, virus shed in urine)
  • Vascular endothelial cells (hemorrhage, DIC, intranuclear inclusions)
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37
Q

What are the clinical signs of CAV-1 infection?

A
  • Slight fever
  • Lethargy
  • Mucous membrane congestion
  • Tender abdomen
  • Jaundice
  • Vomiting
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38
Q

What are laboratory findings associated with CAV-1 infection?

A
  • Pyrexia
  • Leukopenia
  • Lymphocytosis
  • Neutrophilia
  • Increased ALT
  • Coagulopathy
  • Proteinuria
  • Neutralizing antibody (after day 6)
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39
Q

What causes blue eyes with CAV-1 infection?

A

Due to type III hypersensitivity reaction. Can be observed in some animals vaccinated with modified live vaccines.

Occurs 1-3 weeks after infection when immune complexes deposit in the cornea.

RESOLVES SPONTANEOUSLY - no need to treat.

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40
Q

How is CAV-1 infection diagnosed?

A
  • Clinical signs, hematological findings, and liver enzyme changes.
  • Ante mortem confirmation can be done from serology, virus isolation, molecular techniques, immunofluorescence.
  • Post-mortem histopathology.
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41
Q

What are the sources of CAV-1 infection?

A
  • Environment (virus is very resistant)
  • Reservoir in wild carnivores (subclinical) and ectoparasites
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42
Q

What is the role of maternal immunity in CAV-1?

A
  • Pups are protected up to 5-7 weeks.
  • Fully waned by 14-16 weeks.
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43
Q

Describe available CAV-1 vaccines.

A
  • Killed vaccines are safe but need frequent (annual) administration.
  • Modified live vaccines can be given every 3-5 years but can lead to kidney signs or blue eye.

Modern vaccines contain either CAV-1 or CAV-2 but provide cross protection against hepatitis and cough.

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44
Q

What are the viral causes of canine infectious tracheobronchitis?

A
  • Canine parainfluenza virus, CPiV (most common)
  • Canine distemper virus
  • Canine adenovirus 2
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45
Q

What are the risk factors for canine infectious tracheobronchitis?

A
  • High density housing
  • Contact with sick animals
  • Mixing of dogs
  • Stress
  • Bordetella bronchiseptica host range (wildlife, rodents, cats carry bacteria)
  • Preexisting subclinical airway disease
  • Housing with poor hygiene
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46
Q

How is canine infectious tracheobronchitis transmitted?

A
  • Virus is shed through ocular and resp secretions
  • Micro-droplets are aerosolized, can also be direct contact or fomites
  • Highly contagious
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47
Q

How long do the viral and bacterial causes of canine infectious tracheobronchitis shed for?

A

Viruses: 8-10 days following infection
Bordetella: Up to 3 months.

48
Q

What are the two forms of canine infectious tracheobronchitis?

A
  1. Uncomplicated
  2. Complicated
49
Q

Describe uncomplicated canine infectious tracheobronchitis (clinical signs, timeline, treatment).

A

Clinical signs:
- Harsh dry cough
- Watery nasal discharge
- Pharyngitis and tonsillitis
(not systemically ill)

Virus and/or bacteria is replicating in the respiratory epithelium, destroying these cells. Infection is self limiting.
- Body mounts an immune response
- Mild: pass in 1-2 weeks
- Severe: pass in 3-4 weeks

Treatment: Reduce stress and exercise which minimizes irritation to the airways.

50
Q

Describe uncomplicated canine infectious tracheobronchitis (clinical signs, susceptibility, treatment).

A

Occurs in young unvaccinated puppies,
immunocompromised, and elderly animals

Like the uncomplicated form, the virus and bacteria replicate in respiratory epithelium. Body is unable to generate appropriate antibody response
- Viremia
- Secondary bacterial infections
- Signs progress to lethargy, severe fever and inappetence

These dogs require treatment.

51
Q

What control options are there for canine infectious tracheobronchitis?

A
  • Modified live virus vaccines against distemper, CPiV, and CAV-2, which also provides protection against CAV-1
  • When the risk of B. bronchiseptica infection is significant, use of a live, avirulent, intranasal vaccine is preferable to parenteral products containing inactivated bacteria or bacterial extracts
  • A combination of an avirulent B. bronchiseptica and a modified live parainfluenza vaccine is available for intranasal use
52
Q

What family is canine influenza?

A

Orthomyxoviridae

53
Q

What are the types of canine influenza and which species do they affect?

A
  • Type A in animals and humans (cross transmission)
  • Type B only in humans, serological evidence in pigs
  • Type C in humans, occasionally in seals and pigs
  • Type D, primary host is cattle, other animals (pigs) as well, humans are seropositive
54
Q

What are the main target cells of canine influenza?

A
  • Alveolar macrophages
  • Respiratory epithelium
55
Q

How is mucociliary clearance reduced with canine influenza infection?

A

Cilia clump together in areas where the virus buds from the membranes of ciliary shafts.

56
Q

How is canine influenza diagnosed?

A
  • Clinical signs are vague so not reliable for diagnosis
  • Virus isolation, immunoassays, RT-PCR, serology are used
57
Q

How is canine influenza controlled?

A
  • Monovalent or bivalent vaccines are available for both H3N8 and H3N2 canine influenza
  • Vaccination may not all together prevent an infection, but it may reduce the severity and duration of clinical illness
58
Q

What is the difference between the intranuclear inclusions seen in herpesvirus and adenovirus?

A

Herpesvirus - eosinophilic.
Adenovirus - basophilic.

59
Q

Where does canine influenza come from?

A

Mutated equine influenza (H3N8)

60
Q

What species are affected by canine distemper?

A

Lots

Canidae (dog, fox, wolf, raccoon)
Mustelidae ( ferret, mink, skunk, wolverine, marten, badger, otter)
Procyonidae (raccoon, coatimundi)
Viveridae (binturong, palm civet)
Ailuridae (red panda), Ursidae (bear)
Elephantidae (Asian elephant)
Primates (Japanese monkey)
Large Felidae (lions, leopards, cheetahs, tigers)
Others (Caspian and Baikal seals)

61
Q

What is the main reservoir for canine distemper?

A

Unvaccinated domestic and feral dogs act as a reservoir for wildlife due to interspecies transmission.

62
Q

What genome does canine distemper have?

A

Negative sense ss RNA.

63
Q

What family is canine distemper virus?

A

Paramyxoviridae

64
Q

What genus is canine distemper virus?

A

Morbilivirus

Same genus as rinderpest and measles.

65
Q

Different genotypes of CDV are dependent on variation in what gene?

A

H gene

66
Q

Where does CDV replicate?

A

Lymphoid tissues and intestinal lamina propria.

67
Q

What proportion of CDV infections are subclinical?

A

50-70%

68
Q

What diseases are associated with CDV?

A

Acute: GI and respiratory symptoms. (most recover)

Chronic: Neurologic symptoms. (few recover)

Enamel hypoplasia.

Hard Pad disease.

69
Q

What are the target cells for CDV?

A

Lymphocytes, ameloblasts, keratinocytes.

70
Q

How is CDV transmitted?

A

Aerosol (coughing, barking, sneezing, etc.) or fomites

71
Q

What are the clinical signs associated with acute CDV?

A

*Biphasic fever (day 4, then day 14).

Acute: Anorexia, vomiting, diarrhea, fever, conjunctivitis.

72
Q

What are the clinical signs associated with chronic CDV?

A

Chronic: Seizures, ataxia, myoclonus, tremors, death.

CNS signs = chronic.

73
Q

What is a distinct histologic feature with CDV?

A

Appearance of syncytia (cells with multiple nuclei) due to virus ability to dissolve cell membranes.

74
Q

What is the structure and genome of rabies virus?

A

Enveloped virus. Bullet shaped.

Negative sense single stranded RNA virus.

75
Q

What are the two forms of rabies virus and which animals are affected by each form?

A

Two forms:
1. Furious
2. Paralytic

Horses, cattle, bats get paralytic form.

Cats get furious form.

Dogs get both.

76
Q

What is the family and genus of rabies virus?

A

Family: Rhabdoviridae

Genus: Lyssavirus

77
Q

How is rabies virus transmitted?

A

Saliva, CSF, and infected neural tissues through contain the virus.

Transmitted through

  • Bite wounds
  • Skin cuts
  • Mucous membranes
  • Aerosols possible

Virus can be shed by cats and dogs for 1-5 days before clinical signs. Skunks and bats up to 14 days.

78
Q

How does rabies reach the CNS?

A

Bite wound infects muscles. Then, rabies virus moves to synapse between neurons and muscle cell. Enters the neurons at the synapse and moves (anterograde) towards CNS.

Virus can move max 100mm per day so time until it reaches CNS depends on site of infection.

79
Q

What species are resistant to rabies?

A
  • Birds
  • Reptiles
  • Amphibians
80
Q

What is the clinical outcome of rabies? What is the timeline for this?

A

100% fatality. Death in 2-10 days after clinical signs.

Clinical signs within days of reaching CNS.

81
Q

How long is the incubation period of rabies?

A

Days to months.

82
Q

What is the structure and genome of canine parvovirus?

A

Non-enveloped.

Single stranded DNA.

83
Q

What is the family of canine parvovirus?

A

Family: Parvoviridae

84
Q

What are the clinical signs of canine parvovirus?

A
  • Bloody diarrhea
  • Dehydration
  • Weight loss
  • Lymphoid depletion
85
Q

How is canine parvovirus transmitted?

A

Fecal-oral transmission. Fomites common since virus is very stable in environment (>5 months in fomites).

86
Q

How can canine parvovirus be killed?

A

Virus can be killed if exposed to bleach for over 10 minutes.

87
Q

Who is most susceptible to canine parvovirus? What other factors increase susceptibility?

A

Young, unvaccinated dogs most susceptible (1.5-6 mo).

Some breeds more susceptible (black and tan breeds) and concurrent bacterial, protozoal, or helminthic infections increase susceptibility.

88
Q

What are the diseases associated with canine parvovirus?

A
  • Lymphocyte depletion (lymphopenia)
  • Enteritis
  • Neonatal myocarditis (can cause sudden death)
89
Q

What determines the host range of canine parvovirus?

A

The amino acid sequence of the capsid determines host range.

90
Q

Canine parvovirus targets which cells?

A

Targets crypt enterocytes, leads to sloughing of mature enterocytes above which exposes blood vessels and causes bloody diarrhea.

91
Q

What is unique about parvovirus replication?

A

Parvovirus cannot turn on DNA synthesis so needs to target rapidly dividing cells (ex. crypt enterocytes) in order for viral replication to take place.

92
Q

Hard pad disease is associated with which aspect of CDV?

A

Neurologic signs (chronic cdv)

93
Q

What are the reservoirs for rabies virus in Canada?

A

Bats, skunks, raccoons, and foxes.

In Alberta: Bats then skunks then cats.

94
Q

Where is rabies virus absent?

A

New Zealand

95
Q

What are the core dog vaccines?

A
  • Distemper
  • Infectious hepatitis
  • Parvovirus
  • Rabies
96
Q

What viruses can cause canine enteritis?

A
  • Parvovirus
  • Coronavirus
  • Rotavirus
97
Q

What is the rationale behind the vaccination schedule for parvovirus in puppies?

A

Up to a certain age (9 weeks), puppies are protected by maternal antibodies at a level of titer above 1:40. Vaccination with titers above this level will not result in the formation of antibodies (lack of seroconversion) in the puppies since the maternal antibodies will interfere.

At the age of 9-12 weeks, the level of maternal antibodies declines to below 1:40 titers. This point is called the window of susceptibility since maternal antibodies are inadequate to protect against the virus.

Vaccines are given from 9 weeks of age with a high titer concentration to protect the puppies during the window of susceptibility and to allow production of antibodies. A high titer vaccine is necessary since there is still some remaining maternal antibody in the puppy that will interfere with antibody production.

98
Q

What is the average half life of maternal antibodies?

A

9-10 days.

99
Q

What is the genome and structure of canine coronavirus?

A

Enveloped.

Positive sense single stranded RNA virus.

100
Q

What disease is associated with CCoV?

A

Canine viral enteritis. Usually mild or subclinical. Diarrhea is not hemorrhagic.

A similar strain can cause respiratory disease (CRCoV).

101
Q

What are the clinical signs of CCoV infection?

A

Diarrhea (orange in colour, watery)
Neurologic signs

No fever or lethargy.

Spontaneous recovery in 8-10 days.

102
Q

How is CCoV transmitted? What is the incubation? How long is the virus shed?

A

Fecal-oral transmission. Highly contagious.

Incubation 1-3 days.

Shed for 6-9 days up to months post infection.

103
Q

What are the target cells of CCoV?

A

Mature enterocytes.

104
Q

Is there cross protection between respiratory and enteric coronavirus?

A

No

105
Q

How was feline CoV-II created?

A

Canine CoV-II and feline CoV-I combined to form feline CoV-II.

FCoV and CCoV are very closely related!

106
Q

How does CCoV cause diarrhea?

A

Only 1 method!

Immature enterocytes are pushed to top of villus when mature ones die. Causes stunting of villi and loss of enzymes produced by mature enterocytes. The loss of enzymes (such as disaccharidases) and loss of absorptive function leads to accumulation of sugars in lumen of intestine which increases osmotic pressure and leads to water being sucked into intestine.

107
Q

What is the structure and genome of canine rotavirus?

A

Non-enveloped.

Double stranded RNA virus.

Segmented genome.

108
Q

What is the family of canine rotavirus?

A

Family: Reoviridae

109
Q

What are the clinical signs of canine rotavirus?

A

Mild, watery to mucoid diarrhea.

No fever.

Lasts 8-10 days.

110
Q

What is the disease associated with canine rotavirus?

A

Canine viral enteritis.

111
Q

What is unique about canine rotavirus?

A

Produces an enterotoxin NSP4.
ONLY rotavirus produces an enterotoxin!

112
Q

How is canine rotavirus transmitted?

A

Fecal-oral transmission.

Virus is resistant in the environment.

113
Q

What cells does canine rotavirus target?

A

Target cells are mature enterocytes at the tips of villi.

114
Q

How does canine rotavirus cause diarrhea?

A

Two methods!!!

  1. Immature enterocytes are pushed to top of villus when mature ones die. Causes stunting of villi and loss of enzymes produced by mature enterocytes. The loss of enzymes (such as disaccharidases) and loss of absorptive function leads to accumulation of sugars in lumen of intestine which increases osmotic pressure and leads to water being sucked into intestine. (same as CCoV)
  2. Produces an enterotoxin (NSP4) that stimulates enterochromaffin cells to release calcium (Ca2+). The calcium increase triggers EC cells to release 5-hydroxytryptamine (5-HT), also known as serotonin which stimulates the enteric NS, leading to elevated cAMP. Elevated cAMP results in increased secretion of NaCl and water into the intestinal lumen and it also increases intestinal motility.
115
Q

When is rotavirus most common?

A

Most common in puppies less than 12 weeks old.