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Year 2 Small Animal ID > Canine Viral Infections > Flashcards

Canine Viral Infections Flashcards

1
Q

Facts about Canine distemper virus

  • genome
  • what species infected
  • how common in uk?
A
  • RNA virus
  • Envelope
  • Emerging disease – virus need to keep eye on
  • Morbillivirus genus
  • Infects dogs – also other species, including ferrets, badgers and lions and growing
  • Multisystem disease
  • Rare in UK
  • Concern over illegal dog imports (especially rescue dogs)
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2
Q

What are the main viral pathogens causing disease in dogs in the UK

A
  1. Canine distemper virus
  2. Infectious hepatitis
  3. Canine parvovirus,
  4. other canine viruses- SARS_CoV2
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3
Q

PAthogenesis of canine distemper virus

A
  • Oronasal infection – very common route of infection
  • Multiplies in lymphoid tissue of respiratory tract, gains access to blood
  • Widespread multiplication in lymphoid tissue, bone marrow and spleen
  • Virus spread from here to epithelial +/- CNS tissues (entry into CNS tissues depends on the immune response mounted by the host)
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4
Q

Clinical signs of canine distemper virus

A

VARIED
• Subclinical
• Anorexia, depression, pyrexia
• If respiratory epithelia being targeted then get:
1. Ocular and nasal discharge
2. Coughing
3. Conjunctivitis
• Intestinal epithelium primarily affected:
1. Vomiting and diarrhoea
• Skin affected:
1. Hyperkeratosis – nose and feet; “hard pad”
• Neurologic signs seen in proportion of cases
- seen 1-3 wks after other signs – seizures and myoclonus
- Can be severe

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5
Q

Diagnosis canine distemper virus

A
  • History and clinical signs
  • Typically unvaccinated dogs – travel to importation
  • RT-PCR – smears, blood, urine sediment (RT to turn RNA to DNA) (( get this from retro virus!))
  • Virus isolations from secretions is difficult
  • Antibody or viral antigen in CSF is diagnostic
  • For neurological complications of distemper
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6
Q

Treatment canine Distemper

A
  • No antivirals; symptomatic and supportive treatment e.g fluids, anticonvulsants for seizures (like this for most antivirals)
  • Careful nursing
  • Antibacterial cover for secondary infections
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7
Q

Canine distemper adn vaccine

  • what type?
  • when vaccinate?
A
  • Modified live
  • Given as part of core vaccine
  • Classically vaccinate when MDA declines to non-detectable levels: approx 8-12 weeks of age
  • Nowadays higher titred vaccines (more antigen in) allow earlier finish vaccination if necessary
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8
Q

What is canine adenovirus known as

A

Canine Hepatitis

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9
Q

Infectious canine hepatits facts

A
  • Canine adenovirus type 1
  • Very hardy virus; survives weeks in environment so dogs can become infected frm environment
  • Disease now uncommon due to vaccination
  • Mainly seen in unvaccinated dogs, or on ‘puppy farms’
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10
Q

Pathogenesis of infectious hepatitis

A
  • Oronasal infection
  • Viraemia – viruses love to get in blood!!!
  • Virus spreads to many tissues
  • Virus then localises and causes damage in hepatic cells and vascular endothelial cells
  • Virus persists in kidneys and can be excreted in urine for 6 to 9 months
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11
Q

Clinical signs canine hapatitis

A
  • Often dogs < 1 year of age
  • Pyrexia, depression, lethargy
  • Hepatomegaly (large liver)
  • Reluctance to move, abdominal pain
  • Petecchial haemorrhages – bleeding from venipuncture sites due to damage to epithelial cells
  • Vomiting and diarrhoea (haemorrhagic)
  • Coughing
  • Corneal oedema and uveitis – during clinical recovery = “blue eye”
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12
Q

Diagnosis canine hepatitis

A
  • Can see inclusion bodies during histopathology)
  • Virus isolation from faecal samples or oropharyngeal swabs
  • Serology
  • Histopathology of liver tissue at postmortem – cowdry A type intranuclear inclusion bodies
  • PCR
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13
Q

Treatment canine hepatitis

A
  • No specific antivirals
  • Supportive and symptomatic treatments
  • Antibacterial cover for secondary infections if necessary
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14
Q

Prevention canine hepatitis

A

ALL about VACCINATION:
• Vaccination – CAV-2
• CAV-1 vaccines not used due to problems with blue eye – corneal oedema

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15
Q

What is virus classification based on?

A 
•	Virus classification is based on:
–	The genome (RNA or DNA)
–	Number and sense of RNA/DNA strands
–	Morphology (size, symmetry, envelope)
–	Genome sequence similarity
–	Ecology
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16
Q

Canine parvovirus

  • what does it do
  • genome
A
  • First recognised in 1978
  • Attacks rapidly dividing cells
  • Non-enveloped DNA viruses (doesn’t change as much as a RNA
  • No envelope  Stable in environment for prolonged periods of time
  • Cause of profouned diarrhoea in dogs
17
Q

Canine and feline parvo

A

— Tiny virus
— Environmentally resistant
— Highly infectious
— DNA virus, so SMALL it doesn’t even have a DNA polymerase of its own, needs to own DNA polymerase of host cell  rapidly dividing cells
— Invades rapidly dividing cells (intestine, bone marrow)
— Leucopenia
— Severe diarrhoea
— Vomiting
— Largely controlled by vaccination
• Targets actively dividing cells as needs DNA polymerase: small DNA virus needs host machinery as it lack own DNA polymerase
• Villus crypt epithelium  enteritis
• Bone marrow and lymphoid tissue  panleucopenia
• Late gestation/neonatal cerebellum  cerebellar hypoplasia (kittens will have cat food all over face)
• Early pregnancy  foetal death, abortion

18
Q

Canine parvo strains/ varients

A
  • CPV-2 first recognised in 1978. CANINE. If put into cats nothing happens
  • From feline parvovirus?  if put into dogs nothing happens
  • Evolved – now two strains CPV-2a and CPV-2b, which can infect both cats and dogs
  • CPV2c
  • CPV-2c……….. 
19
Q

Pathogenesis of canine parvovirus

A
  • Faecal-oral transmission
  • Virus replication in lymphoid tissue
  • Viraemia
  • Virus replication in intestinal cells – crypts of villi
  • Destruction of normal GI epithelium with profound stunting and loss of villi
  • Therefore lack of ability to absorb
  • Often haemorrhagic diarrhoea
  • Secondary bacterial infection, bacteria translocating from intestine into blood☹
  • Targets actively dividing cells as needs DNA polymerase: small DNA virus needs host machinery as it lack own DNA polymerase
  • Villus crypt epithelium  enteritis
  • Bone marrow and lymphoid tissue  panleucopenia
  • Late gestation/neonatal cerebellum  cerebellar hypoplasia (kittens will have cat food all over face)
  • Early pregnancy  foetal death, abortion
20
Q

Canine parvovirus in utero or neonatal (younger than 8 weeks exposure)

A

infects the rapidly dividing cells of the intestines and the bone marrow. In very young puppies the virus can also infect the cells of the heart.
• Virus replicates in myocardium – myocarditis in animals affected in utero or v soon after borth
• Rare nowadays – protection from MDA

Pregnant queens infected with parvovirus, the virus can spread to the unborn kittens where it can interfere with the developing brain. Kittens may then be born with a condition known as cerebellar hypoplasia

21
Q

Clinical signs canine parvo virus

A

• More severe in unvaccinated young rapidly growing pups (<12wks)
• Inapparent infection to sudden death
• Range of gastrointestinal signs – vomiting, intense, profuse diarrhoea (haemorrhagic)
• Anorexia, depression, pyrexia
• Dehydration
• Sepsis and DIC
• Sudden death
• Depressed and dehydrated (leads to shock)
pyrexic

22
Q

Diagnosis of canine parvo

A
  • Lateral flow
  • History and clinical signs
  • ELISA, culture, PCR
  • Detection of virus in faecal samples – negative results do not mean no infection
  • Be aware, can be virus positive in faecal samples 5-7 days after a live attenuated vaccine
  • Serology – care in interpretation, vaccination and MDA
23
Q

Treatment of canine parvovirus

A
  • Fluid therapy – need to restore fluid and electrolyte balance
  • Antibacterial cover
  • Antiemetic agents if vomiting
  • Interferon
24
Q

Transmission canine parvo vorus

A

• Virus shed in faeces for 10-12 days (5-7 days after onset of clinical signs)
• Direct contact with contaminated faeces
Faecal oraltransmission
• Fomites
• Contaminated environment – resistant virus in environment so if treat me VERY thorough with your cleaning and
• Hair coats of dogs

25
Q

Prevention and control of canine parvo

A

• Vaccination:
- live attenuated vaccine
- based on CPV2 or CPV2b
• Removal of virus from contaminated environment
– Sodium hypochlorite (1 in 30 household bleach)
– Other licensed preparations

26
Q

How are neonates protected from canince parvo

A
  1. mother placenta (5%), colostrum (mainly) (95%)

MDA

27
Q

Immunity gap

A
  • Maternally-derived antibody can block vaccine
  • Timing of first vaccination critical
  • If MDA lasts a short time there is an immunity gap before vaccination has induced immunity
  • If MDA lasts too long then vaccination will not work at the usual time
28
Q

When to vaccinate pups adn kittne against parvo

A

WSAVA recommends all puppies and kittens get 9, 12 AND 16 week vaccinations
• Believe MDA last as long as 16 weeks in some animals
• Most dogs 9 and 12 not 16

How early to start vaccination:
• Some recommend early vaccination to allow earlier socialisation
• More common now to allow socialisation with vaccinated dogs.

29
Q

How often revaccinate

A

• Historically annual boosters
– Not good evidence most antigens longer DOI
– Now vaccinate 9 and 12 weeks, annual booster and then every 3 years
• Parvo vaccines very good and likely give much longer DOI
• Many parvo vaccines in dogs now licensed for every three years.
– Three year boosters becoming more common (for parvo, distemper, adeno)
• Some advocate measuring antibody levels to predict a need for vaccination e.g.

30
Q

Other canine enteric virus

A
  • Canine rotavirus (not important cause of disease as far as we know)
  • Canine calicivirus
  • Canine coronavirus
31
Q

RABIES

A 
•	Infects CNS of most mammals
•	Usually fatal once clinical signs develop
•	We control by vaccination, quarantine and pet travel scheme
•	Transmission
–	Bites, scratches & licking
•	Control
–	Quarantine
–	Vaccination
–	PETS travel scheme

Year 2 Small Animal ID (9 decks)

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