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
Prevention and control of canine parvo
• 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
How are neonates protected from canince parvo
1. mother placenta (5%), colostrum (mainly) (95%) | MDA
27
Immunity gap
* 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
When to vaccinate pups adn kittne against parvo
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
How often revaccinate
• 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
Other canine enteric virus
* Canine rotavirus (not important cause of disease as far as we know) * Canine calicivirus * Canine coronavirus
31
RABIES
``` • 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 ```