Canine parvovirus (CPV) is a highly contagious and relatively common cause of acute, infectious GI illness in young dogs. Although its exact origin is unknown, it is believed to have arisen from feline panleukopenia virus or a related parvovirus of nondomestic animals. It is a nonenveloped, single-stranded DNA virus, resistant to many common detergents and disinfectants, as well as to changes in temperature and pH. Infectious CPV can persist indoors at room temperature for at least 2 mo; outdoors, if protected from sunlight and desiccation, it can persist for many months and possibly years.

1. PARVO VIRAL INFECTION

2. INTRODUCTION
• Most common and prevalent viral infection of dogs
• CPV-2 and -1 are extremely stable and are resistant to adverse
environmental influences
• Original strain of CPV 2 evolved into CPV 2a, 2b, 2c
• CPV originated from feline panleucopenia virus

3. DISTRIBUTION

4. EPIDEMILOGY
• Domestic dogs, bush dogs, coyotes, wolves, foxes
• Experimental infections can be produced in domestic ferrets,
mink, and cats; however, it is generally self-limiting
• Original CPV-2 isolates affected only dogs, whereas the 2a and
2b strains may infect felines
• Infection does not necessarily result in apparent disease

5. • Many dogs that become naturally infected may never develop
overt clinical signs, especially in the presence of residual
maternally derived antibody (MDA)
• Illness is most severe in young, rapidly growing pups that
harbor intestinal helminths, protozoa, and certain enteric
bacteria such as Clostridium perfringens, Campylobacter spp.,
and Salmonella spp
• Incubation period of the original CPV-2 strains in the field was
7 to 14 days; experimentally  4 to 5 days

6. • Acute CPV enteritis can be seen in dogs of any breed, age, or
sex
• Breeds such as, Rottweilers, Doberman pinschers, Labrador
retrievers, American Staffordshire terriers, German
shepherds, and Alaskan sled dog  increased risk

7. ETIOLOGY
• Non enveloped ss DNA virus
• Require rapidly dividing cells for
replication
• Young (6 wks -6 months) unvaccinated or incompletely
vaccinated dogs most susceptible
• Immune status of host, virulence of the virus, environmental
factors etc. determine occurrence of infection

8. TRANSMISSION
• Contact with contaminated faeces in the environment
• Through humans, insects, fomites
• Average infectious dose of unvaccinated dog is 1000 viral
particles
• Infected dog sheds 35 million viral particle per ounce of stool
• Pups born to vaccinated dam are protected for first few
weeks; susceptibility increases as Abs wanes

9. PATHOGENESIS
Viral entry through oro nasal route
Multiplication in LNs in throat
Viremia occurs 1-5 days after infection
Localises in GIT epithelium, small intestine, bone marrow, LNs,
myocardium

10. Infects the germinal epithelium of the intestinal crypts
Destruction & collapse of the epithelium
Villi becomes shortened
Blood loss through diarrhoea, infection, immune mechanism
fails
Virus shed extensively in the feces for a maximum of 7 to 10
days post inoculation

12. CPV kills when;
• Diarrhoea and vomiting leads dehydration and shock
• Loss of intestinal barrier allows bacterial invasion and septic
toxin production
• Excretion of virus starts 3-4 d PI before the start of CS

13. CLINICAL FINDINGS
• GIT, bone marrow and myocardium  mainly; also, skin &
nervous tissue
• Complications of secondary infection or thrombosis

14. Parvovirus Enteritis
• Rapid progress, especially with the new strains
• Severe vomiting , followed by diarrhea, anorexia, and rapid
onset of dehydration
• Feces  yellow-gray and are streaked or darkened by blood
• Fever (104- 105°F) & leukopenia
• Neutrophilia due to infections by opportunistic bacteria
• Death can occur as early as 2 days after the onset of illness

15. Neurologic Disease
• Commonly occurs due to the hemorrhage into the CNS from
disseminated intravascular coagulation or from hypoglycemia
during the disease process, sepsis, or acid-base-electrolyte
disturbances
• Concurrent infection with viruses such as canine distemper virus

16. Cutaneous Disease
• Erythema multiforme
• Ulceration of the footpads,pressure points, and mouth and
vaginal mucosa
• Vesicles in the oral cavity
• Erythematous patches on the abdomen and perivulvar skin

17. Canine Parvovirus-2 Myocarditis
• Occasionally found in pups that do not nurse sufficiently or
are born to isolated, unvaccinated bitches
• Infection in utero or in pups younger than 6 weeks of age
• All pups in a litter are usually affected
• Often die, or they succumb after a short episode of dyspnea,
crying, and retching
• Spectrum of myocardial disease:-
acute diarrhea and death, without cardiac signs;
diarrhea and apparent recovery followed by death,
(weeks or months later) due to congestive heart failure;
 or sudden onset of congestive heart failure (apparently
normal pups - 6 weeks - 6 months

18. • The high titer of MDA in pups prevents neonatal infection
with virus in the early period of life
Thrombosis
• Infected dogs have clinical and laboratory evidence of
hypercoagulability
• May develop thrombosis or phlebitis with catheters or visceral
thrombi

19. Bacteriuria
• Approximately 25% of pups after infection  Asymptomatic
urinary tract infection
• Due to fecal contamination of the external genitalia in
association with neutropenia
• Untreated subclinical urinary tract infection may lead to
chronic urinary infection

20. DIAGNOSIS
• Clinical signs
• Leukopenia – not found in all infected dogs, it is proportional to
the severity of illness
• Abnormal coagulation test - prolongation of active
thromboplastin time and  antithrombin III activity
• Slide agglutination test with porcine RBC – CPV2 in faecal and
intestinal samples.
• Insitu hybridization valuable- specific for virus identification in
formalin fixed/ wax embedded tissue specimen.

21. CPV VIRAL ANTIGEN IN CRYPT AREA OF ILEUM
• Specific identification of parvovirus in tissues can be done by indirect fluorescent
antibody test- antigens of dogs with lethal CPV enteritis

22. ASSAYS FOR CANINE PARVO VIRAL ENTERITIS
ASSAY SPECIMEN TARGET PERFORMANCE
Faecal antigen
ELISA
Faeces CPV antigen Specificity 100%,
low sensitivity
Haemagglutination
assay
Faeces CPV antigen Inexpensive and
rapid
PCR Faeces, tissues CPV DNA Sensitivity and
specificity vary
with designs used
Faecal electron
microscopy
Faeces Virus particles Requires large
amount of viruses,
expensive
Virus isolation Faeces, tissues CPV Used as research
tool, not widely
available

23. PATHOLOGICAL FINDINGS
• Intestinal walls -thickened, segmentally discoloured with
denudation of intestinal mucosa and presence of dark
sometimes bloody, watery material within the stomach and
intestinal lumen.

24. • Intestinal lesions are characterised by necrosis of crypt
epithelium in small intestine
• Villi are shortened/ obliterated due to lack of replacement of
cells collapse of lamina propria.
• Intestinal villi atrophy

25. • CPV-2 lesions – jejenum, ileum, mesenteric LN, other lymphoid
tissues contain intra nuclear inclusion bodies
• Inclusion bodies are mainly seen in epithelial cells, squamous
epithelial cells of upper GIT
• Necrosis & depletion of lymphoid tissue( peyer’s patch,
mesenteric LN, thymus, spleen)

26. • Pulmonary edema, alveolitis – dogs with septicaemia
• Haemorrhage in ileo caecal area

27. • Myocarditis- grossly seen as pale streaks in the myocardium
• Myocardial lesions- non suppurative myocarditis with
multifocal infilteration of lymphocytes and plasma cells and
basophilic inclusion bodies observed in cardiac muscle fibres

28. TREATMENT
• Symptomatic treatment
• To restore fluid and electrolytes and to prevent sec. bacterial
infections
ANTIMICROBIAL AGENTS
• Ampicillin 10 – 20 mg/kg IV, IM, SC 3 – 5 D
• Cefazolin 22mg/kg IV, IM 3 – 5 D
• Ceftiofur 2.2 – 4.4 SC, IV, IM 3 – 5 D
• Gentamicin 6 – 8mg/kg IM, SC, IV 3 – 5 D

29. ANTIEMETIC AGENTS
• Chlorpromazine 0.5 mg/kg IM ,1mg/kg Rectally, 0.2 – 0.5
mg/kg IV
• Metoclopramide 0.2 – 0.4 mg/kg SC,1 – 2 mg/kg IV
• Prochlorperazine 0.1mg/kg IM
• Ondansetron 0.1 – 0.15 mg/kg IV
• Dolasetron 1mg/kg IV, PO
GASTRIC PROTECTANTS
• Cimetidine 5 – 10 mg/kg IM
• Ranitidine 2 – 4 mg/kg SC,IV

30. ANTI-INFLAMMATORY DRUGS
• Flunixine meglumine alone or with glucocorticoid
MISCELLANEOUS THERAPY
• Granulocyte Colony Stimulating Factor (GCSF)- Stimulate
BM to produce WBC
• Transfusion of whole blood
• Plasma transfusion
• ANTI-DIARRHOEALS ARE NOT RECOMMENDED
• Feeding is contraindicated
• All these agents should be given only after correcting the
dehydration

31. PREVENTION
• IMMUNITY AFTER INFECTION : immune to reinfection for at
least 20 months or for a life time.
• Serum antibody titre remain high for prolonged period after
CPV enteritis, even if re exposure does not occur. If serum
antibody titre drops localized infection may occur but viremia
and generalised symptoms are unlikely to occur
• Vaccination of pregnant bitches with attenuated live vaccine is
contraindicated disease in developing foetus
• For attenuated live vaccine there can be transient
lymphopenia for 4-6 days, replicate in intestinal tract and can
briefly shed in faeces

32. VACCINATION
• Modified live vaccine at 6-8, 10-12, and 4-16 wks of age
followed by booster 1 year later & every 3 year
• Abs start developing at 3 days post-vaccination
• High-titre(potentiated)attenuated live CPV vaccine are more
immunogenic and effective
• Vaccinated at 6,9,12 wks of age and annual revaccination

33. CONTROL
• Diluted household bleach (1:30) with water –effective &
economical
• Other agents can be used are potassium peroxymonosulfate,
accelerated hydrogen peroxide,or high level chemicals like
glutaraldehyde - contact time 10 mins
• cleaning the area with these agents during and after the recovery
will help to inactivate all the viruses
• Rodent and insect vector control