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Basics

Basics

Definition

  • CPV-2 infection is an acute systemic illness characterized by vomiting and hemorrhagic enteritis.
  • Often fatal in pups, that may collapse in a “shock-like” state and die suddenly without enteric signs, after only a brief period of illness.
  • The myocardial form was observed in pups during the early outbreaks in the late 1970s when the dog population was fully susceptible, and is now rare.
  • Most pups are now protected against neonatal infection by maternal antibodies.
  • Monoclonal antibodies have revealed antigenic changes in CPV-2 since its emergence in 1978 and CPV2a, b, and c strains have been identified.
  • The original virus is now virtually extinct in the domestic dog population.
  • CPV2c viruses are more virulent than the original isolates, and case mortality rates appear to be higher than in the earliest outbreaks.

Pathophysiology

  • CPV-2 is very closely related to feline panleukopenia virus (FPV) and several other parvoviruses that infect carnivores.
  • Parvoviruses, including CPV-2, require actively dividing cells for growth.
  • After ingestion of virus there is a 2- to 4-day period of viremia, with concomitant growth in lymphatic tissues throughout the body.
  • Early lymphatic infection is accompanied by lymphopenia and precedes intestinal infection and clinical signs.
  • By the third post-infection (PI) day, the rapidly dividing crypt cells of the small intestine are infected.
  • Viral shedding in the feces starts ∼3–4 days PI, and peaks about the time clinical signs first appear.
  • Virus ceases to be shed in detectable amounts by PI days 8–12.
  • Absorption of bacterial endotoxins from the damaged intestinal mucosa is believed to play a role in CPV-2 disease.
  • Intensity of illness appears to be related to the viral dose and the antigenic type.

Systems Affected

  • Cardiovascular-myocarditis with sudden death (now rare).
  • Gastrointestinal-small intestinal crypt cells and adjacent mucosal epithelium; severe hemorrhagic diarrhea, vomiting, dehydration; hypovolemic and septic/endotoxic shock.
  • Hemic/Lymphatic/Immune-thymus, lymph nodes, spleen, Peyer's patches.

Genetics

Unknown

Incidence/Prevalence

Most common in breeding kennels, animal shelters, pet stores, or wherever pups are reared. Rates vary.

Geographic Distribution

Worldwide

Signalment

Species

Dog

Breed Predilections

Certain breeds have been shown to be at increased risk for severe CPV enteritis, including rottweiler, doberman pinscher, American pit bull terrier, Labrador retriever, German shepherd, and Yorkshire terrier. A recent Australian study demonstrated higher case fatality rates in hounds, gundogs and non-sporting pedigree groups than in mixed breed dogs.

Mean Age and Range

  • Illness may occur at any age.
  • Most severe illness occurs in pups 6–24 weeks of age.

Predominant Sex

None

Signs

General Comments

Suspect CPV-2 infection whenever pups have an enteric illness, especially with sudden onset lethargy, vomiting, and/or diarrhea.

Historical Findings

  • Sudden onset of bloody diarrhea, anorexia, and repeated episodes of vomiting.
  • Rapid weight loss.
  • Some pups may collapse in a shock-like state and die without enteric signs.
  • In breeding kennels, several littermate pups may become ill simultaneously or within a short period of time.
  • Occasionally, one or two pups in a litter have minimal or no signs, followed by the death of littermates that presumably encounter greater amounts of virus.

Physical Examination Findings

  • Dehydration, weight loss and abdominal discomfort are consistent features.
  • Often there is severe hemorrhagic diarrhea.
  • Fluid-filled intestinal loops may be palpated.
  • Occasionally enlarged mesenteric lymph nodes are palpable.
  • May have fever or hypothermia.

Causes

Canine parvovirus

Risk Factors

  • Unvaccinated dogs from kennels, animal shelters, pet shops, or elsewhere where dogs have congregated.
  • Pups <4 months of age are at higher risk of severe infection.
  • Co-pathogens such as parasites, viruses, and certain bacterial species (e.g., Campylobacter spp., Clostridium spp.) are hypothesized to exacerbate illness.
  • Severe, often fatal, parvoviral infections have been demonstrated in pups exposed simultaneously to CPV-2 and canine coronavirus.
  • Crowding and poor sanitation increases the risk of infection.

Diagnosis

Diagnosis

Differential Diagnosis

  • Canine coronavirus infection
  • Salmonellosis; colibacillosis; other enteric bacterial infections
  • Gastrointestinal foreign bodies
  • Gastrointestinal parasites
  • Hemorrhagic gastroenteritis
  • Intussusception
  • Toxin ingestion

CBC/Biochemistry/Urinalysis

  • Lymphopenia-characteristic of CPV-2 infection; commonly occurs between PI days 4–6.
  • Severely affected dogs often exhibit severe neutropenia concurrently with the onset of intestinal damage.
  • Hemograms are an important part of the diagnostic regimen.
  • Leukocytosis is common during recovery.
  • Serum chemistry profiles help assess electrolyte disturbances (especially hypokalemia), the presence of azotemia associated with dehydration, panhypoproteinemia, and hypoglycemia.

Other Laboratory Tests

Serologic tests are not diagnostic because dogs often have high titers from vaccination and/or maternal antibodies.

Imaging

  • Abdominal radiographs often reveal generalized small intestinal ileus; exercise caution to prevent misdiagnosis of an intestinal obstruction.
  • Typical ultrasonographic changes include fluid-filled, atonic small and large intestines; duodenal and jejunal mucosal layer thinning with or without indistinct wall layers and irregular luminal-mucosal surfaces; extensive duodenal and/or jejunal hyperechoic mucosal speckling; and duodenal and/or jejunal corrugations.
  • Intussusceptions can also occur.

Diagnostic Procedures

  • May detect virus antigen in stool or intestinal contents at the onset of disease and for 2–4 days afterward by use of commercial solid phase ELISA assays in which sensitivity and specificity appear high.
  • Electron microscopy is another method of detecting fecal virus during the early stages of infection.
  • Samples for virus detection should be submitted during the acute phase of infection; ship specimens refrigerated, not frozen.

Pathologic Findings

  • Gross changes include subserosal congestion and hemorrhage or frank hemorrhage into the small intestinal lumen.
  • Some dogs exhibit intestines that are empty or contain yellow or blood-tinged fluid.
  • Mesenteric lymph nodes are often enlarged and edematous, with hemorrhages in the cortex.
  • Thymic atrophy is common in young dogs.
  • Pulmonary edema and hydropericardium may be the only gross change in pups with myocarditis and acute heart failure.
  • Histopathology reveals intestinal inflammation and necrosis, with severe villus atrophy.

Treatment

Treatment

Appropriate Health Care

  • Symptomatic and supportive (refer to sections on treatment of acute vomiting, acute diarrhea, and hemorrhagic gastroenteritis). Therapies include intravenous fluids, antibiotics, antiemetics and analgesics.
  • Intensity depends on the severity of signs on examination.
  • Goals are to provide intestinal nutrients, restore and maintain fluid and electrolyte balance, and resolve shock, sepsis and endotoxemia.
  • Prompt, intensive in-patient care leads to treatment success.
  • Proper, strict isolation procedures are essential.
  • Exercise care to prevent the spread of CPV-2, a very stable virus.

Nursing Care

  • Hospitalize patients and monitor for dehydration and electrolyte imbalance.
  • Fluids are usually supplemented with potassium chloride, 5% dextrose, and possibly sodium bicarbonate (if severe metabolic acidosis).

Activity

Restrict until symptoms abate.

Diet

Puppies receiving early enteral nutrition via a nasoesophageal tube, compared to puppies that received nil PO until vomiting cease, show earlier clinical improvement, significant weight gain, as well as improved gut barrier function, which could limit bacterial or endotoxin translocation.

Client Education

  • Inform about the need for thorough disinfection, especially if other dogs are on the premises. Strict sanitation is essential.
  • A 1:30 dilution of bleach (5% sodium hypochlorite) destroys CPV-2 in a few minutes.
  • If possible, isolate pups until they reach 3 months of age and vaccinate repeatedly; typical protocol involve vaccination at 6,9, and 12 weeks of age.
  • Pups can be infected with virulent virus before any vaccine will engender immunity.
  • CPV-2 is shed for less than 2 weeks after infection; no carrier state has been substantiated.

Surgical Considerations

  • Exercise caution to prevent misdiagnosis of an intestinal obstruction, especially if vomiting is the only clinical sign.
  • Although uncommon, intussusceptions can occur.

Medications

Medications

Refer to sections on treatment and management of acute vomiting, acute diarrhea, and hemorrhagic gastroenteritis.

Drugs Of Choice

Additional recommended drugs include parenteral antibiotics (ampicillin and gentamicin) and antiemetics (e.g., ondansetron, maropitant).

Precautions

Gentamicin can cause renal toxicity in dehydrated puppies.

Follow-Up

Follow-Up

Patient Monitoring

There seems to be an increased incidence of discospondylitis in pups that had parvovirus infection.

Prevention/Avoidance

  • Inactivated and live vaccines are available for prophylaxis and vaccines differ in their capacity to immunize pups with maternal antibodies.
  • Results of a recent study indicated that vaccination with a modified live vaccine at 4 weeks of age in pups with high maternally-derived antibody concentrations resulted in seroconversion rates of up to 80% that may lead to a reduction in the window of susceptibility with respect to CPV infection and might be used as an adjunct control method in contaminated environments.
  • Control of CPV-2 requires efficacious vaccines, isolation of puppies, and stringent hygiene.

Possible Complications

  • Septicemia/endotoxemia
  • Secondary bacterial pneumonia
  • Intussusception
  • Discospondylitis

Expected Course and Prognosis

  • Prognosis is guarded in severely affected puppies.
  • Prognosis is good for dogs that receive prompt initial treatment and survive the initial crisis of illness-approximately 80% survival rate.
  • A patient is likely to have a poor prognosis if it is purebred, has a low bodyweight, and, after 24 hours of intensive therapy, the following biomarker levels are present: severe persistent leuko- and lymphopenia, a persistently elevated or rising serum cortisol concentration (>8.1 ug/dL), severe hypothyroxinemia (<0.2 ug/dL), hypocholesterolemia (<100 mg/dL), and persistently elevated serum CRP (>97.3 mg/L) and/or TNF concentrations.
  • Conversely, the literature would suggest that puppies with a good prognosis are those that are of mixed breed, >6 months old, and show the following biomarker values: total leukocyte count >4.5 × 103/µL, lymphocyte count >1 × 103/µL, and mature neutrophil count >3 × 103/µL, all associated with a 100% survival when measured at 24 hours post-admission; a serum cortisol <8.1 ug/dL is associated with a 96% survival when measured at 48 hours after admission and a serum thyroxine concentration >0.2 ug/dL associated with 100% survival when measured at 24 hours after admission as well as a HDL-cholesterol of >50.2 mg/dL is associated with a 100% survival when measured at admission.

Miscellaneous

Miscellaneous

Associated Conditions

Coinfection with intestinal helminths and Giardia are indicative of unhygienic housing conditions and can worsen the clinical picture and contribute to morbidity if not treated.

Age-Related Factors

Infection is less likely in dogs older than 1 year of age, but can still occur, especially if the dogs are unvaccinated.

Zoonotic Potential

Parvovirus per se is not zoonotic, but these puppies may harbour coinfections with Giardia parasites which can be zoonotic.

Pregnancy/Fertility/Breeding

Pregnant animals are likely to abort due to the septicemia.

Abbreviation

ELISA = enzyme-linked immunosorbent assay

Author Johan P. Schoeman

Consulting Editor Stanley L. Marks

Acknowledgment The author and editors acknowledge the prior contribution of JoAnn Morrison.

Client Education Handout Available Online

Suggested Reading

Mohr AJ, Leisewitz AL, Jacobson LS, Steiner JM, Ruaux CG, Williams DA. Effect of early enteral nutrition on intestinal permeability, intestinal protein loss, and outcome in dogs with severe parvoviral enteritis. J Vet Intern Med 2003, 17: 791798.

Schoeman JP, Goddard A, Herrtage ME. Serum cortisol and thyroxine concentrations as predictors of death in critically ill puppies with parvoviral diarrhea. J Am Vet Med Assoc 2007, 231:15349.