Objectives. The primary objectives of this session are to learn updates on the diagnosis, treatment, and prevention of parvovirus infections in dogs and cats.

Canine and feline parvoviruses are non-enveloped DNA viruses which require rapidly divided cells to reproduce. Infections in dogs came from feline panleukopenia virus and emerged in the late 1970s. Currently, most worldwide dog cases with clinical diseases are infected with CPV-2b or CPV-2c. The small animal parvoviruses are quite resistant to environmental destruction but are susceptible to bleach. The primary means of transmission is horizontal transmission via oronasal - fecal transmission. Vertical transmission via in utero infection can occur and can leads to myocarditis. CPV-2b and CPV2c can also infect cats.

CPV-2 first enters the oronasal cavity and infects lymphoid tissue followed by viremia for at least 1–5 days. Rapidly dividing cells of the gastrointestinal tract, myocardium, CNS, skin, kidney and other organs are targeted. Most notably, CPV-2 infects the crypt epithelial cells causing villus blunting. Decreased absorption (manifested as diarrhea), necrosis (sloughing of blood) and inflammation result. Lack of gastrointestinal integrity allows normal GI flora to penetrate into the blood stream and can lead to bacteremia with or without sepsis. Canine parvoviruses are shed primarily in feces for 3 to 14 days post infection, often starting before clinical signs appear. Clinical signs usually develop starting 5 to 12 days after exposure. Dogs with maternal or vaccinal antibodies can usually limit viremia and fully immunized dogs have sterilizing immunity.

Any dog or cat can be infected, but disease is thought to be more severe in some breeds like the American Pit Bull Terrier and Rottweilers. Severity of disease depends on virulence of the strain, size of inoculum, age, breed, and host’s defenses. Clinical signs of CPV or FPV infection are most severe in puppies or kittens less than 12 weeks that do not have prior immunity. Most dogs have enteritis characterized by foul smelling bloody diarrhea and vomiting. Leukopenia and fever are also common. Cats may have vomiting without diarrhea and sudden death. Both dogs and cats may also have signs of sepsis like red mucous membranes and can develop disseminated intravascular coagulation. CPV-2 can infect the primary CNS with resultant hemorrhage into brain or spinal cord. In utero infection or infection in pups less than 8 weeks can lead to myocarditis and result in sudden death or congestive heart failure. Depending on the presence of prior immunity, some dogs or cats may have subclinical infections.

Dogs or cats under two years of age with acute bloody diarrhea should be considered at high risk for parvoviruses, particularly if the vaccine history is incomplete. Another differential diagnosis with similar clinical signs is salmonellosis; this should be considered in dogs or cats that look clinically like parvovirus, but are well vaccinated. The clinical diagnosis is usually supported by documenting parvovirus antigen in feces by ELISA or PCR assays which are commonly part of diagnostic PCR panels in the United States.

Treatments. Greater than 90% of dogs with CPV-2 enteritis will survive if administered supportive care shortly after clinical signs develop. Feline panleukopenia often has a higher fatality rate. Fluid replacement, electrolyte balance (particularly potassium), control of hypoglycemia, control of oncotic pressure (hypoalbuminemia can develop), treatment of bacteremia and sepsis (antibiotics), control of nausea and vomiting, and “feeding the gut” as early as possible are paramount to success.

Fluid therapy should be designed to correct losses, hyponatremia and hypokalemia. Oncotic pressure should be maintained with plasma transfusions, hetastarch, or related compounds. Broad spectrum antibiotics with like a first generation cephalosporins are often used in routine cases with therapy escalated to include drugs with a better gram-negative spectrum in pets showing signs of sepsis. Injectable enrofloxacin or amikacin can be added to the protocol to enhance the gram-negative spectrum. Many clinics use second generation cephalosporins like cefoxitin as their primary antibiotic as this drug has an enhanced gram-negative spectrum compared to first generation cephalosporin. Recently it has been shown that maropitant can be used successfully as an antiemetic agent, but also lessens abdominal pain. It is important to “feed the gut” early in cases with enteritis and so at Colorado State University, nasoesophageal or nasogastric tubes are often used to start to deliver elemental diets as soon as possible. Highly digestible diets with or without probiotics are often used in the recovery phase.

A new gastrointestinal recuperation diet, Rebound Recuperation (Virbac) was found to be palatable, as determined by acceptance and preference testing, in healthy dogs during the preoperative and postoperative phases of routine sterilization (Forbes et al., 2015). In a followup study, Rebound Recuperation, was used successfully in a CPV clinical trial performed at Colorado State University (Tenne et al., 2016).

Many different adjunctive therapies like passive immune therapy (hyperimmune serum infections), granulocyte colony stimulating factors, oseltamivir (Tamiflu) are used to attempt to improve survival but has not been shown to be effective in controlled studies. Interferon omega has been beneficial in some puppies. Prognosis is variable. Intussusception may occur as a sequel to severe enteritis and so all dogs or cats should be palpated daily. Not all clients can afford hospitalization and intensive care. Thus, researchers at Colorado State University evaluated an out-patient protocol in dogs with CPV that had an 80% success rate (Venn et al., 2017).

Prevention and public health considerations. Extreme care should be taken to prevent spread to other animals by disinfection with bleach, separation from other hospitalized animals, and vaccination of other dogs in the household. No zoonotic potential is recognized; the parvoviruses of humans are species specific. Vaccination is very effective for both CPV and FPV. Modified live parenteral products are likely to break through maternal antibody interference and should be used for the puppy and kitten series. Vaccines should be administered until at least 16 weeks of age and one more booster after that time could be considered in high risk animals. After a 1-year booster, 3-year intervals for CPV and FPV vaccination is adequate for most animals. Use of serologic test results can be used after the 1-year booster to determine CPV and FPV vaccine need; positive animals do not need to be vaccinated if a validated test is used.

References

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