Canine parvovirus (also referred to as CPV, CPV2, or parvo) is a contagious virus mainly affecting dogs and wolves.

Diarrhea and vomiting result in dehydration that upsets the electrolyte balance and this may affect the dog critically.

[3] Diagnosis is made through detection of CPV2 in the feces by either an ELISA or a hemagglutination test, or by electron microscopy.

PCR has become available to diagnose CPV2, and can be used later in the disease when potentially less virus is being shed in the feces that may not be detectable by ELISA.

[5] Survival rate depends on how quickly CPV is diagnosed, the age of the dog, and how aggressive the treatment is.

Supportive care ideally also consists of crystalloid IV fluids and/or colloids (e.g., Hetastarch), antinausea injections (antiemetics) such as maropitant, metoclopramide, dolasetron, ondansetron and prochlorperazine, and broad-spectrum antibiotic injections such as cefazolin/enrofloxacin, ampicillin/enrofloxacin, metronidazole, timentin, or enrofloxacin.

The fluids are typically a mix of a sterile, balanced electrolyte solution, with an appropriate amount of B-complex vitamins, dextrose, and potassium chloride.

[6] Additionally, fresh frozen plasma and human albumin transfusions can help replace the extreme protein losses seen in severe cases and help assure adequate tissue healing.

Oral antibiotics are administered for a number of days depending on the white blood cell count and the patient's ability to fight off secondary infection.

[7] Preliminary research in kidney cell lines have identified nitazoxanide, closantel sodium, and closantel as drugs which have the most potential as broad-spectrum antiviral agents against canine parvovirus and its various subspecies, raising the prospect that these drugs may yield potential for future treatments of this disease.

[8][9] In May 2023, the USDA granted Elanco Animal Health conditional approval to develop a Canine Parvovirus Monoclonal Antibody (CPMA) which targets the virus instead of its symptoms.

[11] The virus is very similar to feline panleukopenia (also a parvovirus); they are 98% identical, differing only in two amino acids in the viral capsid protein VP2.

[12] It is also highly similar to mink enteritis virus (MEV), and the parvoviruses of raccoons and foxes.

[13] CPV2 was thought to only cause diseases in canines,[5] but newer evidence suggest pathogenicity in cats too.

[12] Certain breeds, such as Rottweilers, Doberman Pinschers, and Pit bull terriers as well as other black and tan colored dogs may be more susceptible to CPV2.

From there, the virus attacks rapidly dividing cells, notably those in the lymph nodes, intestinal crypts, and the bone marrow.

[23] Anaerobic bacteria that normally reside in the intestines can then cross into the bloodstream, a process known as translocation, with bacteremia leading to sepsis.

SIRS leads to a range of complications such as hypercoagulability of the blood, endotoxaemia and acute respiratory distress syndrome (ARDS).

This form is less common and affects puppies infected in the uterus or shortly after birth until about 8 weeks of age.

[3] The virus attacks the heart muscle and the puppy often dies suddenly or after a brief period of breathing difficulty due to pulmonary edema.

On the microscopic level, there are many points of necrosis of the heart muscle that are associated with mononuclear cellular infiltration.

However studies in Vietnam have shown that CPV2 can undergo minor antigenic shift and natural mutation to infect felids.

[31] CPV2 may spread to cats easier than dogs and undergo faster rates of mutation within that species.