Parvoviral enteritis is a highly contagious viral disease that commonly affects young, unvaccinated dogs. Clinical signs include anorexia, lethargy, vomiting, and diarrhea, which is often hemorrhagic. Diagnosis is typically based on history, physical examination findings, and fecal antigen testing. Treatment is largely supportive on an inpatient or outpatient basis because specific therapies are not available.
Parvoviral enteritis is a highly contagious, acute, infectious GI disease of dogs. Infection is relatively common in young and/or unvaccinated dogs.
Etiology and Pathophysiology of Canine Parvovirus Infection
The etiological agent of parvoviral enteritis in dogs is canine parvovirus (CPV). CPV is a nonenveloped, single-stranded DNA virus. Although its exact origin is unknown, CPV is believed to have arisen from feline panleukopenia virus.
In North America, clinical disease is largely attributed to CPV-2b; however, infection with a newer and equally virulent strain, CPV-2c, is increasingly common, having been identified in at least 15 states. No association has been identified between CPV strain and severity of clinical disease.
Pathogenesis of Canine Parvovirus Infection
Replication of canine parvovirus occurs initially in the lymphoid tissue of the oropharynx, with systemic illness resulting for subsequent hematogenous dissemination.
CPV preferentially infects and destroys rapidly dividing cells of the small intestinal crypt epithelium, lymphopoietic tissue, and bone marrow. Destruction of the intestinal crypt epithelium results in epithelial necrosis, villous atrophy, impaired absorptive capacity, and disrupted gut barrier function, with the potential for bacterial translocation and bacteremia.
Lymphopenia and neutropenia develop secondary to destruction of hematopoietic progenitor cells in the bone marrow and lymphopoietic tissues (eg, thymus, lymph nodes, etc) and are further exacerbated by an increased systemic demand for leukocytes.
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Infection in utero, or in pups < 8 weeks old or born to unvaccinated dams without naturally occurring antibodies, can result in myocardial infection, necrosis, and myocarditis. Myocarditis, presenting as acute cardiopulmonary failure or delayed, progressive cardiac failure, can occur with or without clinical signs of enteritis. However, CPV-2 myocarditis is infrequent because most bitches have CPV antibodies from immunization or natural exposure.
Infected dogs shed virus in feces within 4–5 days following exposure (often before clinical signs develop), throughout the period of illness, and for approximately 10 days after clinical recovery.
Epidemiology of Canine Parvovirus Infection
Canine parvovirus infection is acquired through direct oral or nasal contact with virus-containing feces or indirectly through contact with virus-contaminated fomites (eg, environment, personnel, equipment).
Young (6 weeks–6 months old), unvaccinated, or incompletely vaccinated dogs are most susceptible. Among dogs > 6 months old, sexually intact male dogs are more likely than sexually intact female dogs to develop parvoviral enteritis.
Breeds described as at increased risk include the following:
Rottweilers
Doberman Pinschers
English Springer Spaniels
German Shepherd Dogs
Pit bull–type dogs
Assuming sufficient colostrum ingestion, puppies born to a dam with CPV antibodies are protected from infection for the first few weeks of life; however, susceptibility to infection increases as maternally acquired antibodies wane.
Stress (eg, from weaning, overcrowding, malnutrition, etc), concurrent intestinal parasitism, and enteric pathogen infection (eg, Campylobacter spp, Salmonella spp, Giardia spp, coronavirus) have been associated with more severe clinical illness.
Clinical Findings of Canine Parvovirus Infection
Clinical signs of parvoviral enteritis in dogs generally develop within 5–7 days after infection but can appear from 2 to 14 days after infection.
Initial clinical signs may be nonspecific (eg, lethargy, anorexia, fever) with progression to vomiting and hemorrhagic small bowel diarrhea within 24–48 hours. Approximately 25% of dogs may have nonhemorrhagic diarrhea.
Physical examination findings can include depression, fever, dehydration, and intestinal loops that are dilated and fluid filled. Abdominal pain warrants further investigation to exclude the potential complication of intussusception.
At the time of initial evaluation, severely affected animals may have clinical signs potentially consistent with septic shock (collapsed with prolonged capillary refill time, poor pulse quality, tachycardia, and hypothermia).
Although leukoencephalomalacia associated with CPV infection has been reported, CNS signs are more commonly attributable to hypoglycemia, sepsis, or acid-base and electrolyte abnormalities. Inapparent or subclinical infection is common.
Lesions in Canine Parvovirus Infection
Gross necropsy lesions in cases of CPV infection can include the following:
thickened and discolored intestinal walls
watery, mucoid, or hemorrhagic intestinal contents
edema and congestion of abdominal and thoracic lymph nodes
thymic atrophy
in the case of CPV myocarditis, pale streaks in the myocardium
Histologically, intestinal lesions are characterized by multifocal necrosis of the crypt epithelium, loss of crypt architecture, and villous blunting and sloughing. Depletion of lymphoid tissue and cortical lymphocytes (Peyer's patches, peripheral lymph nodes, mesenteric lymph nodes, thymus, spleen) and bone marrow hypoplasia also occur.
Pulmonary edema, alveolitis, and bacterial colonization of the lungs and liver may be observed in dogs that have died of complicating acute respiratory distress syndrome, systemic inflammatory response syndrome, endotoxemia, or septicemia.
Diagnosis of Canine Parvovirus Infection
Suspected based on signalment, history, and clinical signs
Confirmation by fecal parvoviral antigen testing or viral PCR assay
Canine parvoviral enteritis should be suspected in any young, unvaccinated, or incompletely vaccinated dog with relevant clinical signs, especially those living in or newly acquired from a shelter or breeding kennel.
During the course of the illness, most dogs develop moderate to severe leukopenia characterized by lymphopenia and neutropenia. Leukopenia, lymphopenia, and the absence of a band neutrophil response within 24 hours of starting treatment has been associated with a poor prognosis.
Prerenal azotemia, hypoalbuminemia (GI protein loss), hyponatremia, hypokalemia, hypochloremia, hypoglycemia (due to inadequate glycogen stores in young puppies and/or sepsis, potentially a poor prognostic indicator), and increased liver enzyme activities may be noted on the serum biochemical profile.
Commercial ELISAs for detection of antigen in feces are widely available and have good to excellent sensitivity and specificity, even for the more recently evolved CPV-2c strain. All animals with relevant clinical signs should be immediately tested, so appropriate isolation procedures can be initiated.
Most clinically ill dogs shed large quantities of virus in the feces. However, false-negative results can occur early in the course of the disease (before peak viral shedding) because of the dilutional effect of large volume diarrhea, or after the rapid decline in viral shedding that tends to occur within 10–12 days after infection (3-4 days after development of clinical signs).
False-positive results can occur within 4–10 days following vaccination with modified live CPV vaccine.
Alternative ways to detect CPV antigen in feces include PCR assay, electron microscopy, and virus isolation. Serodiagnosis of CPV infection requires demonstration of a 4-fold increase in serum IgG titer throughout a 14-day period or detection of IgM antibodies in the absence of recent (within 4 weeks) vaccination. This testing is rarely used.
Treatment and Prognosis of Canine Parvovirus Infection
Immediate isolation of suspected or confirmed cases
Supportive care
Monoclonal antibody therapy
In cases of parvoviral enteritis in dogs, survival rates are typically best for dogs treated aggressively in the hospital (survival rate > 90%). In some situations, financial limitations may prevent such aggressive therapy.
Outpatient protocols have been reported showing an approximately 80% success rate. Outpatient therapies typically include SC administration of fluids, oral supplementation with electrolyte solutions and nutrition, and parenteral administration of antiemetics (maropitant 1 mg/kg, SC, every 24 hours as needed to control vomiting) and antimicrobials (cefovecin 8 mg/kg, SC, once) (1, 2, 3).
The main goals of treatment for parvoviral enteritis in dogs include restoration of fluid, electrolyte, and metabolic abnormalities and prevention of secondary bacterial infection.
In the absence of substantial vomiting, oral electrolyte solutions can be offered. Administration SC of an isotonic balanced electrolyte solution may be sufficient to correct mild fluid deficits (< 5%) but is insufficient for dogs with moderate to severe dehydration. Most dogs will benefit from IV fluid therapy with a balanced electrolyte solution. Correcting dehydration, replacing ongoing fluid losses, and providing maintenance fluid needs are essential for effective treatment.
Dogs must be monitored for development of hypokalemia and hypoglycemia. If electrolytes and serum blood glucose concentration cannot be routinely monitored, empirical supplementation of IV fluids with potassium chloride (supplemented in fluids at 20–40 mEq/L) and dextrose (supplemented in fluids at 2.5–5%) is appropriate.
If GI protein loss is severe (albumin < 2.0 g/dL, total protein < 4.0 g/dL, evidence of peripheral edema, ascites, pleural effusion, etc), transfusion of fresh frozen plasma can partially replace serum albumin while providing serum protease inhibitors to counter the systemic inflammatory response. Alternatively, concentrated albumin products may be considered if available.
No evidence exists to support the use of serum from dogs recovered from parvoviral enteritis (convalescent or hyperimmune serum) as a means of passive immunization.
Antimicrobials are indicated because of the risk of bacterial translocation across the disrupted intestinal epithelium and the likelihood of concurrent neutropenia. A beta-lactam antimicrobial (eg, ampicillin sodium 22 mg/kg, IV, every 8 hours) will provide appropriate gram-positive and anaerobic coverage. For severe clinical signs and/or marked neutropenia, additional gram-negative coverage (eg, enrofloxacin [10–20 mg/kg, IV, every 24 hours for 5–7 days] or gentamicin [9–12 mg/kg, IV, IM, or SC, every 24 hours for 5–7 days]) is indicated.
Aminoglycoside antimicrobials must not be administered until dehydration has been corrected and fluid therapy established. Enrofloxacin has been associated with articular cartilage damage in rapidly growing dogs 2–8 months old; however, short courses (5–7 days) are not likely to cause clinical issues. Second- or third-generation cephalosporins (eg, cefoxitin, ceftazidime, cefovecin) can also be considered for their relatively wide spectrum of activity against gram-positive and gram-negative bacteria. Antimicrobial therapy is typically only needed for a short duration (eg, 5–7 days).
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Antiemetic therapy is indicated if vomiting is protracted, perpetuates dehydration and electrolyte abnormalities, or limits oral administration of medications and nutritional support. In dogs with parvoviral enteritis, maropitant (1 mg/kg, IV or SC, every 24 hours as needed to control vomiting) and ondansetron (0.5 mg/kg, IV, every 8 hours as needed to control vomiting) appear to be equally effective at controlling vomiting. Metoclopramide (0.2–0.5 mg/kg, IM or SC, every 6–8 hours as needed to control vomiting; or ideally 1–2 mg/kg/day, IV as a CRI) may be considered as an antiemetic as well as for its prokinetic effects, particularly in dogs with substantial gastric stasis.
Vomiting may persist despite antiemetic administration. In these cases, evaluation for other causes of vomiting, such as intussusception, may be warranted.
Antidiarrheals are not recommended because retention of intestinal contents within a compromised gut increases the risk of bacterial translocation and systemic complications.
Previous anecdotal recommendations for nutritional management of parvoviral enteritis in dogs included withholding food and water until cessation of vomiting. However, evidence suggests early enteral nutrition is associated with earlier clinical improvement, weight gain, and improved gut barrier function.
For anorectic dogs, placement of a nasoesophageal or nasogastric tube for continual feeding of a prepared liquid diet (either a commercial liquid diet or a dilute, blended canned diet) should be instituted within 12 hours after hospital admission. Once vomiting has subsided for 12–24 hours, gradual reintroduction of water and a bland, low-fat, easily digestible commercial or homemade (eg, boiled chicken or low-fat cottage cheese and rice) diet is recommended.
Partial or total parenteral nutrition is reserved for dogs with anorexia > 3 days that cannot tolerate enteral feeding.
In one study, fecal microbiota transplantation (taking 10 g of feces from a healthy dog, then diluting in 10 mL of saline solution [0.9% NaCl] and administering rectally 6–12 hours after admission) in dogs with CPV infection was associated with a faster resolution of diarrhea and shorter hospitalization time (median, 3 days), compared with standard therapy (median, 6 days) (4).
Oseltamivir is an antiviral agent usually used to treat influenza virus infections in humans. In a study of naturally occurring parvoviral enteritis in dogs, treatment with oseltamivir (2 mg/kg, PO, every 12 hours for 5 days) did not decrease duration of hospitalization, clinical disease severity, or mortality rate. However, treated dogs did not experience weight loss or a decrease in WBC count, as were observed in untreated control dogs (5). The potential for inducing human or avian influenza viruses to become drug resistant has led some to question the appropriateness of oseltamivir administration to animals.
Other adjunctive treatments, such as recombinant human granulocyte colony-stimulating factor, recombinant bactericidal/permeability-increasing protein, and feline interferon-omega, have not been shown to be beneficial.
A novel CPV monoclonal antibody is now available as a conditionally approved therapy. In an experimental study, dogs received either antibody or saline administration at the time viral shedding was noted in the feces. No other therapies were given. No dogs receiving antibody died, whereas 57% of dogs given saline died (6). Although this may be a promising therapy, further studies in clinical cases will be needed to determine the efficacy and proper timing of administration of this therapy.
Intussusception, bacterial colonization of IV catheters, thrombosis, urinary tract infection, septicemia, endotoxemia, acute respiratory distress syndrome, and sudden death are potential complications of parvoviral enteritis in dogs. Most puppies that survive the first 3–4 days of illness make a full recovery, usually within 1 week. With appropriate supportive care, 70–90% of dogs with parvoviral enteritis will survive. Dogs that recover develop long-term, possibly lifelong, immunity.
Prevention and Control of Canine Parvovirus Infection
Canine parvovirus, as a nonenveloped virus, is resistant to many common detergents and disinfectants, as well as to changes in temperature and pH. CPV can remain viable in the environment for an extended period. Infectious CPV can persist indoors at room temperature for at least 2 months; outdoors, if protected from sunlight and desiccation, the virus can persist for many months and possibly years.
To limit environmental contamination and spread to other susceptible animals, personnel handling dogs with confirmed or suspected parvoviral enteritis must follow strict isolation procedures (eg, isolation housing, gowning and gloving before handling, frequent and thorough cleaning, footbaths, etc). All surfaces should be cleaned of gross organic matter and then disinfected with a solution of dilute bleach (1:30) or a peroxygen, potassium peroxymonosulfate, or accelerated hydrogen peroxide disinfectant. The same solutions may be used as footbaths to disinfect footwear.
To prevent and control CPV, vaccination with a modified live virus vaccine is recommended at 6–8, 10–12, and 14–16 weeks of age, followed by a booster administered 1 year later and then every 3 years. Because of potential damage by CPV to myocardial or cerebellar cells, inactivated rather than modified live virus vaccines are indicated in pregnant dogs or colostrum-deprived puppies vaccinated before 6–8 weeks of age.
The presence of maternally acquired CPV antibodies may interfere with the effectiveness of vaccination in puppies < 8–10 weeks old. However, current modified live CPV vaccines are sufficiently immunogenic to protect puppies from infection in the presence of low levels of interfering maternal antibody, and vaccination of 4-week-old puppies with a high antigen titer vaccine results in seroconversion and may decrease the window of susceptibility to infection. Current vaccines protect equally well against CPV-2 and other strains of the virus.
In a kennel, shelter, or hospital, cages and equipment should be cleaned (including removal of organic material such as feces, urine, and vomit to enhance the activity of disinfectants), disinfected, and dried twice before reuse. Virucidal disinfectants include sodium hypochlorite 5% (bleach) diluted 1:32 in water, potassium peroxymonosulfate, and accelerated hydrogen peroxide. Quaternium ammonium disinfectants are not reliable disinfectants for parvovirus.
The same concepts can be applied to a home situation. Removal of contaminated organic material is important in outdoor situations where complete disinfection is not practical. Disinfectants can be applied outdoors with spray hoses; however, disinfection will be less effective than when applied to clean, indoor surfaces.
Only fully vaccinated puppies (at 6, 8, and 12 weeks) or fully vaccinated adult dogs should be introduced into a home where a dog has recently had parvoviral enteritis. Booster vaccination of in-contact healthy dogs that are up to date on parvovirus vaccination is reasonable, but potentially unnecessary, given the extended duration of immunity to CPV.
Key Points
Parvoviral enteritis is a highly contagious acute GI disease in young, unvaccinated dogs.
Diagnosis is based on signalment, history, clinical signs, and fecal viral antigen testing or viral PCR assay.
Treatment requires supportive care with fluids, antiemetics, antimicrobials, and nutritional support.
For More Information
Also see pet owner content regarding canine parvovirus infection.
References
Sarprong KJ, Lukowski JM, Knapp CG. Evaluation of mortality rate and predictors of outcome in dogs receiving outpatient treatment for parvoviral enteritis. J Am Vet Med Assoc. 2017;251(9):1035-1041. doi:10.2460/javma.251.9.1035
Perley K, Burns CC, Maguire C, et al. Retrospective evaluation of outpatient canine parvovirus treatment in a shelter-based low-cost urban clinic. J Vet Emerg Crit Care (San Antonio). 2020;30(2):202-208. doi:10.1111/vec.12941
Venn EC, Preisner K, Boscan PL, Twedt DC, Sullivan LA. Evaluation of an outpatient protocol in the treatment of canine parvoviral enteritis. J Vet Emerg Crit Care (San Antonio). 2017;27(1):52-65. doi:10.1111/vec.1256
Pereira GQ, Gomes LA, Santos IS, Alfieri AF, Weese JS, Costa MC. Fecal microbiota transplantation in puppies with canine parvovirus infection. J Vet Intern Med. 2018;32(2):707-711. doi:10.1111/jvim.15072
Savigny MR, Macintire DK. Use of oseltamivir in the treatment of canine parvoviral enteritis. J Vet Emerg Crit Care (San Antonio). 2010;20(1):132-142. doi:10.1111/j.1476-4431.2009.00404.x
Larson L, Miller L, Margiasso M, et al. Early administration of canine parvovirus monoclonal antibody prevented mortality after experimental challenge. J Am Vet Med Assoc. 2024;262(4):506-512. doi:10.2460/javma.23.09.0541
