Treating the parvovirus patient - Veterinary Practice
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Treating the parvovirus patient

BLAISE SCOTT-MORRIS of Virbac examines the causes and effects of this highly contagious virus which commonly affects dogs in the UK, along with treatment and vaccination protocols vets should follow

PARVOVIRUS outbreaks are commonly encountered in the UK, with pockets occurring more frequently in certain areas of the country such as Wales and the north-west.

Outbreaks within an area can be devastating for both owners and practices alike, with treatment costly and challenging. However, rapid implementation of intensive treatment can improve prognosis.


Parvovirus is a small non-enveloped DNA virus, which needs actively dividing cells to replicate in, such as those within the gastrointestinal tract and immune system of the dog.7

The challenge with parvovirus is that it is highly contagious via the faecooral route and very resistant in the environment; providing a source of re-infection during outbreaks.

Up-to-date vaccinations are protective but one must remember the role of “herd immunity”. This is when, if a large proportion of individuals within a population is vaccinated, they indirectly protect the unvaccinated individuals. However, if the critical number of vaccinated animals is not maintained, the disease is more likely to spread, possibly even to vaccinated individuals, particularly more susceptible breeds such as Rottweilers and Labradors.7

Clinical signs and diagnosis

Every practitioner is familiar with the acute haemorrhagic gastrointestinal signs associated with parvovirus.

It is important that any puppy with vomiting or diarrhoea is considered at risk, even if they have started their first vaccination course; early detection and treatment can greatly improve the chances of survival.

Differential lists are long due to the vague signs, including dietary indiscretion, idiopathic haemorrhagic gastroenteritis, Salmonella and E. coli infections, intussusception or foreign body and toxins.

In vaccinated puppies, parvovirus diagnosis can be difficult if a high titre vaccine has been used. The vaccinal virus will shed for up to four weeks post-injection in the faeces and can be detected on some in-house tests.

Infective virus may not be shed in the faeces for the first 24-48 hours after onset of clinical signs, is shed for two to seven days, then starts to decrease after seven to 14 days 7, so in-house tests may need to be repeated. Patient side-tests including ELISA, e.g. SNAP Parvo (IDEXX Laboratories) and dry immunochromatographic tests, e.g. Speed Parvo (Virbac), can be useful to make a quick diagnosis. However, parvovirus in animals with clinical signs should not be ruled out on one negative result.


Affected animals are severely dehydrated with electrolyte disturbances, making fluid therapy possibly the most important treatment consideration. Therapy should focus on correcting hydration and replacing ongoing losses while allowing for maintenance fluids.

Electrolyte balance should be monitored closely while rehydration occurs, particularly for the development of hypokalaemia and hypoglycaemia, which will occur rapidly in animals that are vomiting and are less able to compensate, i.e. young/ anorexic patients.

If gastrointestinal protein loss is severe, colloids may be considered; there is a possibility of increased capillary permeability and if colloids are used solely for large volume resuscitation in such animals it will likely result in interstitial oedema. A more detailed discussion of fluid resuscitation is beyond the scope of this article but can be found in medical textbooks.

Due to damage of the intestinal epithelium, and the likelihood of neutropaenia, there is a high risk of bacterial translocation, secondary bacterial infections and possible septicaemia. Therefore antibiotics are indicated.

Broad cover including Gram-positive and anaerobic bacteria is essential. In some cases Gram-negative cover may also be required, so often a multimodal approach is instituted.

It is important to note that some antimicrobials have been linked to disorders in growing animals, e.g. fluoroquinolones are associated with arthropathies related to articular cartilage damage in dogs aged four to 28 weeks.8

Taking into account the clinical condition of the patient and concurrent medical considerations, a risk/benefit analysis can be made to choose the appropriate antimicrobial combination.

Anti-emetics should be considered depending upon the severity of vomiting, as increased emesis can exacerbate dehydration and electrolyte imbalances if left untreated. Agents such as metoclopramide can be administered in sequential doses via constant rate infusion.

Although metoclopramide has prokinetic properties8 which may be beneficial in ileus, it could also predispose to intussusception, so careful monitoring is essential.

Other anti-emetics such as maropitant (Cerenia, Zoetis) may be more effective by preventing both central and peripheral emesis pathways compared with other drugs which only act on one pathway.10

Anti-diarrhoeal agents are not recommended as retention of intestinal contents with potentially compromised intestinal epithelium increases the risk of bacterial translocation and systemic complications.

Nutrition should be included in the therapeutic plan; recent evidence does not support the nil-per-os theory.4,6 Nutrients such as glutamine are important for enterocyte health and contribute to replacing cells during normal epithelial turnover but also the repair of mucosal injury.

Implementing early nutrition may decrease the length of hospitalisation.4 Early enteral nutrition, via nasogastric or oesophagostomy tube, is correlated with earlier clinical improvement and significant weight gain over delaying offering food until vomiting has ceased for 12 hours.6 Early enteral nutrition may also improve gut barrier function, limiting the translocation of bacteria or endotoxins.6

Interferons have anti-viral, antiproliferative (neoplasms) and immunomodulatory properties 8; specifically, interferon omega is released by cells in response to viral infection.

Recombinant feline interferon omega or rFeIFN (Virbagen Omega, Virbac) is authorised in the EU for the reduction in mortality and clinical signs of parvovirus infection in dogs from one month of age at a dose of 2.5mu/kg intravenously once-daily for three days.11

Interferon acts indirectly by inducing anti-viral proteins, protein kinase and 2’5’-oligoadenylate synthetase (2’5’- OAS). rFeIFN significantly improved the severity of enteritis, vomiting and anorexia, with rapid effect, in experimentally induced parvovirus.2

Interferon administration in the field correlates with a 4.4-fold reduction in mortality compared to a placebo 5, when implemented early and combined with relevant supportive treatment such as outlined above. In an unvaccinated population it was found to, with supportive therapy, reduce mortality to less than 3%.5


Attempts have been made to determine prognostic indicators. Measures such as leukocytopaenias, lymphopaenia and hypoalbuminaemia have been associated with prolonged hospitalisation times 3, whilst Goddard et al 1 noted increasing lymphocyte counts between 24 and 48 hours postadmission correlated with survival.


When deciding upon a treatment regime for the parvovirus patient it is important to act quickly, because as the disease progresses, the intestinal microvilli slough, leading to further deterioration, combined with other systemic disturbances.

With this in mind, the most important aspect of treating the parvovirus patient is early recognition of the signs and swift implementation of appropriate treatment, for the best chances of a positive outcome.


  1. Goddard, A., Leisewitz, A. L., Christopher, M. M., Duncan, N. M., Becker, P. J. (2008) Prognostic usefulness of blood leukocyte changes in canine parvoviral enteritis. J Vet Intern Med. 22 (2): 309-316.
  2. Ishiwata, K.1, Minagawa, T., Kajimoto, T. (1998) Clinical effects of the recombinant feline interferon-omega on experimental parvovirus infection in beagle dogs. J Vet Med Sci. 60 (8): 911-917.
  3. Kalli, I., Leontides, L. S., Mylonakis, M. E., Adamama-Moraitou, K., Rallis, T., Koutinas, A. F. (2010) Factors affecting the occurrence, duration of hospitalisation and final outcome in canine parvovirus infection. Res Vet Sci. 89 (2): 174-178.
  4. Liu, D. T.1 , Brown, D. C., Silverstein, D. C. (2012) Early nutritional support is associated with decreased length of hospitalization in dogs with septic peritonitis: A retrospective study of 45 cases (2000-2009). J Vet Emerg Crit Care (San Antonio) 22 (4): 453-459.
  5. Mari, K. D. E., Maynard, L., Eun, H. M., Lebreux, B. (2003) Treatment of canine parvoviral enteriltis with interferon-omega in a placebo-controlled field trial. Veterinary Record 152: 105-108.
  6. Mohr, A. J., Leisewitz, A. L., Jacobson, L. S., Steiner,J. M., Ruaux,C. G., Williams, D. A. (2003) Effect of Early Enteral Nutrition on Intestinal Permeability, Intestinal Protein Loss, and Outcome in Dogs with Severe Parvoviral Enteritis. J Vet Intern Med. 17 (6): 791-798.
  7. Nelson, R. W. DVM, Guillermo Couto, C. (2014). Small Animal Internal Medicine, 5th ed. London: Elsevier. 392-393, 457.
  8. Riviere, J. E., Papich, M. G., (2009) Veterinary Pharmacology and Therapeutics, 9th ed. USA: WileyBlackwell. 1,002-1,003.
  9. Schmitz, S., Coenen, C., Matthias, K., HeinzJürgen, T., Neiger, R. (2009) Comparison of Three Rapid Commercial Canine Parvovirus Antigen Detection Tests with Electron Microscopy and Polymerase Chain Reaction. J Vet Diagn Invest. 21 (3): 344-345.
  10. Sedlacek, H. S., Ramsey, D. S., Boucher, J. F., Eagleson, J. S., Conder, G. A., Clemence, R. G. (2008) Comparative efficacy of maropitant and selected drugs in preventing emesis induced by centrally or peripherally acting emetogens in dogs. J Vet Pharmacol Ther. 31 (6): 533-537.
  11. Virbagen Omega 10 MU for dogs and cats. Summary of Product Characteristics. EMA, 2007.

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