CANINE PARVOVIRUS (CPV) 

Canine parvovirus (CPV) is a member of the genus Parvovirus of the family Parvoviridae. Canine parvovirus infection emerged in the late 1970s most likely as a variant of feline panleukopaenia virus (FPV) or a closely related parvovirus. FPV-like viruses have been isolated from cats, raccoons, mink, and the arctic fox, and are genetically very similar although distinct from CPV-like viruses from dogs and raccoons. Besides the well-known FPV, new antigenic types of CPV, namely CPV-2a and CPV-2b, are also able to replicate and cause disease in cats. These new antigenic types are the predominant types in dog populations worldwide. 

CPV has a worldwide distribution. Serological surveys indicate that severe clinical disease with high mortality is the exception. Most naturally occurring infections with CPV are sub clinical or result in mild signs of disease that do not require veterinary care. Age, stress, breed, intestinal parasites, and concurrent infections all can affect the pathophysiological consequences of infection with CPV so that morbidity and mortality in pups can exceed 90% and 50% respectively. 

Pathogenesis 

Infection in the dog takes place via the oronasal route. Initial viral replication occurs in extra-intestinal lymphoid tissues. Virus is then spread through the blood to other lymphoid tissues where the cycle is repeated, eventually resulting in intestinal epithelial infection. Thus, viraemia always precedes intestinal epithelial infection. 

Infection and destruction of lymphoid tissues are prominent features of parvovirus infection. This is characterized by extensive loss and sometimes depletion of lymphocytes from the cortex of lymph nodes, especially the mesenteric and retropharyngeal nodes. Parvovirus is able to replicate in both T and B-lymphocytes. Intestinal lesions are characterized by extensive necrosis of crypt epithelial cells accompanied by collapse of the lamina propria and a minimal inflammatory infiltrate in both. Lesions are most severe in the ileum and duodenum, with mild lesions in the colon. There is extensive depletion of lymphocytes in the intestinal lymphoid nodules and Peyer's patches. 

The most consistent haematological change in CPV infection is transient lymphopaenia. 

IgA antibodies appear in the intestinal tract and faeces by day 4 after infection with CPV. Some dogs can develop high titres of humoral antibody but little IgA antibodies in the intestinal lumen. These dogs are more likely to have severe disease. 

The severity of intestinal lesions determines the severity of clinical disease, and is in turn dependant on the dose of virus reaching the intestine from the blood. Thereafter, additional virus replication within intestinal lymphoid tissues and the intestinal epithelium further elevates the intestinal virus titre. 

Clinical signs 

The disease is seen mostly in dogs between the ages of 6 weeks to 6 months. Early clinical signs are listlessness, anorexia, vomiting, and fever. The disease progresses to weakness, dehydration, and severe vomition and diarrhea. In advanced cases, septic/hypotensive shock develops. 

Diagnosis 

Clinical signs especially with a poor/no vaccination history are indicative of the disease. 

Laboratory diagnosis

Electron microscopy on fecal specimens. 
Serum antibody titres by the haemagglutination inhibition test or the indirect immunofluorescent antibody test. 
Post mortem examination. 
Virus isolation from either serum or feces. 

Therapy 

Antibiotics 
Amoxicillin 
Gentamycin at 2 mg/kg TID or 3mg/kg BID for 3-5 days. 

Only once patient is re hydrated. 
Check for RTE cells in urine.

Fluid therapy

Replacement or maintenance fluids. 
Colloids.

Anti-emetics 

Metoclopramide:  0.2-0.4 mg/kg tid-qid. 1-2 mg/kg/day as a constant rate infusion. 
Prochlorperazine: at 0.5 mg/kg tid or a piece of a suppository. Has no prokinetic effect.  Ondansetron: at 0.1-1 mg bid-qid. 

Nutrition

Feed once re hydrated, which should be approximately 4-12 hours after admission. 
Feed minimum of 1/3 of nutritional requirements in first 24 hours. 
With severe vomiting, miss out 1-2 hours and/or reduce quantity. 
Naso-oesophageal tube if necessary. 

Additional therapy 

Plasma transfusion at 10-20 ml/kg if albumin < 20 g/l. 
Blood transfusion if not improving and Ht <15-20%. 
Deworm if necessary. 
Sucralfate 1ml/3kg tid-qid with severe vomiting to control flux oesophagitis. 
Cimetidine 10 mg/kg tid or ranitidine 2 mg/kg bid. 
Temgesic 0.01mg/kg tid with severe abdominal pain. 

Monitoring 

Body weight, blood glucose, haematocrit, total serum proteins, and serum potassium should be monitored at admission, after 2 hours of fluids and then on a daily basis in all patients that are still ill.