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.
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
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.
Clinical signs especially with a poor/no vaccination
history are indicative of the disease.
Electron microscopy on fecal
Serum antibody titres by the haemagglutination inhibition
test or the indirect immunofluorescent antibody
Post mortem examination.
Virus isolation from either serum or feces.
Gentamycin at 2 mg/kg TID or 3mg/kg BID for 3-5
Only once patient is re hydrated.
Check for RTE cells in urine.
Replacement or maintenance
mg/kg tid-qid. 1-2 mg/kg/day as a constant
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.
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
Naso-oesophageal tube if necessary.
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.
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.