Internist, Bryanston Veterinary Hospital, Professor, Department of Companion Animal Clinical Studies, Faculty of Veterinary Science, University of Pretoria
Onderstepoort, Bryanston, South Africa
Distemper is caused by a Morbillivirus that affects carnivores and certain Felidae. The disease is characterized by a biphasic temperature reaction, lymphopaenia, generalised catarrhal inflammation, and neurological complications. Canine distemper virus is an immunosuppressive virus that affects both T and B cell function.
Aerosol droplets attach to epithelial cells of the upper respiratory tract. Within 24 hours the virus multiplies in tissue macrophages and spreads via local lymphatics to tonsils and bronchial lymph nodes. From here the virus spreads to bone marrow, thymus and spleen. Within 4-6 days virus multiplication occurs within lymphoid follicles in the spleen, lamina propria of the stomach and small intestine, mesenteric lymph nodes and Kupffer cells. This stage corresponds with the initial fever and lymphopaenia. 8 to 14 days later spread to epithelial and CNS tissues occurs through infected lymphocytes and macrophages. This happens in dogs with insufficient cell mediated immunity and humoral immune response.
Virus, either free or lymphocyte associated, may enter the CNS by entering into mononuclear cells in the meninges, choroid plexus, epithelial cells of the fourth ventricle and ependymal cells lining the ventricular system. From these sites virus may enter the CSF from where it spreads to the cerebral cortex, optic tracts and nerves, cerebral peduncles, and spinal cord. The type of lesion produced and the course of infection within the CNS depends on the age and immunocompetence of the host, as well as the neurotropic and immunosuppressive properties of the virus.
Young dogs can develop acute (non-inflammatory) demyelinating encephalomyelitis. Chronic encephalitis can either be a polioencephalomalacia or a diffuse sclerosing panencephalitis ("Old dog encephalitis"). The pathogenesis of this appears to be based on an immunological reaction against the basic protein in myelin that is triggered by the distemper virus. The lesion is characterised by perivascular lymphocytic/plasmacytic cuffing of vessels at the junction of the grey and white matter. There is a uniform, diffuse sclerosis of the cerebral white matter, as well as demyelination. 'Old-dog encephalitis' is similar to subacute sclerosing panencephalitis caused by measles infection in children.
Chronic neurological disease with distemper is associated with viral persistence. It has been proposed that defective interfering viral particles may play a role in the pathogenesis. Viral infection within neurons is non-productive as nucleocapsids are produced but not released from the surface of the cell. However, under the influence of a triggering mechanism complete virions can again be produced.
The clinical signs of distemper are varied and include:
Sub-clinical to severe multi-systemic signs that can involve the respiratory and gastro-intestinal systems.
Fading puppy syndrome.
Clinical signs especially with a poor/no vaccination history are indicative of the disease. The diagnosis can occasionally be made by finding distemper inclusions in lymphocytes, neutrophils and erythrocytes on peripheral blood smear.
Direct immunofluorescence for presence of antigen from smears of conjunctival, tonsillar and genital epithelium, and buffy coat. Viral inclusions can also be demonstrated by immunoperoxidase staining of skin biopsies.
Serological tests such as serum virus neutralization, ELISA, and IFA. The presence of IgM antibodies in the serum is indicative of either acute infection or recent vaccination. IgM antibodies appear in the sera approximately 7 days following exposure to vaccine virus or natural infection and decline to undetectable levels after approximately 4 weeks. IgG titres begin to decline after five to six months. In the absence of re-exposure, IgG titres can drop to undetectable levels by 14-18 months.
IgG in the CSF can be regarded as a sensitive and specific indicator of distemper encephalitis. IgG is produced locally in the CNS and will not be present in vaccinated dogs. Contamination of the CSF tap with whole blood can be a problem, but simultaneous measurement of parvovirus antibody titres in the CSF and blood can help rule this out. Other typical CSF changes are raised protein and lymphocytic pleocytosis.
There is no specific therapy and thus therapy is dependent on good nursing care, antibiotics for secondary infections, maintenance of fluid and electrolyte balance, nutritional support, and seizure control.
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 subclinical 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 titre.
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 diarrhoea. In advanced cases, septic/hypotensive shock develops.
Clinical signs especially with a poor/no vaccination history are indicative of the disease.
Electron microscopy on faecal specimens.
Serum antibody titres by the haemagglutination inhibition test or the indirect immunofluorescent antibody test.
Post mortem examination.
Virus isolation from either serum or faeces.
Gentamycin at 2 mg/kg TID or 3mg/kg BID for 3-5 days.
Only once patient is rehydrated.
Check for RTE cells in urine.
Replacement or maintenance fluids.
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.
Feed once rehydrated, which should be approximately 4-12 hours after admission.
Feed minimum of 1/3 of nutritional requirements in first 24 hours.
With severe vomition, miss out 1-2 hours and/or reduce quantity.
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.