Distemper

Caused by Canine morbillivirus, a member of the Paramyxoviridae family. Transmission is via aerosol, although it can also be spread through the placenta.

The virus first comes into contact with the epithelium of the upper respiratory tract, where it replicates in the lymphatic tissue. Following that, it continues to multiply in tissue macrophages and T and B lymphocytes, initially spreading (viraemic phase) to the bronchial lymph nodes, and finally localizing in various lymphoid tissues (spleen, thymus, Kupffer cells of the liver, bone marrow, lamina propria of the stomach, etc.).

This stage of infection corresponds to the first fever peak between the third and sixth day after infection. Around seven days after infection, the virus is found in lymphatic tissues and lymphocytes. Between the eighth and ninth day, it spreads to the CNS, which is affected to a different degree and manner (demyelination) depending on the animal and its immune response. In animals with a strong cellular and humoral immune response (effective IgG), the virus is eliminated from the tissue around 14 days after infection without causing symptoms.

The virus may remain for a while longer in some tissues, such as the uvea or the integuments (pads). If the immune response is weak, after 14 days, the virus begins to spread throughout the body (epithelia), affecting the skin, respiratory system, gastrointestinal system, genitourinary system, exocrine and endocrine glands, and central nervous system. This second viremia corresponds clinically with a second episode of intermittent fever, which is usually accompanied by serous nasal discharge, conjunctivitis and anorexia.

If the immune system responds correctly, albeit late, the virus may disappear from some tissues but remain in the CNS, lung, pads, etc. In the acute phase of the disease, the virus is shed in all bodily secretions, starting around the seventh day post-infection and lasting up to 60-90 days, although such long shedding periods are rare.

Some animals may also become asymptomatic carriers with subclinical infection, who shed the virus and contribute to the spread of the disease. There is no evidence that cured animals continue to shed viruses either sporadically or chronically.

Symptoms

From 50% to 70% of infections are subclinical.

The first signs are usually fever, conjunctivitis, discharge from the eyes and nose, dyspnoea and cough, which is dry at first and later becomes productive. Other symptoms can include depression and anorexia, as well as vomiting and diarrhoea that can contain mucous and blood. CNS symptoms can be fulminant, but can also appear from 1 to 3 weeks after the animal has recovered, and consist of vestibular symptoms, hyperesthesia, tetraparesis, convulsions, myoclonus (highly characteristic), and other symptoms depending on the brain area involved. Ocular symptoms usually begin with conjunctivitis and progress to chorioretinitis, keratoconjunctivitis sicca and optic nerve lesions (optic neuritis that can lead to blindness). Benign anterior uveitis and retinal atrophy with scarring are also very common. Keratoconjunctivitis sicca can also occur after a systemic, subclinical infection.

Hyperkeratosis of the pads and nose may also be observed. Common sequelae are anosmia (loss of smell) and dental changes in both temporary and permanent teeth (enamel and dentin hypoplasia, impaction).

Interpretation of laboratory tests

General Tests

• Complete blood count.
  Leukopaenia caused by severe lymphopaenia and neutropaenia. This finding is not specific to distemper. Thrombocytopaenia (as low as 30,000/mm³ in some experimental models).
  Different types of intracellular inclusions, depending on the cell involved, But generally in lymphocytes in peripheral blood and more sporadically in monocytes, neutrophils and erythrocytes.
• Serum proteins
  Decrease in total proteins due to a decrease in albumin levels.

Specific tests

• Direct immunofluorescent assay to detect the virus in a conjunctival smear, CSF, or samples. The virus may disappear from the mucous membranes 15 days after the start of the infection.
• Antibody assay. Difficult to interpret in vaccinated animals. Immunoexpressed animals may have distemper despite a low antibody titre. The presence of antibodies in CSF is pathognomonic of distemper if the blood-brain barrier is intact, since these antibodies are produced intrathecally. Higher antibody titre in CSF than in blood indicates local production of antibodies. To avoid false positives, the sample must be free from blood contamination.

Health measures

The virus is easily inactivated by normal disinfection measures, and also by heat and drying. It is inactivated by UV light, bleach, quaternary ammonia, formaldehyde and heat (30 minutes at 50-60ºC, 1 hour at 37ºC and 3 hours at 20ºC).

Prophylaxis

• In puppies, vaccination schedules should be adapted to the maternal immunity level. Peak titres are achieved within two or three weeks of vaccination.
• Pregnant females should not be vaccinated.

Bibliography

• APPLE. M.J. (1987) Virus Infections of Carnivores. Elsevier pg. 133-159.
• BARRETT, T. (1999) Veterinary Microbiology, Vol. 69, pg. 3-13.
• BONAGURA (1992) Kirk’s Current Veterinary Therapy XI W.B.Saunders pg 455, 1003-1007. BITTEGEKO, S,B. (1995) Journal of American Animal Hospital Association Jan-Feb; 31(1):42-45. BLAIR, E.M. (1998) Veterinary Medicine July pg. 655-658.
• BLIXARKRONE-MOLLER, M. (1991) Journal of Veterinary Diagnostic Investigation Jan.;3(1),3-9. CASTRO, A.E. (1992) Veterinary Diagnostic Virology (Mosby Year Book), pg. 135-138. CORNWELL, H.J.C. (1988) The Veterinary Record. Nov (112), 54-59.
• COYNE, M.J. (2000) Journal of American Animal Hospital Association, Vol 36, nº2.Pg.137-142. ETTINGER (1995)Textbook of Veterinary Internal Medicine (4th ed) W.B.Saunders pg. 400-403, 526-527,623-624, 656-657, 780-781,1204-1205.
• GEMMA, T. (1995) Journal of Veterinary Medical Science (Japan) Aug. 57 (4); 761-763. GREEN (1993) Enfermedades infecciosas de perros y gatos Interamericana Mc Graw Hill pg. 236-250.
• GRÖNE, A. (1999) Veterinary Pathology, Vol. 36, nº 5, pg. 501.
• HAAS, L. (1999) Veterinary Microbiology, Vol. 69, pg. 15-18.
• HAINES, D.M. (1999) Journal of Veterinary Diagnostic Investigation, Vol 11, nº 5, pg. 396-399. IWATSUKI, K. (2000) Veterinary Microbiology, Vol. 71, pg. 281-286.
• JOHNSON, G.C. (1988) Journal of Neuroimmunology Feb. 17 (3), 237-251.
• MORALES, M.J. (1997) Consulta de Difusión Veterinaria Vol 6, nº 44, pg 36-37.
• NESSELER, A. (1999) Veterinary Microbiology, Vol. 69, pg. 23-28.
• OHASHI, K. (1998) Journal of Veterinary Medical Science, Vol. 60, nº 11, pg. 1209-1212. ORTEGA, C. (1989) Medicina Veterinaria Vol. 6, nº 12, pg. 715-721.
• PALMER, D.G. (1990) Research in Veterinary Science (Australia) Sep. 4 (2), 177-181. POTGIETER, L.N. (1989) Journal of Veterinary Diagnostic Investigation Apr.; 1(2), 110-115. RIMA, B.K. (1991) Archives of Virology 121 (1-4) : 1-8.
• SHIN, Y. (1995) Journal of Veterinary Medical Science (Japan) Jun. 57 (3) 439-445.
• SIMON, M.C. (1987) Medicina Veterinaria Vol. 4 nº 4, pg. 211-214.
• WANER,T.(1998) The Veterinary Journal Vol 155, nº2, pg 171-175.
• WILLARD, M.D. (1994) Small Animal Clinical Diagnosis by Laboratory Methods, 2n. ed. W.B. Saunders, pg. 317.
• YOSHIDA, E. (1999) Veterinary Microbiology, Vol. 66, pg. 313-200.
• TIZARD, I. (1998) Journal of American Veterinary Medical Association Vol 213, nº 1,pg 56-57.