Age affected: All ages, human risk.
Causes: Porcine cytomegalovirus (PCMv); poor ventilation.
Effects: Mostly no signs, inappetence, sneezing, fever, infertility, small litters, stillbirth, mummies.
Inclusion body rhinitis is caused by an enveloped cytomegalovirus (herpes virus) which can only be cultured with difficulty and which is most easily isolated by the culture of alveolar macrophages from 3-5 week old pigs. It can be cultivated in vitro in these or porcine testis or fallopian tube cell lines. In alveolar macrophage cultures infected cells enlarge and form basophilic intranuclear inclusions which may be demonstrated by immunofluorescence of Giemsa stain. Isolates appear to belong to one antigenic type, although serological differences have been found amongst recent isolates. Replication of the virus takes place in the nasal mucous glands in non-immune piglets following oronasal infection, in white blood cells (neutrophils) in the blood 14-16 days after infection and finally in epithelial sites such as the nasal mucosa, testicular cells and kidney tubules at 3 weeks of age. Virus may cross the placenta and infect the foetus during the viraemic stage at 14-21 days after infection in non-immune sows. Embryonic death occurs in early gestation. Foetuses exposed late in gestation are born seronegative. Boars can excrete virus in urine and nasal secretions. Serum antibody responses develop but low levels of antibody may not prevent infection of the products of conception.
PCMv is transmitted transplacentally, but is usually transmitted by direct contact between pigs, by aerosol and by contact with fresh urine from infected pigs. Peak virus shedding in a herd with enzootic infection is between 3 and 6 weeks of age. Infection may occur even up to slaughter weight and may be re-activated by stress in carrier pigs. Transmission between farms is normally by the introduction of carrier or affected pigs.
Few clinical signs other than inappetence and fever occur pigs of more than 3 weeks of age in herds where the infection in enzootic. Where individual sows or whole herds are non-immune, pigs may be infected in utero or within 2 weeks birth and may develop rhinitis, sneezing and respiratory distress. Mortality in an affected litter may reach 25%. Piglets may be born dead, die without clinical signs or be pale, anaemic and oedematous in the generalised form of the disease. A reduction in growth rate frequently occurs. Disease may occur in recently-weaned pigs and be associated with inappetence, respiratory distress, conjunctivitis and copious nasal exudate. Severe disease in adults has been recorded when infection enters non-immune herds. Inappetence, fever, coughing and serous, purulent and haemorrhagic nasal discharge have been recorded. Stillbirths and mummified foetuses may result and there may be an increase in returns to service and of small litters.
Inclusion body rhinitis is usually suspected when piglets within 2 weeks of birth develop rhinitis, sneezing and respiratory distress. Mortality in an affected litter may reach 25%. Piglets may be born dead, die without clinical signs or be pale anaemic and oedematous in the generalised form of the disease. Serum antibody can be detected by indirect immunofluorescence or ELISA tests. The clinical signs must be distinguished from those of Bordetella infection and progressive atrophic rhinitis in piglets. Viral isolation can be carried out but with difficulty.
Gross lesions are rarely visible in animals with localised upper respiratory tract infection, but may appear as severe nasal congestion (reddening) of the nasal septum with adherent sticky mucus. Microscopical examination reveals enlarged cells (cytomegaly) with basophilic intranuclear inclusion in cells of the nasal mucous glands and other epithelial sites such as duodenum and renal tubules and may confirm the diagnosis. Generalised lesions in young pigs and foetuses may be seen in the lung where pulmonary oedema occurs, and serous effusions and widespread haemorrhages may be seen, particularly in the kidneys. Growth arrests may be present in the long bones. In field outbreaks, lesions may sometimes be complicated by other agents.
There is no treatment. Secondary infection can be controlled e.g. using parenteral antimicrobial. Where severe infection occurs, neonatal piglets should not be exposed to it. Isolation from infection during the period of major risk (3 to 8 weeks of age) may help reduce clinical signs. Stress and mixing should be avoided in older carrier pigs to reduce recurrence in that age group. The use of all-in, all-out housing systems will reduce the extent of the disease in a herd. As virus can cross the placenta, it can therefore occur in hysterectomy-derived herds. Disease-free herds can be founded if the piglets produced are held isolated and screened serologically for 70 days after birth. Herds free from infection should be isolated as the introduction of carrier pigs is the source of infection.