Primary viral replication in the nasal mucous glands or the lacrimal or harderian gland is followed by viremia. The site of follow-on viral replication depends on the age of the animal. At an age of 3 weeks or more, when most animals experience infection, the virus disseminates to epithelial sites, particularly the glands of the nasal mucosa, harderian and lacrimal glands, renal tubules, and more rarely the epididymis and mucous glands of the esophagus, hepatocytes, and duodenal epithelium. Recovery of virus from pulmonary macrophages of quiescent pigs indicates that the macrophage is a reservoir of infection. Gross pathologic changes in the nasal passages consist of serous rhinitis with acute congestion of the conchal epithelium in the early stages, progressing to catarrhal or even purulent exudate depending on the type and severity of secondary bacterial infection.
Anemia often occurs.
Generalized disease with more extensive and severe lesions is occasionally seen, usually in pigs born alive with congenital infection, but occasionally in older pigs exposed to the virus for the first time. Gross lesions in these pigs include widespread petechiae and edema, including pulmonary edema and congestion, hydrothorax and hydropericardium, multiple firm foci in the ventral lungs, and edema of the throat and tarsal joints. Petechial hemorrhages are seen on the heart, lungs, intestine and particularly the kidneys. The large basophilic intranuclear inclusion bodies, when correlated with appropriate signs, are diagnostic for inclusion body rhinitis. The lesions associated with inclusion body rhinitis with a secondary bacterial infection could mimic the early changes associated with atrophic rhinitis.