Blue eye disease (BED) is the common name for a disease caused by a porcine rubulavirus (Paramyxoviridae; La Piedad Michoacan virus) that is characterized in nursing or growing pigs by central nervous system (CNS) signs and, frequently, by corneal opacities. Signs in sows and boars include various forms of reproductive failure and corneal opacity.
Blue eye disease is only known to occur in swine. In Mexico, the only country that has reported cases, BED occurs throughout the year but is more common in the hotter, drier months (March to July). Swine diseases caused by other paramyxoviruses have occurred in several countries (Japan, Israel, Canada, United States, and Australia) but the diseases they cause are sporadic, rare, and are distinctly different from BED manifesting as transient outbreaks of pneumonia, encephalitis, or reproductive disease.
Blue eye disease first occurred in 1980 in a large swine raising operation in central Mexico. Within a short time it had spread to eleven other states or districts and had become economically important. The first outbreaks occurred mainly in unweaned piglets less than 30 days old, frequently in piglets less than two weeks old. After 1983, severe outbreaks occurred in larger pigs (33-99 lb). Signs of reproductive failure were also observed in mature sows and boars. The scarcity of reports since 1990 suggest BED is less common now.
The agent that causes BED is a paramyxovirus. It grows in chick embryos and hemagglutinates erythrocytes of mammalian and avian origin. It grows and causes cytopathic effect in PK-15 and several other cell culture systems. It stimulates formation of inclusion bodies in PK-15 cells. Formalin destroys infectivity of the virus.
Antisera against seven paramyxoviruses and six parainfluenza viruses do not affect infectivity of the BED virus. This suggests BED virus differs from other paramyxoviruses and causes a unique disease in swine. Other paramyxoviruses are infrequent causes of swine pneumonia and encephalitis.
Subclinically infected pigs are the main reservoir of virus. Virus can also be disseminated by people and vehicles. On farms with a continuous production system, virus persists and is maintained in new groups of susceptible young pigs while adult stock remains well. The disease is largely self-limiting in closed herds. Infected animals develop protective antibodies that usually persist throughout their lifetime.
Natural infection is thought to occur by inhalation based on experimental exposures where intratracheal and intranasal exposure reproduced the disease. The initial site of viral replication is unknown but may be in the nasal mucosa or tonsils. Virus soon spreads to the brain, lung and many other organs, suggesting that viremia occurs. Reproductive problems in dams suggest that the virus crosses the placenta and infects the fetuses.
Corneal opacities (blue eye) sometimes occur late in the course of the disease. The opacities disappear spontaneously, presumably as inflammatory edema resolves. The opacities are, perhaps, the result of an immunologic reaction accompanied by inflammation. Virus may replicate in the eyes since inclusion bodies have been demonstrated there.
Signs vary somewhat with the age groups affected but are mainly those of encephalomyelitis in both young and growing pigs. In young piglets, onset is sudden with prostration and fever. Other signs include ataxia, weakness, muscle tremors, rigidity, nystagmus, abnormal postures, hyperexcitability, squealing, and paddling movements; occasionally there is blindness. Often there is conjunctivitis with adherence of the eyelids. Corneal opacity (blue eye) may occur in 1-10% of young piglets and may be seen in the absence of other signs. Twenty to 65% of litters can be affected. Morbidity within litters is between 20-50%; mortality in affected pigs can reach 90%. Piglets affected early in an outbreak often die within 48 hours; those affected later usually die after a course of four to six days. Mortality occurs over a two to nine week -period.
In pigs greater than 30 days old, signs are more moderate and transient. They include fever, sneezing, coughing and anorexia. CNS signs include listlessness, ataxia and circling. Less than 5% of the pigs are affected and mortality usually is low. However, in pigs weighing 35 to 45 lb, outbreaks with 20% mortality and up to 30% corneal opacity have occurred. Adult animals occasionally develop corneal opacities.
In pregnant swine, returns to estrus may occur and persist in the herd for six to eight months. There also is an increase in stillbirths and mummified fetuses, and occasional abortions. In affected boars, there is a reduction in fertility and an increase in testicular size, usually unilateral, followed by atrophy.
Gross lesions are limited and largely nonspecific. They may include mild anteroventral pneumonia, tonsillitis and mild ascites with some fibrin. Brain congestion and an increase in cerebrospinal fluid may be present. There is conjunctivitis and, perhaps, corneal opacity in one or both eyes. Pericardial and renal hemorrhages also have been reported. In affected boars there is orchitis, epididymitis and testicular atrophy.
Microscopic lesions include a nonsuppurative encephalomyelitis affecting mainly the gray matter of the midbrain, thalamus and cerebral cortex. Intracytoplasmic inclusions in neurons have been reported. Affected eyes have corneal edema and anterior uveitis, perhaps with exudate in the anterior chamber. Intracytoplasmic inclusions may be present in epithelial cells near the drainage angle of the corneoscleral junction.
Clinical signs of encephalomyelitis, along with corneal opacity, suggest a diagnosis of BED. Reproductive problems in either or both sexes, along with numerous corneal opacities, are also suggestive. Microscopic lesions of encephalomyelitis and the presence of intracytoplasmic inclusion bodies in neurons or eyes strongly suggest BED.
The hemagglutinating virus usually can be isolated from the brain or tonsil in PK-15 cells and can be identified by hemagglutination inhibition (HI), virus neutralization (VN) or enzyme-linked immunosorbent assay (ELISA). The HI test is widely used. Direct immunofluorescence has been used to identify the virus in cell culture. BED must be differentiated from other causes of CNS disease, especially pseudorabies.
A rigorous health control program to prevent introduction of virus is the best preventive measure. Maintaining a closed herd and use of the all in/all out system of production may be helpful. Essential replacement stock should be added only after negative serologic tests and a period of quarantine. Commercial vaccines have been produced but there is no report on their efficacy.
BED has been eliminated from infected sites by disposing of infected animals, cleaning and disinfecting the site and using sentinel pigs to confirm elimination of infection. There is no satisfactory treatment of BED and pigs with CNS signs usually die. Pigs having only corneal opacities frequently recover without treatment.