Blue Eye Disease

Also known as: Blue-eye—BE—Blue eye syndrome—Porcine paramyxovirus blue eye disease—PPBED.

Introduction

Blue eye disease is caused by the virus Blue-eye paramyxovirus (BEP). It causes nervous, reproductive and respiratory signs in its domestic host, the pig. The disease is not considered a zoonosis.

Signalment

The disease affects all age ranges of pigs and also causes reproductive disorder in the boar.

Clinical Signs

Generally pigs suffer from anorexia, weight loss, reluctance to move, dehydration, periorbital and conjunctival swelling (chemosis) and purulent/serous ocular discharge and corneal opacity. The virus also causes neurological signs including tetraparesis, opisthotonus, dysmetria, proprioceptive disorders, tremors, nystagmus mydriasis, blindness, decreased or absent menace response and respiratory signs; tachypnea, dyspnea, and open mouthed breathing.

In addition the virus affects different age group and sexes in the following ways:

Piglets and Weaners:

Piglet and weaners suffer from prostration, hind limb stiffness, generalised weakness, muscle fasciculation’s, retarded growth, depression, excitation, head pressing, circling, hyperaesthesia, abnormal behaviour/aggression and coma. In piglets the disease also causes changes in hair coat (dull/rough), ocular erosions, enlarged distended bladder and constipation/reduction in faces or diarrhoea.

Sows:

In sows the disease causes infertility, reproductive failures, embryonic mortality and return to oestrus in the first third of gestation and stillbirths, small litters and mummification in late gestation.

Boars:

In the boar it causes male infertility, lack of libido, haemospermia, and orchitis with epidydimitis and swelling of the genitals.

Epidemiology

The disease is self limiting and closed herds will have sporadic outbreaks of the disease once a herd is infected. The virus can be found in the axon of neurons from its original site of replication, which is thought to be the nasal mucosa and tonsils. It is also found in tissues such as lung, liver, spleen, kidney, lymph node, heart and testis; suggesting that the virus is spread hematogenously.

Distribution

The disease is economically important to Central Mexico and its states.

Diagnosis

Blue-eyed disease can be diagnosed by a combination of history, above clinical signs, serology, lesions and virus isolation.

A week after infection a serological response can be seen using a virus neutralization test and 2 weeks later with a haematoglutination inhibition test.

The diagnosis can be confirmed using virus isolation on PK15 or primary pig kidney, using samples from infected tonsils, brain or lung.

During infection lymphocytosis and monocytosis may be observed.

On post mortem all age ranges have corneal opacity which is mainly unilateral. Piglets show evidence of mild pneumonia, distended bladder and stomach, fibrin strands in the peritoneal cavity and congestion in the brain. Growers show kidney and pericardial haemorrhages as well as brain congestion. Necrosis of the seminiferous tubules and rupture of the epidydimis walls and subsequent abscess and granuloma formation has been documented in boars.

Differential diagnosis:PRRS and Pseudorabies.

Treatment

There is no treatment for Blue eye disease. Supportive medication for respiratory and inflammatory disease should be administered.

Control

There is no approved vaccine for the control of blue eye disease but killed-virus vaccine has been shown to be effective . Preventative health programmes to prevent the spread of the disease are the most effective methods of control. Eliminating blue eye disease from affected herds can be achieved by closing the herd, running an all-in/all-out systems, and following good washing and disinfecting protocols.

References

Blue Eye Disease Learning Resources
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