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 casues 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 occular 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 facsiculations, 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), occular erosions, enlarged distended bladder and constipation/reduction in faces or diarrhoea.
Sows In sows the disease causess infertility, reproductive failures, embryonic mortality and return tooestrus in the first third of gestation and stillbirths, small litters and mummification in late gestation.
Boar In the boar it casues male infertility, lack of libido, haemospermia, and orchitis with epidydimitis and swelling of the genitals.
Epidemiology
The disease is self limited 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 it's 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 it's 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 haemagglutination 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 aswell 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. Medication should be used to control the secondary and associated diseases, which are usually respiratory diseases.
Control
There is not an approved vaccine for the control of blue eye disease. An experimental killed-virus vaccine was shown to be effective in preventing or minimising the clinical signs (Stephano et al., 1992). Preventative health programmes that prevent the entrance of the disease are the most effective method of control. Eliminating blue eye disease from affected herds has been achieved with management practices such as closing the herd to the entrance of new susceptible animals, all-in/all-out systems, washing and disinfecting. The disease appears to be self-limiting if properly managed.
References
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