Jembrana Disease

Also known as

Jembrana disease virus (JDV)

Description

JDV is a recently identified bovine lentivirus that causes an acute and severe disease in Bali cattle (Bos javanicus). Clinical Jembrana disease was not reported in other types of cattle at first, and this led to a belief that the disease is unique to Bali cattle.

Recent research has showed, however, that other types of cattle are also susceptible. Infection of Friesian (a Bos Taurus breed) and crossbred Bali (Bos javanicus x Bos indicus) cattle showed clinical changes and lesions similar to those seen in Bali cattle, although these signs were milder and might have been difficult to detect under field conditions.

The crossbred cattle experimentally infected had the virus present in their bloodstream for 3 months and developed an antibody response to the virus that persisted for at least 46 weeks after infection.

Jembrana disease produces relatively mild signs in European/British Bos Taurus cattle, but is an acute and severe viral disease in Bali cattle, with a fatality rate of approximately 17%. The first documented outbreak occurred in 1964 in the Jembrana district of Bali, Indonesia. Within two years of its appearance, this disease killed an estimated 26,000 of the approximately 300,000 cattle on Bali Island.

After an incubation period of about 5 to 12 days, clinical signs appear, which include loss of appetite, fever, lethargy, enlargement of lymph nodes, diarrhea, anemia and weight loss. The infection results in an acute inflammatory response, and large erosions of the mucous membranes on the bottom surface of the tongue.

Once the acute stage of disease is past (about 7 days), most cattle recover; if they survive the acute phase of infection and do not contract a secondary bacterial infection, prognosis is often good.

This disease has high morbidity (many animals in a group affected) and moderate mortality; some animals succumb to secondary bacterial infections as a result of the immunosuppressive effects of the virus.

During the acute stage of this disease, the virus can be detected in saliva and milk. There is evidence of direct transmission from acutely affected animals in close contact with susceptible cattle, possibly by virus in body secretions—with transmission via intranasal or oral routes.

The level of infectious virus in the blood is high, so it is likely the virus is also transmitted mechanically by blood-feeding insects or ticks.

Recovered cattle are a potential but probably infrequent source of infection; the virus persists in the bloodstream of recovered cattle but the level of infectious virus in blood decreases greatly by 60 days after recovery from the acute disease, and by then the virus cannot be detected in body secretions.

Signs

• Rapid pulse
• Loss or decrease in appetite
• Bloody diarrhea
• Excessive salivation
• Tongue ulcers
• Fever
• Inability to stand
• Enlarged lymph nodes
• Pale mucous membranes
• Anemia
• Depression
• Lethargy
• Watery eyes
• Decreased milk production
• Nasal discharge

Cause

At least one strain of the Jembrana disease virus has been sequenced. This virus belongs to the genus Lentivirus, which includes immunodeficiency viruses such as HIV. Instead of the chronic disease produced by most lentiviruses, however, Jembrana disease produces acute effects.

Jembrana disease was first described in buffaloes (Bubalus bubalis) and Bali cattle (Bos javanicus) in Bali in 1964 following widespread mortalities. The first reported cases occurred in the Jembrana district of Bali and the disease quickly spread to other districts with a Rinderpest-like pathogen suspected. A second outbreak occurred in 1971-72 in the adjacent Tabanan district with similar clinical signs but buffaloes were not affected.

In 1992 the causative agent was identified with electron microscopy, indicating that it was a retrovirus, a type of virus that inserts a copy of its RNA genome into the DNA of the host cell that it invades, thus changing the genome of that cell.

This new virus has genetic and antigenic similarities with bovine immunodeficiency virus (BIV) and was designated as a member of the lentivirus family; it became known as Jembrana disease virus (JDV) in 1993. It is the most recently discovered member of the lentivirus family.

Despite its close genetic relationship to BIV, the development of JDV infection in Bali cattle is very different to that of BIV in cattle and is unusual for a member of this virus family. Attempts to culture JDV have been mostly unsuccessful, which has hampered research efforts into this unusual lentivirus.

Under experimental conditions the fatality rate for JDV infections ranges from 15 to 17% with death of some cattle occurring during the acute phase. Others succumb days or weeks after recovery, usually because they are unable to handle secondary infections. Cattle that recover from Jembrana disease develop immunity which protects against re-infection for up to 22 months.

The immune responses that develop in cattle that recover appear to control the infection; even though the virus persists in them for at least 25 months, there is no disease progression.

Transmission is likely to occur via blood-sucking insects during the acute stage of disease when viral titers are high. This theory is supported by data indicating that infection occurs after close contact between infected and susceptible cattle, and the incidence of Jembrana disease is greater during the wet season in Bali, consistent with high numbers of biting insects.

Transmission from infected to in-contact cattle under experimental conditions has been clearly demonstrated. Other modes of transmission, such as from dam to fetus or via body fluids (milk, semen or saliva) have not been investigated fully, but there is evidence that during the acute phase of infection, JDV is shed into milk from infected cattle, and intranasal, conjunctival and oral infection routes have been experimentally successful.

One of the most likely methods of the spread is by inoculation of cattle with shared needles during vaccination.

Jembrana disease is difficult to differentially diagnose based on clinical signs alone, since the disease is often complicated by secondary bacterial infections. Definitive diagnosis must be confirmed using laboratory tests.

Prevention

The disease can be prevented with an inactivated tissue-derived vaccine prepared from the spleen of an acutely infected animal and mixed with a mineral oil adjuvant. The spread of Jembrana disease is currently controlled by ring vaccination of cattle in outbreak areas.

This entails vaccinating and monitoring all animals around each outbreak area—the ones most likely to be infected next--to form a buffer of immune animals.

Two doses of vaccine are given, with a four-week interval between them. Initial vaccine efficacy trials indicated that the vaccine did not prevent Jembrana disease but reduced the clinical signs of disease. A more recent study in 2009 revealed a reduction in total viral load in vaccinated cattle compared to control animals. Vaccination reduced the average number of infectious days by 33% compared to the control group.

The most significant benefits of vaccination appear after the peak viremia; vaccinated cattle were able to get rid of the circulating virus much faster than the controls.

Treatment

Treatment of secondary infections is the only available treatment method at present.