By: Rahayu Carlis Savitri
Student at Faculty of Veterinary Medicine, Airlangga University
Jembrana Disease or Jembrana disease virus (JDV) first emerged in the Sankaragung area of Bali, Indonesia in December 1964. The name Jembrana comes from the name of the village that first experienced the infection (Adiwinata, 1967). This disease is caused by acute infection with Lentivirus, a member of the Retroviridae family (Kusumawati et al., 2014a). The Jembrana virus is an RNA virus with a single strand, icosahedral in shape, with a base length of 7732 base pairs (bp), and is pathogenic only to Bali cattle (Kertayadnya et al., 1993). Common symptoms of animals affected by Jembrana disease include high fever, lymphadenopathy, lymphopenia, bloody sweat and excessive mucus in the mouth and nose. Death of animals due to JDV occurs 1 to 2 weeks after infection (Wilcox et al., 1997).
The susceptibility of Bali cattle to JDV is often attributed to genetics. However, it's unclear which part of the gene is involved, similar to how the influenza virus in rats is influenced by specific alleles of its genome (Berata, 2015). Jembrana Disease Virus (JDV) doesn't exhibit the typical characteristics of Lentiviruses, which usually cause chronic diseases with long incubation periods. Although it's acute with a short incubation period, several factors precede this. Firstly, in acute cases, there are often lymphoproliferative changes similar to lymphotropic Lentivirus diseases like HIV. Secondly, the disease resembles Simian Immunodeficiency Virus in pig-tailed macaques (SIVSMMPB), with a short incubation period leading to severe lymphopenia followed by rapid lymphoproliferation predominantly involving young lymphocytes (lymphoblasts) in parafollicular lymph nodes, spleen, and primarily in the intestinal lymphoid tissues (Wilcox, 1997).
The biological characteristics of the Jembrana disease virus are as follows:
Student at Faculty of Veterinary Medicine, Airlangga University
Jembrana Disease or Jembrana disease virus (JDV) first emerged in the Sankaragung area of Bali, Indonesia in December 1964. The name Jembrana comes from the name of the village that first experienced the infection (Adiwinata, 1967). This disease is caused by acute infection with Lentivirus, a member of the Retroviridae family (Kusumawati et al., 2014a). The Jembrana virus is an RNA virus with a single strand, icosahedral in shape, with a base length of 7732 base pairs (bp), and is pathogenic only to Bali cattle (Kertayadnya et al., 1993). Common symptoms of animals affected by Jembrana disease include high fever, lymphadenopathy, lymphopenia, bloody sweat and excessive mucus in the mouth and nose. Death of animals due to JDV occurs 1 to 2 weeks after infection (Wilcox et al., 1997).
The susceptibility of Bali cattle to JDV is often attributed to genetics. However, it's unclear which part of the gene is involved, similar to how the influenza virus in rats is influenced by specific alleles of its genome (Berata, 2015). Jembrana Disease Virus (JDV) doesn't exhibit the typical characteristics of Lentiviruses, which usually cause chronic diseases with long incubation periods. Although it's acute with a short incubation period, several factors precede this. Firstly, in acute cases, there are often lymphoproliferative changes similar to lymphotropic Lentivirus diseases like HIV. Secondly, the disease resembles Simian Immunodeficiency Virus in pig-tailed macaques (SIVSMMPB), with a short incubation period leading to severe lymphopenia followed by rapid lymphoproliferation predominantly involving young lymphocytes (lymphoblasts) in parafollicular lymph nodes, spleen, and primarily in the intestinal lymphoid tissues (Wilcox, 1997).
The biological characteristics of the Jembrana disease virus are as follows:
- Short incubation period of about 5-7 days and only affects Bali cattle.
- Resistant to antibiotics.
- Difficult to grow in tissue culture and not resistant to ether.
- Difficult to grow in small animal experiments and doesn't kill mice.
- Possesses reverse transcriptase enzyme.
- Contains various types of proteins such as p100, p45, p33, p16, and major protein p26, which cross-react with antigens and antibodies of bovine immunodeficiency virus (BIV) (Wilcox, 1997).
- Induces temporary immunodeficiency marked by decreased immune response for 2-4 months, decreased CD4/CD8 cell ratio, disappearance of antibody-producing cells, splenomegaly, and death due to secondary infections.
- The Jembrana virus can persist in the blood and tissues of infected animals for a significant period (Berata, 2015).
Detection of Jembrana disease can be done by collecting samples from body secretions of infected animals, including saliva, urine, milk, and semen. Serological tests with enzyme-linked immunosorbent assay (ELISA) are also used for confirmation. The routes of Jembrana virus infection are oral, intranasal, and conjunctival. Detection of Jembrana virus in infected cattle usually occurs around 14 days post-infection, based on observable clinical symptoms. Clinical diagnosis of Jembrana disease is confirmed through necropsy of affected animals and detection of histopathological lesions (Soeharsono, 1995).
High fever, sometimes reaching 42°C, is an early clinical symptom of Jembrana disease. This symptom persists for 5-12 days (average 7 days). Experimental incubation periods of the disease vary between 4-12 days. Swelling of lymph glands is seen in the prescapular, prefemoral, and parotid lymph glands. Diarrhea, often with bloody stools, occurs a few days after the fever starts. In acute cases, especially during the initial outbreak, sudden death can occur. Death can also happen relatively quickly in animals that are still in good condition. Other symptoms include hypersalivation, clear nasal discharge, erosions on oral mucosa and beneath the tongue, blood spots on the skin ("bloody sweat"), and pallor of mucous membranes in the mouth, eyes, and genitalia (Dharma et al., 1992). Consistent and prominent blood changes include leukopenia and lymphopenia (Soesanto et al., 1990). Additionally, thrombocytopenia, eosinopenia, neutropenia, and anemia can occur (Wilcox, 1997). Blood urea levels increase, and plasma protein levels decrease (Soesanto et al., 1990).
There is no specific treatment or prevention for Jembrana disease due to its viral origin. However, vaccination can be done using antigens from animals that have recovered from JDV. The serum containing antigens is induced in other animals to enhance their antibody production and immunity. Attempts to find an effective antigen for JDV vaccination have faced difficulties, as the virus only suppresses the duration and severity of the disease to a certain extent (METHAROM et al., 2001).
References
Kusumawati, A., T.A. Wanahari, R.F. Putri, B.A. Mappakaya and I.D. Tampubolon, 2014a. The structure and function of Jembrana disease virus genome. J. Inf. Mol. Biol. Sci., 2: 26-9. DOI: 10.14737/jimb.2307-5465/2.2.26.29
Kertayadnya G, GE Wilcox, S Soeharsono, N Hartaningsih, RJ Coelen, RD Cook and J Brownlie. 1993. Characteristics of a retrovirus associated with Jembrana disease in Bali Cattle. Journal of Genetics Virology 74, 1765-1773.
Wilcox, G.E. 1997. Jembrana Disease. Australian Veterinary Journal. Vol.75.p.492-497.file A:\Jembrana 2htm.
Berata, I Ketut. 2015. Penyakit Jembrana Musuh Utama Sapi Bali. Laboratorium Patologi FKH Unud; Workshop Binapoktan Udayana, 26 Nop.2015
Adiwinata, T. (1967). Some informative notes on a rinderpest-like disease on the island of Bali. In OIE- FAO Conference on Epizootics in Asia and the Far-East. Tokyo, 2-9 Oct 1967.
Soeharsono, S., G. E. Wilcox, A. A. Putra, N. Hartaningsih, K. Sulistyana And M. Tenaya. 1995. The transmission of Jembrana disease, a lentivirus disease of Bos javanicus cattle. School of Veterinary Studies, Murdoch University, Murdoch WA 6150, Australia. 368-369 html.
Soesanto, M., Soeharsono, S., A.Budiantono, A., Sulistyana, K., .Tenaya, W.M., and Wilcox, G.E. 1990. Studies on Experimental Jembrana Disease in Bali Cattle. II.Clinical Signs and Haematological Changes. J.of.Comp.Pathol. 103 :p.60-69
Dharma, D.M.N. 1992. Studies on the Pathology of Jembrana Disease. Thesis. Graduate School of Tropical Veterinary Science and Agriculture, James Cook University of North Queensland.
Metharom, P., Takyar, S., Xia, H.Q., Ellem, K.A.O., Wilcox, G.E., And Wei, M.Q. 2001. Development of disabled, replicationdefective gene transfer vectors from the Jembrana disease virus, a new infectious agent of cattle. Veterinary Microbiology, 80, 22-43.
High fever, sometimes reaching 42°C, is an early clinical symptom of Jembrana disease. This symptom persists for 5-12 days (average 7 days). Experimental incubation periods of the disease vary between 4-12 days. Swelling of lymph glands is seen in the prescapular, prefemoral, and parotid lymph glands. Diarrhea, often with bloody stools, occurs a few days after the fever starts. In acute cases, especially during the initial outbreak, sudden death can occur. Death can also happen relatively quickly in animals that are still in good condition. Other symptoms include hypersalivation, clear nasal discharge, erosions on oral mucosa and beneath the tongue, blood spots on the skin ("bloody sweat"), and pallor of mucous membranes in the mouth, eyes, and genitalia (Dharma et al., 1992). Consistent and prominent blood changes include leukopenia and lymphopenia (Soesanto et al., 1990). Additionally, thrombocytopenia, eosinopenia, neutropenia, and anemia can occur (Wilcox, 1997). Blood urea levels increase, and plasma protein levels decrease (Soesanto et al., 1990).
There is no specific treatment or prevention for Jembrana disease due to its viral origin. However, vaccination can be done using antigens from animals that have recovered from JDV. The serum containing antigens is induced in other animals to enhance their antibody production and immunity. Attempts to find an effective antigen for JDV vaccination have faced difficulties, as the virus only suppresses the duration and severity of the disease to a certain extent (METHAROM et al., 2001).
References
Kusumawati, A., T.A. Wanahari, R.F. Putri, B.A. Mappakaya and I.D. Tampubolon, 2014a. The structure and function of Jembrana disease virus genome. J. Inf. Mol. Biol. Sci., 2: 26-9. DOI: 10.14737/jimb.2307-5465/2.2.26.29
Kertayadnya G, GE Wilcox, S Soeharsono, N Hartaningsih, RJ Coelen, RD Cook and J Brownlie. 1993. Characteristics of a retrovirus associated with Jembrana disease in Bali Cattle. Journal of Genetics Virology 74, 1765-1773.
Wilcox, G.E. 1997. Jembrana Disease. Australian Veterinary Journal. Vol.75.p.492-497.file A:\Jembrana 2htm.
Berata, I Ketut. 2015. Penyakit Jembrana Musuh Utama Sapi Bali. Laboratorium Patologi FKH Unud; Workshop Binapoktan Udayana, 26 Nop.2015
Adiwinata, T. (1967). Some informative notes on a rinderpest-like disease on the island of Bali. In OIE- FAO Conference on Epizootics in Asia and the Far-East. Tokyo, 2-9 Oct 1967.
Soeharsono, S., G. E. Wilcox, A. A. Putra, N. Hartaningsih, K. Sulistyana And M. Tenaya. 1995. The transmission of Jembrana disease, a lentivirus disease of Bos javanicus cattle. School of Veterinary Studies, Murdoch University, Murdoch WA 6150, Australia. 368-369 html.
Soesanto, M., Soeharsono, S., A.Budiantono, A., Sulistyana, K., .Tenaya, W.M., and Wilcox, G.E. 1990. Studies on Experimental Jembrana Disease in Bali Cattle. II.Clinical Signs and Haematological Changes. J.of.Comp.Pathol. 103 :p.60-69
Dharma, D.M.N. 1992. Studies on the Pathology of Jembrana Disease. Thesis. Graduate School of Tropical Veterinary Science and Agriculture, James Cook University of North Queensland.
Metharom, P., Takyar, S., Xia, H.Q., Ellem, K.A.O., Wilcox, G.E., And Wei, M.Q. 2001. Development of disabled, replicationdefective gene transfer vectors from the Jembrana disease virus, a new infectious agent of cattle. Veterinary Microbiology, 80, 22-43.