environmental in China. Chhetri et al. 2010 identified the factors that associated with spatial clustering of foot-and-mouth disease in Nepal.
Disease mapping and spatial analysis to explore the nature of such spatial distributions has been widely used in risk modeling to identify high-risk areas or
geographically – related risk areas. An objective of such efforts is to identify high risk areas that could subsequently be targeted for control, eradication, and
prevention action Chhetri et al. 2010. Spatial analysis deals with the exploration, description and analysis of data taking into account their geographical distribution
Saez and Saurina 2007 in Allepuz 2008. Spatial analysis involves the analysis of data representing geographical
features which have a location attribute such as absolute location coordinates or relative positioning distance. Disease occurrence produces a spatial point pattern
where each point pattern could be the result of infectiousness or environmental factors. The objectives of spatial analysis are to identify areas of locally increased
risk and of factors resulting in spatial interaction which cause, for example increased transmission probabilities Pfeiffer and Morris 1994.
In Indonesia, studies on the epidemiology of animal disease rarely consider the spatial dimension of disease prevalence. This study presents a study
combining surveillance, laboratory diagnostic method, and GIS for spatial analysis of JD pattern to better understand its epidemiology. This study would
help in developing detection, surveillance, and control strategies of JD in South Kalimantan province, and supporting the local government to conduct the JD
eradication program.
1.2 Objective
The main objective of this study is to conduct a spatial analysis of JD in South Kalimantan Province. This study presents a spatial distribution of JD,
identify the JD cluster, generate JD mapping, and identifying factors associated with the spatial distribution of JD in South Kalimantan Province.
II. LITERATURE REVIEW
2.1 Jembrana Disease
Jembrana Disease JD also known as Ramadewa disease is an acute and severe disease of Bali cattle and endemic in parts of Indonesia Setiyaningsih
2006. The first epidemic was occurred in 1964 at Jembrana District, Bali province. It was estimated to have killed at least 30,000 head of cattle from the
total approximately 300,000 head of Bali cattle. A few years later, it is regarded as endemic throughout the island of Bali, South Sumatera, Lampung, Bengkulu,
West Sumatera, and South Kalimantan Subronto 2003. JD was reported to affect Bali cattle Bos javanicus syn Bos sondaicus and buffaloes Bubalis bubalis, but
only Bali cattle were reported in the later outbreaks in Bali and elsewhere in Indonesia. The disease was diagnosed firstly as a rinderpest–like disease and
subsequently name jembrana disease Soeharsono and Temadja 1996. JD is caused by Jembrana Disease Virus JDV. JDV is a lentivirus
belonging to the Retroviridae family of viruses Burkala et al. 1996. JDV is arranged by several major proteins with approximately molecule weight 45kD,
42kD, 33kD, 26kD, and 16kD consistently. Minor protein sometime found with molecule weight 100kD and 15kD Wilcox et al. 1993. JDV is filterable, the
estimated particle size being 100 – 200 nm. It is inactivated after exposure to 55°C for 15 minutes and to extremes of pH 3.0 and 11.2. JDV is resistant to the
action of sodium deoxycholate 1:1000, diethyl ether, and range of antibiotics. It LV UHDGLO\ LQDFWLYDWHG E\ IRUPDOGHK\GH DQG ȕ-propiolactone. Infectivity in meat
persisted up to 36 hours at 22 - 25°C and for 72 hours at approximate 4°C. JDV stored well for several months at –7°C Ramachandran 1996.
The acute disease associated with JDV infection has a short incubation period of 5 to 12 days and duration of about 7 days, during which affected animals
show signs of fever, lymphadenopathy and lymphopenia Soesanto et al. 1990. The disease is atypical of many lentivirus infections. It produces an acute clinical
disease persisting for up to 12 days, after a short incubation period of less than 12 days Soeharsono et al. 1995
a
. During the acute disease the titer of infectious
virus in blood is high and can be detected in saliva and milk Soeharsono et al. 1995
b
. Animal that infected with JD suffering fever, approximately 40 - 42°C,
followed by fatigue, anorexia, lacrymation, hyper salivation, and secretion of mucous. Infected animal also show the enlargement of the superficial lymph node
especially prescapularis lymph node, prefemoralis lymph node, and parotidea lymph node. About 23 of infected animals indicate hemorrhaging and erosion of
mucosa at nasal, tongue, and mouth. The clinical patognomonis of JD is blood sweating which appear during fever and occur for 2-3 days Subronto 2003.
Another sign is enlargement of spleen. Abortion was recorded in 49 of pregnant cows affected with JD. Abortion occurred at all stages of pregnancy Putra et al.
1983. Figure 1 shows the clinical signs of JD in Bali cattle.
a b
c d
Figure 1. The Clinical Sign of JD in Bali cattle: a enlargement of the superficial
lymph node, b blood sweating, c enlargement of spleen, and d erosion at tongue personal documentation.
Consistent clinical signs include fever, lethargy and lymphodenopathy. Haematological changes during the acute phase include elevated blood urea
concentrations, decreased plasma protein, leucopenia mainly due to a lymphopenia, eosinopenia, and thrombocytopenia Soesanto et al. 1990. The
mortality rate in the experimentally infected cattle was 17 Soeharsono et al. 1996
a
. The mechanism of transmission of JD is poorly understood. There is
evidence of direct transmission from acutely affected animals in close contact with susceptible cattle, possibly by virus in these secretions infecting cattle by
conjunctival, intranasal or oral routes. During the acute disease the titer of infectious virus in blood is high and can be detected in saliva and milk. It is
probable that the virus is also transmitted mechanically by Haematophagous arthropods Soeharsono et al. 1995
b
. The blood sucking insect could transmit JDV from infected animal during fever to susceptible animal Putra and
Sulistyana 1995. Recovered cattle are also a potential source of infection. Recovered cattle are persistently viraemic but the titre of infectious virus in blood
by 60 days after recovery from the acute disease is only about 10
1
IDml Soeharsono et al. 1996
b
. Commonly, JD can be diagnosed by enzyme-linked immunosorbent assay
ELISA and Western Blotting WB to detect the JD antibody. Antibody was not detected by ELISA in majority of infected cattle until 11 weeks after infection and
a maximum antibody response was detected 23 to 33 weeks after infection. Antibody was still detectable 59 weeks after infection Hartaningsih et al. 1994.
Another technique is polymerase chain reaction PCR that can be used to confirm both field and laboratory diagnosis of JD in Bali cattle Tenaya and Hartaningsih
2005.
2.2 Spatial Analysis using Geographic Information System
