Kyasanur Forest Disease
Kyasanur Forest Disease (KFD), also referred to as monkey fever is an infectious bleeding disease in monkey and human caused by a highly pathogenic virus called KFD virus (KFDV). KFDV is of zoonotic origin (originating from animals) and it is transmitted primarily by infective tick, Haemaphysalis spinigera. Rodents, shrews, monkeys and birds upon tick bite become reservoir for this virus. KFDV's common targets among monkeys are langur (Semnopithecus entellus, earlier classified Presbytis entellus) and bonnet monkey (Macaca radiata). A high number of these monkeys' death was seen in the Kyasanur Forest region of Shimoga District of Karnataka State in southern India in 1955. The first epidemic season of KFD in human was observed in Jan - May, 1956 when four villages were affected. In 1957, KFD spread to more than 20 villages and by 2003 it had affected more than 70 villages in four districts adjacent to Shimoga in western Karnataka.
![]() Figure 1. Distribution of KFD in the state of Karnataka in India. Image is modified from ICMR
publication*.
H. spinigera tick is widely distributed in tropical forests of peninsular India and Sri Lanka. In 1957 KFDV was isolated from this tick, the primary vector, and later in sixteen other tick species as well. Apart from ticks, KFDV has also been isolated from certain species of mammals including human. Virulence of KFDV became obvious when numerous infections were reported in laboratory and field personnel who were directly dealing with KFD outbreak. This led to suspension of work with KFDV until an appropriate Biosafety Level-3 laboratory (the level of the biocontainment precautions required to handle pathogens in an enclosed facility) was built at the National Institute of Virology in Pune, India in 2004. However, KFDV is ranked as a high risk category pathogen requiring Biosafety Level-4 handling. This virus belongs to the family of Flaviviridae and is about 45 nm in diameter, enveloped spherical virion particle, and the genome is made of single-stranded, positive sense RNA. Figure 2. Life cycle of KFDV vector tick, Haemaphysalis spinigera. Image
is modified from ICMR publication*.
Deforestation, subsequent cattle grazing in those areas and the low susceptibility of cattle for KFDV lead to conclude cattle being large mammal reservoir for vector maintenance and propagation. It has been observed that around 50% of those affected by KFD were cattle tenders. However, KFD is not directly transmitted by human-human contact. Clinically, KFD symptoms at onset in human are sudden chills, high fever, frontal headache, heightened sensitivity to light, followed by continuous fever for 12 days or longer often associated with diarrhea, vomiting, cough, severe pain in the neck, low back and extremities, accompanied by severe prostration. Papulo-vesicular eruption on the soft palate (blisters on the upper, inner mouth) is an important diagnostic sign in some patients. Bleeding signs such as in the gum, nose (epistasis), cough (hemoptysis), gastrointestinal bleeding resulting in dark feces (melena), fresh blood in the stools are common. The convalescent phase constituting the recovery after KFD's onset is generally prolonged, maybe up to 4 weeks. Relapse of the symptoms, often observed after 1 to 2 weeks of the first febrile period, last for 2 to12 days. The relapse phase displays same symptoms as the first phase and in addition symptoms such as mental disturbance, giddiness and reflex abnormality are often seen. Leucopenia (reduction in the number of white blood cells) and accompanying thrombocytopenia (reduction in the number of blood platelets) are constant hematological features in KFD. Intraalveolar haemorrhage (oozing of blood into the lungs), resulting secondary infection and massive gastrointestinal haemorrhage are terminal complications that could lead to death. Diagnosis
is primarily syndromic and serological. Being a very stable virus in the blood,
isolation of KFDV from patient's serum can substantiate the clinical diagnosis
of KFD. So far, no rapid diagnostic kit
is available, thus precluding early diagnosis. Nor is there any specific
treatment regimen available for KFD patients. A timely supportive therapy, such
as careful precautions for patients with bleeding disorder and maintenance of
hydration, is important and reduces KFD mortality in human. KFD infection and
death rate in human are varying. Approximately 400 – 500 of annual KFD cases
for certain large epidemic years with a 3 – 5% of fatality rate is identified.
A report from Indian council of Medical Research states an occurrence of 40 – 1000 KFD cases each year and a mortality
rate of 4 -15%. Disparate statistics on KFD is not uncommon in the literature,
indicating a dearth of organized statistics. Table 1. Information on KFD cases gathered from various sources for certain segments of epidemic. For 1999, 2002-2004 varying numbers are reported.
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