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. 

KFD epidemic

KFD cases reported































Spearheaded by National Institute of Virology at Pune in India, a vaccine has been made available since 1966. Formalin inactivated KFDV vaccine is prepared by growing the virus in chick embryo fibroblast cells by employing modern cell culture techniques. This vaccine is currently used in the endemic areas of KFD. Over 50 thousand doses of KFDV vaccine are administered annually. Despite this prophylactic effort, reports of large numbers of KFD cases from Karnataka highlights a need for a fresh look into vaccine preparation as well as post-production vaccine handling and overall disease management protocols. Though KFD is still an epidemic that threatens periodically, identification of KFDV and development of a largely effective vaccine, is in itself considered to be a success story in Indian science scenario.

Since 2012 KFD has been reported in new areas beyond the core endemic region in Karnataka. Chamarajanagara district of Karnataka, Nilgiri district of Tamil Nadu and Wayanad and Malappuram districts of Kerala, where new human infections are identified, have geographic proximity to Shimoga (Shivamogga) district. New studies suggest a need for improved vaccination strategies citing low vaccination coverage and low vaccine efficacy. A need for new look in assessing the renewed threat posed by the tick vectors and prioritize the tick control research program in India is also emphasized. 

References and further readings

Work TH, Roderiguez FR, Bhatt PN. Virological epidemiology of the 1958 epidemic of Kyasanur Forest disease. Am J Public Health. 1959;49:869.

Mark Nichter. Kyasanur Forest Disease: An Ethnography of a Disease of Development. 1987;1:406

Pattnaik P. Kyasanur forest disease: an epidemiological view in India. Rev Med Virol. 2006;16:151.

Mehla R, Kumar SR, Yadav P, Barde PV, Yergolkar PN, Erickson BR, Carroll SA, Mishra AC, Nichol ST, Mourya DT. Recent ancestry of Kyasanur Forest disease virus. Emerg Infect Dis. 2009;15:1431.

Ghosh S, Nagar G. Problem of ticks and tick-borne diseases in India with special emphasis on progress in tick control research: a reviewJ Vector Borne Dis. 2014;51:259.

Kiran SK, Pasi A, Kumar S, Kasabi GS, Gujjarappa P, Shrivastava A, Mehendale S, Chauhan LS, Laserson KF, Murhekar M. Kyasanur Forest disease outbreak and vaccination strategy,Shimoga District, India, 2013-2014Emerg Infect Dis. 2015;21:146.

Contributor: Duraiswamy Navaneetham PhD.
Temple University School of Medicine
Philadelphia, PA, USA

March 2010 (last modified Feb. 2015).