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Year : 2017  |  Volume : 23  |  Issue : 1  |  Page : 56-58

Kyasanur forest disease

Department of Speech and Hearing, SOAHS, Manipal University, Manipal, Karnataka, India

Date of Web Publication6-Feb-2017

Correspondence Address:
P G Bhargavi
Department of Speech and Hearing, SOAHS, Manipal University, Manipal - 576 104, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-7749.199504

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Kyasanur forest disease (KFD) a rare viral disease found to be related to the Russian-spring summer virus but differs only because of its hemorrhagic form. KFD is known to be prevalent in the Shimoga District of Karnataka, and it was first identified in the year 1957. Victims of this disease would be those who have been exposed to deceased monkeys in forests or otherwise, have been bitten by an infected tick. Some of the initial phase symptoms include persistent headaches, fever, and muscle weakness. However, the neurological symptoms begin to appear only in the second phase of the viral attack. At this stage, viral encephalopathy, meningoencephalitis, or even meningitis could manifest and lead to vast deficits. Previous literature reviews of this disease have shown no signs of language deficits. A case of a 5-year-old child, confirmed with the KFD, with diffuse encephalopathy as well as other organ functioning deficits, showed deficits in language skills.

Keywords: Childhood aphasia, kyasanur forest disease, recovery

How to cite this article:
Kavi P, Bhargavi P G. Kyasanur forest disease. Indian J Otol 2017;23:56-8

How to cite this URL:
Kavi P, Bhargavi P G. Kyasanur forest disease. Indian J Otol [serial online] 2017 [cited 2022 Jul 2];23:56-8. Available from: https://www.indianjotol.org/text.asp?2017/23/1/56/199504

  Introduction Top

The rare condition termed Kyasanur forest disease (KFD) derives its name from the Shimoga district of Karnataka, India. This virus belongs to the family of Flaviviridae and exposes itself in one or more ways such as deceased monkeys, infected ticks, and unpasteurized milk.[1],[2] The virus was first identified in the year 1957 and has been increasing in terms of incidence, since then.[3] While its discovery, 500 cases were reported between the year 1956 and 1957, of which the mortality rate was 10%.[2],[3] The initial report of the disease stated that it prevailed maximally during the season of summer when the humidity in forests and high altitude areas were favorable for the lifecycle of the virus carriers.[4] The carrier of the virus through ticks is known to dissect on two types of monkeys, known by the nomenclature of black-faced Presbytis entellus and red-faced Macaca radiata.[2] These ticks are present in large numbers across forests of Southern India and Sri Lanka.[4] Diagnosis of approximately 400–500 cases have been seen on an annual basis in the last 50 years.[1] It was also noticed that adults who collected wood in the forest areas were the victims of the disease. In the recent years, children too have been exposed to the virus, without exact evidence as to how they have incurred it. The symptoms of the disease are presented in two classic phases during disease course. The first phase is inclusive of a fever that is sudden in nature and can also be associated with a headache which may occur close to 5–8 days after exposure to a forest.[3] Followed by, a series of signs that can include the spread of the disease in the blood serum, inflammation of the meningeal coverings of the brain, frequent vomiting, and diarrhea. At this stage, the fever would have lasted for up to 14 days. Since its rise in the last five decades, vaccinations have been trailed but have been unsuccessful in its efficiency and the number of human cases are still growing.[4]

  Case Report Top

A 5-year-old child presented with the complaint of being unable to speak (April 12, 2012) but was apparently normal 3 days before. This child had no significant premorbid history but presented with a high fever that persisted for the duration of 10 days and was under the intensive care unit for treatment for the same. A series of medical tests were carried out, to identify the rudimentary cause of the persistent fever, headache, and diarrhea [Table 1].
Table 1: Results of medical investigations

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Following the medical investigations, the child was referred for speech and language evaluation [Table 2] and [Table 3].
Table 2: Pre-morbid history

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Table 3: Results of administration of Receptive and Expressive Emergent Language Scale - 2

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The child's receptive age was age adequate, falling at 4.5–5 years, which was closely linked to the chronological age. Prior to the onset of KFD (before 3 days) child was able to narrate events in sentences. The expressive age was a mere range of 0–1 month, which was depictive of communication through babbling and crying. This indicated that there was a severe effect of meningoencephalitis that resulted from the virus attack, on specifically expressive language skills. Hence, leading to the diagnosis of acquired childhood aphasia. Demonstration therapy was given, and goals taken were to improve the prelinguistic skills and expressive language skills. A total of four therapy sessions were given, and upon termination of it, the child was still unable to verbally express and communicate and only gestural communication was observed. Upon discharge from the hospital, a follow-up tele-assessment was done (September 2012). As reported by the parents, the child had recovered within a span of 3–4 weeks and can communicate well and is attending school.

  Discussion Top

Studies have supported the evidence that speech and language deficits can be caused by different classes of viruses. A study done in Haryana found that three children were inflicted with Japanese encephalitis, who exhibited aphasia, along with rigidity in the neck and trunk muscles.[5],[6] Studies have reported that there may be a large array of neurological deficits resulting from a virus attack, such as psychiatric or behavioral issues.[7] In terms of cognitive deficits, the general sequence of events is most often a severe impairment in anterograde memory and other few domains that may present themselves in a milder severity are a retrograde memory, semantic aphasia, visuospatial function, and executive function. West Nile Virus, which falls under the same family of viruses as does the KFD, displays signs such as headache, pain in the eye, nauseating feeling, anorexia, malaise, and rashes.[8] However, in rare cases acute flaccid paralysis may be observed and cognitive impairments such as slowness of thought and memory deficits.[9] However, there have been no literature reviews supporting that the KFD has an association with aphasia or cognitive impairments.

It is stated that there is proof of decline in intelligence due to diffused brain injury.[7] Cases of viral infections are among those where the recovery period can neither be measured nor guaranteed. There are various factors that can affect the process of recovery and further prognosis. A case of a 4-year-old child in Israel, diagnosed with the infection of the West Nile Virus with meningoencephalitis, this case developed convulsions and motor aphasia, but with appropriate medical intervention, recovered completely.[8],[10] Prognosis for viral infections are poor, and it is reported that prognosis of encephalitis is poor.[1],[4],[5] The communicative and motor skills that have been compromised may or may not be regained.[5] However, in this case report, there was recovery seen in child's language, which could be attributed to factors such as neural plasticity [11] and also due to medical management, which would have assisted in the speedy recovery.

The exact reason for the occurrence of the disease is not known, but the assumption can be made that the disease could have been acquired through a tick bite, or exposure to dead monkeys who have been infested with ticks since the location of their hometown was a forested area. Although literature reviews, it is a well-documented that viral infections can cause acquired childhood aphasia. Now, KFD can be considered as a potential cause leading to language disturbances, as presented in the case report, which was not documented earlier. Perhaps more number of cases would be required to evidence that this particular virus to become a substantial cause of aphasia.

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  References Top

Ferro JM, Martins IP, Pinto F, Castro-Caldas A. Aphasia following right striato-insular infarction in a left-handed child: A clinico-radiological study. Dev Med Child Neurol 1982;24:173-8.  Back to cited text no. 1
Pattnaik P. Kyasanur forest disease: An epidemiological view in India. Rev Med Virol 2006;16:151-65.  Back to cited text no. 2
Mehla R, Kumar SR, Yadav P, Barde PV, Yergolkar PN, Erickson BR, et al. Recent ancestry of Kyasanur forest disease virus. Emerg Infect Dis 2009;15:1431-7.  Back to cited text no. 3
Hécaen H. Acquired aphasia in children and the ontogenesis of hemispheric functional specialization. Brain Lang 1976;3:114-34.  Back to cited text no. 4
Hout AV, Evrard P, Lyon G. On the positive semiology of acquired aphasia in children. Dev Med Child Neurol 1985;27:231-41.  Back to cited text no. 5
Prasad SR, Kumar V, Marwaha RK, Batra KL, Rath RK, Pal SR. An epidemic of encephalitis in Haryana: Serological evidence of Japanese encephalitis in a few patients. Indian Pediatr 1993;30:905-10.  Back to cited text no. 6
Annett M. Laterality of childhood hemiplegia and the growth of speech and intelligence. Cortex 1973;9:4-33.  Back to cited text no. 7
Spiegel R, Miron D, Gavriel H, Horovitz Y. West Nile virus meningoencephalitis complicated by motor aphasia in Hodgkin's lymphoma. Arch Dis Child 2002;86:441-2.  Back to cited text no. 8
Work TH, Roderiguez FR, Bhatt PN. Virological epidemiology of the 1958 epidemic of Kyasanur forest disease. Am J Public Health Nations Health 1959;49:869-74.  Back to cited text no. 9
Lenneberg EH, Chomsky N, Marx O. Biological Foundations of Language. Vol. 68. New York: Wiley; 1967.  Back to cited text no. 10
Arciniegas DB, Anderson CA. Viral encephalitis: Neuropsychiatric and neurobehavioral aspects. Curr Psychiatry Rep 2004;6:372-9.  Back to cited text no. 11


  [Table 1], [Table 2], [Table 3]


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