Dengue fever, a mosquito-borne viral illness, has shown a concerning rise in incidence across India and south east Asia countries in recent years. Classic presentations include fever, muscle aches, bleeding manifestations, and thrombocytopenia [1]. However, thrombocytopenia can occur in various other conditions, posing a diagnostic challenge for physicians. This case report details an unusual cause of thrombocytopenia mimicking dengue fever in an adult male.

A 57-year-old male office worker from Bangalore, India, presented with a 10-day history of intermittent fever, chills and rigors to Emergency Department. Paracetamol provided temporary relief. Seven days prior, he developed a diffuse erythematous rash on both legs, followed by hyperpigmented macules. The rash was painless and non-itchy. Patient went to nearby hospital, where diagnosed with viral fever and thrombocytopenia and prescribed medication. Subsequently, the patient on the day of presenting to emergency experienced an unsettling feeling in the morning, culminating in 1 episode of generalized tonic-clonic seizures (GTCS) followed by a ten-minute period of postictal confusion.

Past medical history was unremarkable. Family history revealed his son's recent admission to the ICU with a diagnosis of viral fever, thrombocytopenia, and multiple organ dysfunction syndrome (MODS), leading to his demise 5 days back within 24 hours of admission to hospital. Notably, the patient and his family had visited Thrissur, Kerala, India 2 days prior to symptoms onset. On examination, the patient was alert and vitals were normal except for heart rate 130/min. 

Physical exam revealed right infra-axillary crepitations on chest auscultation, neck stiffness, Jaundice and Bilateral, irregular, ecchymotic patches on the anterior aspects of both lower legs.

Initial laboratory findings were significant for leucocytosis (WBC 19,950/microliter) with neutrophilia (83%), elevated bilirubin (total 8.28 mg/dL, direct 6.94 mg/dL), low albumin (2.1 g/dL), elevated alkaline phosphatase (311 U/L), and ketonuria with positive bile salts and pigments in the urine.

Imaging studies: a doubtful hypodense lesion on brain CT scan. MRI brain was normal, a homogenous opacity in the left lower lobe on chest X-ray, and normal sinus tachycardia with no ST-T segment changes on ECG. Arterial blood gas was within normal limits. Patient was admitted to ICU for further treatment.

CSF analysis revealed elevated protein, pleocytosis predominantly with lymphocytes, and mildly elevated glucose, consistent with viral meningitis suggestive of viral meningitis, but the Acute Encephalitis Panel was negative. Deteriorating sensorium necessitated intubation within 24 hours. The patient received broad-spectrum antibiotics (Meropenem) and antiviral therapy (Acyclovir) along with supportive measures.  Family history suggestive of a similar illness and travel history to Kerala where there got exposed to dead monkeys raised suspicion for Kyasanur Forest Disease (KFD).  KFD diagnosis was confirmed by positive IgM ELISA on blood testing.  The patient received symptomatic treatment, was successfully extubated on day 5, and discharged on day 10.

There are multiple causes for thrombocytopenia. One of the most common encountered causes being viral infections. Of which Kyasanur Forest disease (KFD) being encountered mostly in endemic areas of Karnataka state, India.

Kyasanur Forest disease (KFD) is caused by Kyasanur Forest disease virus (KFDV), a member of the virus family Flaviviridae. KFDV has a positive-sense, single-stranded RNA genome [1]. First discovered in March 1957 in Kyasanur forest, Karnataka state of India.  It spreads through Vector Haemaphysalis Spinigera (hard tick), which also acts as reservoir. Rodents, shrews, and monkeys are common hosts for KFDV after being bitten by an infected tick. Attack rate from different outbreaks has been found to range from 2–20% and estimated 400–500 cases of KFD occur every year [2].

Human is dead end in the life cycle of virus. Although human-to-human transmission is not known, more than 100 human cases have been reported in the past while working on the virus. National institute of virology Pune started working on the virus again after establishment of a Biosafety Level-3 (BSL-3) laboratory [3].

Biphasic Presentation

Clinical features appear in 2 phases: initial Acute phase and delayed convalescent phase. Acute phase (2-7 days): Clinical features fever with chills, prostration, frontal headache. Convalescent phase (8-12 days): Clinical features of Neck Stiffness, Giddiness, Meningoencephalitis [4].

Laboratory Test

In early stage, Virus isolation and Real-Time PCR useful in diagnosis. Enzyme-linked immunosorbent serologic assay (ELISA) can be performed later.

Laboratory Findings

Leukopenia, Thrombocytopenia, Neutropenia, Eosinopenia, Elevated Liver enzymes [4].

Treatment

There is no specific treatment for KFD. But early hospitalization and supportive therapy is important and help in decreasing morality. Supportive therapy includes the maintenance of hydration and the usual precautions for patients with bleeding disorders as thrombocytopenia and multiple organ failure can occur.

Prevention is by inactivated chick embryo tissue culture vaccine in endemic areas.

1. Dodd, K.A. et al. "Ancient Ancestry of KFDV and AHFV Revealed by Complete Genome Analyses of Viruses Isolated from Ticks and Mammalian Hosts." PLoS Neglected Tropical Diseases, vol. 5, 2011, e1352.

2. Shah, S.Z. et al. "Epidemiology, Pathogenesis, and Control of a Tick-Borne Disease—Kyasanur Forest Disease: Current Status and Future Directions." Frontiers in Cellular and Infection Microbiology, vol. 8, 2018, article 149, doi:10.3389/fcimb.2018.00149.

3. Banerjee, K. "Kyasanur Forest Disease." Arboviruses: Epidemiology and Ecology, edited by T.P. Monath, CRC Press, 1990, pp. 93–116.

4. Mourya, D.T. et al. "Highly Infectious Tick-Borne Viral Diseases: Kyasanur Forest Disease and Crimean-Congo Haemorrhagic Fever in India." WHO South-East Asia Journal of Public Health, vol. 3, no. 1, 2014, pp. 8–21.