Dengue is the most common and widespread arthropod-born arboviral infection in the world today. The geographical spread, incidence and severity of dengue fever (DF) and dengue hemorrhagic fever (DHF) are increasing in the Americas, South-East Asia, the Eastern Mediterranean and the Western Pacific. It is estimated that each year 50 million infections occur, with 500,000 cases of DHF and at least 12,000 deaths [1].

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Figure 1. Muscle biopsy showing nonspecific inflammatory infiltrates.

Neurological complications of dengue are increasingly being recognized in recent years. Myalgia is a common manifestation in DF and one of the criteria of a suspect case according to the WHO 1997 criteria. Though varying degrees of myalgias are commonly seen, muscle weakness is uncommon presenting manifestation. Myositis and/or elevated serum creatinine kinase (CK) were only reported infrequently with few cases with muscle paralysis or acute rhabdomyolysis [2, 3].

A 26 year old male presented with complaints of fever for two days duration, intermittently associated with chills and rigors with no diurnal variation and not associated with any skin rash, body swelling, bleeding or joint pains. There was history of sudden onset weakness of all four limbs of one day duration, incomplete, non-progressive, and associated with severe myalgias. There was no history of any loss of consciousness, seizures, respiratory distress, and bladder or bowel involvement.

Patient was conscious oriented, afebrile with pulse rate of 90/minute regular, blood pressure of 110/70 mmHg and respiratory rate of 20/minute. He had no rash, pallor or jaundice. Respiratory, cardiovascular and abdominal examinations were unremarkable. Neurological examination revealed weakness of all four limbs with power of 3/5 at all joints in upper limbs and lower limbs. Superficial reflexes were present and deep tendon reflexes were diminished in bilateral upper and lower limbs. Active and passive stretching of the muscles was associated with marked tenderness with no obvious swelling. Muscle fasciculation was absent. No local tenderness was present at spine. Rest of examination was normal.

Another patient was fifteen year old male who presented with similar complaints of fever of five days duration, intermittent with chills and rigors and associated with severe myalgias of three days which was aggravated by movement of any limb. There was no history of skin rash, body swelling, joint pains or weakness of any body parts. On examination patient was febrile with a temperature of 102°F, pulse rate of 96/minute, blood pressure of 120/90 mmHg and respiratory rate of 22/minute. He had no rash, pallor or jaundice. Neurological examination revealed weakness of all four limbs with power of 4+/5 at all joints in upper and lower limbs. Active and passive stretching of the muscles was associated with marked tenderness. Rest of neurological examination was unremarkable. Cardiovascular, respiratory and abdominal examination was essentially normal.

Investigations revealed thrombocytopenia and hemoconcentration in both patients with first patient showing an hemoglobin of 15.7 gm%, hematocrit of 45%, total leucocyte count of 4000/mm3, platelet count of 60,000/mm3 and second patient having an hemoglobin of 15.1 gm%, hematocrit of 45%, TLC of 4000/mm3, and platelet count of 80,000/mm3. Creatinine kinase was markedly elevated in both patients with an absolute value of 1772 and 12,590 IU/L, respectively. Patients were positive for dengue NS1 antigen by ELISA. All other tests for common infections like malaria, leptospira, and rickettsia were negative. Ultrasonography abdomen showed gall bladder wall edema and minimal free fluid in first patient while same was normal in second patient. Liver function tests, renal function tests, serum electrolytes and other routine biochemistry were normal in each patient. Their ECG and chest X-ray were normal. Routine urinary examination was normal and there was no hemoglobinuria. Nerve conduction studies done on major nerves of upper and lower limb were essentially normal. Electromyography (EMG) showed fibrillation potentials, positive sharp waves, and complex repetitive discharges in first patient and fibrillation potentials, positive sharp waves only in the other. Muscle biopsy showed nonspecific inflammatory infiltrates in both patients (Figure 1). Patients were treated conservatively and over next few days both patients became afebrile, improved clinically and their hematocrit, platelet count and creatinine kinase reverted to normal

Dengue fever and Dengue hemorrhagic fever are caused by dengue viruses, belonging to the genus flavivirida and transmitted to humans by the bite of Aedes aegypti mosquitoes [5]. Most of the infections are asymptomatic and symptomatic patients present with fever, headache, muscle and joint pains and a characteristic skin rash.

Viral myositis and its complications are well described with several acute viral infections, most notably influenza A and B virus, HIV, coxsackie viruses, and cytomegalovirus [4]. Acute myositis has been previously reported with occasional cases of rhabdomyolysis in dengue fever, but it has largely remained under-diagnosed due to lack of suspicion. Myositis described in dengue fever is of acute onset, short duration and benign nature. Patient presents with complaints like myalgia with or without reversible proximal muscle weakness, specially in lower limbs. Some may present as subclinical myositis with minimal symptoms and elevated serum CK levels and very rarely as rhabdomyolysis. Viral rhabdomyolysis, if diagnosed early, can easily be treated to reduce associated grave complications like acute renal failure.

Here we present two patients of dengue fever who came to us with complaints of myalgia and muscle weakness, having raised creatinine kinase and EMG showing features of myositis. Further muscle biopsy of involved muscle group in both patients showed nonspecific inflammatory infiltrates, confirming our diagnosis of myositis.

The findings in our patients were similar to those by Malheiros et al who reported 15 patients with classic dengue fever, serologically confirmed, during the Brazilian dengue epidemics from September 1986 to March 1987. Muscle biopsy was positive for myositis in 12 patients [6]. In another report by Kalita J et al of 7 patients with dengue fever who presented to their department with acute quadriplegia, serum CK was found to be high. However, nerve conduction and EMG studies were normal in all patients except one whose EMG was myopathic [7].

Though myositis in dengue has been a well-known entity, there is lack of suspicion among physicians, which often leads to it being underdiagnosed. Benign acute myositis should be suspected in every dengue fever patient presenting with complaints of myalgia and muscle weakness. Serum CK level should be checked in every patient and investigations like EMG and muscle biopsy should be done to confirm the diagnosis. This entity when detected early can be managed with ease to reduce morbidity and financial burden.

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