The Journal of Association of Chest Physicians

: 2017  |  Volume : 5  |  Issue : 2  |  Page : 87--88

Chikungunya and the pulmonologist – What we must know

Arjun Khanna, Ankit Kumar Sinha, Kamal Kishore Pandey 
 Galaxy Institute of Pulmonology, Galaxy Hospital, AGCR Enclave, New Delhi, India

Correspondence Address:
Arjun Khanna
Consultant and Head, Galaxy Institute of Pulmonology, Galaxy Hospital, AGCR Enclave, New Delhi

How to cite this article:
Khanna A, Sinha AK, Pandey KK. Chikungunya and the pulmonologist – What we must know.J Assoc Chest Physicians 2017;5:87-88

How to cite this URL:
Khanna A, Sinha AK, Pandey KK. Chikungunya and the pulmonologist – What we must know. J Assoc Chest Physicians [serial online] 2017 [cited 2020 Oct 21 ];5:87-88
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Our country is a hotbed of tropical infections. Every year, outbreaks of infections such as dengue, malaria, and scrub typhus are reported from various parts of the country. This year, another infection, in the form of chikungunya fever, engulfed various parts of the country and we saw more cases of this disease than ever before. Similar to dengue fever, various systemic manifestations of chikungunya were observed. Pulmonary involvement in patients with chikungunya has been reported in the literature.[1] Because this infection has now firmly set its foot in the Indian subcontinent, we must be aware of its myriad pulmonary manifestations.

A 19-year-old, previously healthy male presented to the Emergency Department with high-grade fever and associated chills and rigors over the past 2 days. On examination, the patient had a temperature of 104°F, bilateral conjunctival suffusion, generalized erythematous macular rash all over the body, and also complained of generalized arthralgia, more in the bilateral knee and the ankle joints. Blood pressure was 120/80 mmHg, pulse rate was 120/min, and respiratory rate was 22/min. Chest auscultation revealed bilateral normal vesicular breath sounds. Room air saturation was 100%. In the Emergency Department, the patient was given 650 mg paracetamol orally, and as the fever subsided, his pulse and respiratory rate normalized. The patient’s mother and several other people around his residence had tested positive for chikungunya. The patient was sent home on oral paracetamol and ranitidine. A sample was drawn for chikungunya polymerase chain reaction (PCR)-based antigen detection test, which eventually came out to be positive. The patient presented again after 2 days with persistent fever and increasing shortness of breath. Room air saturation was 94%, with a respiratory rate of 28/min; blood pressure was 110/70 mmHg and pulse rate was 130/min. Chest X-ray performed in the Emergency Department was suggestive of blunting of the bilateral costophrenic angles and left-sided upper lobe pneumonia. Minimal bilateral pitting pedal edema was also noted.

Routine blood investigations revealed a hemoglobin level of 14 g/dl, a total leukocyte count of 14,800/cumm with 85% neutrophils, and platelet count of 1.8 lakh/cumm. Liver and renal function tests were within range. Dengue serology IgM antibodies and NS1 antigen were negative. The patient was started on supplemental oxygen, intravenous ceftriaxone, oral doxycycline, and ribavirin. Over the next 3 days, the patient gradually recovered and was shifted to the ward. The patient had classical post-chikungunya arthralgia, which responded to oral naproxen. We do not know whether the pneumonia was primarily due to chikungunya or a secondary bacterial infection. However, the patient was treated with both antibiotics and antivirals in the form of ribavirin. The exact efficacy of ribavirin in the management of chikungunya infection is debatable.[2]

Chikungunya is an Aedes mosquito-borne disease caused by an alphavirus of the Togaviridae family and has been implicated with epidemics from various parts of the globe.[1] Classical chikungunya is characterized by an acute onset of fever, polyarthralgia, and maculopapular rash. The articular symptoms are very common, debilitating, and may take a long time to resolve. Other systemic manifestations of chikungunya are also reported. The largest data on this disease originate from the Reunion Island, where epidemics of chikungunya are common.[3] The diagnosis of chikungunya is confirmed either by serological testing (IgM antibody titers) or by detecting the presence of the chikungunya virus in the given specimen by reverse transcription-PCR assays.[4]

The most common pulmonary manifestation that has been described in case series is pneumonia. In the largest case series from Reunion Island, pneumonia was seen in 17% of the hospitalized patients.[5] Most of the complications were seen in patients with preexisting comorbidities such as diabetes mellitus and chronic kidney disease. A few of the existing patients had a history of chronic obstructive pulmonary disorder, and three had asthma. Chest pain as a presenting feature of chikungunya was observed in 4% of the patients. During this epidemic, many patients with preexisting obstructive airways disease complained of new onset dyspnea or worsening of various respiratory symptoms. The development of acute chikungunya infection-induced airway hyper-responsiveness was initially hypothesized to be responsible for these symptoms. However, no increase in airway hyper-responsiveness was demonstrated in the pulmonary function tests of these patients. Similar to our patient, as a part of generalized capillary leak syndrome, pleural effusions may be seen in these patients, which may add to the respiratory distress. We could not come across case reports of frank acute respiratory distress syndrome secondary to chikungunya infection.

A study was conducted in tracheal explants to determine the susceptibility of these cultures to infection with nine nonrespiratory viruses including chikungunya.[6] The tracheal cultures did not support the multiplication of the chikungunya virus. Most of the viruses responsible for exacerbation of the obstructive airways diseases are aerocontaminants, with the primary target being the airways epithelium. Chikungunya is an inoculated virus, and unlike the aerocontaminants, it may only secondarily proliferate in the tracheal cells without causing direct damage to the respiratory epithelium. This might explain, in part, why no increase in bronchial hyper-responsiveness was observed in this series with acute chikungunya infection. Why pneumonia is observed in these patients is not clear. Whether this is a primary viral infection of the parenchyma or a secondary bacterial infection can be debated upon. In other viral diseases such as influenza, secondary bacterial infections are common, especially with gram-positive organisms. Similar extrapolation to chikungunya seems plausible, but remains to be proven. The treatment of the pulmonary manifestations of this disease is also not been crystallized. The current literature does not specify whether antivirals such as ribavirin should be used in these patients, or should a more watchful policy of only supportive and symptomatic care be adopted. As these cases increase, more medical studies should be conducted from the Indian subcontinent to answer these yet unanswered questions.

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