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Correspondence

Indian Pediatr 2016;53: 1027-1028

Concomitant Infections Should not Deter Clinicians from Diagnosing Kawasaki Disease

 

Gowda Parameshwara Prashanth and Ganji Shivalingam

Department of Pediatrics, Oman Medical College, Sohar, Sultanate of Oman.
Email: [email protected]
 

  


We recently came across a case of a previously healthy 11-month-old boy admitted with acute gastroenteritis. The child had a 5-day history of passing watery stools, vomiting and fever. Physical examination at admission revealed irritability and signs of some dehydration. There were no signs of meningeal irritation. Investigations revealed hemoglobin 9.2 g/dL, leukocyte count 12×10
9/L (neutrophils 72%), and C-reactive protein (CRP) 54 mg/dl. Stool analysis done as part of national surveillance program using enzyme immunoassay (IDEIA Rotavirus kit, Dako Diagnostics) showed rotavirus antigen. With standard management, diarrhea subsided on day-8 of illness but fever persisted. The child had faint maculopapular rash involving face, congestion of oral mucosa and bilateral cervical lymphadenopathy. There was no conjunctival congestion. Total leukocytes, ESR and CRP at this stage were 18×109/L, 80 and 155 mg/dL, respectively. Bacterial cultures of blood and urine were negative. Liver function tests were normal. Persisting fever 48 hours after parenteral antibiotics (ceftriaxone, 75 mg/kg/day), leukocytosis and elevated CRP coupled with thrombocytosis (platelet count 750×109/L) led to diagnosis of ‘incomplete’ Kawasaki disease. Adminis-tration of intravenous immunoglobulin (2 g/kg over 12 hours) and aspirin (80 mg/kg/day) subsequently lead to normalization of body temperature in 24h and normalization of inflammatory markers (ESR 12 and CRP 10 mg/dL) in the next 48h. Echocardiography done on day–10 and during later follow-up revealed no coronary artery abnormalities.

Infectious etiology of Kawasaki disease (KD) has been long debated. Putatively, at least 1 in 3 cases of KD have concomitant infection which could be systemic or focal [1,2]. In tropical countries where uncommon presentation of common infections is very common, one needs to be vigilant not to miss KD which may follow recovery from infections such as dengue [3]. In fact, apart from rotavirus and dengue, KD is reportedly associated with more than 20 bacterial and viral infections, and also observed post-vaccination [4,5]. Also, seasonal clustering of cases suggests existence of an environmental trigger. However, such temporal associations have not so far been proven to be causal.

Failure to identify a single etiological agent despite 40 years of research implies that KD might represent an aberrant yet predictable immunological phenomenon triggered by exposure to a variety of environmental factors in a genetically predisposed host. The learning point in this case is the clinician’s prudence in the diagnosis and treatment of incomplete KD as a syndrome based on clinical criteria irrespective of other underlying specific and non-specific infectious conditions.

References

1. Sundel RP. Kawasaki disease. Rheum Dis Clin North Am. 2015;41:63-73.

2. Turnier JL, Anderson MS, Heizer HR, Jone PN, Glodé MP, Dominguez SR. Concurrent respiratory viruses and Kawasaki disease. Pediatrics. 2015;136:e609-14.

3. Jagadeesh A, Krishnamurthy S, Mahadevan S. Kawasaki disease in a 2-year-old child with dengue fever. Indian J Pediatr. 2016; 83:602-3.

4. Principi N, Rigante D, Esposito S. The role of infection in Kawasaki syndrome. J Infect. 2013;67:1-10.

5. Abrams JY, Weintraub ES, Baggs JM, Mccarthy NL, Schonberger LB, Lee GM, et al. Childhood vaccines and Kawasaki disease, vaccine safety datalink, 1996-2006. Vaccine. 2015;33:382-7.

 

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