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Indian Pediatr 2016;53: 1027-1028 |
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Concomitant Infections Should not Deter
Clinicians from Diagnosing Kawasaki Disease
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Gowda Parameshwara Prashanth and Ganji Shivalingam
Department of Pediatrics, Oman Medical College, Sohar,
Sultanate of Oman.
Email:
[email protected]
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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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