A 46-day-old male infant presented with fever for 1 day followed by one episode of abnormal movements, associated with decreased feeding and lethargy. The baby was born at term, out of a third-degree consanguineous marriage to a primigravida mother, delivered by caesarean section. The antenatal period was uneventful except for high-grade fever and body pains suffered by the mother 5–6 days before delivery, which was managed conservatively, without any investigations. She was asymptomatic when the baby was presented to us. Baby had a birth weight of 2.3 Kg, cried immediately after birth, and was started on breast feeds, with an uneventful perinatal period, having received birth vaccination. There was no prior illness, intake of drugs, or transfusion before presenting to us. At presentation, the baby was not in active seizures, but lethargic, febrile (101.5°F), with a heart rate of 142/minute and respiratory rate 36/minute, capillary filling time 2 seconds, and SpO2 95%. There was no pallor, cyanosis, icterus, or edema. Length (53 cm) and head circumference (37 cm) of the baby were age-appropriate. The anterior fontanelle was at the level. Cardiorespiratory and abdominal examinations were within normal limits. Neurological examination showed normal tone with no episodes of apnea during the hospital stay. Treatment was started along the lines of meningitis, with intravenous fluids, cefotaxime, amikacin, and levetiracetam. Investigations showed low hemoglobin 8.8 g/dl, leukopenia (3400/mm3, with neutrophils 62%, lymphocytes 29%), and thrombocytopenia (114000/mm3). The C-reactive protein was 78 mg/L; blood sugar was 93 mg/dl. Biochemical parameters showed serum sodium/potassium 138/3.7 meq/L, calcium 9.6 mg/dl, serum bilirubin (total) of 0.8 mg/dl, aspartate transaminase/alanine transaminase 34/23 IU/L, and urea/creatinine of 16/0.3 mg/dl. His cerebrospinal fluid analysis showed 3 lymphocytes, 5–6 red blood cells, protein/sugar of 47/60 mg/dl with sterile culture. Magnetic resonance imaging of the brain was normal. The infant became afebrile after 2 days, with no further convulsions. By day 3 of admission, oral feeds were introduced. Repeat complete blood count showed normalisation of leukocyte count (9500/mm3) and platelet count (253,000/mm3). On day 7, the baby developed generalized macular brown to black hyperpigmentation over the face and nose (chik sign) as well as over the abdomen and extremities Figure 1a and b. The pigmentation was not associated with blanching, exfoliation, vesicle formation, erythema, or oozing. The baby remained hemodynamically stable, without clinical deterioration, continuing on feeds, without bleeding or any other complications. As the mother had fever with body aches just before delivery, we kept the possibility of congenital dengue or chikungunya infections (being endemic to our region) or congenital TORCH infection. Dengue immunoglobulin M (IgM) of the baby and TORCH panel came negative. The prothrombin time and international normalized ratio were 14 seconds and 1.1, respectively. The reverse transcription-polymerase chain reaction (PCR) for chikungunya virus (CHIKV) came positive. We made our final diagnosis of congenital chikungunya infection with encephalopathy.Figure 1: Infantile chikungunya: (a) Diffuse hyperpigmentation (b) Chik signSupportive care was provided. In view of normal neurological examination and neuroimaging, levetiracetam was tapered and stopped. Baby was discharged on the 14th day, afebrile, on full feeds and gaining weight. At first follow-up, 1 week after discharge, hyperpigmentation had started decreasing and had completely resolved at last follow-up, 3 months after discharge, with the baby gaining weight and having a normal neurodevelopment. Chikungunya fever is a mosquito-borne viral illness caused by the CHIKV, manifesting as an acute onset of fever, severe polyarthralgia/arthritis, myalgia, headache, fatigue, and maculopapular rash.1 Congenital and perinatal transmission are likely when the mother acquires CHIKV infection during pregnancy. This infant presented at 45 days of life, so perinatal or vertical transmission is unlikely. Infants with chikungunya often present with more severe and atypical manifestations, such as pronounced skin lesions and neurological involvement, and diagnosis is challenging due to their inability to express symptoms, unlike older children.2 Infants present with fever, cutaneous lesions (flaccid vesicobullous lesions, maculopapular rash, and generalized erythema), encephalopathy (seizures and altered sensorium), gastrointestinal features (vomiting, diarrhea), anemia, thrombocytopenia, coagulopathy, and deranged liver function tests.3,4 The diagnosis can be confirmed by testing for IgM antibodies that develop within 1 week of symptoms. Our case had pigmentary changes which can be an important clue in the diagnosis of chikungunya, especially in endemic countries, and creates awareness regarding infantile chikungunya. Diffuse hyperpigmentation can be a rare manifestation of chikungunya. PCR-based test can help in definitive diagnosis. Hyperpigmentation is self-resolving, and parents need to be reassured. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the legal guardian has given their consent for images and other clinical information to be reported in the journal. The guardian understands that names and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.
Lamge et al. (2026) studied this question.