Chikungunya fever is a reemerging arthropod-borne illness caused by an Arbo virus belonging to family Togaviridae.[1] The term chikungunya is derived from Kimakonde word ‘kungunyala’ which means ‘to become bent’ and refers to stooped posture of the patient due to severe joint involvement.[2] It is endemic to Africa and south east Asia including India and tends to present with cyclical epidemics with variable interval. In India the first case was reported in 1963 from Calcutta and last major outbreak was observed in 2016.[3,4]
Chikungunya fever is transmitted to humans by the urban dwelling, daytime biting Aedes aegypti and Aedes albopictus mosquitoes. Rarely, maternal-to-fetal transmission can occur during intrapartum period and may lead to abortion in first trimester infection. Following an incubation period ranging from 2 to 12 days, the disease presents with sudden onset of high-grade fever, joint pains, and skin rash.[1,5] Constitutional symptoms such as headache, fatigue, and myalgia may be present. The condition is self-limiting and often lasts for less than a week but the joint pains can persist for months to years especially in older persons.
Chikungunya fever presents with cutaneous involvement in 40% to 75% of patients.[5] It can have diverse manifestations such as hyperpigmentation, maculopapular eruption, aphthous-like ulcers, transient nasal erythema, vesiculobullous lesions, acrocyanosis, purpura, vasculitis, lichenoid eruption, erythema multiforme-like lesions, Stevens–Johnson syndrome, and toxic epidermal necrolysis-like lesions and may also cause worsening of preexisting dermatoses.[1,5,6]
Cutaneous hyperpigmentation is one of the most common features of chikungunya fever reported in multiple large case series’ from India.[1,7,8] It typically presents within few days to 2 to 4 weeks after the onset of fever. Pigmentation is predominantly localized but can be generalized in infants.[8] It is sudden in onset and occasionally preceded by maculopapular rash or transient erythema. Characteristically, it presents as asymptomatic brownish-black macules and patches. The most frequent site of involvement is centro-facial area producing the characteristic “chik sign” or “brownie nose.”[7] Pinna, extremities, trunk, shoulders, palms, and oral mucosa (tongue and palate) can also be affected. The various patterns of cutaneous pigmentation associated with chikungunya fever are listed below [Table 1].[1,9,10] Pigmentation in children [Figure 1] develops earlier (within few days of fever and rash onset) and evolves quickly as compared to adults (weeks) [Figure 2]. Ear, chest, abdomen, genital, and lower limb involvement is frequently seen in children.[11] Neonatal facial pigmentation can be an indication in symptomatic patients to look for neurodevelopmental delays in the long term.[12,13] Nail pigmentation is uncommon and may present as diffuse or longitudinal melanonychia, black lunula, and transverse pigmented band. Nail changes can occur without any other mucocutaneous involvement.[7]
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Table 1: Patterns of cutaneous pigmentation associated with chikungunya fever
Figure 1: Diffuse brown pigmentation of face (a) and trunk (b) in a neonate with chikungunya fever.
Figure 2: Dark black macules and patches over face (a) and dorsum of hands (b) in an adult with chikungunya fever.
The exact cause for chikungunya fever induced hyperpigmentation is not known. It has been speculated as a postinflammatory response. Histopathological examination of biopsy samples obtained from hyperpigmented areas reveals intact basal cell layer with diffuse hypermelanosis of whole epidermis. Sparse perivascular lymphocytic infiltrate without melanin incontinence is typically seen in the dermis; however, increased basal layer pigmentation, pigmentary incontinence, and melanophages may also be present.[1,7] Persistence of pigmentation has been attributed by some to the presence of melanophages. An increased intraepidermal dispersion/retention elicited by the virus has been postulated as the reason for pigmentation.[1] Ultraviolet rays are also considered to play a role as face is the commonest site to be affected. Dermoscopy demonstrates brown background, dark brown globules, pseudoreticular pigment network, and bluish-gray globules corresponding to basal layer melanin, increased epidermal melanin, diffuse pigmentation, and free melanin or melanophages, respectively.[14] A pathogenic mechanism similar to cutaneous pigmentation affecting the nail matrix may be responsible for nail lesions.[7]
Diagnosis of chikungunya fever induced pigmentation is essentially clinical and can be confirmed by polymerase chain reaction or serology in the acute phase. IgM antibodies against chikungunya virus become detectable 3 to 5 days after infection and can persist up to 3 months.[9] Hyperpigmentation lasts for a period of few weeks to months and completely subsides spontaneously. Parents of the affected children should be counseled regarding the self-limiting nature of the condition. Depigmenting agents, sunscreen, and photoprotection can be advised for adults.
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