What’s Eating You? Tick Bite Alopecia

Clinical and Histologic Presentation

Tick bite alopecia is well described in the veterinary literature.^7-9 It is possible that the condition is underreported in humans because the cause is often obvious or the alopecia is never discovered. The typical presentation is a roughly oval zone of alopecia that develops 1 to 2 weeks after the removal of a tick from the scalp. Often there is a small central eschar representing the site of tick attachment and the surrounding scalp may appear scaly. In one report of 2 siblings, multiple oval zones of alopecia resembling the moth-eaten alopecia of syphilis were noted in both patients, but only a single attached tick was found.² In some reported cases, hair loss was only temporary, and at least partial if not complete regrowth of hair occurred.^3,4 Follow-up on most cases is not provided, but to our knowledge permanent alopecia has not been described.

Information about the histologic findings of tick bite alopecia is particularly limited. In a report by Heyl,³ biopsies were conducted in 2 patients, but the areas selected for biopsy were the sites of tick attachment. Centrally dense, acute, and chronic inflammation was seen, as well as marked tissue necrosis of the connective tissue and hair follicles. Peripheral to the attachment zone, tissue necrosis was not found, but telogen hairs with “crumpled up hair shafts” were present.³ The histologic findings presented by Castelli et al⁶ were based on a single case of tick bite alopecia; however, the specimen was a generous excisional biopsy, allowing for a panoramic histologic view of the lesion. In the center of the specimen, hair follicles were absent, but residual follicular streamers and follicular remnants were surrounded by lymphocytic inflammation. Sebaceous glands were conspicuously absent, but foci with naked hairs, fibrosis, and granulomatous inflammation were seen. Peripherally, the hair follicles were thinned and miniaturized with an increased number of catagen/telogen hairs. Some follicles showed lamellar fibroplasia and perifollicular chronic inflammation. The inflammatory infiltrate consisted predominantly of helper T cells with a smaller population of B lymphocytes and a few plasma cells.⁶ In 2016, Lynch et al⁵ described a single case of tick bite alopecia and noted pseudolymphomatous inflammation with germinal center formation associated with hair miniaturization and an elevated catagen/telogen count; focal follicular mucinosis also was noted.Our histologic findings are similar to those of Castelli et al,⁶ except that the inflammatory infiltrate was clearly B-cell dominant, with a suggestion of germinal center formation, as noted by Lynch et al.⁵ This inflammatory pattern often can be encountered in a chronic tick bite lesion. Destruction of follicles and associated sebaceous glands and their replacement by follicular scars indicate that at least in the central portion of the lesion some permanent hair loss occurs. The presence of catagen/telogen hairs and miniaturized follicles indicates the potential for at least partial regrowth.

Similar to other investigators who have described tick bite alopecia, we can only speculate as to the mechanism by which clinical alopecia occurs. Given the density of the inflammatory infiltrate and perifollicular inflammation, it seems reasonable to assume that inflammation either destroys hair follicles or precipitates the catagen/telogen phase, resulting in temporary hair loss. The inflammation itself may be due to the presence of tick parts or the antigens in their saliva (or both). The delay between tick attachment and the onset of alopecia can be attributed to the time it takes follicles to cycle into the catagen/telogen phase and shed the hair shaft.