A 54–year–old Haitian Woman with chronic back pain and an implanted neurostimulator placed years ago, presented in the spring with a frontal headache and subjective fevers for 8 days. She noted a nonpuritic nontender rash on her scalp 6 days prior to presentation and then developed a papulovesicular rash on her face, trunk and extremities, sparing the palms and soles. A day prior to the symptoms she had travelled to Coxsackie NY. She had chickenpox and measles as a child. She lived in an apartment building infested by mice, and was unemployed. Physical exam: Temp 101.4, HR 94 and BP 127/76, a normal neurologic exam, a diffuse papular vesicular rash in various stages with nonblanching lesions on the extremities, face, trunk with a single crusted dark lesion on her scalp. Labs revealed a WBC 2.2, Plt 108, AST 99 (nl < 46) and ALT 75 (nl < 46). A head CT was negative and a LP was performed. She was started on vancomycin, ceftriaxone and acyclovir. CSF showed 1 WBC, protein 16 and glucose 46. Doxycycline was started for possible rickettsial disease. A punch biopsy of the rash was performed. Additional lab studies for HIV, Rickettsial, Erlichia, VZV, HSV, Coxsackie and CMV antibodies were sent. On day 3 the biopsy was reported as an intraepidermal vesicle with necrotizing neutrophilic small vessel leukocytoclastic and lymphocytic vasculitis consistent with rickettsialpox. Serologies were positive for Rickettsia akari and negative for other infectious causes. She was discharged home on Doxycycline. The case was reported to the NYC Department of Health and Mental Hygiene.
Rickettsialpox is caused by Rickettsia akari acquired via bites from a mite of the common house mouse. It was first isolated in 1946 from a patient, mites, and an infected house mouse in New York City. It is found in urban settings in the US as well as Russia, South Africa and Korea. After being bitten by a mite, the usual progression of skin lesions is from a papule to a vesicle which will ulcerate and form an eschar over 7–10 days. Within the 3–7 days after the papule forms, constitutional symptoms appear consisting of fevers, chills, and headaches. This is then followed by a generalized papulovesicular rash. Common laboratory findings are leucopenia, thrombocytopenia, and transaminitis. Diagnosis is made by having a high index of suspicion and is confirmed with serologies and skin biopsy. Our patient was a clinical challenge given multiple confounding factors in her history, such as her neurostimulator as a source of indolent bacterial infection and recent travel with exposure to Coxsackie virus, Babesia or other rickettsial diseases. The possibility of disseminated or primary varicella infection, and HSV in an immunocompromised host was included given her rash.
As hospitalists we often see people with vexing clinical situations either as referrals or the first point of contact with medical care, therefore we need to keep a wide differential and be mindful of own unusual local disease.