Spectrum and Treatment of Cat-Scratch Disease

Abstract

Cat-scratch disease (CSD) was first identified in 1931. In 1992, Regnery et al reported isolation of the causative agent, Bartonella henselae, from the blood of a domestic cat and demonstrated antibodies to B. henselae in patients with CSD. Now, CSD has been recognized worldwide as a zoonosis with a wide clinical spectrum. Because CSD is not reportable, its true incidence is unknown; serologic studies performed over the last 10 years suggest that it is emerging, particularly in immunocompromised patients. Epidemiology. Zangwill et al in 1993 noted that individuals with kittens 12 months old were 15 times more likely to develop CSD than owners of adult cats. The organism is transmitted to humans by a kitten scratch, bite, lick or other intimate contact. Demers et al further demonstrated that antibodies to B. henselae are detected by indirect immunofluorescence assay (IFA) in 84% of initial sera of patients with clinical CSD and in 29% of exposed symptom-free family members. Matched controls with no cat exposure lacked such antibodies. Older cats had evidence of past infection but were less likely to be bacteremic or to transmit disease. The cat flea transmits B. henselae from one kitten to another and is hypothesized to be responsible for direct transmission to humans. B. henselae is endemic in warm humid climates. Cats living in U.S. regions with high annual precipitation and high average daily temperatures, such as the Southeast, Hawaii, coastal California, Pacific Northwest and South-Central Plains have an elevated seroprevalence of B. henselae antibodies. Drier, cool environs that do not support high flea density have the lowest seroprevalences. Clinical Manifestations. CSD may present in a typical or atypical fashion in both immunocompetent and immunocompromised patients. Typical disease in immunocompetent persons includes a scratch, bite, lick or other contact with a kitten followed in 3–10 days by a round, red-brown, nontender papule within the scratch line. Regional, unilateral lymphadenopathy occurs 1–3 weeks later with gradual nodal enlargement. Unlike pyogenic lymphadenopathy, CSD does not progress rapidly, and patients are usually well-appearing with mild nonspecific symptoms such as anorexia, malaise, headache, arthralgia, myalgia or abdominal pain. Lymph nodes usually enlarge over 2–3 weeks, stabilize for 2–3 weeks and then resolve over 2–3 weeks. Any stage may be more prolonged; symptoms rarely exceed 6 months. Histologic examination reveals granulomas with central necrosis and multiple microabscesses. Up to 10% of lesions may suppurate and require needle or open drainage. CSD lymphadenopathy does not produce chronic draining fistulous tracts when incised and drained. The most common atypical manifestation is Parinaud’s oculoglandular syndrome (POGS) consisting of unilateral preauricular lymphadenopathy and conjunctivitis. Palpebral conjunctivas demonstrate a 2to 3-mm red-yellow nodule or nodules, the equivalent of the inoculation papule seen with a scratch. Although POGS can be caused by other infections, B. henselae is the most common etiology. POGS is a predictable, self-limited infection with full recovery regardless of treatment in most cases. Fever of unknown origin (FUO) and hepatosplenic CSD represent dissemination that may present in immunocompetent patients as daily spiking fevers lasting weeks to months. Frequently patients have an elevated erythrocyte sedimentaFrom Tripler Army Medical Center, Honolulu, HI Copyright © 2004 by Lippincott Williams & Wilkins ISSN: 0891-3668/04/2312-1161 DOI: 10.1097/01.inf.0000147366.70208.7e CONTENTS Spectrum and Treatment of Cat-Scratch Disease Urinary Tract Infection Treatment and Evaluation: Update