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Cat scratch disease (CSD) is a ubiquitous, self-limited infection characterized by prolonged regional lymphadenitis and often an inoculation site papule, usually after a cat’s (frequently a kitten’s) scratch or bite, and caused primarily by Bartonella henselae. In 10% to 20% of cases, the lymph node will suppurate.1,2 In a minority of cases (approximately 10%), a wide range of extranodal manifestations collectively known as atypical CSD may occur, including fever of unknown origin, as well as visceral, neurologic, and ocular involvement. In immune competent individuals, prognosis is generally good, but infection may be life-threatening and its manifestations different in the immune compromised.


Epidemiology and Pathophysiology


CSD occurs worldwide and is prevalent in warm and humid climates. In temperate zones, CSD occurs primarily during fall and winter, sometimes also during the summer, while in the tropics, it occurs throughout the year.1-3 CSD was, in the past, considered to be mainly a disease of children and adolescents, about 55% males, with approximately 90% of patients younger than 18 to 21 years old.1 Newer studies, however, have reported that 45% and 43% of CSD patients are more than 18 and 20 years of age, respectively.4,5 CSD almost never occurs in children under 2 years of age and is increasingly recognized in all age groups, including the elderly.6 Intrafamilial clustering of CSD occurs rarely,7 though anti-B henselae seropositivity is more frequent in families with a case of CSD than in the general population, indicative of asymptomatic infection.5 Immune deficient people, especially those with HIV, may become severely ill with a unique spectrum of disease.2,8 In 1993, the annual incidence of CSD in the United States was estimated at 9 to 10/100,000 with about 10% hospitalization, and most patients were younger than 21 years old.4 However, indirect transmission of B henselae by red cell transfusion may be possible.19 In 2000, the US annual hospitalization rate for CSD was estimated at 0.6/100,000 and 0.86/100,000 for children under 18 and under 5 years old, respectively; not surprisingly 24% of admissions were for atypical disease, 12% central nervous system (CNS) and 7% visceral.9 Cats, especially kittens under 1 year of age, are the major reservoir and tend to have prolonged, asymptomatic intraerythrocytic bacteremia. They infect humans by scratch, bite, or mucous membrane (conjunctival, respiratory) inoculation.2,5,10-14 The cat flea, Ctenocephalides felis, is associated with increased cat infectivity and with cat-to-cat transmission of B henselae although it probably does not play a major role in cat-to-human B henselae transmission.5,11,15 The observation that in temperate zones CSD incidence peaks in fall and winter while flea infestation of cats primarily occurs during spring and summer argues against the role of the cat flea in human CSD pathogenesis. Felids, dogs, monkeys, and other animals may harbor B henselae, and some have been anecdotally associated with CSD. Inanimate ...

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