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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.
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Epidemiology
and Pathophysiology
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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 ...