Transcript CAT-SCRATCH FEVER Overview Cat-scratch disease is a slowly

CAT-SCRATCH FEVER
Overview
 Cat-scratch disease is a slowly
progressive, self-limiting, chronic
lymphadenopathy that usually occurs in
children.
 Cat-scratch disease, as its name implies,
is transmitted to humans by the scratch
or bite of a cat that has Bartonella
henselae in its saliva and on its nails.
Etiology
 Bartonella
henselae is a rod-shaped
gram-negative organism that causes
cat-scratch disease.
Manifestations
B
henselae can cause several different
diseases depending on the status of a
person’s immune system.
 However, individuals with a normally
functioning immune system who acquire
this organism usually manifest classic catscratch disease with fever and a regional
lymphadenopathy.
 Occasionally, the
organism can cause
symptoms associated with its ability to
infect the brain and retina.
 Immunocompromised hosts
can develop the
diseases illustrated in the figure below as
well as bacillary angiomatosis and peliosis
hepatica.
 Classic
cat-scratch disease has an
incubation period of 1–2 weeks.
 In 50–90% of cases, a 0.5- to 1-cm
brownish papule or pustule forms at
the site of the scratch or bite and is
considered an indicator of cat scratch disease.
 Regional lymphadenopathy follows
within 3–10 days and is often accompanied by fever, malaise, and
 Generally,
the lymph nodes are 1–5 cm
in diameter and proximal to the site
of B henselae inoculation.
 The
most commonly involved nodes
are in the axillary, epitrochlear,
cervical, and supraclavicular areas.
 Over
a period of weeks to months, lymph
nodes may become fluctuant or
suppurative or may spontaneously
regress.
 Full
resolution generally occurs within 1
month, with or without treatment. A
biopsy of lymph nodes will reveal
hyperplasia, granuloma formation, and
suppuration.
 An
increasing number of atypical
manifestations of B henselae infections
are now being recognized as atypical
cat-scratch disease.
 These include complications in the
retina (e.g., Parinaud oculoglandular
syndrome and Leber neuroretinitis),
central nervous system (e.g., catscratch disease encephalopathy and
neuropathy), heart (e.g., endocarditis),
and skin (e.g., erythema nodosum).
 Leber
neuroretinitis is also known as
idiopathic stellate neuroretinitis results
in a loss of visual acuity and a macular
star.
 Patients with Parinaud oculoglandular
syndrome have conjunctival
inflammation with preauricular
adenopathy and a characteristic
granulomatous lesion in the
conjunctiva.
 The
most serious complication of
classic catch-scratch disease is catscratch encephalopathy, with
manifestations of headache, tonicclonic seizures, combative behavior,
and coma.
 These symptoms typically occur
suddenly, 1–8 weeks after the onset of
lymphadenopathy.
 Recovery
is usually complete.
 There
have been no deaths from catscratch disease encephalopathy
confirmed at this time.
 Cat-scratch
disease encephalopathy
occurs in a small number of patients
who have cat-scratch disease.
 Immunocompromised
patients are not
able to keep the Bartonella henselae in
the regional lymph nodes.
 The bacteria can then spread to other
parts of the body via the bloodstream,
resulting in bacillary angiomatosis and
peliosis hepatica.
 Liver biopsies reveal cystic blood filled
spaces in patient with peliosis hepatica.
Epidemiology
 There
are about 25,000 cases of cat-scratch
disease diagnosed each year.
 Most cases of cat-scratch disease occur
during the late summer and early winter
months.
 About 80–90% of cases of cat-scratch disease
occur in patients younger than 21 years of
age.
 B henselae infects kittens and can remain in
the bloodstream for up to 1 year. Bacteremic
cats are more likely to infect their owners
following bites or scratches.
Epidemiology
 Cats
living in the warmer humid
climates of the United States (i.e., the
southeast) are more likely to be
infected with Bartonella henselae.
 Fleas (Ctenocephalides felis) carry B
henselae and can transmit the
bacterium from cat to cat.
 Exposure to kittens is a greater risk
factor for contracting human B
henselae infection than exposure to
adult cats.
Epidemiology
B
henselae can be transmitted to humans
following contact with cats (scratches, bites)
and possibly following contact with cat
fleas.
 Recent studies have shown that B
henselae can live in ticks but as yet there
have been no confirmed cases of tick
transmission this organism to humans.
Pathogenesis
 Cats
are infected with B henselae following the
bite of a flea that carries the bacteria and then
transmits them to humans through a bite or a
scratch.
 B henselae enters the cat’s bloodstream, where it
can live in the erythrocytes for several months to
a year.
 The cat appears to be asymptomatic while B
henselae is in the bloodstream. Researchers do
not completely understand how the organism is
transmitted from the cat’s bloodstream to their
 Once
in the tissue of an immunocompetent
human following a cat scratch or bite, B
henselae are phagocytized by macrophages but
are not killed by the macrophage.
 The bacteria are transported to the lymph
nodes that are in the region of the bite or
scratch. The macrophages produce several
proinflammatory cytokines (e.g., interleukin 1,
[IL-1] and tumor necrosis factor alpha [TNF-])
which recruit neutrophils and macrophages to
the lymph node causing the node to swell.
 The
inflammatory reaction within the node
is granulomatous and consists of a central
zone of necrosis, an inner rim of palisading
macrophages, and an outer rim of
lymphocytes and nonpalisading
macrophages.
 IL-1 induces the fever associated with catscratch disease and activates T-helper
lymphocytes in the node following
presentation of B henselae antigens to the Tcell receptors.
B
henselae occasionally can escape the
lymph node of immunocompetent hosts
and invade the central nervous system,
heart, or skin via the bloodstream,
causing the atypical manifestations
mentioned above.
 There
is very little known about the
pathogenesis of these complications;
however, the complications all resolve
completely with few or no sequelae
following treatment.
 The
activated T-helper lymphocytes
produce TNF-gamma, which induces the
macrophages in the lymph node to produce
nitric oxide.
 Nitric oxide intermediates, following
reaction with oxygen in the tissues, are
produced, which then kill the B henselae in
the lymph node and eliminate the infection.
 The inflammation in the node eventually
resolves and the swelling regresses.
Diagnosis
A
serologic assay (indirect fluorescent antibody
assay) is usually performed to confirm a
diagnosis of classic cat-scratch disease.
 PCR specific for B henselae from a lymph node
biopsy can also be used to confirm a diagnosis
of cat-scratch disease but is not always
available.
 Histopathological
features from a
lymph node biopsy can be helpful but
are not pathognomonic for cat-scratch
disease include granuloma formation,
stellate abscesses, and lymphocytic
infiltrates.
 A Warthin-Starry silver stain or a
Brown-Hopp tissue Gram stain of a
lymph node biopsy revealing the small,
curved, bacilli can aid in diagnosis.
Therapy and Prevention
 The
efficacy of antibiotic therapy currently
has not been proven for classic cat-scratch
disease in immunocompetent hosts.
 Symptomatic care for most patients is
indicated. Swollen lymph nodes will resolve
within 1–6 months.
 The infection usually will resolve in 90% of
patients without treatment, however, there
may be some clinical benefit to treatment
with antibiotics such as azithromycin if
lymph node swelling is extensive.
Table: lists treatment recommendations for
classic and atypical cat-scratch disease.
Disposal of the cat to prevent the
disease is not recommended, since the cat will
only carry B henselae for a limited period of
time; declawing appears to make no
difference. Flea control measures should be
undertaken if there is a cat in the home
environment.
Recommended Treatments for Diseases Caused
by Bartonella henselae
DiseaseTreatment
DiseaseTreatment
Classic cat-scratch disease
None
If lymph node swelling is extensive;
azithromycin
Doxycycline and rifampin
Leber neuroretinitis,
Parinaud oculoglandular
syndrome
Cat-scratch disease
encephalopathy
Endocarditis
Doxycycline and rifampin
Doxycycline and gentamicin
Other medications that have been shown effective in treating
atypical cat scratch disease include ciprofloxacin and trimethoprimsulfamethoxazole.