Clinics in Dermatology (2009) 27, 271280

Bartonellosis
Ciro Maguia, MD , Humberto Guerra, MD, Palmira Ventosilla
Instituto de Medicina Tropical Alexander von Humboldt, Universidad Peruana Cayetano, Heredia,
Apartado Postal 4314, Lima, Per

Abstract Bartonella spp are fastidious bacteria that occur in the blood of man and mammals; they are
usually vector borne but can also be transmitted by animal scratches and bites. The bartonelloses of
medical importance comprise Carrin's disease, trench fever, cat-scratch disease, bacillary
angiomatosis, and peliosis hepatis. Carrin's disease, known as Oroya fever in the acute phase and
verruga peruana (Peruvian wart) in its chronic form, has curious manifestations that, until recently, have
been restricted in their geographic distribution to dwellers of the high, dry Andean valleys, but new sites
of disease are emerging. Trench fever is associated with louse-borne disease and homelessness. Catscratch disease, bacillary angiomatosis, and peliosis hepatis are increasingly being recognized as causes
of human disease, especially in susceptible population groups such as HIV-infected persons. The
Bartonella spp are considered emerging human pathogens. The clinical manifestations, differential
diagnosis, laboratory diagnosis, and treatment of these conditions are discussed.
2009 Published by Elsevier Inc.

Introduction
Bartonella spp are members of the -proteobacteria group
that includes the genera Rickettsia, Ehrlichia, Brucella, and
the plant pathogen Agrobacterium tumefaciens. They are
fastidious bacteria that occur in the blood of man and
mammals. Disease is usually transmitted by hematophagous
insects, such as sandflies (Lutzomyia spp), fleas, and lice, but
can also be transmitted by animal scratches and bites.1
Until recently, the term bartonellosis was applied only
to infections caused by Bartonella bacilliformis that were
endemic in Per, Ecuador, and Colombia.2 Our current
understanding of this genus and our growing appreciation of
the similarities between human infections by different Bar-

tonella spp support the use of this term for all infections
caused by members of the genus Bartonella.1,3
The Bartonella spp are increasingly being recognized as
causes of bacteremia, fever of unknown cause, and culturenegative endocarditis, and are justifiably considered emerging
human infections.4,5 The genus currently has 23 members;
however, only a handful are known to be of medical
significance in humans. These include B bacilliformis, the
cause of Oroya fever and verruga peruana; B henselae, the
etiologic agent of cat-scratch disease, bacillary angiomatosis,
and a cause of fever; B quintana, associated with trench fever,
bacillary angiomatosis (as is B henselae), persistent asymptomatic bacteremia, and culture-negative endocarditis;
B grahami, implicated in neuroretinitis; and B elizabethae.6-8

Carrin's disease
Corresponding author.
E-mail addresses: ciromaguina@yahoo.com, cirom@upch.edu.pe
(C. Maguia).
0738-081X/$ see front matter 2009 Published by Elsevier Inc.
doi:10.1016/j.clindermatol.2008.10.006

Bartonellosis, or Carrin's disease, has been recognized

in the riverine valleys of the Peruvian Andes, because the

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pre-Columbian era.9 Because of its changing epidemiology,
however, Carrin's disease is now emerging as a public
health problem in Per.9-11 It is increasingly being seen in the
nonimmune pediatric age group as well as appearing in new
locales in Colombia and Ecuador.2,12,13
The history of our knowledge of this curious disease is
intimately linked with the history of the Callao to Oroya
railway. Connecting the urban centers with the mines and
fertile altiplano (high plain) above Oroya, the project
would become an engineering marvel. Between 1869 and
1873, however, approximately 7000 railroad workers died,
mostly as a result of acute hemolytic anemia. At an
elevation of 4900 meters above sea level, this line remained
the highest standard gauge railway in the world until the
inauguration in 2006 of the QinghaiTibet railway. The
disease associated with the building of the railroad was
named Oroya fever.14
The link between the acute phase of the disease and the
chronic form was made in a brilliant yet tragic piece of
experimentation. In 1885, a Peruvian medical student, Daniel
Alcides Carrin, requested that a classmate friend inoculate
him using fluid obtained from a wart of a hospitalized
patient. Several days later an acute illness with severe anemia
developed, and as his imminent death approached, Carrin
realized that the wart must have contained the causative
agent of Oroya fever.15,16 After Carrin's death from the
disease, his close friend and confidant was arrested, accused
of murder, and finally acquitted legally amid medical and
public admiration for Carrin's sacrifice.
The causative agent, B bacilliformis, was identified in
1905 by Dr Alberto Barton. The condition was named
bartonellosis, but after Carrin's death it became popularly
known as Carrin's disease.14-18
Humans are the only known reservoir host for B
bacilliformis. Once infected, the human host can remain
persistently bacteremic for many months, even after recovery
from the acute illness. Repeated efforts at isolation of B
bacilliformis from mammals other than man have failed.
Identical strains of other Bartonella spp causing bacteremia
in humans have been found in ground squirrels.19
The established vector species in Per is the sandfly, Lutzomyia verrucarum. Only the female transmits disease when
she takes a blood meal. Their preferred habitats are the narrow
river gorges at elevations between 500 and 3200 meters above
sea level. New emerging endemic areas have been reported in
Per and Ecuador, however, situated in the high forest
between the jungle margin and the altiplano.18,20-22
Climate change, in particular the El Nio southern
oscillation phenomenon, which resulted in an extended rainy
season, high humidity, and higher stable temperatures between
1997 and 1998, have been blamed for the sudden increase in
vector populations and subsequent upsurge in endemic
Carrin's disease that occurred in the wake of El Nio.23
A baseline prevalence of 0.5% for asymptomatic Bartonella bacteremia was found in a Peruvian mountain valley
community endemic for bartonellosis. During a 2-year

C. Maguia et al.
prospective survey of this community, an attack rate of
12.7/100 person-years was found. The highest rates were in
children aged younger than 5 years. A linear decrease in
incidence with increasing age suggests an acquired immunity
after exposure.24 In the study, 70% of cases were found in
18% of households. This cluster pattern, which is seen in
other endemic infectious diseases such as malaria and
leishmaniasis and is termed the 20/80 rule, and implies
that 20% of households or individuals in a susceptible
population account for 80% of the disease burden.25 The
study concluded that the most cost-effective control strategy
should focus on those homes where most cases are clustered.
Early case detection and treatment, focusing on infants and
children, would help break the cycle of infection. Costeffective vector control would include residual insecticide
spraying, fine-mesh screens, and use of bed nets.

Clinical presentation
The illness can be divided into 2 distinct clinical phases.
The initial acute phase of the disease (Oroya fever) is
characterized by fever, hemolytic anaemia, headache, pallor,
myalgia, and arthralgia. The second clinical phase occurs
between 2 weeks and several years after clinical recovery and
is characterized by the eruption of crops of nodular skin
lesions or ferruginous skin lesions, or both, predominantly
on the head and distal extremities.
Variously known as verruga peruana, Peruvian wart (the
literal translation), or verruga andcola, the chronic phase of
the disease may present without any history of an acute
illness. Indeed, in a recent outbreak of Carrin's disease in a
nonendemic area, symptoms of Oroya fever developed in
13.8% of the population and verruga peruana developed in
17.6%. The classic biphasic clinical course was seen in just
4.8% of the population. Antibodies against B bacilliformis
were produced in 77.5% of the population, suggesting
widespread subclinical infection within the population.26
Oroya fever
Oroya fever has an incubation period of about 60 days
(range, 10-210 days). Nonspecific prodromal symptoms
malaise, somnolence, anorexia, myalgia, headache, arthralgia of the spine and extremities, chills, and fevergive way
to a rapid deterioration in which the patient becomes
progressively more pale, jaundiced, dyspneic, and confused.
The differential diagnosis of the disease in its early stages
includes typhoid (enteric) fever, malaria, brucellosis, viral
hepatitis (A to C), tuberculosis, leptospirosis, hematologic
malignancies, parvovirus B19, and aplastic and hemolytic
anemias. As the disease progresses, however, the clinical
picture is dominated by one of severe hemolytic anemia
accompanied by generalized lymphadenopathy and hepatosplenomegaly. In severe cases, pericardial effusion,
myocarditis, endocarditis, delirium, convulsions, coma,
acute respiratory distress, anasarca, and multiorganic failure
may occur.

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273

Oroya fever lasts for between 1 and 4 weeks and varies in

severity from mild to fatal. Mortality rates of up to 44% to
88% in untreated patients have been reported; more recent
hospital-based studies suggest significantly lower mortality
rates than were previously thought, with a mortality rate of
0.7% being reported in a contemporary outbreak among a
nonendemic population in Per.26,27
Most deaths are associated with the presence of secondary
infection.28 Salmonellosis used to be the most frequent fatal
complication in hospitalized patients.29,30 Nowadays, the
range of opportunistic pathogens has broadened to include
other bacteria, mycobacteria, protozoa (Toxoplasma and
amoebae), fungi (Histoplasma, Pneumocystis), and viruses
such as herpes and hepatitis B.1 Infection acquired during
pregnancy may result in transplacental infection, which in
turn may lead to fetal death, abortion, and maternal death.
Fig. 2

Verruga peruana
The eruptive phase is characterized by the appearance of
pleomorphic nodular lesions mainly over the arms and legs,
although the face and trunk may be involved (Figure 1).
Lesions vary in size and number and may appear as red or
purple papules a few millimeters in diameter to pedunculated, sessile, or plaque-like lesions several centimeters
across. New lesions may arise for up to 6 months in untreated
patients. The appearance of these eruptions is frequently
accompanied by mild systemic symptoms such as fever

Fig. 1

Verruga peruana in a young girl.

Mular form of the verruga lesion.

(57%), malaise (53%), osteoarticular pain (47%), and

headache (27%).26,31 The angiomatous nodules are prone
to bleeding, with two-thirds of patients complaining of
bleeding warts in a case series in Per.31
Three classical types of lesions have been recognized.
These are:
1. A miliary form of the disease that presents as small
reddish papules, less than 3 mm in diameter, with or
without a penumbra or collar. The lesions may be itchy
and are frequently multiple.
2. The mular form, in which erythematous nodular tumors
more than 5 mm in diameter are present. These are more
often sessile and eroded.
3. The diffuse form, which presents as diffuse subdermal
nodules.
The eruption usually presents as the miliary form with
many hemangioma-like lesions in the dermis, with or
without a collar. The lesions are normally painless. In the
mular form, however, the nodules are more prominent, and
when juxtaposed near joints, they may become painful and
impede joint function (Figure 2). Prominent lesions located
on the extensor surfaces of arms and legs are prone to
bleeding, ulceration, and the complications of secondary
infection. In addition to the skin, the mucous membrane of
the mouth, conjunctiva, and nose may be involved.32
Inhabitants, especially school children, in endemic areas
often develop the eruptive stage as the sole manifestation of
the disease.26 Accompanying chronic arthralgia is more
common in these children.
The eruptive lesions of verruga peruana normally heal
spontaneously, although the course is often prolonged.
Recurring lesions, in both native and nonnative patients,
is unusual.33
Because of its heterogenous manifestations, the cutaneous
lesions of verruga peruana have a wide differential that
includes pyogenic granuloma, hemangioma, bacillary

274
angiomatosis, Kaposi's sarcoma, fibrosarcoma, leprosy
(cystoid form), malignant lymphoma, reticuloendotheliosis,
yaws, lymphomatoid papillomatosis, angiolymphoid hyperplasia with eosinophilia, varicella, molluscum contagiosum,
Spitz nevus, varicella and sarcoma.31-36

Histopathology
The acute form of Carrin's disease, characterized by a
sudden and profound hemolytic anemia, is without other
gross manifestations, and therefore, the histopathology of
Carrin's disease pertains to the chronic cutaneous form of
verruga peruana.
Verruga peruana lesions are remarkable for the intense
angioblastic proliferation reaction that occurs in a way
similar to that observed in other granulomatous tissue.37-39
The histology of verruga peruana may thus mimic
malignant neoplasias, sarcoma, and lymphoma. 35 In
contrast to pyogenic granulomata, no septa appear that
separate the tissue into lobules. Sheets of cells, comprising mostly endothelial and round cells (dermal dendrocytes), make up most of the cellular infiltrate. Dermal
dendrocytes are interspersed by macrophages, lymphocytes, and plasma cells.
Warthin-Starry and Giemsa staining both permit good
visualization of the Bartonella organisms within tissue
specimens. Specific immunohistochemical staining techniques for B bacilliformis have also been developed. The
organisms are observed within the verrugas as both
intracellular inclusions and as free organisms within the
extracellular matrix.
In the miliary form, lesions are situated at the papillary
and medial dermis, whereas mular form lesions tend to
extend deeper into the hypodermis and may involve
subcutaneous tissue, fascia, and muscle.

Diagnosis
The geographic distribution of Carrin's disease is highly
restricted so that a diagnosis can often be made on clinical
and epidemiologic grounds in patients presenting with the
classical symptoms from an endemic area. Diagnostic
confidence is tempered, however, because other diseases
that present similarly are also endemic in these localities. For
a definitive diagnosis isolation of the causative organism is
therefore required. The most common method used is the
microscopic examination of a Giemsa-stained blood smear.
Bartonella organisms are seen as blue-coloured extraerythrocytic and intraerythrocytic bacilli or coccobacilli, or
both. Although B bacilliformis may parasitize up to 100% of
the erythrocytes, sensitivity using this method can be as low
as 36% in unskilled hands.
B bacilliformis can easily be isolated from blood during
the acute stage and somewhat less easily during the eruptive

C. Maguia et al.
stage. Patients with verrucous and other forms of the
cutaneous lesions have been found to have a higher rate of
positive blood cultures (range, 14-52%), indicating their role
as a likely B bacilliformis reservoir.40
Bartonella organisms are facultative intracellular parasites that invade endothelial cells of lymph nodes and
skin. Histology of biopsy material using Warthin-Starry or
Giemsa methods will demonstrate B bacilliformis in the
extracellular and intracellular space. Failing this, isolation
of Bartonella organisms from the skin lesions of verruga
peruana by microbiologic culture is difficult because of
their slow growth and frequent contamination.41 Bartonella spp are best grown in 5% rabbit or sheep blood agar
incubated at between 25 and 28C in a 5% carbon
dioxide environment. Bartonella organisms produce small,
translucent colonies without hemolysis. Blood cultures
require prolonged incubation from 3 to 6 weeks to
become positive.
Serologic methods used in the diagnosis of Carrin's
disease include enzyme-linked immunosorbent assay
(ELISA), immunoglobulin (Ig) M or IgG indirect immunofluorescence, indirect hemagglutination test, and immunoblot
detection of a specific 17- or 18-kDa antigen.42,43 Newer
techniques, such as Western blot and polymerase chain
reaction (PCR), are both more sensitive and specific, but
expense and lack of infrastructure means that their routine use
is likely to be restricted to central reference laboratories.44,45

Treatment
Oroya fever
The acute febrile phase of Carrin's disease requires
prompt antibiotic treatment. Oroya fever was traditionally
treated with chloramphenicol at 50 mg/kg daily up to 3 g/d.
After defervescence, chloramphenicol was continued at half
the dose for a further 10 days because of its activity against
salmonellosis, a common life-threatening secondary complication of the disease.
In vitro antibiotic susceptibility testing of 4 strains of
B bacilliformis of human origin showed good susceptibility
to multiple antibiotic classes including most -lactams
(amoxicillin, ceftriaxone, ceftazidime), chloramphenicol,
rifampin, the macrolides, cotrimoxazole, tetracyclines,
aminoglycosides, and the fluoroquinolones. 46 More
recently, we have had success using oral ciprofloxacin
(500 mg twice daily for 14 days) in patients aged older than
14 years. The use of oral amoxicillin-clavulanic acid in
patients with uncomplicated acute bartonellosis underwent
a trial in Caraz, Per, with similarly good results; the study
included patients aged younger than 14. Combinations of
two antibiotics are used for the more severe cases; the most
commonly used combination is intravenous ceftriaxone (1 g
daily) with ciprofloxacin.47
Transfusions of packed red blood cells may be needed
to treat the very severe anemia that occurs in about 10%

Bartonellosis
of patients. Once the infection is controlled, recovery
from anemia is surprisingly prompt. For cerebral complications such as coma, convulsions (due to the cerebral
hypoxia), and edema, short courses of dexamethasone
have been used.
Verruga peruana
The duration of the eruptive phase of the disease during 3
to 6 months allows the use of several antibiotics in rotation. It
should be noted, however, that chloramphenicol and penicillin
are ineffective during the eruptive stage of infection.
This stage of the disease has traditionally been treated
with intramuscular streptomycin (15-20 mg/kg daily for
10 days), but the use of this agent is problematic, especially
in children. Since 1975 rifampicin has become the drug of
choice and is given at a daily dose of 600 mg in adults and
10 mg/kg in children for 14 to 21 days.47 Treatment failures
on rifampicin have been reported.48 Rapid resistance to
rifampin can develop when rifampin is used alone; thus,
rifampin alone is not recommended for the treatment of any
Bartonella infection, except verruga peruana.
More recently, oral azithromycin (500 mg for 7 days in
adults, or 10 mg/kg daily in children) has been used with
success.47 Alternative agents that have been used successfully include ciprofloxacin and erythromycin.49

Trench fever
Trench fever was described in soldiers during World
War I and is so-called after the trenches in which they
toiled.50 More than 1 million soldiers suffered during this
epidemic. Other synonyms for the disease are quintana
fever, shinbone fever, shank fever, His-Werner disease, and
Wolhynia fever.
The causative organism was initially considered one of
the Rickettsia spp and was designated R quintana. The
organism proved difficult to culture, but the organism was
isolated in 1961 after prolonged cultivation in blood agar.51
R quintana was briefly reclassified within the genus Rochalimaea but is now considered belonging to the genus
Bartonella.52
B quintana is found worldwide. Humans are the only
known reservoir, and once infected may show persistent
asymptomatic bacteremia lasting years.53 The vector of
B quintana is the human body louse, Pediculus humanus
corporis. Homelessness, poor sanitation, and lack of
personal hygiene strongly correlate with disease.54 The rise
in number of homeless and number people living with AIDS
have made trench fever a reemerging disease.52,54

Clinical presentation
Trench fever is usually mild and is rarely fatal. The
incubation period varies between 5 and 20 days, with a mode
of 8 days.52 The clinical course varies from a mild, afebrile

275
state to a moderately severe illness with a protracted
relapsing course over 4 to 6 weeks punctuated by up to 8
febrile episodes, each of about 5 days duration. Some
patients have just a single febrile episode of about 5 days.
Because of the classic 5-day duration of fever, trench fever is
also known as 5-day fever or quintana fever.
The clinical symptoms include malaise, chills, anorexia,
profuse sweating, headache with postorbital pain, marked
conjunctival injection, myalgia, and arthralgia. Bony pain is
particularly severe in the shins, giving rise to the name of
shinbone fever. Pain may also be felt in the neck and spine.
Erythematous macules or papules measuring up to 1 cm in
diameter that appear in crops over the trunk are common. An
evanescent rash that is more easily visible in lightly
pigmented skin is sometimes present.
B quintana has been demonstrated as a cause chronic
bacteremia in homeless people in France and the United
States.3,53 In a study in Marseilles, France, 14% of the
homeless were found to be chronically bacteremic, without
showing any overt signs or symptoms of disease.53 Bartonella endocarditis, (that may have previously been considered under the euphemism of culture-negative
endocarditis), can be difficult to diagnose because repeat
cultures are frequently negative. Cases of Bartonella
endocarditis have been reported in homeless persons.55
Bartonella endocarditis is most frequently caused by
B quintana or B henselae, or both.
Trench fever may be mistaken for other febrile illness,
including typhoid (enteric) fever, malaria, brucellosis,
leptospirosis, dengue, relapsing fever (caused by Borrelia
spp) and typhus (due to Rickettsia spp). Like trench fever,
both relapsing fever and typhus are louse-borne diseases.

Histopathology
Trench fever causes a transient and usually mild febrile
illness for which there are no specific histopathologic
features.

Diagnosis
Epidemiology is the keystone for making a presumptive
diagnosis of trench fever. The diagnosis is confirmed by the
isolation and identification of B quintana. Culture on
chocolate blood agar plates incubated at 35C in 5% carbon
dioxide provide the optimum growth medium, producing
white, adherent colonies. Automated cell culture systems can
also be used for the isolation of Bartonella organisms from
blood and soft tissue samples of infected patients.
Serologic tests used to detect antibodies against B quintana
include the complement fixation test (CFT), hemagglutination
assay, ELISA, and an immunofluorescent antibody (IFA)
assay, the latter being the test recommended by the United
States Centers for Disease Control and Prevention.

276
Real-time nested PCR assays, for use in patients with
suspected Bartonella endocarditis in whom repeated
blood cultures frequently remain negative, have shown
promising results.56

Treatment
Trench fever is a self-limiting disease. Previously, patients
were treated with chloramphenicol or tetracycline with good
result, showing rapid disappearance of symptoms after
2 days of treatment.
In vitro, B quintana is susceptible to penicillin G,
methicillin, tetracycline, ampicillin, cephalothin, gentamicin,
chloramphenicol, erythromycin, clarithromycin, and azithromycin. Patients with chronic B quintana bacteremia should
be treated with intravenous gentamicin (3 mg/kg once daily
for 14 days) in combination with oral doxycycline (200 mg
daily for 28 days).47

Cat-scratch disease
Cat-scratch disease was first described in 1931, but the
etiologic agent was not elucidated until decades later.
Described as a benign inoculative lymphoreticulosis by
Debr and Mollaret in 1950, this newly recognized
clinical syndrome was later referred to as cat-scratch
disease or maladie des griffes du chat.57 A gram-negative
bacillus isolated from the lesions of cat-scratch disease by
Wear in 1981 was considered to be the causative agent.58
Afipia felis was initially considered as the cause, but
further studies showed that (what was then known as)
Rochalimaea henselae (now B henselae), together with
B clarridgeiae and A felis are all causally associated with
cat-scratch disease.1,59
More than 40,000 cases of cat-scratch disease are
reported annually in the United States, resulting in more
than 2000 hospitalizations. The disease usually occurs in
children and young adults with a median age 15 years
(range, 1-57 years) in the United States.60 Cat-scratch
disease is the most common cause of chronic lymphadenopathy in children and adolescents in the United States.61
Epidemiologic studies have determined that cat-scratch
disease is a seasonal illness, affecting the population mainly
during the autumn and winter.57
The worldwide reservoir of B henselae is the domestic
cat. A substantial proportion of domestic cats are infected,
especially in warm, humid climates where Ctenophalides
felis cat fleas thrive.62 In California, 39% of 205 cats tested
had B henselae bacteremia, with up to 50% in some areas
of North America showing antibodies against B henselae.63
In France, B henselae and B clarridgeiae bacteremia
carriage rates among the feral cat population were 53%.64
Feline bacteremia is prolonged, lasting from months to
more than a year, and cat fleas are capable of transmitting

C. Maguia et al.
B henselae between cats.62 It is also possible that these
vectors transmit disease by contaminating cat scratch or bite
wounds with their feces. Human infection occurs after direct
or indirect scratches, bites, or licks of infected cats or from
the bite of an arthropod vector.

Clinical presentation
Cat-scratch disease usually presents as a benign and selflimiting lymphadenitis after a cat scratch or bite but may
progress to a severe, systemic or recurrent form producing
Parinaud's oculoglandular syndrome, encephalopathy, convulsions, osteomyelitis, retinitis, arthritis, hepatitis, splenitis,
erythema nodosum, pulmonary nodules, and pleurisy.65
Approximately 3 to 10 days after inoculation by a cat
scratch or bite, a papular or pustular cutaneous lesion (0.51 cm in diameter) appears at the puncture site. The lesion
heals over 1 to 23 days with crusting. Regional lymphadenomegaly develops during the next 2 weeks affecting
axillary, cervical, inguinal, or epitrochlear and preauricular
ganglia (Figure 3). The ganglia are initially soft; later they
become firm. Most patients (85%) will present with a
solitary lymphadenomegaly; systemic lymphadenomegaly
is exceptional.57
The lymphadenopathy resolves within a median of
7 weeks, with suppuration occurring in 10% to 15% of
patients. Although some patients experience discomfort,
weight loss, nausea and vomiting, and splenomegaly and
low-grade pyrexia, fever greater than 38C is uncommon.
Persistent lymphadenopathy lasting for 6 to 24 months
occurs in 20% of patients. Lesions heal without scar
formation. Antibiotics do not alter the natural history of
cat-scratch disease.

Fig. 3 Regional adenopathy due to Cat-scratch disease (Bartonella henselae).

Bartonellosis
In a prospective study in Lima, the most common
symptoms were fever (91.6%), malaise (58.3%), headache
(33.3%), and chills (16.6%).66 Evidence of a cat scratch or
bite lesion was found in 75% of patients, and cervical
lymphadenopathy was found in 58%.
The differential diagnosis for cat-scratch disease includes
the lymphatic mycoses, including paracoccidioidomycosis,
histoplasmosis, and sporotrichosis; lymphatic tuberculosis,
HIV infection, syphilis, Epstein-Barr virus infection, lymphoma, and the Kikuchi-Fujimoto and Kimura syndromes.67
Numerous atypical manifestations of cat-scratch disease
have been described. These often lack the characteristic
regional lymphadenitis and inoculation site papules leading to
misdiagnosis. Atypical patterns include Parinaud's syndrome
(unilateral follicular conjunctivitis), encephalitis, myelitis,
peripheral neuropathy, unilateral or bilateral choroidoretinitis,
facial nerve palsy, erythema nodosum, subacute infective
endocarditis, granulomatous hepatitis or splenitis, peliosis,
arthritis, osteomyelitis, mediastinal mass, atypical pneumonia,
pleurisy, and fever of unknown origin.68-70
In a report of 61 cases of encephalopathy associated with
cat-scratch disease, 46% had seizures, 40% showed
aggressive personality disorder behavior, and 50% had
fever greater than 38.2C.71 All patients recovered completely within 12 months, and none sustained any permanent
neurologic sequelae.
Disseminated cat-scratch disease in patients with AIDS is
now well described, occurring in patients with very low CD4
counts of typically 50 cells/mL.72

Histopathology
Early cat-scratch disease shows lymphoid hyperplasia
with arteriolar proliferation. Later in the disease course, these
angiolymphoid nodules give way to produce the hallmark
histologic appearance of granulomatous inflammation with
central necrosis producing a stellate pattern of microabscesses. This appearance is not unlike that seen in other
granulomatous diseases such as tuberculosis, lymphogranuloma venereum, tularemia, and brucellosis. The WarthinStarry stain is used to detect Bartonella organisms that are
best seen during the early stages of the disease before
maturation of the granulomas.

Diagnosis
The diagnosis of cat-scratch disease, which formerly relied
upon clinical criteria, delayed-type hypersensitivity to a crude
skin test material derived from infected human tissue containing antigens of B henselae, and histopathology, can now be
established by an IFA test, ELISA, tissue culture, and PCR of
lymph node aspirate or biopsy material.73,74 Each methodology has is drawbacks. There is considerable serologic crossreactivity between B quintana and B henselae. Bartonella spp

277
are notoriously difficult and slow to grow, and show low
sensitivity results for culture of lymph node aspirate (13%) and
peripheral blood (9%). The most cost-effective diagnostic
strategy therefore relies on a combination of epidemiologic
criteria, clinical manifestations, and serology.
The IFA provides the best results with low-passage
bacterial antigen cocultivated with cells. Agar-grown antigens yield lower titers; however, end point titers vary
between different commercial products such that a fourfold
rise in titer or seroconversion is more convincing than a
single high titer. Specific ELISA for cat-scratch disease will
detect IgM antibodies in 53% during the first 3 months,
reverting to negative thereafter. Although initially negative in
28% of patients with acute illness, IgG antibodies are
detected in 92% after seroconversion, and 25% will continue
to have detectable IgG antibodies at 1 year.

Treatment
Typically, cat-scratch disease responds poorly to antibiotic therapy despite good in vitro sensitivity of the
causative Bartonella species to a range of agents. Whether
therapy should be provided at all is unclear because catscratch disease is ordinarily is a self-limited condition. When
antibiotics have been used, erythromycin and doxycycline
have traditionally been the drugs of choice. Many now
consider azithromycin as the drug of choice, however, after a
double-blind, placebo-controlled trial showed it produced
more rapid resolution of lymphadenomegaly.75
The current recommendation for mild to moderate
disease in immunocompetent patients is no antibiotic
treatment. Treatment with an oral azithromycin regimen
of 500 mg on day 1 and 250 mg once daily on days 2 to 5
should be considered for patients with large, bulky
lymphadenopathy.47
Ocular bartonellosis is treated with oral doxycycline
(100 mg every 12 hours) because of its superior ocular
penetration. A 2- to 4-week course is recommended
in immunocompetent patients, with longer courses of
4 months or longer in immunocompromised patients.47,49
Oral combination therapy using 100-mg doxycycline plus
300-mg rifampicin twice daily is sometimes used and has
produced good outcomes in patients with cat-scratch
disease retinitis.

Bacillary angiomatosis
A 1983 report of a new condition in HIV-infected
patients triggered a new line of clinical and basic research
in a field that, until then, had been virtually ignored.
Bacillary angiomatosis was described as a new syndrome of
reactive vascular proliferation induced by bacteria in
patients with AIDS.76 A 1990 study found that angiomatosis was caused by an agent that was very similar to

278

C. Maguia et al.

Rochalimaea quintana.41 During the same year, a gramnegative bacillus was isolated very similar to R quintana
from immunocompetent and immunosuppressed patients
who presented with fever and bacteraemia.77 These were
later reclassified as the Bartonella spp B quintana and
B henselae. Subsequently, B quintana was also detected in
the liver of patients with peliosis hepatis and in the blood of
patients with endocarditis.

Clinical presentation
Bacillary angiomatosis occurs in AIDS patients with CD4
cell counts of less than 100 cells/mm3. B henselae and
B quintana infection stimulates the proliferation and
migration of endothelial cells, resulting in cutaneous
bacillary angiomatosis.78 Less commonly, similar vascular
proliferations may also occur in the liver (bacillary peliosis)
and spleen, lymph node, lung, bone, gastrointestinal tract,
brain, mouth, nose, and anus.79
Lesions can occur as papules, warts, pedunculated or
subcutaneous nodules, or hyperkeratotic plaques. Ulceration
and bleeding may occur. Lesions may be solitary or multiple,
sometimes disseminated over the entire surface of the
body.80 The typical lesion is a reddish-purple papule about
1 cm in diameter (Figure 4). The differential diagnosis
includes Kaposi's sarcoma, verruga peruana (Peruvian wart),
pyogenic granuloma, angiokeratoma, hemangiomas, and
other dermal neoplasias.
Bony involvement is rare, but when present they are
usually isolated, painless, lytic lesions most commonly
affecting the radius or tibia, sometimes indicated by an
overlying cellulitis. The radiographic findings reveal
destruction of the cortical area with periosteal reaction.
Lesions of the mouth, nose, larynx, conjunctiva, lung, pleura,
peritoneum, and anus have also been described.
Peliosis hepatis. A peculiar form of bacillary angiomatosis affecting the liver was described in 1990.81 Until the

Fig. 4

Bacillary angiomatosis.

AIDS pandemic, peliosis hepatis was a rarity associated with

chronic infection, carcinoma, and the use (and misuse) of
anabolic steroids. Histology is characterized by the formation of hepatic venous pools within the hepatic parenchyma.
Of the 12 patients described, 8 were HIV-infected and 2 had
cutaneous bacillary angiomatosis.
A study of 49 patients with bacillary angiomatosis and
peliosis using molecular techniques found that 53% were
caused by B henselae and 47% were caused by B henselae.
Peliosis hepatis was associated exclusively with B henselae,
whereas subcutaneous and lytic bone lesions were strongly
associated with the presence of B quintana.78 Peliosis
hepatis due to B henselae in an organ transplant recipient has
been described.82
Patients with this peliosis hepatis present with weight
loss, fever, abdominal pain, and hepatosplenomegaly. Raised
alkaline phosphatase levels with a normal or slightly elevated
bilirubin and aminotransferase level are typical.28

Histopathology
The basic histologic architecture of bacillary angiomatosis is that of lobular proliferation of endothelium-lined
blood vessels within the superficial dermis. Granulomata are
rare. Bartonella organisms are seen in clumps using
Warthin-Starry stain.
The pathogenesis of the marked angiogenesis seen in
verruga peruana, bacillary angiomatosis, and peliosis is
thought to involve mitogenic factors secreted by the bacteria
in association with endothelial growth factors and interleukins (IL) derived from macrophages and endothelial cells
(IL-1, IL-8, angiopoietin 2). Inhibition of endothelial
apoptosis, possibly through decreased levels of antiangiogenic IL-12 and interferon- in immunocompromised
persons, may also play a role.

Diagnosis
The diagnosis of bacillary angiomatosis should take into
account the epidemiologic, clinical, and laboratory findings. The laboratory methods include histopathology,
serology, microbiologic culture, and Bartonella DNA
detection by PCR.
Histopathology showing classic lobular neovascular
proliferation would strongly support the diagnosis of
angiomatosis and peliosis hepatis. Granulomas are rarely
seen. Bartonella organisms are seen as aggregations of
intracellular and extracellular cocci or coccobacilli, or both,
that stain with Warthin-Starry and Giemsa methods.
B henselae and B quintana have been cultured from lesions,
but their isolation is difficult and culture is positive in only a
few patients.
The most frequently used serologic technique is IFA; IgG
titers against B henselae of greater than 1 in 64 are
considered diagnostic of disease.

Bartonellosis

Treatment
There are no systematic trials for the antibiotic
treatment of bacillary angiomatosis or peliosis hepatis.
Where antibiotics have been given, the drug regimen most
commonly used has been erythromycin (500 mg, four
times daily) for a minimum of 2 months. This may be
administered by mouth or by intravenous infusion, the
latter being the preferred method in severe disease.
Alternative antibiotics that show equally good minimum
inhibitory concentrations in vitro include doxycycline,
minocycline, azithromycin, clarithromycin, and ciprofloxacin. The higher cost of some of these drugs may
discourage their use when inexpensive alternatives are
readily available.47,49
Doxycycline combined with either erythromycin or
rifampicin is recommended in patients with immunodeficiency. The use of rifampicin, a potent cytochrome p450
enzyme inducer, requires dose adjustment when used in
patients taking highly active antiretroviral therapy and
should be used in caution in these patients. Use of one of
the newer rifamycins is preferred.
Relapses of peliosis hepatis and bacillary angiomatosis of
the bone and skin are not uncommon in treated patients.
Relapses almost always occur when antibiotics are given for
a shorter duration of less than 3 months.31

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