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Running title: Bartonella henselae in central nervous system
Bartonella henselae and Borrelia burgdorferi infections of central nervous system
Edyta Podsiadły*, Tomasz Chmielewski, Stanisława Tylewska-Wierzbanowska
National Institute of Hygiene, 24 Chocimska street, 00-791 Warsaw, Poland
Phone: +48225421261, fax: +48228493335, e-mail:
Key words : mixed infection, central nervous system, B. henselae
To investigate the role of B. henselae in patients with symptoms suggesting neuroborreliosis, serum
and cerebrospinal fluid samples were tested with serological and PCR methods. Among 17
examined patients, in 12 cases B. burgdorferi infections were detected, in 1 case B. henselae
infection was ascertained and in two patients mixed B. burgdorferi and B. henselae infections were
found. These results indicate that mixed infections should be taken into consideration in
establishing diagnosis of neurological disorders. The conclusion needs further studies.
The aim of our study was to investigate the role of B. henselae in central nervous system disorders
among patients with recognized neuroborreliosis. Since B. henselae and B. burgdorferi sensu lato
shared the same tick vector – Ixodes sp. mixed infections should be considered in the differential for
patients who present with neurological symptoms such as seen with borreliosis. Lyme disease is the
most frequent tick-borne disease in the world. Neurologic abnormalities are prominent in this
disease. During the first stage lymphocytic meningitis with cranial or peripheral nerve palsy and
radiculoneuritis accompanied by stiff neck and headache may occur. In some cases a wide spectrum
of clinical manifestations including encephalopathy, polyneuropathy or encephalomyelitis in course
of disease are present (1).
In 11% of patients with cat-scratch disease neurological symptoms are observed. They include
encephalitis, cerebral arterititis and radiculitis (2). Mixed infection of the central nervous system by
B. burgdorferi sensu lato and B. henselae were described (3).
Material and methods
Seventeen paired serum and cerebrospinal fluid samples were studied. Materials from patients with
various clinical symptoms suggesting neuroborreliosis were sent from various Polish hospitals.
Among them, 9 patients had symptoms of meningitis (headache, nauseea, vomiting and mild neck
stiffness), two persons - sclerosis multiplex, two ones had a headache. In the remaining persons, in
one case double vision with difficulty walking, in the second mediastinal lymphadenitis with
pulmonary interstinal changes, in third depression with paresis of face muscles, in the last one
bilateral facial nerve palsy were observed.
Specific antibodies to B. burgdorferi sensu lato in serum were tested with recombinant antigens p21
(OspC), p41i (inner part of flagellin) for IgM and p21, p41i, p18, p100 for IgG class in ELISA test
(BIOMEDICA, Austria). Serum samples were also tested for the presence of B. henselae and B.
quintana specific antibodies. Levels of serum IgM and IgG immunoglobulins were measured with
indirect immunofluorescence test (MRL Diagnostic, USA).
DNA was extracted from the cerebro-spinal fluid samples with QIAamp tissue kit (QIAGEN,
Germany) according to manufacturer recommendations. Extracted DNA was subjected to PCR
amplification of the 16S rRNA for B. burgdorferi sensu lato (5) and 16S-23S rRNA fragment gene
characteristic for Bartonella species (4).
Reactions were performed in a final volume of 50 ml containing: 10 mM Tris-HCl, 50 mM KCl, 3,5
mM MgCl 2 , 0.1% gelatin, 200 mM dNTPs, 50 pmol of each primer and 2 U of Taq DNA
polymerase (Perkin-Elmer Cetus, USA). Aliquots of 5 ml of DNA template were added to each
reaction mixture. PCR was run in a Mini Cycler apparatus (MJ Research, USA).
Fourteen of 17 examined patients had IgM or IgG antibodies to B. burgdorferi. Three patients with
clinical symptoms suggesting neuroborreliosis were seronegative. The 16S rRNA B. burgdorferi
gene fragment was not detected in CSF samples.
B. henselae infection was detected in three patients.
Patient No. 1
She suffered from meningitis. DNA of B. henselae was found in CFS, he had antibodies to B.
burgdorferi. Although specific antibodies to B. henselae were not found in his serum, it may be
regarded as a mixed infection.
Patient No. 2
Patient suffered also from meningitis. He had IgG antibodies to B. henselae and IgM antibodies to
B. burgdorferi at borderline level. What might indicate a probable mixed infection.
Patient No. 3
Patient complained of headache as a lasting symptom after meningitis due to neuroborreliosis. Two
months before neuroborreliosis was recognized serologically and ceftriaxone regimen was applied.
At the time of testing he was seronegative to B. burgdorferi , but antibodies to B. henselae were
found in titer 64. It might suggest a single B. henselae infection.
These results confirm that B. henselae can be an etiological agent of a central nervous system
infection with symptoms resembling neuroborreliosis. Therefore B. henselae infection should be
considered on the differential when evaluating patients suspected of having neuroborreliosis. Mixed
infections of central nervous system with B. burgdorferi and B. henselae should be taken into
consideration especially in patient group with incomplete resolution of Lyme borreliosis symptoms
after treatment. The conclusion needs further investigation.
1. Steere, A. C. 1989. Medical progress. Lyme disease. N. Engl. J. Med. 321 :586-596.
2. Schwartzman, W. A. 1992. Infections due to Rochalimea : The expanding clinical spectrum.
Clin. Infect. Dis. 15 :893-902.
3. Eskow, E. & R.V. Rao & E. Mordechai. 2001. Concurrent infection of the central nervous
system by Borrelia burgdorferi and Bartonella henselae : evidence for a novel tick-borne disease
complex. Arch. Neurol. 58 :1345-7.
4. Jensen, W. A. & M. Z. Fall & J. Rooney, et al. 2000. Rapid identification and differentiation of
Bartonella species using a single-step PCR assay. J. Clin. Microbiol. 38 :1717-22.
Tylewska-Wierzbanowska, S. & T. Chmielewski. 2001. Improvement of laboratory methods for
Lyme borreliosis recognition. Clin. Microbiol. Infect. 7 suppl.1 :194 (P970).
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