Balakrishnan et al. Parasites & Vectors (2016) 9:254
DOI 10.1186/s13071-016-1547-9

SHORT REPORT

Open Access

Vasculitis, cerebral infarction and persistent
Bartonella henselae infection in a child
Nandhakumar Balakrishnan1, Marna Ericson2, Ricardo Maggi1 and Edward B. Breitschwerdt1*

Abstract
Background: The genus Bartonella is comprised of a rapidly increasing number of pathogenic species that induce
a seemingly diverse spectrum of neurological symptoms. During the 12 year period that followed the initial onset
of neurological and gastrointestinal symptoms, an 11 year-old girl experienced a spectrum of neurological
complaints including frequent headaches, visual and auditory hallucinations, anxiety, vision loss involving the lower
left quadrant of both eyes, episodic bouts of generalized paralysis, facial palsy, chronic insomnia, seizures, dizziness,
cognitive dysfunction, and memory loss. PCR assays targeting Bartonella spp. were used to test formalin-fixed,
paraffin embedded brain tissue, patient blood specimens and Bartonella alpha Proteobacteria growth medium
(BAPGM) enrichment blood cultures. PCR positive amplicons were sequenced directly and compared to GenBank
sequences. Bartonella spp. serology was performed by indirect fluorescent antibody testing and confocal laser
scanning microscopy was used to visualize B. henselae organisms in resected brain.
Results: Bartonella henselae DNA was independently PCR amplified and sequenced from the girl’s right parietal
lobe, surgically resected in 2000 and from a blood specimen collected in 2012. Although causation cannot be
established by a case report, prior diagnostic testing resulted in findings that were either inconclusive or within
normal reference ranges and no etiological diagnosis had been obtained to explain the patient’s initial or
progressive neurological symptoms.
Conclusions: As intravascular, intra-erythrocytic and endotheliotropic bacteria, it is possible that B. henselae initially
induced a vasculitis, resulting in secondary cerebral infarction, tissue necrosis and surgical resection. Bartonella
bacteremia, potentially spanning a 12-year time frame, in conjunction with the therapeutic administration of
immunosuppressive drugs may have resulted in a progression and potentiation of the neurological disease that
was partially reversible following antibiotic administration.
Keywords: Neurobartonellosis, Bartonella henselae San Antonio 2 vasculitis

Background
As recently reviewed, an increasing number of Bartonella
species have been identified as zoonotic pathogens that
are transmitted by animal bites or scratches, needle sticks,
blood transfusions, or by arthropods [1–4]. Potentially, because Bartonella spp. can infect erythrocytes, endothelial
cells, pericytes, and various macrophage-type cells, vascular pathology may be much more diverse than is currently
appreciated [5–7]. Due to current limitations associated
* Correspondence: ed_breitschwerdt@ncsu.edu
1
Department of Clinical Sciences and the Intracellular Pathogens Research
Laboratory, Center for Comparative Medicine and Translational Research,
College of Veterinary Medicine, North Carolina State University, Raleigh, NC,
USA
Full list of author information is available at the end of the article

with diagnostic testing for bartonellosis, a high index of
suspicion is required, particularly in patients with occult,
persistent bacteremia, small vessel disease, or non-specific
symptoms, such as fatigue, insomnia and memory loss
[6, 8, 9]. Because of the rapid discovery of new, pathogenic Bartonella spp., the expanding number of arthropods proven or suspected in transmission, the large
numbers of infected animal reservoir hosts in nature, and
the broad spectrum of neurological abnormalities reported
in recent years, neurobartonellosis may be a much more
prevalent disease in both immunocompetent and immunocompromised patients throughout the world than is
currently recognized [6].

© 2016 Balakrishnan et al. Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0
International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and
reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to
the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver
(http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Balakrishnan et al. Parasites & Vectors (2016) 9:254

Case report
In March 2000, an 11-year-old girl residing in Ottawa,
Canada developed sudden-onset, headaches, difficulty
walking, left sided paresis and an ataxic gait. The family
resided in a rural environment and their home backed
onto an extensive ravine. Shortly before the onset of
neurological symptoms, a feral dog was adopted from
the local humane society. Historically, the owner did not
observe fleas or ticks and the dog did not bite the child.
However, shortly after adoption, the dog developed a
large abscess with purulent discharge in the neck region,
which the child cleaned daily. A few weeks later, the girl
developed flu-like symptoms followed by progressive
neurological abnormalities. Concurrently, she reported
gastrointestinal symptoms, including abdominal pain,
bloating and constipation, which persisted throughout
the patient’s subsequent illness. A Magnetic resonance
imaging (MRI) scan identified a large, focal, demyelinating mass lesion located in the right parietal lobe. Based
upon the MRI and examination of frozen brain tissue
sections obtained at surgery, the mass was presumptively
diagnosed by a neuropathologist as a glioblastoma. The
mass and a portion of the right parietal lobe were surgically resected. Based upon formalin-fixed paraffin embedded (FFPE) tissue histopathology, the diagnosis was
revised to a reactive inflammatory process consistent with
vasculitis, secondary cerebral infarction, and tissue necrosis. The histopathological examination revealed abrupt demarcations between necrotic areas, with accompanying
destruction of axons and myelin. Adjacent brain tissue
contained wide-spread perivascular lymphoplasmacytic infiltration with extension into the vessel wall, resulting in
intimal proliferation and sparse hemosiderin deposition in
both venules and small arteries. There was no evidence of
selective perivascular demyelination. The majority of the
perivascular lymphocytes were T cells, with a few scattered
B cells. Mindbomb E3 ubiquitin protein ligase 1(MIB1)
staining was minimal, except among lymphocytes, and
the tissue was immunonegative for Epstein-Barr virus
(EBV). During the next 3 years, the patient was intermittently treated for a presumptive autoimmune neurological
disease with high dose intravenous corticosteroids. Her
diagnoses included idiopathic vasculitis, Guillain-Barre
syndrome, multiple sclerosis, and acute disseminated encephalomyelitis (ADEM).
In 2003, the patient experienced frequent headaches,
chest pain, visual and auditory hallucinations, anxiety,
ocular floaters, severe depression, and fatigue. Additional
episodes of partial paralysis occurred in 2004 and 2009.
A few weeks prior to each of the three episodes, the patient experienced a non-febrile respiratory illness. In July
2004, after returning home from a sailing camp, the girl
developed neurocognitive abnormalities, after which
there was rapid deterioration in muscle strength with

Page 2 of 6

left sided paralysis, homonymous hemianopia, seizures,
dysphagia, laryngitis, and severe confusion. After initiation
of intravenous immunoglobulin (IVIG) the patient slowly
recovered; however, it was several months before she became ambulatory, and her gait never normalized. During
this time, the patient reportedly developed severe allergic
reactions when ingesting gluten, corn, lactose or pork.
In March 2009, the patient again developed progressive
paresis that was treated with low dose IVIG for 3 days.
Despite initial improvement in neurological status, she developed generalized seizures and status epilepticus a few
days later, requiring plasma exchange and pharmacologicalinduction of a coma, lasting for 10 days. After awakening from the coma, the patient exhibited tetraplegia,
dysphasia, and marked facial palsy. During hospitalization,
treatment consisted of IVIG and fluconazole (Diflucan)
for oral Candidiasis. Serum IgA, IgM and IgG levels were
consistently low, and based upon repeated testing had
never normalized. Due to her unusual clinical presentation and disease progression, a diagnosis of tumefactive
multiple sclerosis was rendered at this time. Shortly following this hospitalization, the family physician suspected
Lyme disease, with equivocal Western immunoblot results
(IgM positive, IgG negative), the patient was treated with
penicillin. Combination therapy with fluconazole, penicillin and IVIG appeared to facilitate rapid improvement in
neurological status, including improved ambulation, decreased headaches, and improved cognitive function.
Overall, there was a cumulative deterioration in neurological status following each of the three distinct paralysis episodes (2000, 2004, 2009); however, there was no
observable disease progression between these episodes.
After 2009, the patient’s neurological disabilities resulted
in limited daily activities and required physical support
and full-time care. In October of 2011, based upon the
patient’s historical symptoms, a physician in Vancouver
clinically suspected co-infections consisting of Lyme
disease, babesiosis and neurobartonellosis. Because of a
history of night sweats (starting in 2000), the patient
was treated with atovaquone (Mepron) 1 tsp. twice
daily, azithromycin (Zithromax) 500 mg, intravenously
once daily and ceftriaxone (Rocephin®) 2 g intravenously 5 days each week for 8 weeks. After initiation of
this treatment regimen, the patient experienced dramatic
improvement, including partial resolution of facial palsy
within 2 weeks, resolution of severe jaw and chest pain,
cessation of night sweats, clearer thinking and speech, and
a decrease in the frequency of floaters; all historical problems reported since illness onset. On February 14, 2012,
the mother contacted the corresponding author by email
and requested that her daughter be entered into an Institutional Review Board (North Carolina State University,
College of Veterinary Medicine, IRB #164-08-05, NCSUCVM IRB) approved research study.

Balakrishnan et al. Parasites & Vectors (2016) 9:254

Methods
Serology

For this study, all serum samples were tested by indirect fluorescent antibody (IFA) assays using a panel of
Bartonella antigens. Briefly, antibody responses to Bartonella henselae strain Houston I, B. henselae strain San
Antonio 2 (SA2 strain type), B. vinsonii subspecies berkhoffii genotype I, B. vinsonii subspecies berkhoffii genotype II,
B. vinsonii subspecies berkhoffii genotype III, and B. koehlerae were tested by IFA as previously described [4–6].
Seropositive samples were defined as having endpoint titers
≥1:64 using a twofold dilution scale of 1:16 – 1:8192.
Molecular testing

Bartonella testing was performed using the Bartonella
alpha proteobacteria growth medium (BAPGM) platform, as previously described [4–8]. The primer sequences targeting Bartonella genus specific 16-23S
intergenic transcribed spacer (ITS) and B. koehlerae
species specific 16-23S ITS were used [4–8]. BAPGM
cultures were processed in a biosafety cabinet with
HEPA filtration in a limited access Biosafety Level II
laboratory. To assess for potential contamination during
blood sample processing into BAPGM, an un-inoculated
BAPGM culture flask was processed simultaneously and
in an identical manner with each batch of patient blood
and serum samples tested.
DNA extraction from formalin fixed paraffin-embedded
(FFPE) brain tissues were tested by PCR for the presence
of Bartonella spp. DNA. Multiple 30μm sections of FFPE
brain tissue was excised using a microtome. Previously,
we described Bartonella spp. DNA carryover, during animal necropsy and during the subsequent processing of tissue samples [10]. Hence, special precautions were taken in
our laboratory when sampling paraffin blocks to minimize
the DNA cross contamination. A negative control paraffin
block, containing no tissue, was cut in between each tissue
block and processed in an identical manner as samples to
determine if any DNA carryover was occurring through
the use of the microtome. Tissues were processed in small
batches and the work surface was thoroughly cleaned
using ethanol and DNAse between each tissue block
tested, to avoid Bartonella spp. DNA carry over between the samples. DNA was extracted using QIAamp
FFPE Tissue Kit (Qiagen, Valencia, CA) following manufacturer’s instructions. Elution buffer was used as a reagent control with each set of DNA extractions. DNA
concentrations and purity were determined using a
spectrophotometer (Nanodrop, Wilmington, DE). Extracted DNA was stored at -20 °C.
Laser confocal immunohistochemistry

To visualize B. henselae, brain tissue sections were
processed using immunostaining as described previously

Page 3 of 6

[11]. Briefly, 20μm paraffin-embedded brain tissue sections were incubated with monoclonal Bartonella henselae antibody (Abcam Cambridge, MA) at 1:100
dilution followed by donkey anti-mouse IgG conjugated to Alexa Fluor 594 (Jackson ImmunoResearch
West Grove, PA) at 1:400 dilution. Secondary antibody
control includes buffer and donkey anti-mouse IgG conjugated to Alexa Fluor 594 (1:400 dilution) only.

Results and discussion
By IFA testing using previously described antigens and
techniques, the patient was not seroreactive to B. henselae (Houston 1 strain type), B. henselae (SA2 strain
type), B.vinsonii subsp. berkhoffii genotypes I, II and III
and B. koehlerae. Using a triple draw approach [12] and
previously described PCR assays targeting Bartonella
genus specific 16-23S ITS and B. koehlerae species specific 16-23S ITS elements, B. henselae (376/380 base
pairs, 99 %) DNA was amplified and sequenced from
one of three of the patient’s blood specimens. At the
time of sample collection, the patient was being treated
with azithromycin and ceftriaxone. BAPGM enrichment
blood cultures were PCR negative following 7 and
14 day incubation periods and no subculture isolate was
obtained. Subsequently, B. henselae (448/448 base
pairs, 100 %) was amplified from the surgically obtained, April 2000 FFPE brain tissue. Intracellular
localization of B. henselae in surgically resected FFPE
brain tissue was visualized by confocal laser scanning
microscopy (Fig. 1).
When BAPGM enrichment PCR testing was performed
in March, 2012, the girl was still experiencing severe
cognitive problems, essential tremors and had musculoskeletal pain and weakness. Based on amplification
of B. henselae from blood and brain tissue, her family
physician initiated antibiotic treatment with intravenous
ceftriaxone (2g intravenously daily), metronidazole
(Flagyl, 250 mg twice daily), and azithromycin (500 mg
daily) for 9 weeks. During the first 2 weeks of therapy, the
patient experienced worsening symptoms, including
cognitive decline, seizures, generalized muscle and joint
pain, after which there was gradual improvement in
overall cognitive function. By August 2012, muscle tone,
visual stress and memory had improved dramatically. By
October 2012, the patient’s mother reported continued
improvement in neurological status. Subsequently, the
patient developed a flu-like illness; however, unlike the
three previous respiratory episodes and for the first time
in 12 years she developed a fever (104 °F), and did not
subsequently develop paralysis.
In October 2012, the patient was retested in conjunction
with the NCSU-CVM IRB study. Prior to sample collection, the patient was not receiving antibiotics. Based upon
repeated IFA testing, she was not seroreactive against B.

Balakrishnan et al. Parasites & Vectors (2016) 9:254

Page 4 of 6

Fig. 1 Bartonella henselae immunoreactivity detected in brain tissue biopsy using laser scanning confocal microscopy. Panel a shows no
immunoreactivity (secondary antibody control). Panel b (arrows) shows immunoreactive B. henselae. Stained samples were imaged using laser
scanning confocal microscopy. Z-stack projections for both images are in-focus projections of 17 0.43μm optical sections for a total thickness of
7 μm. (Olympus PlanApo 63×/1.40 oil objective)

henselae (Houston 1 strain type) B. henselae (SA2 strain
type), B. vinsonii subsp. berkhoffii genotypes I, II and III
and B. koehlerae antigens. Using the triple draw approach
(3 samples sets pulled every other day) [12], B. henselae DNA was not amplified from blood, serum, and
post-enrichment 7 and 14 day BAPGM enrichment blood
cultures. No subculture isolates were obtained. Due to the
chronicity and complexity of the patient’s illness and
because based upon prior instances of rapid neurological deterioration, she refused additional treatment
with immunosuppressive drugs. On follow up, facial
palsy has resolved, neurocognitive function and physical
movement have marginally improved, and her thought processes, (i.e. memory and ability to plan and follow complex
operations) have remained stable. MRIs performed in
2015 and 2016 showed frontal lobe disintegration
without evidence of progressive pathology in other
portions of the brain.
Since 2000, when this patient was initially examined,
there has been a substantial increase in the body of
clinical literature describing a spectrum of symptoms
in patients infected with B. henselae. Despite progress,
Bartonella species in general, and B. henselae in particular, remain incompletely understood in the context
of cellular and vascular tropism, neuropathogenesis,
and the role that persistent intravascular infection
plays in disease expression [6]. During the 12 year
period following the initial onset of neurological and
gastrointestinal symptoms, this patient experienced a
wide spectrum of neurological abnormalities including
frequent headaches, visual and auditory hallucinations,
anxiety, vision loss involving the lower left quadrant
of both eyes, episodic bouts of generalized paralysis, facial
palsy, chronic insomnia, seizures, dizziness, cognitive
dysfunction, and memory loss. During this time frame,

differential neurological diagnoses included gliobastoma
(initial mass lesion), vasculitis of undetermined etiology,
Guillain-Barre syndrome, acute disseminated encephalomyelitis (ADEM), and multiple sclerosis. Based upon
retrospective testing of the parietal lobe mass lesion that
was surgically resected in 2000, a diagnosis of neurobartonellosis seems justified in this patient. Based upon DNA
sequence comparison, B. henselae was successfully PCR
amplified from the FFPE brain tissue and from a blood
specimen obtained in 2012. Using a previously described
technique [11], B. henselae organisms could be visualized
in FFPE surgical brain tissue by laser scanning confocal
microscopy. Additional indirect support for a diagnosis of
neurobartonellosis was provided by the historical deterioration in neurological status that followed administration
of immune suppressive drugs, as compared to gradual improvement in neurological status after the initiation of
antimicrobial therapy.
The extent to which repeated, corticosteroid-induced
suppression of immune function contributed to additional or progressive neurological damage is unknown.
However, there are case reports in which patients treated
with immunosuppressive drugs based upon a “positive”
autoimmune disease test result subsequently developed
B. henselae endocarditis [13, 14]. There are also recent
case reports that describe the medical complexities associated with differentiating occult, intravascular infection
with a Bartonella sp. from autoimmune diseases [15].
The extent to which repeated administration of IVIG
prevents or enhances disease progression in patients
with occult infection also deserves critical consideration.
IVIG administration to a child with Guillain-Barre syndrome did not halt the progressive paralysis prior to an
apparent reversal in the disease process after initiation
of antibiotic therapy [16].

Balakrishnan et al. Parasites & Vectors (2016) 9:254

It is also unclear whether persistent intravascular,
microglial, or cerebrospinal fluid (CSF) infection contributed to the various neurological symptoms or to the
three paresis/paralysis episodes experienced by this patient between 2000 and 2009. Based upon in vitro and in
vivo evidence, B. henselae is an intraerythrocytic and
endotheliotropic bacteria [17]. However, no studies have
addressed the potential localization of the bacterium
within the vasculature versus brain parenchymal tissues
or CSF of human patients. Unfortunately, despite substantial efforts on the part of several research groups, a
pathologically relevant rodent model for bartonellosis or
neurobartonellosis has not been established. Thus,
prospective patient studies are needed to document
intravascular and/or CSF infection with B. henselae,
in conjunction with direct therapies to eliminate the
infection and determine subsequent patient outcomes.
Combined utilization of molecular-based diagnostic
testing, in conjunction with conventional microbiological approaches, are increasingly used in the clinical
setting for the detection of fastidious and non-fastidious
pathogens. While the location of Bartonella during the
nonbacteremic phase of infection is currently unknown,
endothelial cells and bone marrow have been hypothesized as primary niches in both incidental and reservoir
hosts [18, 19]. Negative BAPGM enrichment blood
culture is often attributed to history of antibiotic treatment before sampling as reported in this patient. A crosssectional study by Maggi et al. [20] found that 75 % of
Bartonella-infected humans did not have IFA antibodies
to the infecting Bartonella species or genotype. Although
unproven, chronic intravascular infection with Bartonella
spp. may induce a degree of immunological anergy,
resulting in an undetectable level of organism-specific
antibodies in naturally-infected human patients or other
mechanisms may contribute to seronegativity.
The source of B. henselae infection was not established
for this patient. Although cats are most often implicated
in the transmission of B. henselae to humans (Cat Scratch
Disease), dogs have been infrequently reported as a source
of infection. Shortly before the onset of a flu-like illness,
this child did participate in cleaning purulent material
from an abscess in the dog’s neck region, which could
have potentially contained viable bacteria. Bartonella
henselae can be isolated from the lymph nodes of dogs
and humans with granulomatous lymphadenitis [21]
Recently, French investigators implicated B. henselae
and three Bartonella spp. not previously isolated from
humans, as a cause of undifferentiated chronic illness,
potentially transmitted by ticks [22]. The numerous
modes of transmission in conjunction with the increasingly large number of animals in which B. henselae
bacteremia has been confirmed supports a more overarching disease designation (bartonellosis), rather than the

Page 5 of 6

historical designation of B. henselae-induced Cat Scratch
Disease.

Conclusion
If B. henselae contributed to the onset and progression
of this patient’s illness, a delay in diagnosis and administration of immunosuppressive drugs may have resulted
in a progression and potentiation of the neurological disease, which might have been more effectively managed
pre-surgically by directed antimicrobial therapy. In a
2004 Nature publication by Merrell & Falkow [23], Helicobacter pylori and B. henselae were used to exemplify
the role of “stealth pathogens” in chronic disease causation. Stealth pathogens are characterized by slow bacterial replication time (approximately 22h for B.
henselae), a long incubation period (potentially months
to years), induction of chronic symptomatology, a
non-sterilizing immune response, indirect modes of transmission (all Bartonella spp. are known or thought to be
transmitted by one or more arthropod vector), and a
persistently infected “carrier state”. Based upon evolving
evidence, B. henselae appears to fulfill all criteria for a
stealth, intravascular, and endotheliotropic pathogen that
can induce a chronic neurological symptoms.
Consent
Written informed consent was obtained from the patient
for publication of this report and the accompanying
images.
Competing interests
In conjunction with Dr. Sushama Sontakke and North Carolina State
University, Dr. Breitschwerdt holds U.S. Patent No. 7,115,385; Media and
Methods for cultivation of microorganisms, which was issued October 3,
2006. He is the chief scientific officer for Galaxy Diagnostics, a company that
provides advanced diagnostic testing for the detection of Bartonella species
infection in animals.
Authors’ contributions
NB and RM performed the BAPGM enrichment blood culture, PCR testing of
the patient’s blood and tissue specimens, DNA sequencing and alignments,
and helped generate the first draft of the manuscript. ME performed the
confocal immunohistochemistry. EBB coordinated various aspects of the
investigation and drafted the final manuscript. All authors read and
approved the manuscript.
Acknowledgements
The authors would like to thank Julie Bradley for technical assistance and
Barbara Hegarty for careful review of the manuscript. This case study was
supported in part by the State of North Carolina and donations to the Vector
Borne Disease Research Fund, North Carolina State University Veterinary
Medical Foundation. Publication of this manuscript was sponsored by Bayer
Animal Health in the framework of the 11th CVBD World Forum Symposium
Author details
1
Department of Clinical Sciences and the Intracellular Pathogens Research
Laboratory, Center for Comparative Medicine and Translational Research,
College of Veterinary Medicine, North Carolina State University, Raleigh, NC,
USA. 2Cutaneous Imaging Center, Department of Dermatology, University of
Minnesota, Minnesota, USA.

Balakrishnan et al. Parasites & Vectors (2016) 9:254

Page 6 of 6

Received: 15 April 2016 Accepted: 27 April 2016

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