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Ahmed M Hassan
King Abdulaziz University
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All content following this page was uploaded by Mohamed Abdel Rahman Arbab on 14 October 2015.
Correspondence:
Mohamed A.R Arbab M.D, Ph.D.
Department of Surgery, Faculty of Medicine, University of Khartoum.
P.O Box 13456 Khartoum.
Email: mohamedarbab@hotmail.com Field Code Changed
Abstract Formatted: Font: 11 pt, Font color: Auto,
Complex Script Font: 11 pt
A 13 and 35-year-old female patients presented in humans. It was first reported in 1990 and
because of fatigability, nocturnal febrile described as a new species in 1992. The
illness,generalized body aches and worsening pathogen is mainly carried by cats and can
headache. In the course of the illness both cause in humans wide spectrum of clinical
patientsdeveloped worsening headache and syndromes that include cat scratch disease,
attacks of epileptic seizure. Brain MRI imaging bacillary angiomatosis, endocarditis and
showedintraaxial cerebral heterogeneous relapsing bacteremia. Central nervous system
irregular masseswith involvement has included encephalopathy,
focalencephalomalacia,cystic component, glial myelopathy, meningitis, cerebral arteritis, optic
reaction and dystrophic calcification. neuritis and radiculopathy (Brazis et al. 1986),
Histological results of the resected pathology (Carithers and Margilet 1991), (Lewis and
revealed highly vascular mass with features Tucker 1986), (Pickerill and Milder 1986),
suggestive of Bartonella henselae. In this (Selby and Walker 1979).
report, the initial course of the disease was that
of febrile illness, a common problem in a Although about 40% of cats carry the bacteria
tropical country, furthermore the symptoms in their saliva but they do not themselves show
were not suggestive of cat scratch disease. manifestations of the disease. Cat scratch
disease mostly is a self-limiting disease that
Key words: Bartonella henselae; brain; resolves without treatment; however, in
cerebral mass immune compromised patients it can cause
serious illness.In this paper, we report 2cases
Introduction of young females who had bizarre symptoms
Bartonella henselae, a bacterial pathogen that lasted for periods of 8 weeks andone year.
known to cause central nervous system disease Development of neurologic symptoms
necessitated imaging of the brain which
revealed intra- axial brain masses with cystic followed by headache, failing vision and
component mimking cerebral neoplasms. The convulsions. The patient was initially been
post-operative diagnosis ofBartonella henselae investigated for the febrile illness without
was made. conclusive diagnosis. Development of
neurologic symptoms necessitated brain MRI
Case 1 imaging. The images showed intra-axial thick-
A previously healthy 35-year –female walled cystic lesion with perilesional edema
developed general fatigability, nocturnal low (Fig. 1). The patient was subjected to surgery
grade fever, worsening headache, generalized where a thick-walled cystic mass with gliotic
body aches and pains. These symptoms have white to yellowish content was encountered.
been going on for one year. One month before The tumor specimens from both cases 1 and 2
presentation to the neurosurgical department, werefixed in neutral formalin saline and
the patient developed neck pain, left ear pain stained with Hematoxylin and Eosin, Warthin
with hyperacuasia and one attack of Starry stain and Masson Fontana and Melan-A
generalized epileptic seizure. The patient for melanin. Aggregates of small black
reported in the past history of the illness vague filamentous structures suggested Bartonella
abdominal pains and diarrhea and general ill organisms were confirmed by a mono-clonal
health that necessitated blood transfusion. The antibody specific for B henselae. It was Mouse
patient denied history of any skin scratching or monoclonal antibody: Anti-Bartonella
joints pain. henselae (Cat Scratch Fever) antibody
MRI brain showed a left temporal [H2A10] (ab704) Abcam Call (888) 77-
heterogeneous irregular mass lesion with focal ABCAM (22226. It was obtained from the
encephalomalacia, glial reaction and dystrophic USA
calcification(Fig. 1). The patient was operated The cell phenotypes in the lesions were
upon. Left craniotomy flap was reflected. The identified by indirect Immunoperoxidase stains
dura was then opened, this was found adherent that included CD3, CD20, and CD68. IgG and
to the underlying pia-arachnoid. A bright - Complement C3a, C3b and C5a were also
yellowish firm nodular mass with a tuft of stained for. CD34 was used for identification of
numerous tiny vessels was encountered. The blood vessels.
tumor mass was gradually resected and the
vascular part secured by coagulation and freed Results
from the Sylvain vessels.
The histologic sections showed inflammatory
The patient had uneventful post-operative lesions composed of chronic inflammatory
recovery. cells composed of lymphoid cells and
macrophages (Fig. 2). Some of the latter
Case 2 contained hemosiderin positive for iron stain.
A 19 years old female presented because of The lesionswere negative for GFAB. Marked
febrile illness that lasted few weeks to be vascularity of the lesion was a remarkable
finding (Fig. 3. There were foci of necrosis.
Warthin Starry stain showed small linear Cerebral bacillary angiomatosis has been
organisms in small groups and aggregates. The reported in human immunodeficiency virus-
features were characteristic of Bartonella infected patients(Spach et al. 1992).However,
henselae (Fig. 4) the patients in this study were found to be
immune-competent.
Discussion
Of particular clinical importance, in the present
In this report, both patients had states of ill report the Bartonella infection manifested as
health for periods that extended from few cerebral neoplasms as shown in the MRI. Role
weeks up to more than one year. Both of infectious agents in tumor genesis has been
patientswere immune competent. The low reported (Hansen et al 2007), (Moss et al
grade fever, generalized body aches and pains 2007).
in a tropical country enlist a number of
differential diagnoses. In the two Vasoproliferative tumors induced by
patientsneither lymph-adenopathy nor skin Bartonellaspecies were reported as benign and
scratching was reported.Remarkable low can be cured with antibiotic(Rudikoff et al.
hemoglobin in the course of the disease that 1989).
necessitated blood donation could be attributed
to either poor nutritional status of the patient However, in our cases the state of clinical
during her illness or could be part of the presentation and the absence of supportive
pathogenesis of the disease. evidence of possibility of B. hensaele disease
gave no chance for therapeutic trail.
Emergence of headache, visual deterioration,
ear pain, hyperacuasis and convulsive attacks In conclusion Bartonella hensaele infection of
were the early neurologic symptoms that lead the brain can manifest as cerebral neoplasms
ultimately to the diagnosis of the disease. and do not necessarily present as classical cat
scratch disease.Furthermore the relatively late
Bartonella is known as the only genus of presentation of patients with this disease and
bacteria that induces pathological angiogenesis establishment of cerebral neoplasm call for
in mammalian host. The mechanism of surgical intervention.
Bartonella –induced angiogenesis was not well
understood. It was found that these bacteria References
invade human brain vascular pericytes and [1.] Brazis PW, Stokes HR, Ervin FR. Optic
induces increase pericyte production of neuritis in cat scratch disease. J Clin
vascular endothelial growth factor NeurolOpthalmol. 1986; 6:172-174.
(VEGF)(Varanat et al. 2013).
This can explain the pathologic remarkable [2.] Carithers HA, Margileth AM. Cat
vascularity in our cases. Cases of encephalitis scratch disease. Acute encephalopathy
or neuroretinitis havebeen reported with and other neurologic manifestations.
Bartonella henselae infection. Am J Dis Child. 1991; 145:98-101.
Fig 1.
MRI axial cuts A & B (case 1) and C (case 2) showing intraaxial cerebral heterogeneous irregular
masses with focal encephalomalacia, cystic component, glial reaction and dystrophic calcification
AB
Fig 2.
A shows inflammatory cells consisting of lymphocytes and macrophages. Some of the latter had a
clear cytoplasm. In one area there was a focus of necrosis surrounded by chronic inflammatory
cells (H&E X40
A B
Fig 3.
A lesion shows marked angiomatosis as seen in the figure on the left (H&E X40)
B Many macrophages contained brown granular material (Upper figure. H&E X40)) that was
positive for hemosiderin as shown in the slide at the bottom (Prussian blue stain X40)
Fig 4. A Warthin-Starry stain showed numerous bacilli. Some are arranged in clumps.