brucellosis is a zoonotic disease caused by intracellular gram - negative bacteria of the brucella genus . brucella melitensis is known to be the most common etiological agent of human brucellosis in turkey . neurobrucellosis is a rare , severe form of systemic infection with a broad range of clinical syndromes . the broad spectrum of clinical involvement and nonspecific signs and symptoms may interfere with an early diagnosis of this disease . among its varied presentations , we present a rare case of neurobrucellosis with an isolated brain mass , mimicking a cerebral tumor in which the specific diagnosis was made via bacterial isolation in the blood and seroagglutination in the cerebrospinal fluid ( csf ) . a 20-year - old woman presented with left arm and leg numbness and weakness for 1  month . one week before admission , the symptoms had become particularly severe ; they had been accompanied by a mild headache . the diagnosis of brucellosis was first made 4  months previously . at that time , she was treated with rifampicin 600  mg / day and doxycycline 200  mg / day for 45  days . she had remained free of symptoms until 1  month previously . upon examination , the differential blood count indicated 85.6% neutrophils and 4.8% lymphocytes . the c - reactive protein ( crp ) value ( 40  mg / dl ) and sedimentation rate ( 38  mm / h ) were elevated . an initial serological titer for brucella was positive at 1:640 via wright s agglutination test . then , blood cultures were sent for brucella . magnetic resonance imaging ( mri ) showed a 1.5    1.5 cm enhancing nodular lesion with moderate surrounding edema in the right parietal lobe ( fig .  1 ) . the final examination of the pathological specimens showed a nongranulomatous encephalitis that consisted of diffuse lymphocytic infiltrates and perivascular lymphocytic cuffing ( fig .  2 ) . these observations led us to investigate the etiology of encephalitis . then , a lumbar puncture was performed . examination of the csf showed no pleocytosis , a protein concentration of 48  mg / dl , and a glucose level of 52  mg / dl . csf samples were sent for gram and ziehl - neelsen staining and bacterial , mycobacterial , and fungal cultures . polymerase chain reaction ( pcr ) testing for mycobacterium tuberculosis was performed as well . all results , as well as those of the csf serologies for cytomegalovirus ( cmv ) , epstein barr virus ( ebv ) , herpes simplex virus type 1 and 2 ( hsv-1 and hsv-2 ) , rubella , and toxoplasmosis , were negative . serum serologies for human immunodeficiency virus , serum hepatitis c , cmv , ebv , hsv-1 and hsv-2 , rubella , borrelia burgdorferi , toxoplasmosis , and syphilis , except for serum hepatitis b , were negative . wright s agglutination test in the csf was positive at 1:320 titers . eventually , brucella melitensis was isolated in the blood culture . based on these findings therapy with rifampin ( 600  mg / day ) , trimethoprim  sulfamethoxazole ( 6403,200  mg / day ) , and ceftriaxone ( 2  g / day ) was started and continued for 3  weeks . thereafter , therapy with rifampin ( 600  mg / day ) and trimethoprim  sulfamethoxazole ( 6403,200  mg / day ) was maintained , but ceftriaxone was replaced with doxycycline ( 200  mg / day ) , and the new antimicrobial combination was planned to be continued for 6  months . on hospital day  14 , the patient s symptoms had apparently subsided . during the next 6  months , the patient will be followed up closely with serological , microbiological , and mri imaging assays until complete recovery.fig . 1a axial t1-weighted gadolinium - enhanced image shows a strongly enhancing 1.5    1.5 cm nodule in the right parietal cortex surrounded by vasogenic edema . b axial t2-weighted image demonstrates vasogenic edema surrounding a low - signal central nodulefig . a hematoxylin and eosin ( h&e)-stained brain section shows scattered lymphocytic infiltrates and perivascular lymphocytic cuffing . b brain section stained for leukocyte common antigen demonstrates perivascular lymphocytic cuffing a axial t1-weighted gadolinium - enhanced image shows a strongly enhancing 1.5    1.5 cm nodule in the right parietal cortex surrounded by vasogenic edema . b axial t2-weighted image demonstrates vasogenic edema surrounding a low - signal central nodule nongranulomatous encephalitis . a hematoxylin and eosin ( h&e)-stained brain section shows scattered lymphocytic infiltrates and perivascular lymphocytic cuffing . brucellosis is still a significant health problem in many parts of the world , especially in the mediterranean and middle east regions . brucella melitensis infection is endemic in certain areas of turkey , such as the eastern and southeastern anatolia regions . our case also had an etiological agent of infection , called b. melitensis , and said patient had lived in the southeastern anatolia region of turkey . central nervous system ( cns ) involvement in brucellosis or neurobrucellosis is rare . because of its nonspecific manifestations and broad spectrum of clinical syndromes , neurobrucellosis mass lesions in the brain are extremely uncommon and can be documented radiologically and pathologically . in the present study , we encountered brucella encephalitis , presenting as a solitary brain mass , mimicking a cerebral tumor , but there was no meningeal inflammation . to date , neurobrucellosis with a solitary intracranial mass mimicking a cerebral tumor has been documented in only two adult patients [ 1 , 3 ] . in only one of these cases was the definitive diagnosis of neurobrucellosis made via bacterial isolation ; brucella melitensis was cultured in postoperative brain tissue specimens . our patient is the second case of neurobrucellosis to be misdiagnosed as a brain tumor before the identification of encephalitis caused by brucella melitensis . the differential diagnosis of a mass - occupying lesion with enhancement after the administration of a contrast agent is a brain tumor or abscesses . in our patient , mri imaging revealed an enhanced lesion with vasogenic edema in the right parietal lobe , interpreted as a cerebral tumor . in this case , the diagnosis of nongranulomatous encephalitis was made after a neurosurgical cerebral biopsy . the other adult patients with neurobrucellosis mimicking a brain tumor showed the histopathological findings of marked granulomatous encephalitis in previous studies [ 1 , 3 ] . nongranulomatous encephalitis was reported only in a child with focal cerebral involvement from neurobrucellosis . despite optimal antimicrobial treatment , brucellosis presents as an infectious disease with a tendency to progress to a chronic state , accompanied by relapses . as per pathogenesis of neurobrucellosis , because of direct invasion of bacteria through the cns during the acute bacterial period or the capability of brucella bacteria to survive for prolonged durations in phagocytes , it may develop after a long time following a disturbance in host immunity . noncompliance to treatment is another important factor that increases the risk of chronicity [ 8 , 9 ] . the other potentially treatable conditions that may mimic viral encephalitis are abscesses , subdural empyema ( bacterial , listerial , fungal , mycoplasmal ) , tuberculosis , toxoplasmosis , tumor , systemic lupus erythematosus , toxic encephalopathy , vascular disease , fungal infections ( mucormycosis ) , rickettsia , and cryptococcus . remarkably , here the specific diagnosis of neurobrucellosis is based on seroagglutination ( positive wright s agglutination or coombs test at 1:160 titers ) in the csf and blood and csf cultures ( positive in < 15% of the cases ) , which have relatively low sensitivities . because isolation of the organism in the csf and serum is rarely possible , the diagnosis is usually made by seroagglutination in the csf . furthermore , the culture of surgical or biopsy specimens may reveal a localized infection caused by brucella species , such as neurobrucellosis [ 3 , 12 ] . brucellosis requires high suspicion to dismiss the diagnosis in endemic areas . in our case , the definitive diagnosis of neurobrucellosis was established by isolating brucella melitensis in the blood culture and a positive wright s agglutination test in the csf at 1:320 titers . brucella - related cerebral masses can be treated medically , reducing the potential long - term neurological complications of resection . in our case , we unexpectedly found neurobrucellosis as the cause of a solitary intracranial mass lesion . therefore , our patient underwent a mass resection before medical therapy . in conclusion , despite its rareness , it is crucial that neurobrucellosis be considered in the context of a solitary intracranial mass lesion in the differential diagnosis of cerebral tumors , particularly in endemic areas . hence , patients having these lesions , with either granulomatous or nongranulomatous encephalitis , should be studied for brucella with blood and csf cultures and serological tests in the serum and csf .
among the diverse presentations of neurobrucellosis , solitary intracranial mass lesions are extremely rare . to the best of our knowledge 
 , we describe here the second case of neurobrucellosis mimicking a cerebral tumor caused by brucella melitensis . 
 the mass lesion was clinically and radiologically indistinguishable from a brain tumor . 
 the diagnosis was established by isolating brucella melitensis in a blood culture and a positive wright s agglutination test on the cerebrospinal fluid at 1:320  titers . 
 paraffin sections of the cerebral mass showed nongranulomatous encephalitis . 
 we suggest that patients with an isolated intraparenchymal mass lesion with nongranulomatous encephalitis should also be studied for brucellosis in endemic areas .