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Intracranial tuberculosis due to mycobacterium bovis
Comqmterized Ra&/. Vol. II, No. 3, pp. 151-154, Printed in the U.S.A. All rights reserved
0730-4862/87 $3.00 + 0.00 1987 Pergamon Journals Ltd
1987 Copyright
0
INTRACRANIAL TUBERCULOSIS DUE TO MYCOBACTERIUM BO VIS STEVENS. GUEST,’CARLOSJ. BvIT,‘* WILLIAM J. MEISLER,’ ANTHONY C. STEVENS’and GARY L. SIMON’ Departments
of ‘Medicine and ‘Radiology, The George 901 23rd Street, N.W., Washington,
Washington University DC 20037, U.S.A.
(Received 4 September 1986; received for publication 17 December
Medical
Center,
1986)
Abstract-A case of intracranial
tuberculosis due to Mycobacterium bouis is presented. Computed tomography (CT) identified multiple enhancing lesions which by biopsy proved to be intracranial tuberculomas. The CT appearance, epidemiology and bacteriology as well as pharmacotherapy of this uncommon entity are discussed. Computed
tomography
Intracranial
tuberculosis
Mycobacterium bovis Central
nervous
system
infections
INTRODUCTION
Infection with A4ycobacterium bouis is seldom encountered in the United States [l, 21. Compulsory pasteurization of milk and eradication of infected cattle has dramatically reduced human illness with this organism [l]. However, other nations with less rigorous eradication programs still have significant morbidity and mortality from Mycobacterium bovis [3]. We report a case of a Nigerian male who presented with fever and rapidly deteriorating neurologic condition. Computed tomography (CT) of the brain revealed multiple enhancing lesions that proved to be due to Mycoblzcterium bovis tuberculomas. CASE
REPORT
A 31-year-old previously healthy Nigerian male who had recently migrated to the United States was admitted to The George Washington University Hospital after a 2-week history of headache, neck pain and increasing lethargy. Past medical history revealed no known history of tuberculosis or other systemic disease. On admission, the patient was very lethargic, though arousable. He had an oral temperature of 38.3”C, pulse rate of 84 beats/min, blood pressure of 120/85 mmHg and respiratory rate of 16/min. Meningismus was present and fundoscopic examination showed no papilledema. There were no focal neurol’ogic findings. Fundoscopic examination showed no papilledema. The remainder of the physical examination was normal. The WBC count was 49OO/cu mm with 78% neutrophils, 14% lymphocytes, 8% monocytes. The hemoglobin was 14.4 g/gL. Serum electrolytes and other chemistries were normal. Chest roentgenogram revealed moderate mediastinal adenopathy and multiple parenchymal lesions, consistent with granulomas. A contrast enhanced CT scan of the brain revealed multiple enhancing lesions of variable size (Fig. 1) with displacement of the third ventricle across the midline. Moderate dilatation of the lateral and third ventricles was noted. Response to an intermediate strength PPD skin test, as well as to candida and mumps antigen was negative. During the first 48 hours of hospitalization his mental status rapidly deteriorated and he became more confused and less responsive. A biopsy of one of the intracranial lesions was performed. Acid fast bacilli were noted on stains of the biopsy specimen. Bacterial and fungal stains were negative. The patient was started on Rifampin, Isoniazid and Ethambutol as well as Decadron. His mental status progressively deteriorated and by the seventh day of hospitalization he was unresponsive to any stimuli and his pupils were non-reactive. Repeat CT scans of the brain revealed progressively worsening hydrocephalus with all ventricles enlarged which failed to improve after ventriculostomy placement. He continued to receive anti-tuberculous therapy but remained unresponsive and expired * please address reprint requests and correspondence Center,
901 23rd
Street,
N.W.,
Washington,
to: Carlos J. Skit, DC 20037, U.S.A. 151
M.D., The George
Washington
University
Medical
152
STEVENS. GUEST rf al.
Intracranial
tuberculosis
due to Mycobac&Gm
bor;is
153
5 weeks after admission. Approximately 4 weeks after inoculation acid fast bacilli grew from the biopsy specimen, which were identified as Mycobacterium bovis. Colonies were sensitive to Rifampin, Isoniazid and Etham butol. DISCUSSION Before compulsory pasteurization of milk in the 1920’s, Mycobacterium bovis tuberculosis was relatively common in humans [4]. In recent years it has been relatively rare, accounting for 0.2-l% of all cases of tuberculosis in several North American reports [I, 2,5]. Most of these sporadic cases have been felt to represent a recrudescence of infection acquired during childhood or reactivation of the attenuated strain of Mycobacterium bovis contained in the BCG vaccine [5]. Intracranial tuberculomas secondary to Mycobacterium bovis have been reported in only one other recent case [6]. That patient had been immunosuppressed secondary to Hodgkins disease. Our patient had no known preceding illness which might have resulted in immunosuppression. He was lymphopenic and anergic when skin tests were applied on admission but no testing for HTLV III/LAV bovis bacillus while was available at that time. It is presumed that he acquired the Mycobacterium in Nigeria where infected cattle are monitored to a lesser extent than in the United States and unpasteurized milk is available. Intracranial tuberculomas have a variable CT appearance. The lesions may be single or multiple,
(b) Fig. 2. Post contrast axial scans 2 weeks following admission demonstrating enlargement of the lateral (a) and third and fourth ventricles (b). A ventriculostomy tube is noted with its tip in the third ventricle. Enhancement of the basal cisterns is also noted.
STEVEN
154
S. GUEST et al.
infratentoral of supratentorial, isodense or hyperdense on a nonenhanced scan, and are associated with varying degrees of associated edema and mass effect [7]. Following the administration of intravenous contrast, two patterns of enhancement have been described, a peripheral ring surrounding diffuse form of enhancement [7]. CT in our patient showed a central lucent region and a “nodular”, multiple, minimally hyperdense, supratentorial and infratentorial lesions of variable size without surrounding edema (Fig. 1). Following the administration of intravenous contrast some lesions showed diffuse enhancement while others showed peripheral enhancement. On subsequent scans contrast enhancement surrounding the basal cisterns as well as progressive hydrocephalus ultimately involving all of the ventricles was noted (Fig. 2). These findings suggested tuberculous meningeal involvement. Mycobacterium bovis infection should be suspected if acid fast bacilli are obtained that reveal slow dysgonic growth on glycerol containing media but uninhibited growth on glycerol free agars [8]. Mycobacterium bovis isolates are niacin and nitrate negative and growth is inhibited by thiopene-2carboxylic acid (TCH) [ 1,8]. Standard anti-tuberculosis therapy employed although a higher incidence of drug resistance has been occasionally reported [8]. In the past decade there has been a large influx of individuals into the United States from developing countries. In the proper clinical setting (specifically, a history of consumption of unpasteurized milk) Mycobacterium bovis infection should be added to the differential of intracranial enhancing lesions and early cerebral biopsy should be considered. SUMMARY Computed tomography detected multiple enhancing intracranial lesions in an acutely ill patient. A diagnosis of Mycobacterium bovis tuberculosis was established by biopsy of one of the lesions. This is a rare infection that should be suspected in the proper clinical setting. REFERENCES 1. A. G. Karlson and D. T. Carr, Tuberculosis caused by Mycobacterium boois, Ann. Im. Med. 73, 979 2. B. Damsker, E. J. Bottone and S. S. Scheierson, Human infections with Mycobacferium bouis, Ann. Rec. 446 (1974). 3. P. N. Tandon and S. N. Pathale, Intracranial tuberculomas, in Tropical Neurology, J. D. Spillane, Ed, p. Press (1973). 4. J. H. Steele and A. F. Ranney, Animal tuberculosis, Am. Rev. Tuberc. 77, 908 (1968). 5. W. D. Wigle, M. S. Ashley, E. M. Killough and M. Cosens, Bovine tuberculosis in humans in Ontario,
(1970). Respjr. ~i.~. 110,
51. Oxford
Univ.
Am. Ret’. Respir.
Dis. 106, 528 (1972).
6. P. D. Heath
and J. W. Grant,
Intracranial
infection
due to Mycobacterium
both
in Hodgkin’s
disease,
Br. Med. J. 288
465 (1984).
I. M. A. Whelan and J. Stern, Intracranial 8. P. G. Jones and J. Silva, Mycobacterium
tuberculoma, Radiology 138, 75 (1981). bouis meningitis, J. Am. Med. Assoc. 247, 2270 (1981).
About the Author-STEVEN S. GUEST is a senior resident in Internal Medicine at the George Washington University Medical Center. Originally from Montgomery, Alabama, Dr Guest received a B.A. from Emory University and an M.D. from Vanderbilt University. He plans a career in international health-infectious disease. About the Author-CARLOS J. SIVIT received a B.S. degree from the George Washington University and his M.D. from the University of Virginia. Dr Sivit completed a pediatrics residency at Vanderbilt University Hospital and is currently a senior resident in Diagnostic Radiology at George Washington University Medical Center. He plans a career in pediatric radiology. About the Author-WILL.IAM MEISLER is Assistant Professor of Diagnostic Radiology at the George Washington University Medical Center. Dr Meisler received a B.A. and M.D. from Columbia University followed by residency training in Diagnostic Radiology at Columbia-Presbyterian Medical Center. He completed a neuroradiology fellowship at New York University. He is a member of the Radiologic Society of North America as well as a senior member of the American Society of Neuroradiology. About the Author-CHRIS STEVENSis a senior resident in Internal Medicine at the George Washington University Medical Center. Dr Stevens received his B.A. degree from the University of North Carolina at Chapel Hill. He received an M.D. from the University of Miami. After completion of his residency training he plans to pursue a career in gastroenterology. About the Author-GARY L. SIMON is Associate Professor of Medicine and Associate Chairman of the Department of Medicine. He received an M.D. and completed his residency training in Internal Medicine at the University of Maryland. He completed an Infectious Diseases fellowship at Tufts University.
0730-4862/87 $3.00 + 0.00 1987 Pergamon Journals Ltd
1987 Copyright
0
INTRACRANIAL TUBERCULOSIS DUE TO MYCOBACTERIUM BO VIS STEVENS. GUEST,’CARLOSJ. BvIT,‘* WILLIAM J. MEISLER,’ ANTHONY C. STEVENS’and GARY L. SIMON’ Departments
of ‘Medicine and ‘Radiology, The George 901 23rd Street, N.W., Washington,
Washington University DC 20037, U.S.A.
(Received 4 September 1986; received for publication 17 December
Medical
Center,
1986)
Abstract-A case of intracranial
tuberculosis due to Mycobacterium bouis is presented. Computed tomography (CT) identified multiple enhancing lesions which by biopsy proved to be intracranial tuberculomas. The CT appearance, epidemiology and bacteriology as well as pharmacotherapy of this uncommon entity are discussed. Computed
tomography
Intracranial
tuberculosis
Mycobacterium bovis Central
nervous
system
infections
INTRODUCTION
Infection with A4ycobacterium bouis is seldom encountered in the United States [l, 21. Compulsory pasteurization of milk and eradication of infected cattle has dramatically reduced human illness with this organism [l]. However, other nations with less rigorous eradication programs still have significant morbidity and mortality from Mycobacterium bovis [3]. We report a case of a Nigerian male who presented with fever and rapidly deteriorating neurologic condition. Computed tomography (CT) of the brain revealed multiple enhancing lesions that proved to be due to Mycoblzcterium bovis tuberculomas. CASE
REPORT
A 31-year-old previously healthy Nigerian male who had recently migrated to the United States was admitted to The George Washington University Hospital after a 2-week history of headache, neck pain and increasing lethargy. Past medical history revealed no known history of tuberculosis or other systemic disease. On admission, the patient was very lethargic, though arousable. He had an oral temperature of 38.3”C, pulse rate of 84 beats/min, blood pressure of 120/85 mmHg and respiratory rate of 16/min. Meningismus was present and fundoscopic examination showed no papilledema. There were no focal neurol’ogic findings. Fundoscopic examination showed no papilledema. The remainder of the physical examination was normal. The WBC count was 49OO/cu mm with 78% neutrophils, 14% lymphocytes, 8% monocytes. The hemoglobin was 14.4 g/gL. Serum electrolytes and other chemistries were normal. Chest roentgenogram revealed moderate mediastinal adenopathy and multiple parenchymal lesions, consistent with granulomas. A contrast enhanced CT scan of the brain revealed multiple enhancing lesions of variable size (Fig. 1) with displacement of the third ventricle across the midline. Moderate dilatation of the lateral and third ventricles was noted. Response to an intermediate strength PPD skin test, as well as to candida and mumps antigen was negative. During the first 48 hours of hospitalization his mental status rapidly deteriorated and he became more confused and less responsive. A biopsy of one of the intracranial lesions was performed. Acid fast bacilli were noted on stains of the biopsy specimen. Bacterial and fungal stains were negative. The patient was started on Rifampin, Isoniazid and Ethambutol as well as Decadron. His mental status progressively deteriorated and by the seventh day of hospitalization he was unresponsive to any stimuli and his pupils were non-reactive. Repeat CT scans of the brain revealed progressively worsening hydrocephalus with all ventricles enlarged which failed to improve after ventriculostomy placement. He continued to receive anti-tuberculous therapy but remained unresponsive and expired * please address reprint requests and correspondence Center,
901 23rd
Street,
N.W.,
Washington,
to: Carlos J. Skit, DC 20037, U.S.A. 151
M.D., The George
Washington
University
Medical
152
STEVENS. GUEST rf al.
Intracranial
tuberculosis
due to Mycobac&Gm
bor;is
153
5 weeks after admission. Approximately 4 weeks after inoculation acid fast bacilli grew from the biopsy specimen, which were identified as Mycobacterium bovis. Colonies were sensitive to Rifampin, Isoniazid and Etham butol. DISCUSSION Before compulsory pasteurization of milk in the 1920’s, Mycobacterium bovis tuberculosis was relatively common in humans [4]. In recent years it has been relatively rare, accounting for 0.2-l% of all cases of tuberculosis in several North American reports [I, 2,5]. Most of these sporadic cases have been felt to represent a recrudescence of infection acquired during childhood or reactivation of the attenuated strain of Mycobacterium bovis contained in the BCG vaccine [5]. Intracranial tuberculomas secondary to Mycobacterium bovis have been reported in only one other recent case [6]. That patient had been immunosuppressed secondary to Hodgkins disease. Our patient had no known preceding illness which might have resulted in immunosuppression. He was lymphopenic and anergic when skin tests were applied on admission but no testing for HTLV III/LAV bovis bacillus while was available at that time. It is presumed that he acquired the Mycobacterium in Nigeria where infected cattle are monitored to a lesser extent than in the United States and unpasteurized milk is available. Intracranial tuberculomas have a variable CT appearance. The lesions may be single or multiple,
(b) Fig. 2. Post contrast axial scans 2 weeks following admission demonstrating enlargement of the lateral (a) and third and fourth ventricles (b). A ventriculostomy tube is noted with its tip in the third ventricle. Enhancement of the basal cisterns is also noted.
STEVEN
154
S. GUEST et al.
infratentoral of supratentorial, isodense or hyperdense on a nonenhanced scan, and are associated with varying degrees of associated edema and mass effect [7]. Following the administration of intravenous contrast, two patterns of enhancement have been described, a peripheral ring surrounding diffuse form of enhancement [7]. CT in our patient showed a central lucent region and a “nodular”, multiple, minimally hyperdense, supratentorial and infratentorial lesions of variable size without surrounding edema (Fig. 1). Following the administration of intravenous contrast some lesions showed diffuse enhancement while others showed peripheral enhancement. On subsequent scans contrast enhancement surrounding the basal cisterns as well as progressive hydrocephalus ultimately involving all of the ventricles was noted (Fig. 2). These findings suggested tuberculous meningeal involvement. Mycobacterium bovis infection should be suspected if acid fast bacilli are obtained that reveal slow dysgonic growth on glycerol containing media but uninhibited growth on glycerol free agars [8]. Mycobacterium bovis isolates are niacin and nitrate negative and growth is inhibited by thiopene-2carboxylic acid (TCH) [ 1,8]. Standard anti-tuberculosis therapy employed although a higher incidence of drug resistance has been occasionally reported [8]. In the past decade there has been a large influx of individuals into the United States from developing countries. In the proper clinical setting (specifically, a history of consumption of unpasteurized milk) Mycobacterium bovis infection should be added to the differential of intracranial enhancing lesions and early cerebral biopsy should be considered. SUMMARY Computed tomography detected multiple enhancing intracranial lesions in an acutely ill patient. A diagnosis of Mycobacterium bovis tuberculosis was established by biopsy of one of the lesions. This is a rare infection that should be suspected in the proper clinical setting. REFERENCES 1. A. G. Karlson and D. T. Carr, Tuberculosis caused by Mycobacterium boois, Ann. Im. Med. 73, 979 2. B. Damsker, E. J. Bottone and S. S. Scheierson, Human infections with Mycobacferium bouis, Ann. Rec. 446 (1974). 3. P. N. Tandon and S. N. Pathale, Intracranial tuberculomas, in Tropical Neurology, J. D. Spillane, Ed, p. Press (1973). 4. J. H. Steele and A. F. Ranney, Animal tuberculosis, Am. Rev. Tuberc. 77, 908 (1968). 5. W. D. Wigle, M. S. Ashley, E. M. Killough and M. Cosens, Bovine tuberculosis in humans in Ontario,
(1970). Respjr. ~i.~. 110,
51. Oxford
Univ.
Am. Ret’. Respir.
Dis. 106, 528 (1972).
6. P. D. Heath
and J. W. Grant,
Intracranial
infection
due to Mycobacterium
both
in Hodgkin’s
disease,
Br. Med. J. 288
465 (1984).
I. M. A. Whelan and J. Stern, Intracranial 8. P. G. Jones and J. Silva, Mycobacterium
tuberculoma, Radiology 138, 75 (1981). bouis meningitis, J. Am. Med. Assoc. 247, 2270 (1981).
About the Author-STEVEN S. GUEST is a senior resident in Internal Medicine at the George Washington University Medical Center. Originally from Montgomery, Alabama, Dr Guest received a B.A. from Emory University and an M.D. from Vanderbilt University. He plans a career in international health-infectious disease. About the Author-CARLOS J. SIVIT received a B.S. degree from the George Washington University and his M.D. from the University of Virginia. Dr Sivit completed a pediatrics residency at Vanderbilt University Hospital and is currently a senior resident in Diagnostic Radiology at George Washington University Medical Center. He plans a career in pediatric radiology. About the Author-WILL.IAM MEISLER is Assistant Professor of Diagnostic Radiology at the George Washington University Medical Center. Dr Meisler received a B.A. and M.D. from Columbia University followed by residency training in Diagnostic Radiology at Columbia-Presbyterian Medical Center. He completed a neuroradiology fellowship at New York University. He is a member of the Radiologic Society of North America as well as a senior member of the American Society of Neuroradiology. About the Author-CHRIS STEVENSis a senior resident in Internal Medicine at the George Washington University Medical Center. Dr Stevens received his B.A. degree from the University of North Carolina at Chapel Hill. He received an M.D. from the University of Miami. After completion of his residency training he plans to pursue a career in gastroenterology. About the Author-GARY L. SIMON is Associate Professor of Medicine and Associate Chairman of the Department of Medicine. He received an M.D. and completed his residency training in Internal Medicine at the University of Maryland. He completed an Infectious Diseases fellowship at Tufts University.