- Email: [email protected]
Nocardia farcinica brain abscess in an immunocompetent patient treated with antibiotics and two surgical techniques
1675
Case Reports / Journal of Clinical Neuroscience 16 (2009) 1675–1677
in the subfascial drain post-operatively – in retrospect, taking the drain off suction or clamping the drain may have slowed CSF drainage. High output drainage of CSF, especially through a drain on suction, can cause this rare but potentially devastating complication. Surprisingly, the literature does not support the reasonable assumption that older patients are more prone to cerebellar haemorrhage due to cerebral and cerebellar atrophy. In the most recent and detailed review of 14 patients with this haemorrhage by Hashidate et al. the mean patient age was 54.4 years.13 Fortunately, the majority of case reports describe a favourable long-term prognosis for patients in which spinal surgery is complicated by cerebellar haemorrhage. Only one mortality has been reported,10 likely due to aggressive, emergent and ultimately successful management of this potentially life-threatening complication. Prompt recognition of the responsible pathology and rapid, appropriate management – operative or non-operative – remains the key to patient recovery. References 1. Chadduck WM. Cerebellar hemorrhage complicating cervical laminectomy. Neurosurgery 1981;85:718–22.
2. Karaeminogullari O, Atalay B, Sahin O, et al. Remote cerebellar haemorrhage after a spinal surgery complicated by dural tear: case report and literature review. Neurosurgery 2005;57(Suppl. 1):E215. 3. Friedman JA, Ecker RD, Piepgras DG, et al. Cerebellar hemorrhage after spinal surgery. Neurosurgery 2002;50:1361–4. 4. Thomas G, Jayaram H, Cudlip S, et al. Supratentorial and infratentorial intraparenchymal hemorrhage secondary to intracranial CSF hypotension following spinal surgery. Spine 2002;27:E410–2. 5. Andrews RT, Koci TM. Cerebellar herniation and infarction as a complication of an occult postoperative lumbar dural defect. Am J Neuroradiol 1995;16:1312–5. 6. Farag E, Abdou A, Riad I, et al. Cerebellar hemorrhage caused by cerebrospinal fluid leak after spine surgery. Anesth Analg 2005;100:545–6. 7. Khan MH, Rihn J, Steele G, et al. Postoperative management protocol for incidental dural tears during degenerative lumbar spine surgery. Spine 2006;31:2609–13. 8. Cammisa FP, Girardi FP, Sangani PK, et al. Incidental durotomy in spine surgery. Spine 2000;25:2663–7. 9. Wang JC, Bohlman HH, Riew KD. Dural tears secondary to operations on the lumbar spine. J Bone Joint Surg 1998;80:1728–32. 10. Cornips EMJ, Staals J, Stavast A, et al. Fatal cerebral and cerebellar hemorrhagic infarction after thoracoscopic microdiscectomy. J Neurosurg Spine 2007;6: 276–9. 11. Eismont FJ, Wiesel SW, Rothman RH. Treatment of dural tears associated with spinal surgery. J Bone Joint Surg Am 1981;63:1132–6. 12. Satake K, Matsuyama Y, Iwata H, et al. Cerebellar haemorrhage complicating resection of cervical intramedullary tumour. Spinal Cord 2000;38:504. 13. Hashidate H, Kamimura M, Nakagawa H, et al. Cerebellar hemorrhage after spine surgery. J Orthop Sci 2008;13:150–4.
doi:10.1016/j.jocn.2009.03.030
Nocardia farcinica brain abscess in an immunocompetent patient treated with antibiotics and two surgical techniques Tzu-Tsao Chung a, Jung-Chung Lin b, Cheng-Ta Hsieh a, Guann-Juh Chen a, Da-Tong Ju a,* a b
Department of Neurological Surgery, Tri-Service General Hospital, National Defense Medical Center, No. 325, Section 2, Cheng-Kung Road, Neihu District, Taipei 114, Taiwan Department of Internal Medicine, Division of Infectious Diseases and Tropical Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan
a r t i c l e
i n f o
Article history: Received 12 January 2009 Accepted 24 March 2009
a b s t r a c t Nocardia farcinica brain abscesses rarely occur in immunocompetent hosts. We present a patient with an N. farcinica brain abscess. This was confirmed by 16S ribosomal RNA sequencing and was successfully treated using one medical and two different surgical techniques, highlighting the important role of surgical intervention if antibiotic treatment fails.
Keywords: Brain abscess Nocardia farcinica 16S rRNA
1. Introduction Brain abscesses resulting from infections caused by Nocardia species in an immunocompetent patient are rarely reported.1–3 The optimum surgical intervention is still controversial.1 Here, we report a patient who had a Nocardia brain abscess that was treated using a combination of stereotactic aspiration, craniotomy with drainage of the abscess and antibiotic therapy. The importance of using a surgical intervention in a Nocardia brain abscess is highlighted. 2. Case report Two days prior to admission, a 65-year-old immunocompetent male with a history of excessive alcohol consumption experienced * Corresponding author. Tel.: +886 2 8792 7177; fax: +886 2 8792 7178. E-mail address: [email protected] (D.-T. Ju)
Ó 2009 Elsevier Ltd. All rights reserved.
intermittent focal seizures in his left-sided limbs. At the time of admission, the physical and neurological examinations were positive for meningismus and papilledema. His laboratory examinations for leukocyte count, C-reactive protein levels and erythrocyte sedimentation rate were normal. A contrast-enhanced CT scan of the head revealed a rim-enhancing lesion with obvious perifocal edema in the right parietal region (Fig. 1A). An MRI of the brain revealed a 2.5 cm lobulated mass surrounded by significant perifocal edema in the right parietal region on T1-weighted MRI, and hyperintensity on T2-weighted MRI, with rim enhancement observed after the administration of gadolinium (Fig. 1B). On day 7 post-admission, the patient underwent a craniotomy with stereotactic aspiration for pathological assessment and diagnosis of the lesion. During the operation, yellowish pus was aspirated and a cerebral abscess was diagnosed. Although serial culture and gram staining did not detect any organisms, intravenous ceftriaxone (2.0 g every 12 hours for 8 weeks) was recommended empirically. Unfortunately, the patient experienced
1676
Case Reports / Journal of Clinical Neuroscience 16 (2009) 1675–1677
Fig. 1. (A) An axial contrast-enhanced CT scan of the head taken at the time of admission showing a lobulated, rim-enhancing lesion with perifocal edema located in the right parietal region. (B) Coronal T1-weighted MRI scan of the brain after the administration of gadolinium on admission showing a 2.5 cm rim-enhancing lobulated mass in the right parietal region. (C) A coronal T1-weighted MRI scan of the brain taken 52 days after admission showing that the abscess had increased to 3.4 cm in diameter. (D) A follow-up coronal T1-weighted MRI scan of the brain, taken 6 months after discharge, showing complete resolution of the cerebral abscess.
intermittent high fever and focal left-sided seizures. Re-imaging 52 days later revealed that the abscess had increased from 2.5 cm to 3.4 cm in diameter, and had disseminated to the right frontal region along the subdural space of the frontal convexity and falx cerebri (Fig. 1C). Five days later, on day 57 of admission, the patient underwent a repeat craniotomy with removal of the abscess. A 16S ribosomal RNA (rRNA) gene–based universal polymerase chain reaction (PCR) and sequencing of the obtained rRNA identified Nocardia farcinica. The antibiotic regimen was changed to oral trimethoprim–sulfamethoxazole (TMP–SMX; 160/800 mg, two every 12 hours) and continued for 6 months. Follow-up MRI scanning performed at 6 months showed complete resolution of the cerebral abscess (Fig. 1D). 3. Discussion Nocardia brain abscess is an opportunistic infection that occurs most often in immunosuppressed patients.4 However, this type of abscess is rare in immunocompetent individuals.1,5,6 Nocardia species are gram-positive aerobic actinomycetes that have a branching rod morphology.7 Nocardia (N.) asteroids, N. farcinica and N. nova are the most common species associated with human disease,8 with the respiratory tract being the most common site of Nocardia infection. Hematogenous dissemination to the brain, kidneys,
joints, bones and eyes can subsequently occur.9 Long-term corticosteroid use, malignancy and localized pulmonary disease are the most commonly recognized risk factors for Nocardia infection.10 In a series of 11 patients who had Nocardia brain abscesses, heavy alcohol use was implicated as a predisposing factor for cerebral nocardiosis.1 Focal neurological deficits and seizures are the most common clinical manifestations observed in patients who have Nocardia brain abscesses;1,6 however, these patients seldom present with toxic symptoms such as fever, chills or dyspnea.1 As a result, these findings may not alert physicians to the possibility of an infection. In such a setting, CT brain scans may be used in order to identify one or more rim-enhancing lesions.9 However, based on clinical and radiological findings, a Nocardia brain abscess may be misdiagnosed as a neoplasm. Further assessment using T2-weighted MRI, which may reveal multiple concentric rims, diffusion-weighted images showing hyperintensity of the lesion, and peaks on proton MRI spectroscopy of lactate (1.3 ppm) and amino acids (0.9 ppm) all suggest the presence of a brain abscess.2 As Nocardia species are difficult to culture and grow slowly, it is difficult to diagnose a Nocardial infection using culture-based methods; moreover, growth may be obscured or contaminated by faster growing competitors.5 The 16S rRNA gene universal PCR method is a fast and reliable way to identify Nocardia spp.5,7 In the current report, a specimen was heated at 95 °C for 15 minutes
Case Reports / Journal of Clinical Neuroscience 16 (2009) 1677–1681
for use as a template. Amplification was carried out in a reaction mixture of PCR buffer, a primer and the template. The PCR product (about 900 base pairs) was sequenced and compared to sequences in the National Center for Biotechnology Information database. Homology to the N. farcinica 16S rRNA gene was evident. Given the difficulties surrounding correct diagnosis, and the treatment challenges that include resistance to antibiotics and the a propensity for rapid spread of the infection, Nocardia brain abscess, especially caused by N. farcinica, is associated with a high mortality rate of up to 20% for immunocompetent patients and 55% for immunocompromised patients.4,6,9 Treatment options supporting antibiotic therapy include stereotactic aspiration of the abscess and craniotomy with drainage of the lesion.1,4,6 A review of 131 patients who had Nocardia brain abscesses reported mortality rates when treated initially with craniotomy and excision of 24%, aspiration and drainage of 50% and non-surgical therapy of 30%.6 These authors recommended the use of aspiration or craniotomy and excision for brain abscesses larger than 2.5 cm, abscesses that enlarged after 2 weeks of antibiotic treatment and abscesses that fail to shrink after 4 weeks of antibiotic therapy. A Nocardia brain abscess of less than 2 cm in diameter can be treated using antibiotic therapy alone when the patient is immunocompetent and clinically stable. Aspiration plus antibiotic therapy is a suitable initial treatment for those patients who have multiple deep lesions.1 Due to the excellent tolerance and cerebrospinal fluid penetration, TMP–SMX is the preferred initial treatment of N. farcinica brain abscesses. Amikacin, carbapenem (imipenem and meropenem), sulfonamide, minocycline, ciprofloxacin or a third-generation cephalosporin are also effective antibiotic agents.1,2,6,8–10 A regimen of 3–6 weeks of parenteral drugs followed by 12 months of oral antibiotic therapy is recommended to prevent relapse.9 In summary, an N. farcinica brain abscess is an infrequent entity rarely observed in immunocompetent patients. Early diagnosis and
1677
appropriate antibiotic therapy are important for a good outcome. Surgical intervention should be considered if the abscess enlarges, if antibiotic treatment fails, or the diagnosis remains unrecognized.
Acknowledgements This study was supported by grants from the Tri-Service General Hospital (TSGH-C97-83 & C97-84) and National Defense Medical Center (DOD97-21-02).
References 1. Lee GY, Daniel RT, Brophy BP, et al. Surgical treatment of nocardial brain abscesses. Neurosurgery 2002;51:668–71. 2. Malincarne L, Marroni M, Farina C, et al. Primary brain abscess with Nocardia farcinica in an immunocompetent patient. Clin Neurol Neurosurg 2002;104:132–5. 3. Menku A, Kurtsoy A, Tucer B, et al. Nocardia brain abscess mimicking brain tumour in immunocompetent patients: report of two cases and review of the literature. Acta Neurochir (Wien) 2004;146:411-14. 4. Kilincer C, Hamamcioglu MK, Simsek O, et al. Nocardial brain abscess: review of clinical management. J Clin Neurosci 2006;13:481–5. 5. Tatti KM, Shieh WJ, Phillips S, et al. Molecular diagnosis of Nocardia farcinica from a cerebral abscess. Hum Pathol 2006;37:1117–21. 6. Mamelak AN, Obana WG, Flaherty JF, et al. Nocardial brain abscess: treatment strategies and factors influencing outcome. Neurosurgery 1994;35:622–31. 7. Sonesson A, Oqvist B, Hagstam P, et al. An immunosuppressed patient with systemic vasculitis suffering from cerebral abscesses due to Nocardia farcinica identified by 16S rRNA gene universal PCR. Nephrol Dial Transplant 2004;19:2896–900. 8. Kennedy KJ, Chung KH, Bowden FJ, et al. A cluster of nocardial brain abscesses. Surg Neurol 2007;68:43–9. 9. Sabuncuoglu H, Cibali Acikgo ZZ, Caydere M, et al. Nocardia farcinica brain abscess: a case report and review of the literature. Neurocirugia (Astur) 2004;15:600-603. 10. Lerner PI. Nocardiosis. Clin Infect Dis 1996;22:891–903.
doi:10.1016/j.jocn.2009.03.029
Late onset Rasmussen’s encephalitis with triple pathology J.Y. Cheong a,*, C. Wong b, A. Bleasel b, W. Varikatt c, T. Ng c, M.A. Dexter a a
Department of Neurosurgery Westmead Hospital, Hawksbury Road, Westmead, New South Wales 2145, Australia Department of Neurology, Westmead Hospital, Westmead, New South Wales, Australia c Department of Anatomical Pathology, ICPMR, Westmead Hospital, Westmead, New South Wales, Australia b
a r t i c l e
i n f o
Article history: Received 13 January 2009 Accepted 20 February 2009
Keywords: Delayed Onset Encephalitis Epilepsy Epilepsia partialis continua Rasmussen’s encephalitis Therapy
a b s t r a c t Rasmussen’s encephalitis is a devastating illness characterized by intractable focal seizures due to chronic localised encephalitis. We report on a rare variant of delayed onset Rasmussen’s encephalitis with triple pathology. A 27-year-old male, who was initially diagnosed with seizures when he was 16 years old, presented with focal seizures that became refractory to multiple anticonvulsants. Multiple investigations, including subdural electrode monitoring, revealed foci of onset in the right frontotemporal region. The patient underwent right front-temporal lobectomy. Post-operatively, the seizures became more severe and he developed new epilepsia partialis continua. Treatment with intravenous immunoglobulin was unsuccessful. He subsequently underwent a right hemispherectomy that rendered him seizure free. The three pathologies identified were old ischemic changes, type II cortical dysplasia and stage II Rasmussen’s encephalitis.
* Corresponding author. Fax: +61 2 9648 4963. E-mail address: [email protected] (J.Y. Cheong)
Ó 2009 Elsevier Ltd. All rights reserved.
Case Reports / Journal of Clinical Neuroscience 16 (2009) 1675–1677
in the subfascial drain post-operatively – in retrospect, taking the drain off suction or clamping the drain may have slowed CSF drainage. High output drainage of CSF, especially through a drain on suction, can cause this rare but potentially devastating complication. Surprisingly, the literature does not support the reasonable assumption that older patients are more prone to cerebellar haemorrhage due to cerebral and cerebellar atrophy. In the most recent and detailed review of 14 patients with this haemorrhage by Hashidate et al. the mean patient age was 54.4 years.13 Fortunately, the majority of case reports describe a favourable long-term prognosis for patients in which spinal surgery is complicated by cerebellar haemorrhage. Only one mortality has been reported,10 likely due to aggressive, emergent and ultimately successful management of this potentially life-threatening complication. Prompt recognition of the responsible pathology and rapid, appropriate management – operative or non-operative – remains the key to patient recovery. References 1. Chadduck WM. Cerebellar hemorrhage complicating cervical laminectomy. Neurosurgery 1981;85:718–22.
2. Karaeminogullari O, Atalay B, Sahin O, et al. Remote cerebellar haemorrhage after a spinal surgery complicated by dural tear: case report and literature review. Neurosurgery 2005;57(Suppl. 1):E215. 3. Friedman JA, Ecker RD, Piepgras DG, et al. Cerebellar hemorrhage after spinal surgery. Neurosurgery 2002;50:1361–4. 4. Thomas G, Jayaram H, Cudlip S, et al. Supratentorial and infratentorial intraparenchymal hemorrhage secondary to intracranial CSF hypotension following spinal surgery. Spine 2002;27:E410–2. 5. Andrews RT, Koci TM. Cerebellar herniation and infarction as a complication of an occult postoperative lumbar dural defect. Am J Neuroradiol 1995;16:1312–5. 6. Farag E, Abdou A, Riad I, et al. Cerebellar hemorrhage caused by cerebrospinal fluid leak after spine surgery. Anesth Analg 2005;100:545–6. 7. Khan MH, Rihn J, Steele G, et al. Postoperative management protocol for incidental dural tears during degenerative lumbar spine surgery. Spine 2006;31:2609–13. 8. Cammisa FP, Girardi FP, Sangani PK, et al. Incidental durotomy in spine surgery. Spine 2000;25:2663–7. 9. Wang JC, Bohlman HH, Riew KD. Dural tears secondary to operations on the lumbar spine. J Bone Joint Surg 1998;80:1728–32. 10. Cornips EMJ, Staals J, Stavast A, et al. Fatal cerebral and cerebellar hemorrhagic infarction after thoracoscopic microdiscectomy. J Neurosurg Spine 2007;6: 276–9. 11. Eismont FJ, Wiesel SW, Rothman RH. Treatment of dural tears associated with spinal surgery. J Bone Joint Surg Am 1981;63:1132–6. 12. Satake K, Matsuyama Y, Iwata H, et al. Cerebellar haemorrhage complicating resection of cervical intramedullary tumour. Spinal Cord 2000;38:504. 13. Hashidate H, Kamimura M, Nakagawa H, et al. Cerebellar hemorrhage after spine surgery. J Orthop Sci 2008;13:150–4.
doi:10.1016/j.jocn.2009.03.030
Nocardia farcinica brain abscess in an immunocompetent patient treated with antibiotics and two surgical techniques Tzu-Tsao Chung a, Jung-Chung Lin b, Cheng-Ta Hsieh a, Guann-Juh Chen a, Da-Tong Ju a,* a b
Department of Neurological Surgery, Tri-Service General Hospital, National Defense Medical Center, No. 325, Section 2, Cheng-Kung Road, Neihu District, Taipei 114, Taiwan Department of Internal Medicine, Division of Infectious Diseases and Tropical Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan
a r t i c l e
i n f o
Article history: Received 12 January 2009 Accepted 24 March 2009
a b s t r a c t Nocardia farcinica brain abscesses rarely occur in immunocompetent hosts. We present a patient with an N. farcinica brain abscess. This was confirmed by 16S ribosomal RNA sequencing and was successfully treated using one medical and two different surgical techniques, highlighting the important role of surgical intervention if antibiotic treatment fails.
Keywords: Brain abscess Nocardia farcinica 16S rRNA
1. Introduction Brain abscesses resulting from infections caused by Nocardia species in an immunocompetent patient are rarely reported.1–3 The optimum surgical intervention is still controversial.1 Here, we report a patient who had a Nocardia brain abscess that was treated using a combination of stereotactic aspiration, craniotomy with drainage of the abscess and antibiotic therapy. The importance of using a surgical intervention in a Nocardia brain abscess is highlighted. 2. Case report Two days prior to admission, a 65-year-old immunocompetent male with a history of excessive alcohol consumption experienced * Corresponding author. Tel.: +886 2 8792 7177; fax: +886 2 8792 7178. E-mail address: [email protected] (D.-T. Ju)
Ó 2009 Elsevier Ltd. All rights reserved.
intermittent focal seizures in his left-sided limbs. At the time of admission, the physical and neurological examinations were positive for meningismus and papilledema. His laboratory examinations for leukocyte count, C-reactive protein levels and erythrocyte sedimentation rate were normal. A contrast-enhanced CT scan of the head revealed a rim-enhancing lesion with obvious perifocal edema in the right parietal region (Fig. 1A). An MRI of the brain revealed a 2.5 cm lobulated mass surrounded by significant perifocal edema in the right parietal region on T1-weighted MRI, and hyperintensity on T2-weighted MRI, with rim enhancement observed after the administration of gadolinium (Fig. 1B). On day 7 post-admission, the patient underwent a craniotomy with stereotactic aspiration for pathological assessment and diagnosis of the lesion. During the operation, yellowish pus was aspirated and a cerebral abscess was diagnosed. Although serial culture and gram staining did not detect any organisms, intravenous ceftriaxone (2.0 g every 12 hours for 8 weeks) was recommended empirically. Unfortunately, the patient experienced
1676
Case Reports / Journal of Clinical Neuroscience 16 (2009) 1675–1677
Fig. 1. (A) An axial contrast-enhanced CT scan of the head taken at the time of admission showing a lobulated, rim-enhancing lesion with perifocal edema located in the right parietal region. (B) Coronal T1-weighted MRI scan of the brain after the administration of gadolinium on admission showing a 2.5 cm rim-enhancing lobulated mass in the right parietal region. (C) A coronal T1-weighted MRI scan of the brain taken 52 days after admission showing that the abscess had increased to 3.4 cm in diameter. (D) A follow-up coronal T1-weighted MRI scan of the brain, taken 6 months after discharge, showing complete resolution of the cerebral abscess.
intermittent high fever and focal left-sided seizures. Re-imaging 52 days later revealed that the abscess had increased from 2.5 cm to 3.4 cm in diameter, and had disseminated to the right frontal region along the subdural space of the frontal convexity and falx cerebri (Fig. 1C). Five days later, on day 57 of admission, the patient underwent a repeat craniotomy with removal of the abscess. A 16S ribosomal RNA (rRNA) gene–based universal polymerase chain reaction (PCR) and sequencing of the obtained rRNA identified Nocardia farcinica. The antibiotic regimen was changed to oral trimethoprim–sulfamethoxazole (TMP–SMX; 160/800 mg, two every 12 hours) and continued for 6 months. Follow-up MRI scanning performed at 6 months showed complete resolution of the cerebral abscess (Fig. 1D). 3. Discussion Nocardia brain abscess is an opportunistic infection that occurs most often in immunosuppressed patients.4 However, this type of abscess is rare in immunocompetent individuals.1,5,6 Nocardia species are gram-positive aerobic actinomycetes that have a branching rod morphology.7 Nocardia (N.) asteroids, N. farcinica and N. nova are the most common species associated with human disease,8 with the respiratory tract being the most common site of Nocardia infection. Hematogenous dissemination to the brain, kidneys,
joints, bones and eyes can subsequently occur.9 Long-term corticosteroid use, malignancy and localized pulmonary disease are the most commonly recognized risk factors for Nocardia infection.10 In a series of 11 patients who had Nocardia brain abscesses, heavy alcohol use was implicated as a predisposing factor for cerebral nocardiosis.1 Focal neurological deficits and seizures are the most common clinical manifestations observed in patients who have Nocardia brain abscesses;1,6 however, these patients seldom present with toxic symptoms such as fever, chills or dyspnea.1 As a result, these findings may not alert physicians to the possibility of an infection. In such a setting, CT brain scans may be used in order to identify one or more rim-enhancing lesions.9 However, based on clinical and radiological findings, a Nocardia brain abscess may be misdiagnosed as a neoplasm. Further assessment using T2-weighted MRI, which may reveal multiple concentric rims, diffusion-weighted images showing hyperintensity of the lesion, and peaks on proton MRI spectroscopy of lactate (1.3 ppm) and amino acids (0.9 ppm) all suggest the presence of a brain abscess.2 As Nocardia species are difficult to culture and grow slowly, it is difficult to diagnose a Nocardial infection using culture-based methods; moreover, growth may be obscured or contaminated by faster growing competitors.5 The 16S rRNA gene universal PCR method is a fast and reliable way to identify Nocardia spp.5,7 In the current report, a specimen was heated at 95 °C for 15 minutes
Case Reports / Journal of Clinical Neuroscience 16 (2009) 1677–1681
for use as a template. Amplification was carried out in a reaction mixture of PCR buffer, a primer and the template. The PCR product (about 900 base pairs) was sequenced and compared to sequences in the National Center for Biotechnology Information database. Homology to the N. farcinica 16S rRNA gene was evident. Given the difficulties surrounding correct diagnosis, and the treatment challenges that include resistance to antibiotics and the a propensity for rapid spread of the infection, Nocardia brain abscess, especially caused by N. farcinica, is associated with a high mortality rate of up to 20% for immunocompetent patients and 55% for immunocompromised patients.4,6,9 Treatment options supporting antibiotic therapy include stereotactic aspiration of the abscess and craniotomy with drainage of the lesion.1,4,6 A review of 131 patients who had Nocardia brain abscesses reported mortality rates when treated initially with craniotomy and excision of 24%, aspiration and drainage of 50% and non-surgical therapy of 30%.6 These authors recommended the use of aspiration or craniotomy and excision for brain abscesses larger than 2.5 cm, abscesses that enlarged after 2 weeks of antibiotic treatment and abscesses that fail to shrink after 4 weeks of antibiotic therapy. A Nocardia brain abscess of less than 2 cm in diameter can be treated using antibiotic therapy alone when the patient is immunocompetent and clinically stable. Aspiration plus antibiotic therapy is a suitable initial treatment for those patients who have multiple deep lesions.1 Due to the excellent tolerance and cerebrospinal fluid penetration, TMP–SMX is the preferred initial treatment of N. farcinica brain abscesses. Amikacin, carbapenem (imipenem and meropenem), sulfonamide, minocycline, ciprofloxacin or a third-generation cephalosporin are also effective antibiotic agents.1,2,6,8–10 A regimen of 3–6 weeks of parenteral drugs followed by 12 months of oral antibiotic therapy is recommended to prevent relapse.9 In summary, an N. farcinica brain abscess is an infrequent entity rarely observed in immunocompetent patients. Early diagnosis and
1677
appropriate antibiotic therapy are important for a good outcome. Surgical intervention should be considered if the abscess enlarges, if antibiotic treatment fails, or the diagnosis remains unrecognized.
Acknowledgements This study was supported by grants from the Tri-Service General Hospital (TSGH-C97-83 & C97-84) and National Defense Medical Center (DOD97-21-02).
References 1. Lee GY, Daniel RT, Brophy BP, et al. Surgical treatment of nocardial brain abscesses. Neurosurgery 2002;51:668–71. 2. Malincarne L, Marroni M, Farina C, et al. Primary brain abscess with Nocardia farcinica in an immunocompetent patient. Clin Neurol Neurosurg 2002;104:132–5. 3. Menku A, Kurtsoy A, Tucer B, et al. Nocardia brain abscess mimicking brain tumour in immunocompetent patients: report of two cases and review of the literature. Acta Neurochir (Wien) 2004;146:411-14. 4. Kilincer C, Hamamcioglu MK, Simsek O, et al. Nocardial brain abscess: review of clinical management. J Clin Neurosci 2006;13:481–5. 5. Tatti KM, Shieh WJ, Phillips S, et al. Molecular diagnosis of Nocardia farcinica from a cerebral abscess. Hum Pathol 2006;37:1117–21. 6. Mamelak AN, Obana WG, Flaherty JF, et al. Nocardial brain abscess: treatment strategies and factors influencing outcome. Neurosurgery 1994;35:622–31. 7. Sonesson A, Oqvist B, Hagstam P, et al. An immunosuppressed patient with systemic vasculitis suffering from cerebral abscesses due to Nocardia farcinica identified by 16S rRNA gene universal PCR. Nephrol Dial Transplant 2004;19:2896–900. 8. Kennedy KJ, Chung KH, Bowden FJ, et al. A cluster of nocardial brain abscesses. Surg Neurol 2007;68:43–9. 9. Sabuncuoglu H, Cibali Acikgo ZZ, Caydere M, et al. Nocardia farcinica brain abscess: a case report and review of the literature. Neurocirugia (Astur) 2004;15:600-603. 10. Lerner PI. Nocardiosis. Clin Infect Dis 1996;22:891–903.
doi:10.1016/j.jocn.2009.03.029
Late onset Rasmussen’s encephalitis with triple pathology J.Y. Cheong a,*, C. Wong b, A. Bleasel b, W. Varikatt c, T. Ng c, M.A. Dexter a a
Department of Neurosurgery Westmead Hospital, Hawksbury Road, Westmead, New South Wales 2145, Australia Department of Neurology, Westmead Hospital, Westmead, New South Wales, Australia c Department of Anatomical Pathology, ICPMR, Westmead Hospital, Westmead, New South Wales, Australia b
a r t i c l e
i n f o
Article history: Received 13 January 2009 Accepted 20 February 2009
Keywords: Delayed Onset Encephalitis Epilepsy Epilepsia partialis continua Rasmussen’s encephalitis Therapy
a b s t r a c t Rasmussen’s encephalitis is a devastating illness characterized by intractable focal seizures due to chronic localised encephalitis. We report on a rare variant of delayed onset Rasmussen’s encephalitis with triple pathology. A 27-year-old male, who was initially diagnosed with seizures when he was 16 years old, presented with focal seizures that became refractory to multiple anticonvulsants. Multiple investigations, including subdural electrode monitoring, revealed foci of onset in the right frontotemporal region. The patient underwent right front-temporal lobectomy. Post-operatively, the seizures became more severe and he developed new epilepsia partialis continua. Treatment with intravenous immunoglobulin was unsuccessful. He subsequently underwent a right hemispherectomy that rendered him seizure free. The three pathologies identified were old ischemic changes, type II cortical dysplasia and stage II Rasmussen’s encephalitis.
* Corresponding author. Fax: +61 2 9648 4963. E-mail address: [email protected] (J.Y. Cheong)
Ó 2009 Elsevier Ltd. All rights reserved.