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CASE REPORT
Year : 2012  |  Volume : 60  |  Issue : 3  |  Page : 325-327

Intracranial actinomycosis: Varied clinical and radiologic presentations in two cases


1 Department of Neurosurgery, Postgraduate Institute of Medical Education and Research, Chandigarh, India
2 Department of Histopathology, Postgraduate Institute of Medical Education and Research, Chandigarh, India

Date of Submission19-Mar-2012
Date of Decision19-Mar-2012
Date of Acceptance14-May-2012
Date of Web Publication14-Jul-2012

Correspondence Address:
Sandeep Mohindra
Department of Neurosurgery, Postgraduate Institute of Medical Education and Research, Chandigarh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.98527

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 » Abstract 

Two patients with primary actinomycotic brain infection are presented here. The first case had 2 predisposing factors, cardiac septal defect and chronic mastoiditis, whereas the second patient was a chronic smoker, belonging to a desert region. Both the patients were successfully managed with surgical debridement and prolonged administration of antibiotics.


Keywords: Actinomycosis, radiology, treatment


How to cite this article:
Mohindra S, Savardekar A, Rane S. Intracranial actinomycosis: Varied clinical and radiologic presentations in two cases. Neurol India 2012;60:325-7

How to cite this URL:
Mohindra S, Savardekar A, Rane S. Intracranial actinomycosis: Varied clinical and radiologic presentations in two cases. Neurol India [serial online] 2012 [cited 2019 May 24];60:325-7. Available from: http://www.neurologyindia.com/text.asp?2012/60/3/325/98527



 » Introduction Top


Actinomycosis is a chronic suppurative bacterial infection, usually affecting cervicofacial region, abdomen, or lungs. [1] Secondary involvement of brain is occasionally noted. [2] However, occurrence of primary central nervous system actinomycosis remains controversial. [2] In the present communication, 2 unusual cases of actinomycotic brain infection are presented.


 » Case Reports Top


Case 1

A 33-year-old woman, operated a decade ago for an atrial septal defect presented with severe headache and projectile vomiting of about 8-week duration. She had undergone right mastoidectomy for chronic suppurative mastoiditis 7 years ago. On examination, the patient was fully conscious and well-oriented to time, place, and person without any focal neurologic deficit. Cranial computed tomography (CT) scan and magnetic resonance imaging (MRI) showed a mass lesion involving right frontal lobe, with intense perilesional cerebral edema, causing subfalcine herniation [Figure 1]a-c. The mass lesion was approached via right frontal craniotomy. Intraoperatively, dull white, odorless purulent material, admixed with avascular necrotic material was excised. Margins of mass lesion were thick, firm, and leathery and partial excision could be achieved. Postoperatively, the patient got relieved of raised intracranial pressure and was started on antibiotics. The histopathology of excised specimen showed extensive areas of necrosis and chronic mixed inflammation comprising lymphocytes, plasma cells, histiocytes, and neutrophils. Gram-positive and para-amino salicylic acid (PAS)-positive bacteria were also identified, the morphology of which was consistent with actinomycosis. The patient was administered parenteral clindamycin and cloxacillin for 6 weeks, and was continued on enteral therapy for 6 months. During ongoing drug therapy, MRI scan at 3 months showed intensely contrast-enhancing tumor-resection margins at the operative site [Figure 1]d-f. Considering it to be a partially treated infection, the patient was continued on the same drug combination for another 3 months. At 6 months, there was no contrast-enhancing lesion and followup MRI scan performed at 4 years showed right frontal gliosis and no evidence of disease [Figure 2]a-f.
Figure 1: (a) Contrast-enhanced computed tomography scan showing ill-defined right frontal mass lesion, with intense perilesional edema and midline shift; (b) plain magnetic resonance imaging (MRI) scan showing better defined lesion abutting against corpus callosum, containing necrotic material; (c) MRI scan, T2 weighted, showing intense perilesional edema; (d– f) MRI scan (plain, contrast enhanced, and T2 weighted) at 3 months of followup shows intensely contrast-enhancing tumor-resection margins at the operative site

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Figure 2: (a– f) Magnetic resonance imaging scan (plain, contrast enhanced and T2 weighted) shows no contrast-enhancing lesion. There is gliosis of right frontal lobe and ipsilateral ventricle is pulled toward the operative site

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Case 2

A 50-year-old chronic smoker and alcoholic man presented with complaints of generalized tonic-clonic seizures of 18 months duration. He had progressively increasing intensity of headache for 1 year, without any vomiting. On examination, he was dull, drowsy, arousable with left-sided hemiparesis. Plain and contrast CT scan showed a right frontal dural-based contrast-enhancing mass lesion, causing intense cerebral edema and midline shift [Figure 3]a and b. The patient underwent right frontal craniotomy and excision of dural-based mass lesion, which was avascular, firmly attached to duramater, having an ill-defined plane of cleavage from cerebral parenchyma. Pericranial patch was applied after excising the pathologic dura. The patient was administered crystalline penicillin (160 lac/ day) and clindamycin (2700 mg/day) for 6 months. Followup CT scan showed no evidence of disease after 3 months of antibiotic administration [Figure 3]c. At 2 years of followup, patient remains asymptomatic. The histopathologic examination of the excised lesion revealed multiple neutrophilic abscesses with central colonies of filamentous bacteria. There was marked fibroblastic, Splendore-Hoeppli reaction around the bacterial colonies, indicating actinomycotic brain infection [Figure 3]d-f.
Figure 3: (a,b) Axial computed tomography (CT) scan, showing duralbased, intensely contrast-enhancing lesion; (c) followup CT scan after excision of lesion and 2 months of antibiotics administration; (d) photomicrograph showing granule surrounded by dense acute inflammatory infiltrate (H and E, ×200); (e) photomicrograph showing granule composed of aggregates of thin filaments surrounded by eosinophilic, club-like, Splendore– Hoeppli material (H and E, ×400); (f) photomicrograph showing focal giant cell reaction around filamentous bacteria (H and E, ×200)

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 » Discussion Top


Actinomycosis remains a rare, chronic, but curable bacterial brain infection. [3],[4] The offending organism is gram-positive, non-acid-fast branching filamentous bacteria with anaerobic or microaerophilic requirements. [5] Secondary spread to brain from cervicofacial region, abdomen, or lungs remains the more common form of presentation. [1] Risk factors include dental problems, head trauma, chronic mastoiditis, sinusitis, cardiac septal defect, or actinomyces infection of intrauterine devices. [3],[6] The first patient had 2 of the known risk factors (cardiac septal defect and chronic mastoiditis), whereas no predisposing factors were noted in the second patient. As both the patients had primary brain actinomycoses infection, they posed a real diagnostic challenge. For the secondary cases, the meticulous search and discovery of visceral lesions provide a significant lead to this rare diagnostic entity. [7]

Brain abscess (67%) remains the most common type of actinomycotic brain infection, followed by meningoencephalitis (13%), actinomycetoma (7%), subdural empyema (6%), and epidural abscess (6%). [3],[4] Our first patient presented with brain abscess, but the diagnosis could only be reached on histopathology. [6] The possible role of the 2 predisposing factors in this patient, operated several years before, is more of a speculation. The second patient presented as dural-based tumor, with mass effect, previously reported from our institute, more than 2 decades ago. [4] Actinomycotic osteomyelitis of cranial vault, invading duramater and underlying brain, presenting as meningioma was described. [4] The present case had solid mass lesion, firmly adhering to duramater, invading the cerebral parenchyma, without any bony involvement. As no extracranial site was involved, the case qualifies to be categorized as primary actinomycosis of brain. The inoculation of brain may have occurred after hematogenous spread of bacilli from lungs as he was a chronic smoker, without causing primary lung involvement.

Management involves surgical drainage of purulent material, so as to establish the correct diagnosis, decrease the bacterial load, and treatment with antibiotics for prolonged duration. [8],[9],[10],[11] Penicillin remains the drug of choice, and may be administered parenterally or enterally. As half-life of enterally administered penicillin is very short, drug compliance remains an important issue regarding its usage. [7] In combination, clindamycin and cloxacillin are the most preferred drugs. Even when the literature describes poor outcome in cases with symptomatology more than 2 months, both our cases made eventless recovery. Overall mortality of 28% and morbidity of 54% is cited in the published literature. [3] The duration of antibiotic administration is not clearly mentioned. In the present patients, MRI scans at 3 months clearly showed partial resolution of actinomycotic cerebral infection, whereas it seemed adequate disease control in second case. Nevertheless, it seems prudent to administer 6 months of antibiotics to actinomycotic brain infection. [12]

 
 » References Top

1.Millan JM, Escudero L, Roger RL, de la Fuente M, Diez I. Actinomycotic brain abscess: CT findings. J Comput Assist Tomogr 1985;9:976-8.  Back to cited text no. 1
    
2.Salvati M, Ciappetta P, Raco A, Artico M, Artizzu S. Primary intracranial actinomycosis. Report of a case and review of the literature. Zentralbl Neurochir 1991;52:95-8.  Back to cited text no. 2
[PUBMED]    
3.Smego RA Jr. Actinomycosis of the central nervous system. Rev Infect Dis 1987;9:855-65.  Back to cited text no. 3
[PUBMED]    
4.Khosla VK, Banerjee AK, Chopra JS. Intracranial actinomycoma with osteomyelitis simulating meningioma. J Neurosurg1984;60:204-7.  Back to cited text no. 4
[PUBMED]  [FULLTEXT]  
5.Wang S, Wolf RL, Woo JH, Wang J, O'Rourke DM, Roy S, et al. Actinomycotic brain infection: registered diffusion, perfusion MR imaging and MR spectroscopy. Neuroradiology 2006;48:346-50.  Back to cited text no. 5
[PUBMED]  [FULLTEXT]  
6.Sundaram C, Purohit AK, Prasad VS, Meena AK, Reddy JJ, Murthy JM. Cranial and intracranial actinomycosis. Clin Neuropathol 2004;23:173-7.  Back to cited text no. 6
[PUBMED]    
7.Brunon J, Pialat J, Brun Y, Sindou M, Fischer C, Perrin G. Actinomycotic brain abscess. [Article in French]. Neurochirurgie 1980;26:31-8.  Back to cited text no. 7
[PUBMED]    
8.Dailey AT, LeRoux PD, Grady MS. Resolution of an actinomycotic abscess with nonsurgical treatment: Case report. Neurosurgery 1993;32:134-7.  Back to cited text no. 8
[PUBMED]  [FULLTEXT]  
9.He CW. Actinomycosis of the brain. Case report. J Neurosurg 1985;63:131-3.  Back to cited text no. 9
[PUBMED]  [FULLTEXT]  
10.Puzzilli F, Salvati M, Ruggeri A, Raco A, Bristot R, Bastianello S, et al. Intracranial actinomycosis in juvenile patients. Case report and review of the literature. Childs Nerv Syst 1998;14:463-6.  Back to cited text no. 10
[PUBMED]  [FULLTEXT]  
11.Puzzilli F, Salvati M, Bristot R, Bastianello S, Ruggeri A, Lunardi P. Actinomycosis of the central nervous system: Surgical treatment of three cases. J Neurosurg Sci 1998;42:165-71.  Back to cited text no. 11
[PUBMED]    
12.Sharma BS, Banerjee AK, Sobti MK, Kak VK. Actinomycotic brain abscess. Clin Neurol Neurosurg 1990;92:373-6.  Back to cited text no. 12
[PUBMED]    


    Figures

  [Figure 1], [Figure 2], [Figure 3]



 

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