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Table of Contents    
Year : 2019  |  Volume : 67  |  Issue : 4  |  Page : 1123-1126

Actinomyeces Cerebral Abscess Masquerading as Tuberculosis: Delayed Presentation following Head Trauma and Scalp Infection

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
3 Department of Radio-diagnosis and Imaging, Postgraduate Institute of Medical Education and Research, Chandigarh, India

Date of Web Publication10-Sep-2019

Correspondence Address:
Prof. Manoj K Tewari
Department of Neurosurgery, Postgraduate Institute of Medical Education and Research, Chandigarh - 160 012
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.266291

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How to cite this article:
Kumar M, Bajaj A, Tripathi M, Radotra BD, Tewari MK, Ahuja CK. Actinomyeces Cerebral Abscess Masquerading as Tuberculosis: Delayed Presentation following Head Trauma and Scalp Infection. Neurol India 2019;67:1123-6

How to cite this URL:
Kumar M, Bajaj A, Tripathi M, Radotra BD, Tewari MK, Ahuja CK. Actinomyeces Cerebral Abscess Masquerading as Tuberculosis: Delayed Presentation following Head Trauma and Scalp Infection. Neurol India [serial online] 2019 [cited 2021 Jan 23];67:1123-6. Available from:


Actinomycosis of the brain is a rare chronic suppurative infection. The close clinic–histologico–radiological mimicry with tuberculosis frequently leads to delay in definitive diagnosis and effective management. Actinomyeces account for nearly 2% of all intracranial pyogenic infections. The most common intracranial infective lesion is the brain abscess (75%) followed by meningoencephalitis (13%), actinomycetoma (7%), subdural empyema (6%), and epidural abscess (6%).[1],[2]

A 45-year-old female presented with complaints of headache, generalized tonic clonic seizures (GTCS) for six months, decreased verbal output, and right hemiparesis for three months. She also complained of intermittent low-grade fever. About 22 years ago, she underwent drainage of a left frontoparietal scalp abscess following a trivial head injury by fall of an object over the head. On admission, the patient had features of raised intracranial pressure, right upper motor neuron facial palsy, and right hemiparesis (2/5). There was a 5 × 4 cm nontender, soft boggy swelling over the left parietal region, which on aspiration revealed methicillin resistant staphylcoccus aureus. Imaging revealed multiple conglomerate ring enhancing lesions, with calcification and significant perilesional edema in left high parietal lobe [Figure 1]a, [Figure 1]b, [Figure 1]c, [Figure 1]d, [Figure 1]e, [Figure 1]f. Magnetic resonance spectroscopy (MRS) revealed a lipid-lactate peak at 1.3 ppm. There was a small extradural collection with pachymeningeal enhancement and adjacent calvarial thickening. The scalp abscess was also communicating with intracranial abscess [Figure 1]c. Based on the imaging and clinical presentation, a diagnosis of tuberculosis was proposed.[3] To relieve mass effect and ascertain diagnosis, left parietal craniotomy with subtotal excision of the lesion was performed. Intraoperatively, the lesion was fibrous in consistency with areas containing creamy white pus. Histopathological analysis revealed fibro-collagenous tissue with neutrophilic infiltrate and areas of hemorrhage. Tubercular work up (acid fast stain, culture, and polymerase chain reaction) was negative. Extensive colonization with actinomycosis was seen [Figure 2]. Patient received antibiotics (Ampicillin and Sulbactum) for eight weeks. At two-months of follow-up, patient improved in his neurological status. The patient did not give consent for follow-up imaging and lost to follow up.
Figure 1: (a-e): Multiple conglomerate lesions seen in left high parietal region with hypointense calcified wall (arrows in a and b) and diffuse ring enhancement (black arrow in c). Large ring enhancing lesion is seen in deep white matter (arrow in d) with considerable edema (arrow in e) and mass effect. Internal debris is noted posteriorly (black arrows in e and f). Scalp abscess is present in the overlying region (long white arrow in c) with calvarial thickening and pachymeningeal enhancement

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Figure 2: (a and b) H and E stain shows a central abscess cavity containing actinomycotic colonies (black arrows) walled off by inflammatory infiltrate (yellow star) and thick fibrous capsule (black star); (c) High power view to show the Actinomyeces colonies composed of branched networks of rod-shaped bacterial filaments and peripheral intensely eosinophilic Splendore-Hoeppli phenomenon (yellow arrows); (d) Gram stain demonstrates positive staining of the bacterial colonies with more intense staining at the periphery (white arrows)

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A prior history of head trauma, surgery, oral infections, cardiac structural abnormality, and immune system disorders is predisposing for this rare infection.[4] Actinomyeces shows no regard to the anatomical barriers and tend to spread to the contiguous areas along fascial planes or lymphatic drainage. The history of scalp drainage in nearly same area on the skull might be the antecedent event later flaring in the form of an intra pathology. The present case has multiple conglomerate intracranial lesions, firmly adhering to the dura mater, and invading cerebral parenchyma with bone and scalp involvement. As there was already a scalp swelling, the intracranial infection was most likely a direct invasion of the pathogen. Nearly in all the cases, Actinomyeces are part of a polymicrobial flora, and practically never found as an isolated organism in the culture studies. In present case, the presence of staphylococcus aureus may have facilitated actinomycotic infection, but this cannot be definitely concluded.

The management of cranial actinomycosis remains challenging. In a non-endemic area, actinomycosis remains a masquerader with significant clinico–patho–radiological mimicry with a myriad of other granulomatous inflammatory and infective pathologies. The demonstration of sulfur granules clumped with actinomyeces filaments in exudates or histology strongly supports the diagnosis in the above case. Similar to tubercular bacilli, actinomyeces grow slowly, and cultures need to be observed for at least 14–21 days to allow adequate detection.[5] This request should be raised with the pathologist if the clinical suspicion is strong. Though the definitive diagnosis is established by culture examination, ancillary methods such as fluorescent-conjugated monoclonal antibody and 16S rRNA gene polymerase chain reaction have shown improved identification in the presence of mixed infections. Neuroimaging may not clinch diagnosis, but it delineates the dimensions and extent of the disease. The most common imaging appearance is a ring-enhancing lesion with a thick wall with solid nodular or mass lesions termed as “actinomycetoma.”[6] There may be associated osteomyelitis, sinusitis, or ear infection with sinister epidural or subdural empyema similar to the present case. A left parietal abscess with multiple conglomerate lesions in close vicinity and lipid-lactate peak on MRS suggested a tubercular infection. The delayed occurrence of actinomycotic intracranial abscess following trauma has been reported in the literature [Table 1]. In our case, there was surgical trauma two decades ago, which could explain it in the absence of infective foci elsewhere in the body.
Table 1: Intracranial actinomycosis following trauma/surgery

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Ideal therapy for intracranial actinomycosis is debatable. In view of diagnostic pitfalls, broad spectrum antibiotics are administered for short durations. This makes the management further complicated as the isolation of the causative organisms from the patients who have recently received antibiotics for 7–10 days becomes difficult.[11] The chronicity of disease process with antibiotic therapy enhances fibrosis, which makes detection of sulfur granules further difficult. Aggressive debridement should be done. This reduces mass effect, provides histological diagnosis, helps increase oxygen tension and reduces microaerophilic environment in the infected tissue, which is lethal for Actinomyeces.[12] High-dose penicillin after surgical debridement is the treatment of choice for actinomycosis. The alternative treatment options are tetracycline, erythromycin, and clindamycin.[11],[13],[14] The duration of the therapy should be guided by the severity of infection and regular assessment of clinic–pathologic remission. Actinomycotic collection is a surgical disease which should be proven on histopathology. Long-course antibiotics should be administered to get good results.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

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Fabbri G, Guardigni V, Sarubbo S, Cultera R, Contini C. Brain abscess sustained by actinomycesmeyeri in an immunocompetent patient. J Neurol Neurophysiol 2014;5:1.  Back to cited text no. 8
Akhaddar A, Elouennass M, Baallal H, Boucetta M. Focal intracranial infections due to Actinomyces species in immunocompetent patients: Diagnostic and therapeutic challenges. World Neurosurg 2010;74:346-50.  Back to cited text no. 9
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Peabody JW Jr, Seabury JH. Actinomycosis and nocardiosis. A review of basic differences in therapy. Am J Med 1960;28:99.  Back to cited text no. 11
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