Brain Abscess in the Current Decade (2010–2019) in India—A Review

Abstract

Brain abscess outcomes have improved in recent years due to advancements in cranial imaging, microbiological techniques, minimally invasive neurosurgical procedures, and effective antibiotic treatments. However, the incidence of brain abscess remains unchanged in developing countries. We searched PubMed and Google Scholar for references using the key words “brain abscess” and “India” and reviewed both retrospective and prospective studies published in peer-reviewed journals in the current decade to understand the present status. The review shows that the patients’ ages, the predominance of male patients, the symptoms and locations of brain abscesses, and the types of bacteria associated with them have remained unchanged over the past decade. The most common predisposing condition in recent years has been chronic suppurative otitis media with a mortality rate of 7 to 10%. Middle ear infection is often neglected and not treated aggressively in Asian countries. It requires multidisciplinary treatment strategies to address the primary source of infection and better health awareness to prevent the development of brain abscess.

 

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Keywords

brain abscess - chronic suppurative otitis media (CSOM) - prevention

Introduction

Brain abscess is a focal collection of pus in the brain parenchyma surrounded by a well-vascularized collagenous capsule.[1] It is life-threatening condition with long-term neurological sequelae in 9 to 36% of patients.[2] With the advancements in imaging and microbiological techniques, neurosurgical procedures, and effective antibiotic treatments, brain abscess mortality has decreased in recent years.[3] However, the incidence of brain abscess remains unchanged in developing countries, particularly among populations of lower socioeconomic status due to chronic suppurative otitis media (CSOM) and immunosuppression.[4] [5] We searched PubMed and Google Scholar for references using the key words “brain abscess” and “India” and reviewed both retrospective and prospective studies published in peer-reviewed journals in this decade to understand the current status. There were eight brain abscess ([Table 1]) and six otogenic brain abscess ([Table 2]) journal articles. The number of years of study from various institutions in [Table 1] ranges from 1.5 to 28 years and the number of patients in these studies ranges from 8 to 89 per year with an average of 24 brain abscess cases per year. Lakshmi et al reported the average number of brain abscess specimens received for microbiological analysis was 21 per year.[6]

Table 1 Publications on brain abscess in India in the current decade (2010–2019)

Reference and place of study	Duration and (y)	No. of patients	Age range (average)	Gender (%)		No. of culture positive (%) and organisms	Predisposing factors (%)	Location (%)	No. of died patients (%)
				Male	Fe-male
Abbreviations: CSOM, chronic suppurative otitis media; CHD, congenital heart disease; GNB, gram negative bacteria; No., number.
Tomar et al, 20117 Chhatrapati Sahuji Maharaj Medical University, Lucknow, Uttar Pradesh	Aug 2009–Dec 2010 (1.5)	30	9–47 (25)	24 (69)	11 (31)	22 (73). Pyogenic: 18 (82) Streptococci: 10 (33) Staphylococci: 1 (3) Bacteroides sp.: 2 (6) Nocardia: 1(3); Fungal:1 (3) Mycobacteria: 3 (10) Mixed infection 4: (13)	CSOM: 15 (50) CHD: 3 (10) Postoperative/traumatic: 2(6) Pulmonary tuberculosis: 2 (6)	Temporal: 10 (33) Cerebellar: 9 (30) Frontal: 3 (10) Parietal: 4 (13) Temporoparietal: 4 (13)
Lakshmi et al, 20116 Nizam’s Institute of Medical Sciences, Hyderabad, Telangana	1987–2010 (24)	352	2–80 (28)			247 (70); Pyogenic:232 (94) S taphylococcus aureus: 68 (28) Streptococcus: 35(14) Enterococcus: 34 (14) GNB:62(25) parasitic 2(0.5) Anaerobes: 39 (16) Mixed infections: 30 (12) Fungal: 5 (1) Nocardia: 3(0.8) Mycobacteria: 9 (5)	CSOM: 135 (38) CHD: 32 (9) Post-traumatic/operative: 42(12) Pulmonary: 9 (3) Sepsis: 33 (9) Sinusitis: 8 (2)	Temporal: 81 (23) Cerebellar: 26 (7) Frontal: 81 (23) Parietal: 102 (29) Occipital: 12 (3) Others: 11 (3) Multiple: 39 (11)
Muzumdar et al, 20118 Seth GS Medical College & King Edward Memorial Hospital, Mumbai, Maharashtra	1999–2006 (7)	289	1.5–62 (32)	204 (71)	86 (29)	76 (26) Streptococcus:19 (25) Staphylococcus: 18 (24) Klebsiella: 17 (22) P revotella aeruginosa:16(21)	CSOM: 120 (42) Pulmonary/CHD: 17 (6) Post-traumatic/operative: 12 (4) Sinusitis: 15 (5)	Temporal: 111 (38) Cerebellar: 74 (25) Frontal: 61 (21) Parietal: 19 (7) Occipital: 7 (2) Multiple: 17 (6)	8 (3)
Sarmast et al., 20129 Sher I Kashmir Institute of Medical Sciences, Srinagar, Jammu and Kashmir (SKIMS)	Oct 2001–2011 (10)	114	0.5–70 (31)	83 (73)	31 (27)	93 (82) S. pneumoniae: 22(24) Staphylococcus:29(31) Streptococcus: 16(17) P. aeruginosa:11(12) Enterobacter 4: (4) K lebsiella pneumoniae: 3 (3) Haemophilus influenzae:6 (6) B acteroides fragilis: 1 (1) Peptostreptococcus: 1 (1) Mixed infection: 4 (3)	CSOM: 57 (50) CHD: 4 (4) Post-traumatic/operative: 21(18) Pulmonary: 8 (7) Sinusitis: 6 (5) Adjacent local infection: 3(2)	Temporal: 33 (29) Cerebellar: 16(14) Frontal: 17 (15) Parietal: 12 (10) Occipital: 6 (5) Temporoparietal: 28(24) Parieto-occipital: 9 (7)	8 (7)
Bajpai et al, 201410 Sanjay Gandhi Post Graduate Institute of Medical Sciences& King George Medical University Lucknow, Uttar Pradesh		90	(24)	67 (74)	23 (26)	64 (71) S. aureus:13 (20) S. intermedius:8 (12) Enterococcus sp.:4 (7) Escherichia coli:7 (11) P. aeruginosa: 4 (7) P. mirabilis:2 (3) B. fragilis:8 (12) Fusobacterium sp.: 6 (10) Peptostreptococcus sp.:5 (9) Mixed infection: 7(8)	CSOM: 34 (49) CHD: 3 (4) Head trauma: 8(11) Dental infection: 5(7) Sinusitis: 6(6) Pulmonary tuberculosis: 4 (5) HIV: 2 (2) Diabetes: 1(1)	Temporal: 11 (12) Cerebellar: 12 (13) Frontal: 23 (25) Parietal: 21 (23) Occipital: 3(3) Temporoparietal: 6 (6) Frontoparietal: 5 (5) Temporo-occipital: 1 (1)
Kothari et al, 201511 King Edward Memorial Hospital & Seth Gordhandas Sunderdas Medical College, Mumbai, Maharashtra	1998–2006 (8)	715				Tuberculosis: 426 (60) Pyogenic: 280 (39) Fungal: 9 (1)	CSOM: 189 (67) CHD: 50 (18) Post-traumatic: 14 (5) Miscellaneous: 27(10)	Temporal: 111(39) Cerebellar: 72 (26) Frontal: 54(19) Parietal: 19 (7) Occipital: 7 (2) Multiple: 17 (6)	39 (5)
Naik et al 201512 Osmania Hospital, Hyderabad, Telangana	June 2009–2012 (3)	24	2–70	20 83	4 17	11 (46) Staphylococcus: 4 (17) Streptococcus: 3 (13) Klebsiella: 2 (9) Mixed infection: 2 (9)	CSOM:10 (42) CHD: 5 (20) Post-traumatic/operative: 5 (20)	Temporal: 3 (13) Cerebellar: 7(29) Parietal: 6 (25) Frontal: 3(13) Occipital: 1 (4) Temporoparietal: 2 (8) Multiple: 2 (8)
Sudhaharan et al, 201613 Nizam's Institute of Medical Sciences, Hyderabad, Telangana	1987–2014 (28)	430		35 (73)	13 (27)	116:(27); anaerobes: 48 (41) Peptostreptococcus: 26(54) Bacteroides: 18 (37) Peptococcus: 5 (10) Veillonella: 3 (6) P. melaninogenicus: 1(2) Mixed 14: (3)	CSOM: 36(75) CHD: 5 (10) Trauma: 4 (8) Pulmonary:1 (2)	Temporal: 13(27) Cerebellar: 10(21) Frontal: 12 (25) Parietal: 4 (8) Occipital: 2(4) Frontoparietal: 6 (12)	1 (2)

Table 2 Publications on otogenic brain abscess in India in the current decade (2010–2019)

Reference and place of study	Duration (y)	No. of patients/samples	Age range in years (average)	Gender (%)		Symptoms and predisposing factors	No. of culture positive and isolated organisms (%)	Location (%)		No. of died patients (%)
				Male	Female			Temporal	Cerebellar
Abbreviations: NA, not available; No., Number; T-P, temporoparietal.
Borade et al, 201114 Dr. Vaishampayan Memorial Govt. Medical College, Solapur, Maharashtra	Jan 1997–Dec 2010 (4)	72	6–54 (16 y)	40 (55)	32 (45)	Cholesteatoma: 62 (86) Granulations: 10 (14)	(20) Escherichia coli, Pseudomonas Proteus spp. Staphylococcus Streptococcus	12(17)	60 (83)	5 (7)
Suligavi et al, 201515 SN Medical College, Agra, Uttar Pradesh	2008–2013 (6)	8	8–51 (21 y)	5 (63)	3 (37)	Headache: (100) Vomiting: (63) Seizures: (38)	Pseudomonas sp.: 1 B acteroides fragilis:1	6 (75)	2 (25)	0
Borgohain et al, 201516 Gauhati Medical College & Hospital, Guwahati, Assam	July 2013–Dec 2014 (1.5)	17	5–20 (14 y)	12 (75)	4 (25)	Headache, nausea, and vomiting: (100)	12 (71) Klebsiella: 5 (38) Pseudomonas: 7 (54)	1 (6)	16 (94)	NA
Bhattacharjee et al, 2016.17 Silchar Medical College, Silchar, Assam	Sept 2014–2015 (1)	33	9–65 (21 y)	18 (54)	15 (46)	Headache: (90) Fever: 25 (76) Seizures: 55 Cholesteatoma: (76)	Proteus mirabilis and Enterococcus: 17 (52) P. aeruginosa: 16 (48)	25 (76)	8 (24)	0
Mukherjee et al, 201618 KPC Medical College & Hospital, Kolkata, West Bengal	May 2009–April 2014 (5)	22	8–58 (26 y)	17 (77)	5 (23)	Headache: (100) Fever: 13 (59) Altered sensorium: 9 (41)	NA	7 (32)	15 (68)	0
Melkundi and Melkundi, 201719 MR Medical College and Gulbarga Institute of Medical Sciences, Gulbarga, Karnataka	2006–2015 (10)	20	4–32 (18 y)	16 (80)	4 (20)	NA	NA	6 (30) T-P 5 (25)	8 (40)	2 (10)

 

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Common Symptoms

As shown in [Table 1], the majority of brain abscess patients in India was males, which is in line with findings of studies across the globe.[20] [21] [22] The average age of the patients was 20 to 30 years, which is similar or a decade lower compared with studies in other countries.[2] [5] [23] Headache was found to be the most common symptom. Other symptoms include fever, focal neurologic deficit, seizure, nausea, and vomiting.[8] [9] [10] [11] Studies in other countries have reported similar symptoms.[24] The classic triad of fever, headache, and focal neurologic deficit was observed in half of the patients, and the mean duration of the symptoms before diagnosis was approximately 8 days.[25] [26] [27]

 

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Neuropathology

Brain abscess begin as localized areas of cerebritis in the brain parenchyma in response to an infection. The computed tomography (CT) or magnetic resonance imaging (MRI) studies show that the brain abscess development can be divided into four stages: early cerebritis (Days 1–3), late cerebritis (Days 4–9), early capsule formation (Days 10–13), and late capsule formation (after Day 14). A well-developed abscess consists of five distinct histological zones: a necrotic center, a peripheral zone of inflammatory cells, a dense collagenous capsule, a layer of neovascularization, and cerebral edema external to the capsule.[27]

More than 90% of the brain abscesses reported in [Tables 1] and 2 were single and were located in the frontal and temporal lobes and the cerebellum, and occasionally in the parietal and occipital lobes. The most common predisposing condition was middle ear infection (8–75%), as shown in [Table 1]. Other common predisposing conditions were congenital heart disease (CHD; 4–20%), post-traumatic, and neurosurgical procedures (4–20%). Other studies have reported CSOM as the main predisposing factor, followed by post-traumatic and CHD.[5] [24] [28] Middle ear infections are associated with abscess formation in the temporal or cerebellar lobes ([Table 2]). In addition, intraventricular rupture of brain abscess has been reported, resulting in acute deterioration and death.[29] [30] Other factors that contribute to intracranial complications are the virulence of organisms and the host’s immunity status.[15] Whole genome sequencing of Streptococcus intermedius TYG1620 isolated from a human brain abscess showed the presence of the type VII secretion system, which might be associated with strain-specific pathogenicity, including abscess formation.[31] The host inflammatory response, which increases with bacterial cell lysis following the administration of antibiotics, can cause damage to the surrounding normal brain parenchyma, which exceeds the brain area occupied by the infecting organism.[32] It has been shown that several inflammatory cytokine (tumor necrosis factor-α [TNF-α], interferon-γ, interleukin-1β [IL-1β], IL-10, IL-17, IL-23) levels are significantly higher in a brain abscess than in blood, and their expression in the abscess is influenced by the bacterial pathogen and the duration of symptoms.[10]

 

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Etiology

This review found that 26 to 82% of the brain abscess samples were culture-positive ([Table 1]). The most frequently identified bacteria were Streptococci (12–42%), Staphylococci (3–31%), Enterococci (7–14%), and gram-negative bacteria (9–23%), including Escherichia coli, Klebsiella, Enterobacter, Citrobacter, Proteus, and Pseudomonas. Anaerobic bacteria (2–41%) such as Peptostreptococcus, Bacteroides, Peptococcus, Fusobacterium, and Veillonella were also isolated in some studies. Nocardia and fungi were seen in 1 to 3% of samples. Mycobacterium tuberculosis was isolated from 5% (9 cases) and 10% (3 cases) of brain abscess samples in two studies.[6] [7] Only one study showed 60% tubercular abscess outnumbering pyogenic abscesses probably due to endemicity of tuberculosis in India.[11] Mixed infections were observed in 3 to 13% of samples. A retrospective analysis of 317 brain abscess samples collected over a 3-year period (January 2012 to December 2014) at the National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore, found rare pathogens in 19 samples (12%), including Cryptococcus neoformans, Aspergillus flavus, Mucor, Salmonella, and Pantoea.[33] Molecular characterization of methicillin-resistant S. aureus (MRSA) showed community-acquired (CA-MRSA), hospital-acquired (HA-MRSA), and livestock-associated (LA-MRSA) strains in brain abscess samples.[34] CSOM was mostly caused by gram-negative bacteria, including E. coli, Klebsiella, Pseudomonas, and Proteus ([Table 2]). The distribution of bacterial pathogens identified in brain abscesses has been shown to be relatively similar in different continents and to have remained stable over the past 60 years.[2]

 

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Diagnosis

Imaging techniques such as cranial CT and MRI were used in most studies to confirm the clinical diagnosis and for follow ups. In some cases, imaging techniques enabled safe and successful medical treatment without surgical intervention.[8] [9] MRI, when combined with diffusion-weighted images (DWI) and apparent diffusion coefficients (ADC) images, differentiates pyogenic brain abscess from nonpyogenic abscesses, neoplasm, cystic, or necrotic tumors.[7] [8] Magnetic resonance spectroscopy (MRS) analysis differentiated between brain abscesses and tumors, as well as between anaerobes and aerobes.[35]

Comprehensive microbiological investigations of brain abscesses were conducted in most studies, including wet mounts, Gram’s staining, Ziehl–Neelsen staining, and conventional aerobic and anaerobic cultures. BACTEC aerobic and anaerobic media were used in some studies to isolate bacterial pathogens.[7] [10] In other studies, anaerobic incubation was performed in jars using commercial GasPak systems.[6] [13]The isolates were identified by standard biochemical tests. Smears and cultures were also performed for mycobacteria, nocardia, and fungi when requested. This review shows that the incidence of negative cultures was 18 to 73% ([Tables 1] and [2 ]), which is similar to other reports.[21] [36] Polymerase chain reaction(PCR) was not performed routinely, but PCR amplification and sequencing of 16S ribosomal RNA (rRNA) in one study showed the presence of bacterial DNA in 37% of the culture-negative samples.[35] Other reports demonstrated the usefulness of 16S rRNA PCR sequencing in bacterial identification in culture-negative samples and samples containing fastidious bacteria.[37] [38] Multiple sequencing by metagenomics increases the number of identified bacteria in brain abscess samples, and next-generation sequencing (NGS) identifies infectious agents with higher confidence where microbiology fails to detect the presence of microbes.[39] [40]

 

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Management

Patients were managed with combined medical (e.g., antibiotic, steroid, and anticonvulsant) and surgical (aspiration and excision) treatments and monitored with weekly CT or MRI scans until the abscess completely disappeared. Empirical intravenous broad-spectrum antibiotic treatments were immediately initiated upon diagnosis and were further modified according to microbiological isolation and antibiotic sensitivity. Antibiotics that are active against both aerobes and anaerobes such as a third-generation cephalosporin, metronidazole and vancomycin to cover streptococci, staphylococci, strict anaerobes, and Enterobacteriaceae were used. Aminoglycosides were used for Pseudomonas infection. Long-term therapy with cotrimoxazole or sulfadiazine was used for nocardia abscesses and antituberculosis drugs were used for treating tuberculous abscesses. Flucytosine, amphotericin B, and voriconazole were used for fungal infections.[8] Antibiotic therapy was continued for 6 weeks or longer, depending on the therapeutic response and the neuroimaging findings.[8] [9] [11] Abscesses in the cerebritis stage measuring less than 2 cm in diameter and multiple deep-seated abscesses were treated with medical regimens alone.[9] Surgery was performed for large abscesses and in patients with a poor response to medical treatment. Most patients underwent abscess aspiration through a single burrhole.[11] If the size of the abscess shown in CT or MR images after the first aspiration increased or was not reduced despite antibiotic therapy, the aspiration was repeated. Patients with a poor response to repeated aspirations and post-traumatic abscesses underwent complete abscess excision through craniotomy.[1] [8] Stereotactic aspiration is associated with few complications compared with excision that involves hemorrhage, cerebrospinal fluid (CSF) leakage, seizure, and stroke.[41] When the efficacies of aspiration and excision were compared for the management of pyogenic brain abscesses, excision was found to be better with respect to duration of antibiotic use, length of hospital stay, and overall cost of treatment.[42] However, excision is said to have a poor outcome when the abscess is deep-seated and in the cerebritis stage.[41] In CSOM cases, patients underwent craniotomy for abscess removal followed by radical mastoidectomy under single anesthesia in the same session or mastoidectomy was done after the patient’s general and neurological conditions were stabilized.[17] [19] High-dose corticosteroid treatment was administered to patients with life-threatening cerebral edema or cerebral herniation and tapered over a period of 4 weeks.[8] Anticonvulsants were administered as prophylactics, and the duration of therapy was individualized and guided by electroencephalographic (EEG) reports.[9] [11] The mortality rate in brain abscess patients was 2 to 7%, and up to 10% in patients with middle ear infection ([Tables 1] and [2 ]).

 

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Prevention

Eradication of potential sources of infection before the abscess fully develops is a reasonable preventive strategy. Middle ear infection, which is often neglected and not treated aggressively, remains the most frequent predisposing condition in India ([Tables 1] and [2]) and other Asian countries.[43] [44] [45] [46] Multidisciplinary treatment strategies to address the primary source have helped to improve outcomes in otogenic brain abscesses.[19] Congenital cyanotic heart disease (CCHD) in the majority of children in Asia remains either uncorrected or only partially palliated. Uncured CCHD is a high-risk factor for the occurrence, persistence, and recurrence of a brain abscess.[47] [48] Prompt diagnosis of CCHD and corrective surgery might help to reduce the development of brain abscesses in children.[49] Head trauma has become an important predisposing factor with the increasing incidence of traffic accidents, which requires safety measures.[23] Tooth extraction and treatment for sinusitis may also help to remove the focus of infection and prevent further spread of bacteria.[50] The duration of hospitalization increases the risk of nosocomial infections concomitant with higher mortality.[36] Infection control strategies in intensive care units (ICUs) may help to improve brain abscess outcomes.[20] Health awareness in terms of ear and oral hygiene may help to reduce the overall incidence of brain abscess.[51] [52]

 

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Conclusion

The incidence of brain abscess continues to be high in India due to CSOM, particularly among socioeconomically vulnerable populations with poor health consciousness ([Tables 1] and [2]). New developments include hyperbaric oxygen therapy, which improves brain abscess outcomes.[53] Gene therapy is another prospect, as there is an association between single nucleotide polymorphisms in TNF-α, IL-1β, Intercellular Adhesion Molecule 1 (ICAM-1), and monocyte chemoattractant protein-1 (MCP-1) genes and increased risk of brain abscess development.[54] [55] Identifying pathogens associated with brain abscess using NGS might contribute to early detection and appropriate treatment.

 

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Conflict of Interest

None declared.

• References

• 1 Brook I. Microbiology and treatment of brain abscess. J Clin Neurosci 2017; 38: 8-12
• 2 Brouwer MC, Coutinho JM, van de Beek D. Clinical characteristics and outcome of brain abscess: systematic review and meta-analysis. Neurology 2014; 82 (09) 806-813
• 3 Brouwer MC, van de Beek D. Epidemiology, diagnosis, and treatment of brain abscesses. Curr Opin Infect Dis 2017; 30 (01) 129-134
• 4 Khullar P, Datta NR, Wahi IK, Kataria S. Brain abscess mimicking brain metastasis in breast cancer. J Egypt Natl Canc Inst 2016; 28 (01) 59-61
• 5 Mian MA, Abbasi S, Khan FA, Usman M. Association of etiological and pathological features of brain abscess with outcome. Journal of Rawalpindi Medical College (JRMC) 2017; 21 (01) 29-32
• 6 Lakshmi V, Umabala P, Anuradha K. et al. Microbiological spectrum of brain abscess at a tertiary care hospital in South India: 24-year data and review. Pathol Res Int 2011; 2011: 583139
• 7 Tomar V, Yadav A, Rathore RK. et al. Apparent diffusion coefficient with higher b-value correlates better with viable cell count quantified from the cavity of brain abscess. AJNR Am J Neuroradiol 2011; 32 (11) 2120-2125
• 8 Muzumdar D, Jhawar S, Goel A. Brain abscess: an overview. Int J Surg 2011; 9 (02) 136-144
• 9 Sarmast AH, Showkat HI, Bhat AR. et al. Analysis and management of brain abscess; a ten year hospital based study. Turk Neurosurg 2012; 22 (06) 682-689
• 10 Bajpai A, Prasad KN, Mishra P, Singh AK, Gupta RK, Ojha BK. Distinct cytokine pattern in response to different bacterial pathogens in human brain abscess. J Neuroimmunol 2014; 273 (1-2) 96-102
• 11 Kothari M, Goel A, Muzumdar D. Brain abscess: heuristics, principles, pathobiology, practice. Neurol India 2015; 63 (03) 329-337
• 12 Naik RRM, Rao AL, Venugopal G. et al. Clinical study of brain abscess and its treatment with repeated aspirations and outcome. J EvolMed DenSci 2015; 4 (08) 1325-1331
• 13 Sudhaharan S, Chavali P, Vemu L. Anaerobic brain abscess. Iran J Microbiol 2016; 8 (02) 120-124
• 14 Borade VR, Jaiswal SA, Nemade HO. Transmastoid approach to otogenic brain abscess: 14 years experience. Ind J Otol 2011; 17 (04) 155-158
• 15 Suligavi SS, Gokale S, Jain P, Doddamani SS, Patil MN. Otogenic brain abscess: our experience. J Evol Med Den Sci 2015; 4 (13) 2087-2091
• 16 Borgohain R, Talukdar R, Ranjan K. Otogenic brain abscess: a rising trend of cerebellar abscess an institutional study. Indian J Otol 2015; 21: 286-289
• 17 Bhattacharjee A, Singh RP, Nazrin J. Monitoring the evolution of otogenic brain abscess - changing trends in management. IOSR JDenMedSci 2016; 15: 36-47
• 18 Mukherjee D, Das C, Paul D. Single-stage trans-mastoid drainage of otogenic brain abscess: a single-institution experience. Indian J Otolaryngol Head Neck Surg 2016; 68 (02) 179-184
• 19 Melkundi S, Melkundi RS. Otogenic brain abscess and its management with review of literature. Int J Otorhinolaryngol Head Neck Surg 2017; 3 (02) 180-183
• 20 Ong CT, Tsai CF, Wong YS, Chen SC. Epidemiology of brain abscess in Taiwan: a 14-year population-based cohort study. PLoS One 2017; 12 (05) 0176705
• 21 Chowdhury FH, Haque MR, Sarkar MH, Chowdhury SMNK, Hossain Z, Ranjan R. Brain abscess: surgical experiences of 162 cases. Neuroimmunol Neuroinflamm 2015; 2 (03) 153-161
• 22 Amir S. Brain abscess: a clinical experience in a tertiary care hospital. Pak J Surg 2017; 33 (03) 203-207
• 23 Ndubuisi CA, Ohaegbulam SC, Mezue WC, Chikani MC, Nkwerem SP, Ozor II. Management of brain abscess: changing trend and experience in Enugu, Nigeria. Niger J Surg 2017; 23 (02) 106-110
• 24 Azam F, Iftikhar-Ul-Haq M. Mushtaq. Clinical manifestation of brain abscess. Pak J Neurol Surg 2011; 15: 99-101
• 25 Hsu CW, Lu CH, Chuang MJ. et al. Cerebellar bacterial brain abscess: report of eight cases. Acta Neurol Taiwan 2011; 20 (01) 47-52
• 26 Ahmad S, Rehman L, Afzal A, Rizvi R. Outcome of burr-hole aspiration of brain abscess. Pak J Med Sci 2017; 33 (05) 1161-1165
• 27 Sonneville R, Ruimy R, Benzonana N. et al. ESCMID Study Group for Infectious Diseases of the Brain (ESGIB). An update on bacterial brain abscess in immunocompetent patients. Clin Microbiol Infect 2017; 23 (09) 614-620
• 28 Wiwanitkit S, Wiwanitkit V. Pyogenic brain abscess in Thailand. N Am J Med Sci 2012; 4 (06) 245-248
• 29 Savardekar AR, Krishna R, Arivazhagan A. Spontaneous intraventricular rupture of pyogenic brain abscess: a short series of three cases and review of literature. Surg Neurol Int 2016; 7 (Suppl. 39) S947-S951
• 30 Sáez-Llorens X, Nieto-Guevara J. Brain abscess. Handb Clin Neurol 2013; 112: 1127-1134
• 31 Hasegawa N, Sekizuka T, Sugi Y. et al. Characterization of the pathogenicity of Streptococcus intermedius TYG1620 isolated from a human brain abscess based on the complete genome sequence with transcriptome analysis and transposon mutagenesis in a murine subcutaneous abscess model. Infect Immun 2017; 85 (02) e886-16.pii:
• 32 Esen N, Kielian T. Toll-like receptors in brain abscess. Curr Top Microbiol Immunol 2009; 336: 41-61
• 33 Ravikumar R, Nivedita P, Mridula RP, et al. Emerging pathogens causing brain abscess as seen in a Neurocare Centre, NIMHANS, Bangalore, South India. Paper presented at: XIX International Congress for Tropical Medicine and Malaria; September 18–22, 2016; Brisbane, Australia
• 34 Bahubali VKH, Vijayan P, Bhandari V, Siddaiah N, Srinivas D. Methicillin-resistant Staphylococcus aureus intracranial abscess: an analytical series and review on molecular, surgical and medical aspects. Indian J Med Microbiol 2018; 36 (01) 97-103
• 35 Bajpai A, Prasad KN, Mishra P, Gupta RK, Singh AK, Ojha BK. Multimodal approach for diagnosis of bacterial etiology in brain abscess. Magn Reson Imaging 2014; 32 (05) 491-496
• 36 Miniar T, Amel BA, Khalil S. et al. Pyogenic brain abscess in children: a Tunisian multi-center experience. Afr Health Sci 2018; 18 (03) 560-568
• 37 Jenkins C, Ling CL, Ciesielczuk HL. et al. Detection and identification of bacteria in clinical samples by 16S rRNA gene sequencing: comparison of two different approaches in clinical practice. J Med Microbiol 2012; 61 (04) 483-488
• 38 Lleo MM, Ghidini V, Tafi MC, Castellani F, Trento I, Boaretti M. Detecting the presence of bacterial DNA by PCR can be useful in diagnosing culture-negative cases of infection, especially in patients with suspected infection and antibiotic therapy. FEMS Microbiol Lett 2014; 354 (02) 153-160
• 39 Al Masalma M, Lonjon M, Richet H. et al. Metagenomic analysis of brain abscesses identifies specific bacterial associations. Clin Infect Dis 2012; 54 (02) 202-210
• 40 Salzberg SL, Breitwieser FP, Kumar A. et al. Next-generation sequencing in neuropathologic diagnosis of infections of the nervous system. Neurol Neuroimmunol Neuroinflamm 2016; 3 (04) e251
• 41 Ratnaike TE, Das S, Gregson BA, Mendelow AD. A review of brain abscess surgical treatment–78 years: aspiration versus excision. World Neurosurg 2011; 76 (05) 431-436
• 42 Sarmast AH, Showkat HI, Kirmani AR. et al. Aspiration versus excision: a single center experience of forty-seven patients with brain abscess over 10 years. Neurol Med Chir (Tokyo) 2012; 52 (10) 724-730
• 43 Menon S, Bharadwaj R, Chowdhary A, Kaundinya DV, Palande DA. Current epidemiology of intracranial abscesses: a prospective 5 year study. J Med Microbiol 2008; 57 (Pt 10) 1259-1268
• 44 Kafle P, Sharma M, Shilpakar S. et al. Pediatric brain abscess clinical profile, management and outcome at tertiary care centre in Nepal. Journal of College of Medical Sciences-Nepal 2018; 14 (02) 102-106
• 45 Lee CG, Kang SH, Kim YJ. et al. Brain abscess in Korean children: a 15-year single center study. Korean J Pediatr 2010; 53 (05) 648-652
• 46 Zhang C, Hu L, Wu X, Hu G, Ding X, Lu Y. A retrospective study on the aetiology, management, and outcome of brain abscess in an 11-year, single-centre study from China. BMC Infect Dis 2014; 14: 311
• 47 Udayakumaran S, Onyia CU, Kumar RK. Forgotten? not yet. Cardiogenic brain abscess in children: a case series-based review. World Neurosurg 2017; 107: 124-129
• 48 Lee HS, Kim JH, Kim YH, Lee S. Surgically treated community-acquired brain abscess: bacteriological analysis based on predisposing infections. Jpn J Infect Dis 2018; 71 (03) 191-196
• 49 Ziaullah RZ. Brain abscess in children with cyanotic congenital heart disease-clinical presentation and outcome. JSMC 2017; 7 (02) 107-111
• 50 Brouwer MC, van de Beek D. Management of bacterial central nervous system infections. Handb Clin Neurol 2017; 140: 349-364
• 51 Akashi M, Tanaka K, Kusumoto J, Furudoi S, Hosoda K, Komori T. Brain abscess potentially resulting from odontogenic focus: report of three cases and a literature review. J Maxillofac Oral Surg 2017; 16 (01) 58-64
• 52 Lajolo C, Favia G, Limongelli L. et al. Brain abscess of odontogenic origin in children: a systematic review of the literature with emphasis on therapeutic aspects and a new case presentation. Acta Otorhinolaryngol Ital 2019; 39 (02) 67-74
• 53 Gossman W, Tommeraasen MA, Cooper JS. Hyperbaric evaluation and treatment of intracranial abscess. Treasure Island (FL):. StatPearls Publishing 2019
• 54 Mishra P, Prasad KN, Singh K, Sahu RN, Ojha BK. Association of ICAM-1 (K469E) and MCP-1 -2518 A>G gene polymorphism with brain abscess. J Neuroimmunol 2016; 292: 102-107
• 55 Mishra P, Prasad KN, Singh K, Bajpai A, Sahu RN, Ojha BK. Tumor necrosis factor-αand interleukin-1βgene polymorphisms and risk of brain abscess in North Indian population. Cytokine 2015; 75 (01) 159-164

Publikationsverlauf

Artikel online veröffentlicht:
13. Mai 2021