Brain Abscesses in the Tropics

Abstract

Purpose of Review

This review aims to elucidate the etiologies of brain abscesses in the tropics. Despite the similarities in causes of brain abscesses across global regions, tropical settings manifest distinguishing characteristics, prominently observed on computed tomography or magnetic resonance imaging.

Recent Findings

In tropical climates, the leading conditions predisposing individuals to brain abscesses are polymicrobial bacterial infections originating from paranasal sinuses, dental sources, and otitis media. However, the tropics present unique etiologies to be aware of, including Trypanosoma cruzi (Chagas disease), free-living amoebas like Balamuthia mandrillaris, infections from Burkholderia pseudomallei (melioidosis), fungi such as Talaromyces marneffei, and Mycobacterium tuberculosis. Given the differential diagnoses, which include neoplastic, inflammatory, and demyelinating diseases, a stereotactic biopsy coupled with a microbiological assessment remains valuable for accurate diagnosis.

Summary

In tropical regions, brain abscesses are a concern when confronted with mass-occupying or other types of brain lesions. Successful clinical management of brain abscesses typically combines surgical intervention and extended anti-microbial treatment. However, specific parasitic invasions like Chagas disease, free-living amoebas, and Entamoeba histolytica necessitate targeted anti-parasitic therapies. Furthermore, international policy efforts should focus on prevention measures in resource limited regions with heightened risks and disease burden.

Introduction

The etiology of brain abscesses in persons living in the tropics is the same as those identified in non-tropical settings, with a few exceptions. This spectrum reflects the many potential underlying sources of infection (Table 1) [1••, 2•]. Bacteria, fungi, or parasitic infections (protozoal or helminthic) may enter the intracranial space to establish foci of infection in the epidural or subdural spaces or reach the brain parenchyma [2•]. When the infection reaches the brain parenchyma through the hematogenous route or via regional veins and lymphatics from oral or otic sources, it causes single or multiple abscesses. The initial stage of the infection leading to a brain abscess is cerebritis, followed by perivascular inflammation and central necrosis, producing edema in the surrounding brain parenchyma [3]. As the necrotic center enlarges, a capsule thickens through neovascularization and collagen deposition. Neovascularization with disruption of the blood–brain barrier manifests as ring-enhancing mass lesions on neuroimaging studies. The resulting clinical syndromes depend on the location of the abscess and the predisposing condition, but it is often the result of mass occupying effect and surrounding cerebral edema. The differential diagnosis of ring-enhancing lesions includes neoplasms, demyelinating diseases, vascular lesions, radiation necrosis, and others [1••, 3]. We discuss the pathogenesis, etiology, diagnosis, and treatment of brain abscess in the tropics.

Table 1.

Sources of infection and associated microbiology in patients diagnosed with a brain abscess

Underlying conditions	Infectious pathogens
Penetrating trauma or post-neurosurgical procedures	Pseudomonas aeruginosa, Klebsiella pneumoniae, Enterobacter spp.
	Clostridium spp.
	Staphylococcus aureus
	Staphylococcus epidermidis
Otitis media or otomastoiditis	Bacteroides spp.
	Prevotella spp.
	Fusobacterium spp.
	Streptococcus pneumoniae
	Haemophilus influenzae
	Streptococcus milleri
Dental infections	Fusobacterium necrophorum
	Actinomyces spp.
	Bacteroides spp.
	Peptostreptococcus
Immunocompromised persons (HIV/AIDS)	Nocardia spp.
	Listeria monocytogenes, Cryptococcus neoformans
	Trypanosoma cruzi
	Mycobacterium tuberculosis
	Toxoplasma gondii
	Pseudomona pseudomallei
	Talaromycosis
Paranasal sinusitisa	Streptococcus spp. and Prevotella spp.
Lung abscess and/or empyema	Fusobacterium spp.
	Actinomyces spp.
	Nocardia spp.
	Prevotella spp.
	Streptocci spp (e.g.. Viridans group Streptococci)
Bacterial endocarditis	Staphylococcus aureus
	Viridians group Streptococci (e.g., Streptococcus mitis)
	Streptococcus spp.

Adapted and modified from Franco-Paredes, C. Academic Press, Elsevier 2016, P. 24. [60]

^aParanasal sinusitis may be associated with suppurative intracranial infection

Pathogenesis and Predisposing Medical Conditions

Pathogenic infection mechanisms depend on predisposing conditions, which can broadly be divided into abscesses affecting immunocompetent versus immunocompromised patients [1••, 3]. In the tropics, the etiological determinants of brain abscesses continue to be notably modulated by the immunological status of the afflicted individual. Brain abscesses in immunocompetent patients are predominantly caused by bacterial infections, accounting for approximately 95% of cases [3]. Once the blood–brain barrier is breached, the brain becomes highly susceptible to these infections [4]. Notably, many bacteria, including anaerobes, can be involved in polymicrobial infections, further complicating the pathogenesis [5••, 6]. Bacterial entry into the brain principally occurs via contiguous spread and hematogenous dissemination. Contiguous spread accounts for 40–50% of cases, commonly originating from local infections such as otitis, mastoiditis, and sinusitis or due to cranial trauma and neurosurgical procedures [7, 8]. When the infection results from a contiguous spread, it often involves skin-colonizing bacteria like Staphylococcus aureus and S. epidermidis, or gram-negative bacilli. Also, streptococcus species frequently cause abscesses from parameningeal infection sites, such as the middle ears, mastoids, and sinuses. However, staphylococcal and polymicrobial abscesses, including those by anaerobes and gram-negative bacilli, are also seen.

Hematogenous dissemination accounts for 30–40% of brain abscesses, particularly in cases with underlying conditions like infective endocarditis [8, 9••, 10]. Common predisposing factors for this spread include pulmonary circulation shunts — seen in conditions like congenital heart disease or arteriovenous fistulas in hereditary hemorrhagic telangiectasia patients — and dental infections [11–14]. When infections disseminate via the hematogenous route, they often involve distant foci such as the skin, paranasal sinuses, and teeth. In these cases, the microbial culprits are typically Staphylococcus and Streptococcus species [7]. It is worth noting that brain abscesses resulting from paranasal sinus or dental infections can be polymicrobial [15]. Often, it is important to consider the possibility of a combination of lung and brain abscesses occurring concomitantly (Table 2). The prime example of this is the case of infections caused by Nocardia spp.

Table 2.

Lung and brain abscess syndromes

Category	Specific pathogen
Bacterial	Melioidosis (Burkholderia pseudomallei)
	Nocardia spp.
	Actinomyces spp.
Mycobacterial	Mycobacterium tuberculosis
	Mycobacterium avium-intracellulare
	Mycobacterium abscessus
Fungal	Blastomycosis
	Aspergillosis
	Histoplasmosis
	Coccidiodomycosis
	Cryptococcosis
	Talaromycosis
Parasitic	Paragonimus westermani
	Strongyloides stercolaris

Adapted and modified from Franco-Paredes, C. Academic Press, Elsevier 2016, P. 25 [60]

About 10–20% of brain abscesses in immunocompetent patients remain cryptogenic [16]. Moreover, meningitis rarely culminates in brain abscess development, with such outcomes seen in less than 0.05% of patients [17]. Brain abscesses manifest with notably higher frequency in immunocompromised patients [9••]. Such compromised states of immunity often arise from conditions like HIV infection or immunosuppressive therapy, particularly among patients undergoing solid-organ or hematopoietic stem-cell transplantation. In immunocompromised, non-bacterial agents, such as fungi or parasites, become significant causative agents of abscesses [9••]. In HIV-infected individuals, the predisposition to infections by Toxoplasma gondii and Mycobacterium tuberculosis is significantly pronounced [18, 19]. In developing countries, infections are the leading cause of HIV-associated focal brain lesions [20].

Nocardial brain abscesses present a considerable clinical challenge and frequently coexist with systemic diseases [21]. Patients who have received solid-organ transplants face not only the risk of nocardial brain abscesses but also the threat of fungal abscesses, often stemming from infections by species like Aspergillus or Candida, although Aspergillus typically presents in the brain as a mass and less commonly as an abscess [22]. Among solid-organ transplant recipients, fungi are implicated in most cases of cerebral abscess [23]. Recently, brain abscesses caused by Volvariella volvacea have emerged as a fungal pathogen in Asia [24]. These findings underscore the heightened vulnerability of immunocompromised patients to a diverse array of cerebral infections in the tropics.

Moreover, in the tropics, the pathogenesis, epidemiology, and risk factors associated with brain abscesses are shaped by distinct environmental and socio-economic determinants. Direct environmental exposure plays a pivotal role in disease transmission; for example, interaction with soil or water contaminated with Burkholderia pseudomallei can lead to infections like Melioidosis [25, 26]. Moreover, the health infrastructure in these regions, often characterized by limited resources and decreased access to essential medical interventions, can exacerbate the severity of primary infections. As a result, conditions such as otitis media, if not promptly or effectively treated due to restricted access to appropriate medical care, can escalate into severe complications like otogenic brain abscesses [27, 28]. This issue becomes particularly salient in developing nations located within the tropics [28]. It is also relevant when considering migrant populations traveling through endemic regions or areas with heightened risk of environmental exposure to infectious agents associated with brain abscesses [29]. Additionally, regions in the tropics are often the epicenters for endemic diseases that further predispose individuals to brain abscesses. For instance, the high prevalence of HIV in regions like sub-Saharan Africa introduces an intricate layer of complexity to clinical presentations, given the interplay between the virus and agents responsible for brain abscesses [7, 30]. Hence, a holistic understanding of region-specific dynamics is important when considering pathogenesis and subsequent management or prevention of brain abscesses in the tropics.

Etiology of Brain Abscesses in the Tropics

Although bacteria are responsible for > 95% of brain abscesses, causative agents of brain abscesses vary broadly and largely depend on the infection etiology [6]. While contiguous extension is the more common cause of brain abscesses, hematogenous diffusion of systemic infection is still responsible for around 30% of abscesses—substantially diversifying the pathogenic culprits of brain abscesses [6].

Due to the anatomic adjacency of the brain to the oral cavity, oral infections, otitis media, frontal sinusitis, or directly invasive trauma and surgery can result in contiguous extension [31, 32]. When cultured, odontogenic cerebral abscesses contain oral flora, resulting in a mixed polymicrobial infection. Examples of commensal organisms to the oral cavity include streptococci (Viridans group Streptococci (VGS)), Actinomyces spp., and Fusobacterium spp. Actinobacillus spp. and Staphylococci are not native to the human oral cavity but are found in acute odontogenic infections [32].

Otogenic brain abscesses have been rare since the introduction of antibiotics, but life-threatening central nervous system complications of acute or chronic otitis media persist in developing countries [33]. Otitis-associated brain abscesses in immunocompetent individuals can be polymicrobial and tend to be dominated by Streptococci (including Streptococcus pneumoniae), Enterobacteriaceae, and Staphylococcus aureus [6]. Of note, enteric gram-negative Bacilli such as Proteus spp. including Proteus vulgaris are causative organisms of brain abscesses secondary to otitis media [33]. Along with the Proteus spp., other enteric gram-negative rods, including Escherichia coli, Klebsiella spp., and Pseudomonas spp. are isolated in 23–33% of patients and often in patients with infective ear disease [7].

Bacterial brain abscesses as complications of sinusitis also tend to be polymicrobial, with Streptococcus spp. and Staphylococcus spp. as the most isolated organisms [31]. Infections, including brain abscesses that arise from head or neurosurgery, tend to be composed of skin-colonizing bacteria such as S. aureus and S. epidermidis [7]. Overall, within bacteria, the most common causative agent of cerebral abscess is streptococci, accounting for 70% of brain abscesses, followed by Staphylococci, which is responsible for 10–20% of abscesses [7].

Hematogenous spread is more common in immunocompromised individuals. It is associated with distant infection (cellulitis), cardiac valvular disease (such as endocarditis or structural heart defects), HIV infection, melioidosis, Klebsiella mucoid, and solid-organ transplantation. With hematogenous-sourced brain abscess development, Streptococci and Staphylococci remain the most common causative pathogens. In a study assessing 178 patients with bacterial brain abscesses in Taiwan, the single most common predisposing factor for brain abscess development was congenital heart disease—identified in 12.4% of total patients—and bacterial endocarditis was confirmed in 7.3% of total patients [34].

Septic emboli from infective endocarditis (IE) are known to lead to ischemic infarction and the development of brain abscesses [35]. In cases of IE, Streptococci and Staphylococci are again the most common pathogenic culprits of brain abscesses, though HACEK endocarditis is a rare but possible cause of brain abscess formation [36].

In cases of underlying HIV infection, brain abscesses are more frequently caused by Toxoplasma gondii but may also be caused by Mycobacterium tuberculosis—especially in endemic regions [7, 18]. Although HIV-infected individuals are at higher risk of central nervous system tuberculomas and tuberculous abscesses, these are also possible in HIV-negative patients [18].

Melioidosis—a bacterial infection caused by Burkholderia pseudomallei—is another known cause of brain abscesses more common in the tropics. Melioidosis—or Whitmore’s disease—is caused by contact with contaminated soil and water. Melioidosis cases typically take place in endemic areas (especially northern Australia and Thailand) or non-endemic regions but with a history of travel to the endemic areas where individuals would have been in contact with soil or water contaminated with B. pseudomallei that can remain latent and reactivate after an extended period [1••, 37].

Another known causative pathogen of brain abscessation is the mucoid phenotype of Klebsiella pneumoniae. Mucoid Klebsiella—also known as hypervirulent Klebsiella pneumoniae (kvKp)—tends to infect healthy, younger individuals in the community and can lead to life-threatening liver and brain abscesses, endophthalmitis, meningitis, and more [38]. Because of this, hvKP has emerged as a concerning global pathogen. Though hvKp was first recognized in Taiwan and remains more common in the Asian Pacific Rim, infections occur globally [39]. Although Klebsiella is a rare yet rising cause of community-acquired brain abscessation, it has a mortality rate of up to 27%, increasing to 38% with complicating intraventricular empyema [40].

Fungal and parasitic pathogens represent a more minor yet critical cause of brain abscesses in the tropics and immunocompromised individuals. Fungal agents leading to cerebral abscessation in the tropics include Aspergillus, Cryptococcus, and dimorphic fungi (including Histoplasma capsulatum, Blastomyces dermatitidis, and Coccidioides spp.). While fungi remain a minority in causative pathogens, reports indicate that fungal infections of the central nervous system have been increasingly more common over the past two decades [41]. Moreover, although rare, the mortality rates of fungal pathologies are staggering—with invasive central nervous system aspergillosis in immunocompromised individuals at nearly 100% and immunocompetent individuals at 67% mortality [42]. Within dimorphic fungi, the most common pathogen is Histoplasma capsulatum—which infects nearly 40 million humans worldwide and endemically persists in Latin America, Africa, Asia, and the US [41]. While less prevalent than Histoplasmosis, other dimorphic fungi such as Coccidioides (endemic in Mexico and South America), Blastomycosis (endemic in Africa and Central America), and Talaromyces marneffei (endemic in Southeast Asia) are other severe causes of brain abscessation in the tropics [41]. Cryptococccomas usually develop in immunocompromised individuals and can present with headaches, altered mental status, confusion, and vomiting [43•].

Regarding parasitic causes of brain abscesses, Toxoplasmosis is the most common but not the only parasitic organism responsible for cerebral abscessation. Parasitic agents other than Toxoplasma gondii include free-living amoebas (such as Naegleria fowleri, Balamuthia mandrillaris, and Acanthamoeba spp.), American trypanosomiasis (Trypanosoma cruzi), Trypanosoma brucei rhodesiense, and sleeping sickness (Trypanosoma bruce gambiense). Free-living amoebas and African trypanosomiasis or sleeping sickness tend to cause multiple brain abscesses, while American trypanosomiasis or Chagas disease typically causes a focal, non-cystic lesion [44]. Although these are less frequent, clinical suspicion should rise with epidemiologic indicators such as travel history or country of origin [44]. Notably, Echinococcus is another parasitic cause of brain abscesses in the tropics. It is distinct from other parasitic etiologies because, while many other parasitic brain abscesses can be managed with needle aspiration and anti-parasitic medications, Echinococcus abscesses require a specialized approach. The preferred treatment is surgical excision to avoid cyst rupture, and in high-risk locations, the puncture-aspiration-injection-reaspiration method may be used, despite limited research on this rare cause of brain abscesses.

Diagnosis and Treatment

Intraparenchymal abscesses are an elusive clinical diagnosis to make under even the best of circumstances, primarily due to variations in presenting symptoms. Headache is the most frequently reported symptom, with an incidence of 69%, followed by fever (53%), neurological deficits (48%), and nausea/vomiting (47%); fever has been reported in 25% of patients, with papilledema (35%) and nuchal rigidity (32%) frequently noted, as well [7]. The classical clinical triad of brain abscess of headache, focal deficit, and fever has increasingly fallen out of favor, as observed in just 20% of patients on initial presentation [7]. Notably, brain abscess secondary to hematogenous spread may present symptoms directly associated with the primary source of infection.

Unsurprisingly, advanced imaging is critical to diagnosis due to the non-specific nature of abscess symptoms. The presence of predisposing factors such as a contiguous source of infection (mastoiditis, otitis, sinusitis, meningitis, and odontogenic infection), recent history of neurologic surgery, head trauma, or cardiopulmonary disease, older age, and immunocompromised status should all heighten clinical suspicion and increase urgency of imaging [1••, 7]. Although the median time from symptom onset to diagnosis is 8.3 days, early intervention is vital to prevent the development of devastating neurological consequences and reduce mortality [7]. Multidisciplinary approaches are also recommended to identify pathogenesis as distant sources of infection may require additional operative source control.

Diagnostic considerations specific to tropical countries include increased infectious disease burden with disease expected to grow in step with global warming and climate change [45, 46], a historically higher incidence of infectious diseases specifically leading to immunocompromised status, rarer and thus more challenging to identify causative organisms and a relative paucity of regional literature.

Radiological Approaches and Findings

MRI is considered the gold-standard imaging modality for brain abscess due to its superior ability to delineate soft tissue changes and better characterize the extent of the infection [47]. Specific benefits of MRI are increased ability to identify additional lesions, clearer depiction of surrounding edema, and decreased toxicity from contrast agents [47, 48].

Intraparenchymal abscesses typically present on contrast-enhanced computerized tomography (CT) as lesions characterized by a hyperdense rim, central hypodensity, and surrounding edema. On MRI, on the other hand, brain abscesses present as ring-enhancing masses with a hyper-intense center on T2, diffusion restriction on DWI, and a hypointense smooth rim on T2WI. Very early indications of an early abscess include vascular congestion, petechial hemorrhage, and edema, which presents on MRI as high T2WI with scare contrast enhancement. As the abscess forms, an incompletely enhancing rim develops with complete ring enhancement, indicating the presence of a mature abscess. Most abscesses will present with ring enhancement (95%), while about a quarter will present with dual rim sign [40]. Notably, restricted diffusion sequences (DWI and ADC) on MRI have been used to differentiate abscesses from other space-occupying lesions with a sensitivity of 94% and specificity of 95%, historically a more challenging distinction for clinicians to make [49].

However, although MRI is considered a more sensitive modality, numerous studies note that CT is more widely available. CT is generally sufficient to identify mature abscesses and to follow treatment outcomes; however, CT lacks sensitivity for early abscess formation. Significantly, patients with abscesses are at heightened risk of developing herniation and ventricular extension with eventual obstructive hydrocephalus, devastating findings readily apparent on MRI and CT alike. Most cases of bacterial abscess present as a single lesion, primarily located in the frontal (31%) or temporal lobes (27%) at the junction of gray and white matter [7, 47], although abscesses may also occur in any other location, as well.

Finally, although imaging is increasingly able to detect the presence of abscess, biopsy is also necessary to confirm the presence of abscess and determine causative organisms through stereotactic or open tissue collection.

Laboratory Diagnosis

Laboratory testing is of mixed benefit in the early diagnostic process. Leukocyte counts are commonly elevated (60%), as are CRP (60%) and ESR (72%), although these findings are classically non-specific [7]. Thus, while elevated inflammatory and stress markers may increase suspicion of infection, negative bloodwork does not preclude the possibility of abscess and should not significantly delay imaging.

Blood cultures have revealed causative organisms in 28% of cases and should be collected early in the infectious workup before administering any antibiotics. Twenty-four percent of patients who underwent cerebrospinal fluid culture yielded positive results [7]. However, the possibility of extant brain herniation should always be evaluated with imaging before obtaining a lumbar puncture. Cultures should also be collected from the abscess itself via biopsy to identify the specific offending pathogen(s).

Combined pyogenic and blood cultures have helped determine that most abscesses are bacterial, with only parasitic infections accounting for 0.1% and fungal infections for 1%. Thirteen percent of abscesses are cryptogenic, with no causative organism ever identified. CSF cultures are rarely recommended due to the associated risks. Universal PCR in brain tissue or next-generation sequencing can be necessary ancillary diagnostic tools when no etiologic agent is identified through the standard workup. However, its price and accessibility are very limiting factors for their implementation.

Treatment Modalities

Brain abscesses are regularly treated through a dual pharmacologic and surgical approach, with specifics depending on the abscess’s etiology and extent. However, any suspected abscess necessitates urgent neurosurgical and infectious disease involvement. Pharmacologic treatment is with antibiotic, anti-fungal, or anti-parasitic therapy. Empiric broad-spectrum antibiotic therapy for bacterial brain abscess classically consists of a third-generation cephalosporin with metronidazole, with vancomycin added in cases where there is heightened suspicion for methicillin-resistant Staphylococcus aureus (MRSA) [3, 9••, 50]. Other antibiotics may be used pending the specific microbial etiology, although the extent of penetration through the blood–brain barrier should be considered carefully when selecting an agent. Typically, anti-microbial therapy ranges from 4 to 8 weeks in length, and parenteral administration has been historically preferred, although studies are increasingly looking at outcomes with partial oral antibiotic treatment [51]. Additional anti-microbials may be added for fungal and parasitic abscesses once the etiology is identified, although fewer data and treatment recommendations are available for these sources.

If the infection is not yet encapsulated on imaging, anti-microbials alone may be given as therapy. There is also evidence that abscesses < 2.5 cm may respond to pharmacotherapy alone, although if the abscess is accessible and there is low suspicion for echinococcus, aspiration for diagnostic purposes should still be performed [52]. However, surgical excision or drainage is typically performed after the complete formation of an abscess of any size. Available techniques include craniotomy and complete abscess excision, aspiration via a burr hole, neuro-endoscopic aspiration, and stereotactic guided aspiration. Although aspiration has become an increasingly prevalent technique, more recent meta-analyses have revealed that surgical excision offers lower rates of re-operation when compared to aspiration without substantial differences in morbidity, mortality, or functional outcomes [52–54].

Although there is understandable hesitancy to perform an open craniotomy, this technique is still considered a first-line treatment for patients with large multi-lobulated abscesses and/or intracranial hypertension. Other indications for open procedure include external ventricular drain placement, necessity of monitoring intracranial pressure, abscess rupture into the ventricles, and in select cases of large abscess with accompanying hydrocephalus [6, 9••, 52, 53].

Just as prompt identification and treatment of brain abscess leads to improved outcomes, so does early and aggressive management of elevated intracranial pressure reduce mortality [34, 55–57]. Although adjuvant corticosteroid therapy remains controversial due to risks including decreased antibiotic penetration of the abscess, encapsulation retardation, increased necrosis, CT scan disturbance, and rebound effect, steroids may be used cautiously in cases of markedly increased intracranial pressure or significant cerebral edema with midline shift [58]. No studies have yet been performed on dosage and timing; however, it is generally thought that shorter courses are preferred. Other measures to reduce intracranial pressure include hyperosmolar therapy, hyperventilation, and ventricular shunting [3, 57, 58]. Seizure prophylaxis, though once a mainstay of treatment, remains controversial [6, 58, 59].

Clinical Outcomes

With the advancement of neuro-imaging and neurosurgical techniques, morbidity and mortality have been markedly reduced in recent decades. Mortality is now in the range of 5–15% [7, 52]. The most common long-term neurological consequences include focal deficits, residual seizures, and permanent changes in mental cognition. Poor prognosticators for outcomes include late diagnosis, multiple lesions or lesions that are difficult to reach operatively, expansion and intraventricular rupture, coma, fungal etiology, and very old or very young [52]. These numbers are anticipated to decline with further imaging and treatment option developments.

Prophylaxis and Preventive Strategies

As most patients present with predisposing conditions, early or even prophylactic treatment of contiguous infection, as well as infectious foci that may lead to hematogenous seeding, is critical for the prevention of abscess formation; unfortunately, however, a dearth of literature and recommendations address abscess-specific prophylaxis. Clinicians should recognize that brain abscess is a devastating sequela of advancing infection and have a low threshold for further evaluation provided that imaging resources are readily available. As in many areas of medicine, there is a delicate balance to strike here between resource stewardship and the understanding that early recognition and intervention of brain abscesses leads to markedly improved outcomes.

Conclusions

Numerous meta-analysis studies have noted that brain abscess outcomes have improved substantially over recent decades, primarily due to advances in neuroimaging and neurosurgical techniques. However, significantly more studies describe bacterial brain abscesses than fungal or parasitic ones. It is suspected that fungal and parasitic abscesses are underrecognized and underreported; their treatments, prognosis, and outcomes are expected to differ substantially from bacterial abscesses due to different pathogenesis. More research is needed on these types of abscesses specifically, which are more likely to present in tropical regions where the infectious disease burden is higher, as is the number of people with predisposing immunological conditions.

Finally, many treatment modalities that have decreased morbidity and mortality in brain abscesses may be inconsistently available in global populations. Healthcare systems within the tropics are heterogeneous, and thus, outcomes are expected to be. The preponderance of data available is from healthcare centers in developed countries and is unlikely to represent all populations appropriately. It is essential to consider obtaining brain biopsy specimens for etiological diagnosis and to consider specific etiologies among patients living in the tropics presenting with a brain abscess.