A. Clinical manifestations
The clinical course of brain abscess ranges from indolent to fulminant. Most clinical manifestations are not due to the systemic signs of infection, but rather to the size and site of the abscess. Headache is the most common presenting symptom. Other symptoms and signs include changes in mental status, focal neurological deficits, fever, seizures, and increase intracranial pressure.
According to animal studies, four stages of brain abscess formation evolution were observed: early cerebritis (days 1–3), late cerebritis (days 4–9), early capsule formation (days 10–13) and late capsule formation (day 14 and later). The early cerebritis stage is characterized by an acute inflammatory infiltrate with visible bacteria on Gram stain and marked oedema surrounding the lesion. The centre of the lesion becomes necrotic during the late cerebritis stage. With early capsule formation, the necrotic centre begins to decrease in size with simultaneous development of a collagenous capsule in which it increased in density and thickness during the late capsule formation stage.
The aetiological agents of brain abscess depend on the underlying predisposition.
|Otitis media, mastoiditis||Streptococci (aerobic and anaerobic), Bacteroides and Prevotella spp., Enterobacteriaceae.|
|Sinusitis||Streptococci (aerobic and anaerobic), Bacteroides, c, Staphylococcus aureus, Haemophilus spp.|
|Dental infection||Mixed anaerobes with Fusobacterium, Prevotella, Actinomyces, and Bacteroides spp., streptococci.|
|Penetrating trauma orpost-surgery||Staphylococcus aureus, streptococci, Enterobacteriaceae, Propionibacterium acnes.|
|Lung abscess, empyema, bronchiectasis,||Anaerobes such as Fusobacterium, Actinomyces, Bacteroides, also streptococci, Nocardia spp.|
|Infective endocarditis||Staphylococcus aureus, streptococci.|
|HIV infection||Toxoplasma gondii, Nocardia spp., Mycobacterium spp., Listeria monocytogenes, Cryptococcus neoformans.|
Imaging studies (CT and MRI) are the most important investigations in the diagnosis of brain abscess. The characteristic CT appearance of brain abscess is that of a hypodense centre with a peripheral uniform ring enhancement after the injection of contrast. This is surrounded by a variable hypodense area of brain oedema. However, CT may not be able to pick up the early cerebritis phase. MRI is superior and more sensitive than CT and offers significant advantages in the early detection of cerebritis. In T1-weighted images, the abscess capsule often appears as a discrete rim that is isointense to mild hyperintense, together with contrast enhancement with the paramagnetic agent (Figure 1).
Figure 1. Contrast enhanced T1 cerebral MRI showing left parietal brain abscess with a hyperintense, contrast enhancing rim.
Stereotactic CT-guided aspiration or incision and drainage (I & D) performed in the operating theatre are essential to aid microbiological diagnosis. Gram stain and culture of the abscess fluid can help identify the pathological organism and thus guide anti-microbial therapy.
Antibiotics with coverage of both aerobic and anaerobic bacteria (initially empirical, based on assessment of underlying predisposing factors) and measures for prevention of complications (e.g. use of anti-convulsants in patients with seizures, intravenous mannitol and intravenous steroids in patients with cerebral oedema) should be initiated as soon as possible. Occasionally, serological investigations such as serum cryptococcal antigen and Toxoplasma antibody might be helpful in identifying the causative pathogens.