Intracranial suppuration










Spread from a contiguous focus
Otitis media, mastoiditis; 40% of all brain abscesses
Sinusitis, frontal
Dental infections (10%), typically with molar infections; abscesses usually frontal but may be temporal
Meningitis; rarely complicated by brain abscess (must be considered in neonates with Citrobacter diversus meningitis, of whom 70% develop brain abscess)
Hematogenous spread from a distant focus of infection
Empyema, lung abscess, bronchiectasis, cystic fibrosis, wound infections, pelvic infections, intra-abdominal sepsis
Trauma
After penetrating head trauma, brain abscess develops in about 3%, more commonly after gunshot wounds
Neurosurgical procedures; complicated by brain abscess in only 6 to 17 per 10 000 clean neurosurgical procedures
Cryptogenic
Asymptomatic pulmonary arteriovenous malformation (AVM), a consideration in cases of cryptogenic brain abscess
Cyanotic congenital heart disease is present in 5% to 10% of brain abscesses and is the most common predisposing factor in some pediatric series



The age distribution of patients with brain abscess varies with its cause. A brain abscess from an otogenic focus typically occurs in patients younger than 30 and shows a male predominance. Brain abscess secondary to sinusitis typically occurs in men in their second to third decade of life.


Pathogenesis

The location of a brain abscess is dependent on its predisposing cause. Abscess from a contiguous focus usually occurs in the cortical area of the brain near its causal site. The most common foci of contiguous infections are otitis or sinusitis. Infection from a contiguous site can spread either directly through intervening tissues, bone, and meninges or indirectly through retrograde thrombophlebitis of the diploic or emissary veins. An abscess may also result from an otogenic infection by spread through pre-existing channels such as the internal auditory canal or cochlear, and vestibular aqueducts. The majority of otogenic brain abscesses are located in the temporal lobe, followed by the cerebellum. Approximately 90% of cerebellar abscesses are secondary to an otogenic infection. Brain abscesses due to sinusitis are almost always found in the frontal lobe.


Brain abscesses secondary to hematogenous dissemination are often multiple and are located in the territory of the middle cerebral artery at the gray–white junction. They have a distant focus of infection, which is most often within the chest. These abscesses are poorly encapsulated and have a high mortality.


Brain abscesses rarely accompany bacteremia if the blood–brain barrier is intact. For example, despite the presence of persistent bacteremia in bacterial endocarditis, brain abscess is rare (nine brain abscesses reported in 218 cases of infective endocarditis).


Causes

Organisms isolated from brain abscesses are outlined in Table 77.2. Although a single organism is detected in the majority of bacterial brain abscesses, nearly 30% are of mixed infection. Streptococci, Enterobacteriaceae, and anaerobes are most commonly found. In contrast, Staphylococcus aureus is commonly isolated in pure culture.



Table 77.2 Pathogens in brain abscess































Agent Frequency (%)
Streptococci (S. intermedius, including S. anginosus) 60–70
Bacteroides and Prevotella spp. 20–40
Enterobacteriaceae 23–33
Staphylococcus aureus 10–15
Fungia 10–15
Streptococcus pneumoniae <1
Haemophilus influenzae <1
Protozoa, helminthsb (vary geographically) <1





a Yeasts, fungi, Aspergillus, agents of mucor, Candida, cryptococci, coccidiodoides, Cladosporium trichoides, Pseudallescheria boydii.



b Protozoa, helminths, Entamoeba histolytica, schistosomes, paragonimus, cysticerci.


Fungal brain abscesses have increased in incidence due to the prevalent use of immunosuppressive agents, corticosteroids, and broad-spectrum antibiotics. Candida species are the most common fungi in autopsy series. Risk factors for invasive Candida infection include the use of corticosteroids, broad-spectrum antimicrobials, and hyperalimentation. Cerebral aspergillosis occurs in 10% to 20% of all cases of invasive aspergillosis, although the brain is rarely the only site of infection. Most cases occur in neutropenic patients with underlying hematologic malignancy. Fungi of the Zygomycetes most often cause rhinocerebral mucormycosis, particularly in patients with diabetes mellitus and ketoacidosis, hematologic malignancies, or patients on immunosuppressive therapy. Isolated cerebral mucormycosis is most commonly seen in injection drug users. Scedosporium apiospermum is a common mold found in soil. Brain abscess with this organism is often associated with near drowning, trauma, or immunosuppression. While numerous other etiologic agents of fungal brain abscess exist, it is also important to highlight the recent rise in Cryptococcus gatti brain abcesses in immunocompetent hosts with epidemiologic exposure in the Pacific Northwest. Patients usually have outdoor exposure and may have a delayed time to diagnosis given that cryptococcal infection is not frequently considered among an otherwise immunocompetent population.


There are several protozoa and helminths that produce brain abscess. The most common is Toxoplasma gondii, which typically causes an intracerebral mass or encephalitis in immunosuppressed hosts. While clinically more descript as an inflammatory lesion rather than suppuration, the larval form of Taenia solium, causative of neurocysticercosis, is of considerable burden in Central and South America. Also found among immunocompetent hosts, cysticercosis is the most common cause of acquired seizure in the developing world.


Infections more often found in patients with defects in cell-mediated immunity include T. gondii, Nocardia asteroides, Cryptococcus neoformans, mycobacteria, and Listeria monocytogenes. Neutrophil defects are associated with an increased incidence of infections caused by Enterobacteriaceae, Pseudomonas, and fungi. Patients with acquired immunodeficiency syndrome (AIDS) may develop focal central nervous system (CNS) lesions as a result of a variety of pathogens (Table 77.3).



Table 77.3 Causes of parenchymal CNS lesions in patients with AIDS











Toxoplasma gondii
Most common focal lesion
Occurs in about 10% of all AIDS patients
>1 lesion seen on MRI with surrounding edema, mass effect, and ring enhancement
Most common location is the basal ganglia; most Toxoplasma IgG positive
Primary lymphoma
Occurs in about 2% of AIDS patients
Lymphoma is B cell in origin
Lesions are hyperdense or isodense on CT with edema, mass effect, and variable enhancement
Caused by Epstein–Barr virus
Progressive multifocal leukoencephalopathy
Occurs in 2% to 5% of AIDS patients
Lesions occur at gray–white junction and adjacent white matter; usually hypodense without mass effect Caused by JC virus (Papovavirus)
Less common
Cryptococcus neoformansa
Histoplasma capsulatuma
Coccidioides immitisa
Other fungi – Aspergillus, Candida, agents of mucormycosis
Mycobacterium tuberculosisa
Mycobacterium avium complex
Cytomegalovirusb
Metastatic malignancy, notably Kaposi’s sarcoma
Acanthamoeba
Bacterial brain abscess of Listeria, Nocardia, Salmonella
Syphilisa



Abbreviations: CNS = central nervous system; AIDS = acquired immunodeficiency syndrome; MRI = magnetic resonance imaging; CT = computed tomography; IgG = immunoglobulin G.




a More commonly meningitis.



b More commonly encephalitis.


Clinical manifestations

The clinical course of patients with brain abscess varies dramatically. In approximately 75% of patients, symptoms are present for fewer than 2 weeks. Importantly, the prominent symptoms are secondary to mass effect, not infection (Table 77.4). Headache, the most common symptom, may be hemicranial or generalized. Varying degrees of altered mental status are present in most patients. Furthermore, fever may be absent in as many as 50% of all cases.



Table 77.4 Clinical manifestations of brain abscessa























Headache 70% Nuchal rigidity 25%
Fever 50% Papilledema 25%
Altered mental status >50% Focal neurologic findings 50%
Seizures 25–35%





a Fewer than half have classic triad of fever, headache, and neurologic deficits.


Brain abscesses in certain anatomic locations may cause additional symptoms. For example, cerebellar abscesses are often associated with nystagmus, ataxia, vomiting, and dysmetria. Frontal lobe abscesses induce headaches, drowsiness, inattention, and decline in mental function. Temporal lobe abscesses are associated with early ipsilateral headaches and, if in the dominant hemisphere, aphasia. Intrasellar abscesses simulate pituitary tumors. Brainstem abscesses often cause facial weakness, headache, fever, hemiparesis, dysphagia, and vomiting.


Laboratory findings

Most laboratory tests are not diagnostic for brain abscess (Table 77.5). Lumbar puncture is contraindicated in patients with known or suspected brain abscess. Not only are cerebrospinal fluid (CSF) findings nonspecific, but patients may herniate after the procedure. In one series, 41 of 140 patients deteriorated within 48 hours after lumbar puncture, and 25 died. Similar results have been reported in other studies.



Table 77.5 Laboratory tests and imaging studies







Laboratory testsa
WBC: moderate leukocytosis present in about 50% (only 10% WBC >20 000) and normal WBC in 40%
Moderate increase in ESR
Chest x-ray film is useful in detecting the origin of hematogenous brain abscess
EEG abnormal in most patients, lateralizes to side of lesion
Imaging studies
CT scan: useful in evaluating the brain, sinuses, mastoids, and middle ear
MRI: appears more sensitive early in illness and in detecting cerebral edema
99mTc very sensitive; useful where CT or MRI not available



Abbreviations: WBC = white blood cell count; ESR = erythrocyte sedimentation rate; EEG = electroencephalograph; CT = computed tomography; MRI = magnetic resonance imaging.




a Lumbar puncture is contraindicated in patients with known or suspected brain abscess.


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Jun 18, 2016 | Posted by in INFECTIOUS DISEASE | Comments Off on Intracranial suppuration

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