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1 osteomyelitis, septic arthritis, or epidural/brain abscess).
2 remature infant with sepsis, meningitis, and brain abscess.
3 Epilepsy is a common complication of brain abscess.
4 y bacteria are the most frequent etiology of brain abscess.
5 ks of mortality and new-onset epilepsy after brain abscess.
6 ecommendations for neurosurgical drainage of brain abscess.
7 e part of the anaerobic community that cause brain abscess.
8 crophorum who developed a right frontal lobe brain abscess.
9 agent of CNS parenchymal infections, such as brain abscess.
10 ested case-control study of risk factors for brain abscess.
11 tion between innate and adaptive immunity in brain abscess.
12 was unsuccessfully treated for a C. bantiana brain abscess.
13 ks of mortality and new-onset epilepsy after brain abscess.
14 plantation, and who later developed multiple brain abscesses.
15 on of infected teeth, and community-acquired brain abscesses.
16 ontogenic bacteremia, and community-acquired brain abscesses.
17 ormed as the method of choice for confirming brain abscesses.
18 n reveal inflammatory changes and developing brain abscesses.
19 ight frontal lobe, which could correspond to brain abscesses.
20 a prospective nationwide study on bacterial brain abscesses.
21 e establishment of spontaneous polymicrobial brain abscesses.
22 cerebrally infected with S. aureus to induce brain abscesses.
23 tis, 60 (4%) had hemorrhages, and 2 (1%) had brain abscesses.
24 munity-acquired pneumonia (CAP) and multiple brain abscesses.
25 uable method to identify bacterial agents of brain abscesses.
26 -resistant mold, was cultured from bilateral brain abscesses.
27 ich often progresses to establish multifocal brain abscesses.
28 delta T cells were also a source of IL-17 in brain abscesses.
29 c central nervous system infection including brain abscesses.
30 filled macrophages within the ventricles and brain abscesses.
31 confirmed CNS melioidosis; 20 (38.5%) had a brain abscess, 18 (34.6%) had encephalomyelitis, 4 (7.7%
34 was observed in 21 of 362 (6%) patients with brain abscess and 179 of 3257 (5%) population controls (
37 medications between patients diagnosed with brain abscess and individuals from the general populatio
38 nimals consistently demonstrated more severe brain abscesses and higher CNS bacterial burdens compare
40 g to the anaerobic community responsible for brain abscess, and M. oralis may participate in the path
44 d a well-characterized model of experimental brain abscess as a tool to query effects of the CNS infl
46 e describe the recovery of M. hominis from a brain abscess associated with a postpartum infection.
50 sting that a population of cells forming the brain abscess capsule originate from a bone marrow precu
51 s and invasive dental procedures and risk of brain abscess caused by oral cavity bacteria from 1989 t
54 The case of a patient who presented with a brain abscess caused by Streptomyces infection following
55 rt the case of a previously healthy boy with brain abscesses caused by M/emm type 12 GAS and review t
57 sion of select inflammatory mediators during brain abscess development including inducible NO synthas
59 d for its ability to influence the course of brain abscess development when treatment was initiated 3
60 majority of the cellular infiltrate in early brain abscess development, subsequent analysis focused o
61 he contribution of virulence determinants in brain abscess development, the abilities of S. aureus st
62 CNS host response during the early stages of brain abscess development, whereas MyD88-independent pat
67 comprising all adults (aged >=18 years) with brain abscess due to oral cavity bacteria in Denmark fro
70 ly restricted, since all previous reports of brain abscesses due to this organism have been for patie
72 Unexpectedly, ciglitazone also accelerated brain abscess encapsulation, which was typified by the h
74 e of central nervous system involvement with brain abscess formation in a patient with chronic granul
76 continued innate responses during late-stage brain abscess formation is not known but is important, b
81 hundred thirteen of 362 (59%) patients with brain abscess had visited their dentist within 1 year be
83 t is unknown whether patients diagnosed with brain abscess have an increased risk of psychiatric diso
84 ion, the influx of fibrocyte-like cells into brain abscesses immediately preceded the onset of fibrot
87 thogenesis of S. aureus-induced experimental brain abscess in TLR2 knockout (KO) and wild-type (WT) m
88 reus is one of the major etiologic agents of brain abscesses in humans, occasionally leading to focal
91 showed that C. koseri causes meningitis and brain abscesses in the neonatal rat model, and we utiliz
92 Streptococcus intermedius, a common cause of brain abscesses, in both CSF samples as well as in the f
93 ld in 253 of 280 (90%), and risk factors for brain abscess included immunocompromise in 95 of 287 (33
94 cribe a case of polymicrobial infection in a brain abscess including two rapidly growing Mycobacteriu
97 s of Citrobacter spp. causing meningitis and brain abscess is not well characterized; however, as wit
100 enesis of C. freundii causing meningitis and brain abscess may relate to invasion of and intracellula
101 omised persons.Among the 30-day survivors of brain abscess (median follow up 7.6 years [IQR 2.2-15.5]
102 omised persons.Among the 30-day survivors of brain abscess (median follow-up 7.6 years [IQR 2.2-15.5]
104 and chemokine expression in an experimental brain abscess model in the rat during the acute stage of
105 e modulatory effects in a mouse experimental brain abscess model, we found that minocycline significa
107 ed pneumonitis (n = 7), myocarditis (n = 5), brain abscesses (n = 5), chorioretinitis (n = 3), lymph
108 ubstantial contributors to the occurrence of brain abscess neurosurgery (12%); solid cancer (11%); ea
109 oprotein receptor-1 (LOX-1) was increased in brain abscesses of both TLR2 KO and WT mice compared to
111 crophages, and neutrophils isolated from the brain abscesses of MyD88 KO mice produced significantly
113 d CD8(+) T cell infiltrates were elevated in brain abscesses of TLR2 KO mice at days 3, 7, and 14 pos
114 y protein-2, was significantly attenuated in brain abscesses of TLR2 KO mice compared to WT mice duri
116 unctions in a compensatory manner to control brain abscess pathogenesis, with cells other than glia a
127 ielded archaea, mostly methanogens, in 28/32 brain abscess samples, and no archaea in 71 negative con
131 rchaea-specific qPCR yielded archaea in 8/18 brain abscess specimens and 1/27 controls (P < .003), an
133 ied 44 bacteria that had never been found in brain abscess specimens, including 22 uncultured bacteri
136 ncertainty about the role of neurosurgery in brain abscess treatment is reflected in surveys and obse
137 of tissue injury, with significantly larger brain abscesses typified by exaggerated edema and necros
138 was restricted to those with a diagnosis of brain abscess using International Statistical Classifica
139 r, and 6-30 year mortality of patients after brain abscess was 21%, 16% and 27% as compared to 1%, 6%
140 r, and 6-30 year mortality of patients after brain abscess was 21%, 16%, and 27% as compared to 1%, 6
141 the importance of MyD88-dependent signals in brain abscesses, we compared disease pathogenesis using
147 al hematoma, acute infarcts, and Aspergillus brain abscesses were the predominant etiologies during t
148 ts aged 18 years or older at the time of the brain abscess with at least 1 year of prior enrollment w