Bacteraemia associated with multiple septic localizations caused by Klebsiella pneumoniae sequence type ST660.

We report a case of Klebsiella pneumoniae bacteraemia in an 80-year-old man in France with no history of travel to Asia, complicated by endogenous endophthalmitis, multiple cerebral microbleeds and hepatic microabscesses, associated with a Bentall endocarditis. Hypervirulence pathotype was suggested based on clinical picture, bacterial isolate genomic sequence and hypermucoidy. Interestingly, the isolate had the non-K1/K2-capsular serotype locus KL113-like, carried a KpVP-1-like virulence plasmid, and belonged to the emerging sublineage SL660 (comprising the sequence type ST660).

Effects of intestinal flora on cerebral hemorrhage area and brain tissue inflammation in acute hemorrhagic stroke.

To explore the impacts of intestinal flora on cerebral hemorrhage area and brain tissue inflammation in acute hemorrhagic stroke, seventy-two male C57BL/6 mice were randomly separated into 6 groups (n=12), the experimental group (EG, day 1, day 3 and day 7) and the control group (CG, day 1, day 3 and day 7). The mouse cerebral hemorrhage model was established by collagenase injection, and the EG received 0.4 mL fecal filtrate of healthy mice once a day, and the CG received the same amount of normal saline transplantation. The mNSS score, hematoma volume and cerebral edema content were used to evaluate nerve function injury and brain injury degree at each time point after operation. The expressions of inflammatory factors were detected by western blot. We found that at each time point after operation, compared with the CG, nerve function deficit scores of mice in the EG declined (P<0.05), the water content of mice brain tissue in the EG declined (P<0.05), and the protein expressions of inflammatory factors in the EG were decreased (P<0.05). Relative to the CG, the volume of hematoma in the EG declined on day 3 along with day 7 after operation (P<0.05). In conclusion, intestinal flora can reduce cerebral hemorrhage area and brain tissue inflammation, and then improve the performance of nerve function deficit in acute hemorrhagic stroke.

Cost and Utility of Microbiological Cultures Early After Intensive Care Unit Admission for Intracerebral Hemorrhage.

BACKGROUND: Fever is common among intensive care unit (ICU) patients. Clinicians may use microbiological cultures to differentiate infectious and aseptic fever. However, their utility depends on the prevalence of infection; and false-positive results might adversely affect patient care. We sought to quantify the cost and utility of microbiological cultures in a cohort of ICU patients with spontaneous intracerebral hemorrhage (ICH). METHODS: We performed a secondary analysis of a cohort with spontaneous ICH requiring mechanical ventilation. We collected baseline data, measures of systemic inflammation, microbiological culture results for the first 48 h, and daily antibiotic usage. Two physicians adjudicated true-positive and false-positive culture results using standard criteria. We calculated the cost per true-positive result and used logistic regression to test the association between false-positive results with subsequent antibiotic exposure. RESULTS: Overall, 697 subjects were included. A total of 233 subjects had 432 blood cultures obtained, with one true-positive (diagnostic yield 0.1 %, $22,200 per true-positive) and 11 false-positives. True-positive urine cultures (5 %) and sputum cultures (13 %) were more common but so were false-positives (6 and 17 %, respectively). In adjusted analysis, false-positive blood and sputum results were associated with increased antibiotic exposure. CONCLUSIONS: The yield of blood cultures early after spontaneous ICH was very low. False-positive results significantly increased the odds of antibiotic exposure. Our results support limiting the use of blood cultures in the first two days after ICU admission for spontaneous ICH.

Infective endocarditis--rare cause of intracerebral haemorrhage.

Cerebral haemorrhage occurs rarely in infective endocarditis. Here, we present a case of young female with severe intracerebral haemorrhage. Later, she found to be a case of infective endocarditis with mitral valve prolapse and on investigation blood culture grew S. aureus.

A Glycyrrhizin Derivative with a More Potent Inhibitory Activity against High-Mobility Group Box 1 Efficiently Discovered by Chemical Synthesis Inspired by the Bioconversion Products of an Endophytic Fungus Isolated from Licorice.

Glycyrrhizin (GL) from licorice alleviates intracerebral hemorrhage (ICH) injuries by interacting with high-mobility group box (HMGB) 1, an inflammatory factor. We found that GL is bioconverted by endophyte coexisting with licorice and succeeded in isolating two derivatives. The aim of this study was to identify the compound with more potent HMGB1 inhibitory activity inspired by these GL derivatives. We took advantage of a ketone introduced by an endophyte at the C-3 position and attempted methyl esterification at the C-30 position because it was suggested that the water or lipid solubility of the molecule plays an important role. Among three derivatives synthesized, the product that is both ketonized and esterified showed more potent HMGB1 inhibitory activity than GL in macrophages and significantly improved adverse events occurred in ICH in vivo. These results suggest that modification of the hydrophilicity of GL, particularly at the C-3 and C-30 positions, enhances the HMGB1 inhibitory activity.

[Stroke-induced nosocomial pneumonia in the acute period of cerebral hemorrhage: clinical pathogenic and age-associated aspects].

The article presents the clinical features of stroke-induced nosocomial pneumonia and interleukin-1alpha level monitoring in serum and cerebrospinal fluid of 100 patients with cerebral hemorrhage on the 1st, 3rd and 10th day. The authors show that 66% of patients with cerebral hemorrhage develop nosocomial pneumonia since the end of 2nd up to 5th day of conservative hospital treatment, more frequently in the serious cases with high level of neurological deficiency. The most important risk factors of stroke-induced nosocomial pneumonia are chronic focal infection, diabetes mellitus, cardiac failure, smoking, obesity. Since the first day of stroke the interleukin-1alpha level both in serum and cerebrospinal fluid exceeds 25-30 times its content in healthy people and increases more in the presence of nosocomial pneumonia. Interleukin-1alpha level can serve as an early risk marker of lethal outcome in patients with cerebral hemorrhage.

Diet-Induced High Serum Levels of Trimethylamine-N-oxide Enhance the Cellular Inflammatory Response without Exacerbating Acute Intracerebral Hemorrhage Injury in Mice.

Trimethylamine-N-oxide (TMAO), an intestinal flora metabolite of choline, may aggravate atherosclerosis by inducing a chronic inflammatory response and thereby promoting the occurrence of cerebrovascular diseases. Knowledge about the influence of TMAO-related inflammatory response on the pathological process of acute stroke is limited. This study was designed to explore the effects of TMAO on neuroinflammation, brain injury severity, and long-term neurologic function in mice with acute intracerebral hemorrhage (ICH). We fed mice with either a regular chow diet or a chow diet supplemented with 1.2% choline pre- and post-ICH. In this study, we measured serum levels of TMAO with ultrahigh-performance liquid chromatography-tandem mass spectrometry at 24 h and 72 h post-ICH. The expression level of P38-mitogen-protein kinase (P38-MAPK), myeloid differentiation factor 88 (MyD88), high-mobility group box1 protein (HMGB1), and interleukin-1ß (IL-1ß) around hematoma was examined by western blotting at 24 h. Microglial and astrocyte activation and neutrophil infiltration were examined at 72 h. The lesion was examined on days 3 and 28. Neurologic deficits were examined for 28 days. A long-term choline diet significantly increased serum levels of TMAO compared with a regular diet at 24 h and 72 h after sham operation or ICH. Choline diet-induced high serum levels of TMAO did not enhance the expression of P38-MAPK, MyD88, HMGB1, or IL-1ß at 24 h. However, it did increase the number of activated microglia and astrocytes around the hematoma at 72 h. Contrary to our expectations, it did not aggravate acute or long-term histologic damage or neurologic deficits after ICH. In summary, choline diet-induced high serum levels of TMAO increased the cellular inflammatory response probably by activating microglia and astrocytes. However, it did not aggravate brain injury or worsen long-term neurologic deficits. Although TMAO might be a potential risk factor for cerebrovascular diseases, this exploratory study did not support that TMAO is a promising target for ICH therapy.

In utero exposure to Ureaplasma spp. is associated with increased rate of bronchopulmonary dysplasia and intraventricular hemorrhage in preterm infants.

AIMS: We determined the association between short-term neonatal morbidities, such as bronchopulmonary dysplasia (BPD) and intraventricular hemorrhage (IVH), and Ureaplasma spp. in amniotic fluid, placental and amniotic membrane of preterm infants. METHODS: This study enrolled 257 patients who were born by cesarean section at <34 weeks' gestation. Patients were divided into two groups according to detection of Ureaplasma spp. by culture-based and/or polymerase chain reaction (PCR) techniques. RESULTS: Significant differences were observed between both groups for all IVH (P=0.032) and IVH grades III or IV (P=0.013), as wells as for BPD [odds ratio (OR) 5.46, 95% confidence interval (CI) 2.02-14.77], oxygen requirement at 28 days postnatal age (OR 1.93, 95% CI 1.00-3.70), and for death between 28 days and 36 postmenstrual weeks or BPD (OR 4.20, 95% CI 1.77-9.96). Ureaplasma spp. was a significant predictor (P<0.001) of BPD after correcting for birth weight (P=0.003) and positive pressure ventilation (P=0.001). CONCLUSIONS: In our study population Ureaplasma spp. was associated with BPD and IVH in preterm infants even after adjustment for multiple risk factors.

Cerebral microbleeds in vascular dementia from clinical aspects to host-microbial interaction.

Vascular dementia is the second leading cause of dementia after Alzheimer's disease in the elderly population worldwide. Cerebral microbleeds (CMBs) are frequently observed in MRI of elderly subjects and considered as a possible surrogate marker. The number and location of CMBs reflect the severity of diseases and the underlying pathologies may involve cerebral amyloid angiopathy or hypertensive vasculopathy. Accumulating evidence demonstrated the clinicopathological discrepancies of CMBs, the clinical significance of CMBs associated with other MRI markers of cerebral small vessel disease, cognitive impairments, serum, and cerebrospinal fluid biomarkers. Moreover, emerging evidence has shown that genetic factors and gene-environmental interactions might shed light on the underlying etiologies of CMBs, focusing on blood-brain-barrier and inflammation. In this review, we introduce recent genetic and microbiome studies as a cutting-edge approach to figure out the etiology of CMBs through the "microbe-brain-oral axis" and "microbiome-brain-gut axis." Finally, we propose novel concepts, "microvascular matrisome" and "imbalanced proteostasis," which may provide better perspectives for elucidating the pathophysiology of CMBs and future development of therapeutics for vascular dementia using CMBs as a surrogate marker.

Intracerebral Hemorrhage Related With Penicillium Species Following Deceased-Donor Liver Transplant.

Early or late posttransplant opportunistic infections are among the leading complications after liver transplant. The source of early posttransplant opportunistic infections is usually the patient, the implantation of an infected graft, contamination during a surgical procedure, or invasive interventions performed at the intensive care unit. A 10-year-old male patient with Wilson disease (Pediatric End-Stage Liver Disease Score of 42, Child-Pugh score of 12, total bilirubin 40 mg/dL, platelet count 55000/mL, hemoglobin level 6.3 g/dL, albumin level 1.7 g/dL, urinary copper level 4305 µ/24 h) was closely monitored in the pediatric intensive care unit of our liver transplantation center for care of a worsened general status. A deceased-donor liver transplant was performed using a right lobe liver graft (ex vivo split) obtained through the national organ sharing network. The patient developed rightward deviation of eyes and altered consciousness after the procedure and underwent cranial magnetic resonance imaging and computerized tomography examinations. The cranial magnetic resonance image, taken on the third postoperative day, revealed lesions consistent with embolic infarction, and the computed tomography scan, taken on the eighth day, showed intracerebral hemorrhage. Decompressive craniotomy, which included hematoma drainage and catheter placement, was performed. Culture and histopathologic examinations of the hematoma material revealed a Penicillium species of fungi. However, the patient died before a definitive diagnosis was made. The aim of this report is to raise awareness on early posttransplant opportunistic infections of the central nervous system presenting with intracranial hemorrhage following liver transplant.

Association between infectious burden and cerebral microbleeds: a pilot cross-sectional study.

OBJECTIVE: Cerebral microbleeds (CMBs) is a subtype of cerebral small vessel disease. Their underlying pathogenesis remains unclear. The aim of this study was to investigate the association between infectious burden (IB) and CMBs. METHODS: Seven hundred and seventy-three consecutive patients who were hospitalized in the Department of Neurology in General Hospital of Western Theater Command without severe neurological symptoms were recruited and selected in this pilot cross-sectional study. CMBs were assessed using the susceptibility-weighted imaging sequence of magnetic resonance imaging. Immunoglobulin G antibodies against common pathogens, including herpes simplex virus (HSV)-1, HSV-2, cytomegalovirus (CMV), Chlamydia pneumoniae (C. pneumoniae), Mycoplasma pneumoniae (M. pneumoniae), Epstein-Barr virus (EBV), Helicobacter pylori (HP), and Borrelia burgdorferi (B. burgdorferi), were measured by commercial ELISA assays. IB was defined as a composite serologic measure of exposure to these common pathogens. RESULTS: Patients with and without CMBs were defined as the CMBs group (n = 76) and the non-CMBs group (n = 81), respectively. IB was significantly different between the CMBs and non-CMBs groups. After adjusted for other risk factors, the increased IB was independently associated with the presence of CMBs (P = 0.031, OR = 3.00, 95% CI [1.11-8.15]). IB was significantly positively associated with the number of CMBs (Spearman ρ = 0.653, P < 0.001). The levels of serum inflammatory markers were significantly different between the CMBs and non-CMBs groups and among the categories of IB. INTERPRETATION: IB consisting of HSV-1, HSV-2, CMV, C. pneumoniae, M. pneumoniae, EBV, HP, and B. burgdorferi was associated with CMBs. All the findings suggested that pathogen infection could be involved in the pathogenesis of CMBs.

Excessive antibiotics use increased in-hospital mortality in intracerebral hemorrhage patients with stroke-associated infection.

Intracerebral hemorrhage (ICH) is associated with higher incidence of stroke-associated infection (SAI) as well as antibiotic use. However, there were few methods for judging proper antibiotic use in clinical manner. We introduce an index of antibiotic use, called personal antibiotic use density (PAUD), to evaluate the relation between antibiotic use and prognosis of ICH patients with SAI. A total of 162 in 570 ICH patients were observed to diagnose as SAI. Comparing with the survival patients, PAUD, ICH volume, National Institutes of Health Stroke Scale (NIHSS) score and ICH score were significantly higher among those who died, while the Glasgow Coma Scale score and the length of stay were significantly lower (P < 0.05). PAUD was identified as an independent risk factor of in-hospital death (OR 2.396, 95% CI 1.412-4.067, P = 0.001). In-hospital mortality was significantly lower in the low (P = 0.027) and intermediate PAUD (P < 0.001) groups than that in the high PAUD group. Cumulative in-hospital survival was significantly higher in low and intermediate PAUD groups (log rank test, P < 0.001). PAUD correlated positively with NIHSS score (r = 0.224, P < 0.001) and in-hospital mortality (r = 0.268, P = 0.001). The study indicated that PAUD is closely related to in-hospital prognosis of ICH patients with SAI. Higher PAUD may not be associated with better prognosis, but instead, higher risk of death.

Annexin A2 depletion exacerbates the intracerebral microhemorrhage induced by acute rickettsia and Ebola virus infections.

Intracerebral microhemorrhages (CMHs) are small foci of hemorrhages in the cerebrum. Acute infections induced by some intracellular pathogens, including rickettsia, can result in CMHs. Annexin a2 (ANXA2) has been documented to play a functional role during intracellular bacterial adhesion. Here we report that ANXA2-knockout (KO) mice are more susceptible to CMHs in response to rickettsia and Ebola virus infections, suggesting an essential role of ANXA2 in protecting vascular integrity during these intracellular pathogen infections. Proteomic analysis via mass spectrometry of whole brain lysates and brain-derived endosomes from ANXA2-KO and wild-type (WT) mice post-infection with R. australis revealed that a variety of significant proteins were differentially expressed, and the follow-up function enrichment analysis had identified several relevant cell-cell junction functions. Immunohistology study confirmed that both infected WT and infected ANXA2-KO mice were subjected to adherens junctional protein (VE-cadherin) damages. However, key blood-brain barrier (BBB) components, tight junctional proteins ZO-1 and occludin, were disorganized in the brains from R. australis-infected ANXA2-KO mice, but not those of infected WT mice. Similar ANXA2-KO dependent CMHs and fragments of ZO-1 and occludin were also observed in Ebola virus-infected ANXA2-KO mice, but not found in infected WT mice. Overall, our study revealed a novel role of ANXA2 in the formation of CMHs during R. australis and Ebola virus infections; and the underlying mechanism is relevant to the role of ANXA2-regulated tight junctions and its role in stabilizing the BBB in these deadly infections.

Subcortical intracerebral hemorrhage caused by mucormycosis in a patient with a history of bone-marrow transplantation.

We report on a rare case of a patient with rhinocerebral mucormycosis that presented as intracerebral hemorrhage (ICH). A 54-year-old man who was immunosuppressed had ophthalmoplegia. Four days later, ICH developed in his left frontal lobe. The ICH was surgically removed totally. Pathology specimen surgically obtained from brain surface adjacent to hematoma cavity showed blood vessels filled with Mucor mycelium. Combined with surgical findings, venous occlusion by Mucor mycelium might be the cause of ICH in the patient.

[Manifestations of systemic mycoses and related infections in the central nervous system]. / Szisztémás mycosisok és hasonló infekciók központi idegrendszeri manifesztációi.

UNLABELLED: In daily practice mycotic infections of the CNS have become more and more frequent. The main causes are the wide-ranging use of corticosteroids, immunosuppressive, cytostatic drugs and antibiotics, the spreading of AIDS, the increasing number of surviving immature newborns. To illustrate the diagnostic difficulties, the authors report several cases. CASE REPORTS: 1. Multifocal hemorrhagic infarcts of the brain, caused by generalized aspergillosis in mantle cell malignant lymphoma. 2. Cerebral microabscesses, caused by systemic candidiasis in a premature infant. 3. Fatal actinomycosis, mimicking a space occupying tumour in the thigh and with an abscess in the brain, radiologically indicated as a metastasis. The cause of death was actinomycotic pneumonia. 4. A successfully treated and recovered patient with recurrent pneumonia and multiplex brain abscesses, caused by filamentous microorganism of a Nocardia species revealed by histological examination of the neurosurgical specimen. DISCUSSION AND CONCLUSIONS: We have to be aware for the development of the mycotic and related infections of endangered patients. Aspergillosis and candidiasis play the most significant role in the involvement of the central nervous system. Actinomycosis and nocardiosis are more sensitive to treatment, so their diagnosis is of life-saving importance. The therapeutic chances of high risk patients with aspergillosis and candidiasis will be definitively better, if the infection is recognized and appropriately treated before the involvement of the CNS.

Whole genome sequence of an Escherichia coli ST410 isolate co-harbouring blaNDM-5, blaOXA-1, blaCTX-M-15, blaCMY-2, aac(3)-IIa and aac(6')-Ib-cr genes isolated from a patient with bloodstream infection in China.

OBJECTIVES: Mortality associated with carbapenemase-producing Enterobacteriaceae is high as there are few therapeutic options. Escherichia coli sequence type 410 (ST410) is currently an international high-risk clone and is responsible for a large number of clinical infections. Here we report the draft genome sequence of a ST410 clinical E. coli isolate (ECS9) co-harbouring blaNDM-5, blaOXA-1, blaCTX-M-15, blaCMY-2, aac(3)-IIa and aac(6')-Ib-cr genes, obtained from a patient with bloodstream infection in China. METHODS: The genome of E. coli ECS9 was sequenced using an Illumina HiSeqTM 4000 instrument with a 150-bp paired-end approach. Generated sequence reads were assembled using Velvet 1.2.10. Contigs were annotated using Rapid Annotation using Subsystem Technology (RAST), and further whole-genome sequence data analyses were performed. RESULTS: Escherichia coli ECS9 belongs to multilocus sequence typing (MLST) ST410. The total number of assembled bases was 4 935 145 bp, with 5077 protein-coding sequences. The presence of the blaNDM-5, blaOXA-1, blaCTX-M-15 and blaCMY-2 genes was detected in addition to other antimicrobial resistance genes conferring resistance to fluoroquinolones, aminoglycosides, trimethoprim, sulfonamides and tetracyclines. CONCLUSION: To our knowledge, this is the first report of anE. coli ST410 strain co-harbouring blaNDM-5, blaOXA-1, blaCTX-M-15, blaCMY-2, aac(3)-IIa and aac(6')-Ib-cr, obtained from a bloodstream infection in China. The presented genome sequence of carbapenemase-producing E. coli strain ST410 could provide further insight into the acquisition of multiple resistance genes by this successful lineage.

PI3Kγ (Phosphoinositide 3-Kinase-γ) Inhibition Attenuates Tissue-Type Plasminogen Activator-Induced Brain Hemorrhage and Improves Microvascular Patency After Embolic Stroke.

Genetic and pharmacological inhibition of the PI3Kγ (phosphoinositide 3-kinase-γ) exerts anti-inflammatory and protective effects in a number of inflammatory and autoimmune diseases. SHRs (spontaneously hypertensive rats) subjected to embolic middle cerebral occlusion were treated with AS605240 (30 mg/kg) at 2 or 4 hours, tPA (tissue-type plasminogen activator; 10 mg/kg) at 2 or 6 hours, or AS605240 at 4 hours plus tPA at 6 hours. Infarct volume, brain hemorrhage, neurological function, microvascular thrombosis, and cerebral microvessel patency were examined. We found that treatment with AS605240 alone at 2 hours or the combination treatment with AS605240 at 4 hours and tPA at 6 hours significantly reduced infarct volume and neurological deficits at 3 days after stroke compared with ischemic rats treated with saline, AS605240 alone at 4 hours, and tPA alone at 6 hours. Moreover, the combination treatment effectively prevented the delayed tPA-induced cerebral hemorrhage. These protective effects are associated with reduced disruption of the blood-brain barrier, reduced downstream microvascular thrombosis, and improved microvascular patency by AS605240. Inhibition of the NF-κB (nuclear transcription factor-κB)-dependent MMP (matrix metalloproteinase)-9 and PAI-1 (plasminogen activator inhibitor-1) in the ischemic brain endothelium may underlie the neurovascular protective effect of AS605240. In addition, the combination treatment significantly reduced circulating platelet P-selectin expression and platelet-leukocyte aggregation compared with ischemic rats treated with saline or tPA alone at 6 hours. In conclusion, inhibition of PI3Kγ with AS605240 reduces delayed tPA-induced intracerebral hemorrhage and improves microvascular patency, which likely contributes to neuroprotective effect of the combination treatment.

The effect of S. pneumoniae bacteremia on cerebral blood flow autoregulation in rats.

In the present study, we studied the effect of bacteremia on cerebral blood flow (CBF) autoregulation in a rat model of pneumococcal bacteremia and meningitis. Anesthetized rats were divided into five groups (A to E) and inoculated with pneumococci intravenously and normal saline intracisternally (group A, N=10); saline intravenously and pneumococci intracisternally (group B, N=10); pneumococci intravenously and pneumococci intracisternally (group C, N=5); saline intravenously, antipneumococcal antibody intravenously (to prevent bacteremia), and pneumococci intracisternally (group D, N=10); or saline intravenously and saline intracisternally (group E, N=10), respectively. Positive cultures occurred in the blood for all rats in groups A, B, and C, and in the cerebrospinal fluid for all rats in groups D and E. Twenty-four hours after inoculation, CBF was measured with laser-Doppler ultrasound during incremental reductions in cerebral perfusion pressure (CPP) by controlled hemorrhage. Autoregulation was preserved in all rats without meningitis (groups A and E) and was lost in 24 of 25 meningitis rats (groups B, C, and D) (P<0.01). In group A, the lower limit was higher than that of group E (P<0.05). The slope of the CBF/CPP regression line differed between the meningitis groups (P<0.001), being steeper for group B than groups C and D, with no difference between these two groups. The results suggest that pneumococcal bacteremia in rats triggers cerebral vasodilation, which right shifts the lower limit of, but does not entirely abolish, CBF autoregulation in the absence of meningitis, and which may further aggravate the vasoparalysis induced by concomitant pneumococcal meningitis.

Endovascular treatment of primary infectious aneurysm in childhood: a case report.

Infectious aneurysms constitute 4% of all intracranial aneurysms. The microorganisms responsible are most commonly streptococcus viridans, staphylococcus aureus and combined bacterial infections. Nonetheless, cases with no reproduction in their cultures are rather frequent. A 6-year-old patient admitted with complaints of sudden headache, nausea, vomiting and high temperature. Intracerebral hematoma and saccular aneurysm located at the distal posterior cerebral artery were diagnosed as a result of the laboratory investigations and neuroradiological examinations. Infectious aneurysm was considered due to the clinical findings, morphology and location of the aneurysm. Although the causative microorganism was detected in blood culture, no focus could be detected. The aneurysm was hindered by endovascular intervention. In this manuscript, we discuss the infrequently seen childhood infectious aneurysm in the light of the pertinent literature.

Cerebral hemorrhage in infective endocarditis caused by Actinobacillus actinomycetemcomitans.

Cerebral hemorrhage occurs rarely in endocarditis caused by Actinobacillus actinomycetemcomitans. A 51-year-old man with a prosthetic mitral valve, who had been prophylactically treated (7 years) with warfarin, presented with intermittent fever. On admission, a Levine grade II/VI systolic cardiac murmur was detected. A transthoracic echocardiogram was negative for valve vegetation. Cefepime (1 g every 8 hours) was administered intravenously. On day 4, culturing of Gram-negative bacilli from blood and a transesophageal echocardiogram revealed a small oscillating filament attached to lateral mitral prosthetic ring on the atrial side. Ceftriaxone (2 g once daily) was started. Gait instability and left-side weakness developed abruptly 2 weeks later; brain magnetic resonance imaging revealed a hematoma over the right parietal-occipital lobe. Ceftriaxone was adjusted to 2 g every 12 hours. Actinobacillus actinomycetemcomitans was identified 3 weeks later. Recovery was achieved, with significant interval improvement and resolution of the cerebral lesions evident on CT.