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.

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.

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.

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.

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.

Ventilator-associated pneumonia in patients with cerebral hemorrhage: Impact on mortality and microbiological characterization / Neumonía asociada a ventilación mecánica en pacientes con hemorragia cerebral: mortalidad y caracterización microbiana

Ventilator-associated pneumonia (VAP) is a major complication among critically ill patients who depend on mechanical ventilation. Few reports have focused on intracerebral hemorrhage patients with VAP. Our main objective was to investigate the bacteria distribution characteristics and the impact of ventilator-associated pneumonia mortality in critical cerebral hemorrhage patients. This retrospective study included 89 cases of cerebral hemorrhage patients with VAP admitted to the ICU of Huashan Hospital. We used the chi-square test to compare qualitative variables and Student's t-test to compare means between groups of normally distributed quantitative variables. Multiple logistic regression analysis was used to assess mortality-independent predictors in the ICU. A total of 42% patients with cerebral hemorrhage were diagnosed with VAP in the ICU during the study period, and the mortality rate was 18%. Acinetobacter baumannii (n=58), Klebsiella pneumoniae (n=52), and Pseudomonas aeruginosa (n=21) were the most common pathogenic bacteria. Blood volume >30ml, tracheal ventilation mode and head of bed elevation were independent factors associated with increased mortality. Glasgow Coma Scale (GCS), Acute Physiology and Chronic Health Evaluation II (APACHE II) score and the time from bleeding to intubation were other potentially important factors. While the number of infecting bacteria may not be directly related to death, it can increase antibiotic consumption and length of intensive care unit (ICU) stays. Blood volume >30ml, tracheal ventilation mode and head of bed elevation were directly related to the death of critical cerebral hemorrhage patients with ventilator-associated pneumonia

La neumonía asociada a ventilación mecánica (NAV) es una complicación mayor entre los pacientes críticos que dependen de la ventilación mecánica. Pocos artículos se han centrado en los pacientes de hemorragia cerebral con NAV. Nuestro objetivo principal fue investigar las características de la distribución bacteriana y el impacto de la mortalidad de la neumonía asociada a ventilación mecánica en pacientes críticos de hemorragia cerebral. Este estudio retrospectivo incluyó 89 casos de pacientes de hemorragia cerebral con NAV ingresados en la unidad de cuidados intensivos (UCI) del Hospital Huashan. Utilizamos la prueba χ2 para comparar las variables cualitativas, y la t de Student para comparar las medias entre grupos de las variables cuantitativas normalmente distribuidas. Utilizamos análisis de regresión logística múltiple para valorar los factores predictivos independientes de la mortalidad en la UCI. Diagnosticamos NAV en el 42% de los pacientes con hemorragia en la UCI durante el periodo de estudio, y la tasa de mortalidad fue del 18%. Acinetobacter baumannii (n=58), Klebsiella pneumoniae (n=52) and Pseudomonas aeruginosa (n=21) fueron las bacterias patogénicas más comunes. El volumen sanguíneo >30ml, el modo de ventilación traqueal y la inclinación del cabecero de la cama fueron factores independientes asociados al incremento de la mortalidad. La Glasgow Coma Scale (GCS) y el Acute Physiology and Chronic Health EvaluationII (APACHE II), así como el tiempo transcurrido entre el sangrado y la intubación, fueron otros factores potencialmente importantes. A pesar de que el número de bacterias infecciosas puede no estar directamente relacionado con la muerte, puede incrementar el consumo de antibióticos y la duración de la estancia en la UCI. El volumen sanguíneo >30ml, el modo de ventilación traqueal y la inclinación del cabecero de la cama guardaron una relación directa con la muerte de los pacientes críticos de hemorragia cerebral con neumonía asociada a ventilación mecánica

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.

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.

Complete genome sequence of Acinetobacter baumannii A1296 (ST1469) with a small plasmid harbouring the tet(39) tetracycline resistance gene.

OBJECTIVES: Acinetobacter baumannii is considered an important nosocomial pathogen worldwide owing to its increasing antibiotic resistance. This study aimed to determine the complete genome sequence of A. baumannii strain A1296 and to perform a comparative analysis among A. baumannii. METHODS: The complete genome sequence of A. baumannii A1296 was sequenced on two SMRT cells using P6C4 chemistry on a PacBio Single Molecule, Real-Time (SMRT) RS II instrument. The A1296 genome sequence was annotated using Prokaryotic Genome Automatic Annotation Pipeline (PGAAP), and the sequence type and resistance genes of the strain were analysed. RESULTS: Here we present the complete genome sequence of A. baumannii strain A1296, belonging to a novel sequence type (ST1469) and isolated from patient in China, that was sensitive to multiple antibiotics. The genome of A. baumannii A1296 was 3810701bp in length, including one circular chromosome and two plasmids. The tet(39) resistance gene was located on the small plasmid in this A. baumannii strain. CONCLUSIONS: The genome sequence of A. baumannii strain A1296 can be used as a reference sequence for comparative analysis aimed at elucidating the acquisition, dissemination and mobilisation of resistance genes among A. baumannii.

Cerebral haemorrhage as a clinical manifestation of human ehrlichiosis.

A 16-year-old young man presented to the emergency room with new-onset generalised tonic-clonic seizures. Examination showed a Glasgow score of 13 and predominantly crural left hemiparesis. Imaging demonstrated a right frontoparietal haemorrhage of non-vascular origin with perilesional oedema. Surgical drainage was carried out, but rebleeding occurred within 24 hours following surgery, and again 1 week after discharge. On reinterrogation and examination, Ehrlichia canis infection was suspected and empirical management with doxycycline was begun. Improvement was evident 72 hours after antibiotic initiation, and PCR confirmed the diagnosis; thus, doxycycline was continued for 6 months. After 2 years, seizures recurred and treatment was reinstated with good clinical response. However, seizures reappeared whenever treatment discontinuation was attempted. Lacking alternatives, doxycycline was maintained up to the third year following the initial episode. Subsequently, the patient showed complete resolution without neurological sequelae up to his last follow-up visit, 12 months following treatment cessation.

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.

Oral Cnm-positive Streptococcus Mutans Expressing Collagen Binding Activity is a Risk Factor for Cerebral Microbleeds and Cognitive Impairment.

Cerebral microbleeds (CMBs) are an important risk factor for stroke and dementia. We have shown that the collagen binding surface Cnm protein expressed on cnm-positive Streptococcus mutans is involved in the development of CMBs. However, whether the collagen binding activity of cnm-positive S. mutans is related to the nature of the CMBs or to cognitive impairment is unclear. Two-hundred seventy nine community residents (70.0 years) were examined for the presence or absence of cnm-positive S. mutans in the saliva by PCR and collagen binding activity, CMBs, and cognitive function were evaluated. Cnm-positive S. mutans was detected more often among subjects with CMBs (p < 0.01) than those without. The risk of CMBs was significantly higher (odds ratio = 14.3) in the group with S. mutans expressing collagen binding activity, as compared to the group without that finding. Deep CMBs were more frequent (67%) and cognitive function was lower among subjects with cnm-positive S. mutans expressing collagen binding activity. This work supports the role of oral health in stroke and dementia and proposes a molecular mechanism for the interaction.

Empirical Combination Antibiotic Therapy Improves the Outcome of Nosocomial Meningitis or Ventriculitis in Neuro-Critical Care Unit Patients.

BACKGROUND: Nosocomial meningitis and ventriculitis (MEN) are serious complications in neuro-critical care unit (NCCU) patients. Few data are available on the risk factors and mortality rates among NCCU patients with these disorders caused by multi-drug-resistant (MDR) pathogens. Our aim was to identify the risk factors for MEN caused by such pathogens and in-hospital deaths in critically ill neurologic patients and to evaluate the impact of empirical combination antibiotic therapy (ECAT) on the outcomes of these patients. METHODS: We conducted a retrospective study of critically ill neurologic patients having nosocomial MEN who were admitted to the NCCU in a university teaching hospital from January 2003 to December 2013, with MEN being defined using the modified U.S. Centers for Disease Control and Prevention criteria for nosocomial infections. RESULTS: In total, 6,149 consecutive NCCU patients were screened; 132 had MEN. Logistic regression analysis demonstrated that MDR MEN was related to infection with gram-negative (GN) bacteria (odds ratio 3.16; 95% confidence interval [CI] 1.08-9.25; p = 0.036), and inadequate initial antibiotic therapy (odds ratio 9.80; 95% CI 3.79-25.32; p < 0.001). The ECAT was associated with a lower mortality rate (hazard ratio 0.35; 95% CI 0.14-0.86; p = 0.022) in Cox proportional hazard regression analysis. The other variable independently associated with a greater mortality rate was a greater Simplified Acute Physiology Score II (hazard ratio 1.07; 95% CI 1.01-1.13; p = 0.018). CONCLUSIONS: Initial combination therapy improves the in-hospital mortality rate among NCCU patients with nosocomial MEN. Inadequate initial antibiotic therapy and GN infection were associated with MDR MEN.

Cerebral imaging in infectious endocarditis: A clinical study.

BACKGROUND: Because neurological failure is the most frequent extra-cardiac complication in Infectious Endocarditis (IE), a brain computerised tomography (CT) scan is usually performed. The benefits of magnetic resonance imaging (MRI) have not been clearly established. This study aims to clarify the prevalence and type of cerebral lesions in IE detected using MRI and to compare them with those detected using CT scans. METHODS: In the Grenoble University Hospital, patients diagnosed with definite or possible endocarditis according to Duke's criteria were screened from 2010-2012. Brain CT and MRI were performed as soon as possible after diagnosis. RESULTS: Of the 62 patients with IE who underwent at least one cerebral imaging within 3 weeks of diagnosis, Streptococcus (29) and Staphylococcus (14) were the main micro-organisms present. Twenty-eight (45%) patients underwent cardiac surgery. Eight (13%) died before discharge. Twenty (32%) had neurological symptoms. A brain CT-scan was performed on 53 (85%) patients and a MRI was performed on 43 (69%) patients. CT was pathological in 26 (49%) patients, whereas 32 (74%) MRI demonstrated abnormalities. The MRI lesions were classified as follows: ischaemia (48%), microbleeds (34%), haemorrhages (16%), abscesses (9%) and microbial aneurysms (4%). Of the 37 patients who underwent both MRI and CT examinations, ischaemia (48% vs 35%) and microbleeds (34%) demonstrated the difference between the two imaging methods. CONCLUSION: Through the early diagnosis of cerebral damage, even in asymptomatic cases, MRI may have a role in the IE management, influence any surgical decision and assist in prognosis assessment.

Cerebral hemorrhage due to tuberculosis meningitis: a rare case report and literature review.

Tuberculosis (TB) is a common disease to threaten human health. TB of the central nervous system (CNS) is rare but the most serious type of systemic TB because of its high mortality rate, serious neurological complications and sequelae. In this case report, we describe a woman who presented with walking instability, intracerebral hemorrhage and leptomeningeal enhancement due to tuberculosis meningitis. The patient had no significant medical history and the initial clinical symptoms were walking instability. On analysis, the cerebrospinal fluid was colorless and transparent, the pressure was more than 400 mm H2O, there was lymphocytic pleocytosis, increased protein, and decreased glucose levels present. No tuberculosis or other bacteria were detected. The patient's brain computed tomography image showed intra-cerebral hemorrhage (ICH) and contrast magnetic resonance imaging showed ICH in the right frontal lob, and leptomeningeal enhancement. CNS TB is rare but has a high mortality rate. As this disease has no unique characteristics at first presentation such as epidemiology and obvious clinical manifestation, a diagnosis of CNS TB remains difficult.

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.

Scrub typhus and cerebrovascular injury: a phenomenon of delayed treatment?

Abstract. Three patients diagnosed with scrub typhus through serology and polymerase chain reaction tests, experienced delayed administration of effective antibiotics after the appearance of symptoms, presented with subdural hemorrhage, intracerebral hemorrhage, or cerebral infarction in the late acute phase. Orientia tsutsugamushi should be considered as a causal or provoking factor for cerebrovascular accidents in regions where scrub typhus is endemic, especially in those who receive delayed treatment.

[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.

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.