Search

Background: Neurolisteriosis ranks among the most severe neurological infections. Its radiological features have not been thoroughly studied. We describe here the neuroradiological features of neurolisteriosis and assess their prognostic value., Methods: Patients with microbiologically proven neurolisteriosis were enrolled from November 2009 to October 2013 in MONALISA study. Magnetic resonance and computed tomography images were studied by 2 independent neuroradiologists. Predictors of 3-month mortality were determined using logistic regression., Results: Seventy-one patients were included; 42 were men (59%). Mean age was 64 years. Sixty patients (85%) reported signs of encephalitis, with clinical brainstem involvement in 16 (23%). Images were abnormal in 87% of cases (62/71). Main neuroradiological images were meningeal enhancement (25/71, 35%), abscess(es), or nodular image(s) evocative of abscess (10/71, 14%), hemorrhages (11/71, 15%), contrast-enhancing ventricles, or hydrocephalus (7/71, 10%). White-matter images (42/71, 59%), dilated Virchow-Robin spaces (22/71, 31%), and cerebral atrophy were also reported (34/71, 48%). Brainstem involvement (meningeal enhancement, abscess) was reported in only 7/71 cases (10%). Three-month survival was lower in patients with hydrocephalus or contrast-enhancing ventricles (1/7 [14%] than without [47/64, 73%], P = .005) and in patients with parenchymal images (abscess[es], nodule[s]\, or white matter images; 25/46 [54%] vs 23/25 without [92%], P = .004). Parenchymal images were associated with lower 3-month survival in the multivariable model (odds ratio 5.60, 95% confidence interval [1.42-29.6], P = .02)., Conclusions: Neurolisteriosis presents as a combination of neuroradiological images, none being specific. Radiological signs of rhombencephalitis are uncommon, whereas, unexpectedly, hemorrhagic images are frequent. The negative prognostic value of parenchymal neuroradiological images was evidenced., Clinical Trials Registration: NCT01520597.

Background: Lyme encephalopathy, characterized by nonspecific neurobehavioral symptoms including mild cognitive difficulties, may occur in patients with systemic Lyme disease and is often mistakenly attributed to central nervous system (CNS) infection. Identical symptoms occur in many inflammatory states, possibly reflecting the effect of systemic immune mediators on the CNS., Methods: Multiplex immunoassays were used to measure serum and cerebrospinal fluid (CSF) cytokines in patients with or without Lyme disease to determine if there are specific markers of active CNS infection (neuroborreliosis), or systemic inflammatory mediators associated with neurobehavioral syndromes., Results: CSF CXCL13 levels were elevated dramatically in confirmed neuroborreliosis (n = 8), less so in possible neuroborreliosis (n = 11) and other neuroinflammatory conditions (n = 44). Patients with Lyme (n = 63) or non-Lyme (n = 8) encephalopathy had normal CSF findings, but had elevated serum levels of interleukins 7, 17A, and 17F, thymic stromal lymphopoietin and macrophage inflammatory protein-α., Conclusions: CSF CXCL13 is a sensitive and specific marker of neuroborreliosis in individuals with Borrelia-specific intrathecal antibody production. However, it does not distinguish individuals strongly suspected of having neuroborreliosis, but lacking confirmatory intrathecal antibodies, from those with other neuroinflammatory conditions. Patients with mild cognitive symptoms occurring during acute Lyme disease, and/or after appropriate treatment, have normal CSF but elevated serum levels of T-helper 17 markers and T-cell growth factors, which are also elevated in patients without Lyme disease but with similar symptoms. In the absence of CSF abnormalities, neurobehavioral symptoms appear to be associated with systemic inflammation, not CNS infection or inflammation, and are not specific to Lyme disease.

Background: Neonatal encephalopathy (NE) is a leading cause of child mortality and longer-term impairment. Infection can sensitize the newborn brain to injury; however, the role of group B streptococcal (GBS) disease has not been reviewed. This paper is the ninth in an 11-article series estimating the burden of GBS disease; here we aim to assess the proportion of GBS in NE cases., Methods: We conducted systematic literature reviews (PubMed/Medline, Embase, Latin American and Caribbean Health Sciences Literature [LILACS], World Health Organization Library Information System [WHOLIS], and Scopus) and sought unpublished data from investigator groups reporting GBS-associated NE. Meta-analyses estimated the proportion of GBS disease in NE and mortality risk. UK population-level data estimated the incidence of GBS-associated NE., Results: Four published and 25 unpublished datasets were identified from 13 countries (N = 10436). The proportion of NE associated with GBS was 0.58% (95% confidence interval [CI], 0.18%-.98%). Mortality was significantly increased in GBS-associated NE vs NE alone (risk ratio, 2.07 [95% CI, 1.47-2.91]). This equates to a UK incidence of GBS-associated NE of 0.019 per 1000 live births., Conclusions: The consistent increased proportion of GBS disease in NE and significant increased risk of mortality provides evidence that GBS infection contributes to NE. Increased information regarding this and other organisms is important to inform interventions, especially in low- and middle-resource contexts., (© The Author 2017. Published by Oxford University Press for the Infectious Diseases Society of America.)

Background: We aimed to provide the first comprehensive estimates of the burden of group B Streptococcus (GBS), including invasive disease in pregnant and postpartum women, fetal infection/stillbirth, and infants. Intrapartum antibiotic prophylaxis is the current mainstay of prevention, reducing early-onset infant disease in high-income contexts. Maternal GBS vaccines are in development., Methods: For 2015 live births, we used a compartmental model to estimate (1) exposure to maternal GBS colonization, (2) cases of infant invasive GBS disease, (3) deaths, and (4) disabilities. We applied incidence or prevalence data to estimate cases of maternal and fetal infection/stillbirth, and infants with invasive GBS disease presenting with neonatal encephalopathy. We applied risk ratios to estimate numbers of preterm births attributable to GBS. Uncertainty was also estimated., Results: Worldwide in 2015, we estimated 205000 (uncertainty range [UR], 101000-327000) infants with early-onset disease and 114000 (UR, 44000-326000) with late-onset disease, of whom a minimum of 7000 (UR, 0-19000) presented with neonatal encephalopathy. There were 90000 (UR, 36000-169000) deaths in infants <3 months age, and, at least 10000 (UR, 3000-27000) children with disability each year. There were 33000 (UR, 13000-52000) cases of invasive GBS disease in pregnant or postpartum women, and 57000 (UR, 12000-104000) fetal infections/stillbirths. Up to 3.5 million preterm births may be attributable to GBS. Africa accounted for 54% of estimated cases and 65% of all fetal/infant deaths. A maternal vaccine with 80% efficacy and 90% coverage could prevent 107000 (UR, 20000-198000) stillbirths and infant deaths., Conclusions: Our conservative estimates suggest that GBS is a leading contributor to adverse maternal and newborn outcomes, with at least 409000 (UR, 144000-573000) maternal/fetal/infant cases and 147000 (UR, 47000-273000) stillbirths and infant deaths annually. An effective GBS vaccine could reduce disease in the mother, the fetus, and the infant., (© The Author 2017. Published by Oxford University Press for the Infectious Diseases Society of America.)

Background: The tuberculosis epidemic is still a global emergency, and its spread in the past 20 years has been fueled by the acquired immune deficiency syndrome pandemic and increasing drug resistance. International travel and migration may increase the incidence of tuberculosis in industrialized countries., Methods: We reviewed the clinical charts of patients admitted to the infectious diseases unit of Ospedali Riuniti (Bergamo, Italy) to identify patients with intracranial mass lesions caused by Mycobacterium tuberculosis., Results: During the past 6.5 years, 5 of 30 patients with a mass of infectious origin in the brain had tuberculous brain lesions diagnosed. All 5 were human immunodeficiency virus (HIV)-negative adults and African immigrants. No patient had concomitant meningitis, 1 had a concomitant pulmonary disease, and 3 subjects reported a past history of tuberculosis. At presentation, no patient had fever and 3 had seizures. Examination of cerebrospinal fluid revealed normal findings for 4 of 4 subjects, and neuroimaging showed multiple intracranial mass lesions in 4 of 5 patients. The diagnosis was definite for 2 subjects (based on analysis of brain specimens) and presumptive for 3 subjects (1 had concomitant pulmonary tuberculosis, and 2 had clinical response to therapy). Results of susceptibility tests for M. tuberculosis were available for 2 patients: both isolates were resistant to isoniazid, and 1 was also resistant to streptomycin. Duration of medical treatment ranged from 11 to 23 months, and 2 subjects underwent surgical procedures at the time of diagnosis. All 5 patients recovered., Conclusions: Clinicians in western countries should consider the possible role of tuberculosis in causing mass lesions in the brain, particularly in immigrants from regions where tuberculosis is endemic.

We describe a patient with multiple cerebral lesions that initially were believed to be tumor metastases but were later found to be caused by Nocardia asteroides, after magnetic resonance spectroscopy (MRS) findings suggested that the lesions were infective in origin. This case report demonstrates the ability of MRS, a noninvasive imaging modality, to aid in the diagnosis of brain infection.

Three previously normal patients with cryptococcal meningitis had intracranial lesions on computed tomography and magnetic resonance imaging that persisted for >5 years after successful cure with antifungal drugs. Persistence of lesions on neuroimaging should not be misinterpreted as evidence of active cryptococcosis.

Histoplasmosis is a common cause of systemic mycosis in areas of the United States where it is endemic. Central nervous system and genitourinary histoplasmosis is rare, especially in immunocompetent hosts. We describe a case of disseminated histoplasmosis in a normal host that was associated with cerebral and prostatic histoplasmosis presenting as fever of undetermined origin, weight loss, and severe debilitating altered mental status. The patient subsequently developed acute renal failure that manifested as obstructive uropathy during antifungal therapy with amphotericin B. Transurethral resection of the prostate resulted in improved renal function during continuation of amphotericin B therapy. Pathological analysis of the prostate revealed necrotizing granulomas with intralesional fungal organisms. Blood and urine cultures were positive for Histoplasma capsulatum. Diagnostic issues and management are discussed. Treatment resulted in return of normal cognitive and motor function. This case is compared with the 8 previously reported cases of H. capsulatum prostatitis.

Extrapulmonary involvement with Pneumocystis carinii has been described in 0.5%-2.5% of persons with AIDS. One hundred nine patients with AIDS and confirmed extrapulmonary pneumocystosis were identified, and seven of these patients (including our patients) had central nervous system (CNS) pneumocystosis. Of these seven patients, six had prior AIDS-related complications, and three had previous P. carinii pneumonia. Six patients had CNS symptoms, one of whom underwent a focal neurological examination. No cases were diagnosed before death. The involved sites were the cerebral cortex (2 patients), meninges (2), pituitary gland (1), putamen (1), and nonspecified locations (3). In two patients, organisms were seen around blood vessels, and in five patients there was concurrent neuropathology. In summary, CNS involvement with P. carinii usually occurs as a late complication of AIDS and probably represents hematogenous dissemination.

Disseminated infection with Histoplasma capsulatum frequently involves the nervous system, but the CNS process is generally not clinically apparent. We report an unusual case of a renal transplant recipient with long-standing immunosuppression who presented with clinical evidence of mass lesions in both his cerebral cortex and his spinal cord. Findings of CSF examination were normal, but stereotaxic biopsies of his cortical lesions demonstrated yeast forms and cultures of biopsy specimens yielded H. capsulatum. Clinical defects referable to both the cortical and spinal lesions decreased in severity after the patient received antifungal therapy. Our case illustrates that disseminated histoplasmosis can present in myriad ways and that widespread disease in the CNS can be occult in immunocompromised patients.

Patients with AIDS are prone to developing infections with opportunistic pathogens. Recently, a new mycobacterium, Mycobacterium genavense, has been found to cause infection in patients with AIDS. Previously published reports indicate that patients who are infected with this organism present with the same clinical features as do patients with disseminated infection due to organisms of the Mycobacterium avium complex. We describe an unusual case of a patient with AIDS who presented with grand mal seizures and a mass lesion in his brain, which was found to be caused by infection with M. genavense. No evidence of disseminated infection could be found in this patient. We discuss the microbiology of this organism and review the literature on M. genavense infections. Clinicians should be aware of this organism so that efforts at culture and identification will be made.

CSF samples taken from three patients with primary hypogammaglobulinemia and chronic brain disease were positive for enterovirus RNA by use of a technique based on the polymerase chain reaction (PCR) to amplify viral genomic sequences. Repeated attempts to culture viruses from the CSF from these patients were unsuccessful, possibly because the patients were treated regularly with intravenous immunoglobulin, which may have contained enough specific antibody to partially neutralize the viruses. Our data suggest that enteroviruses are responsible for diverse CNS features in patients with primary hypogammaglobulinemia and that for these patients the diagnosis should be pursued using PCR technology.