Staphylococcal Toxic Shock Syndrome 2000–2006: Epidemiology, Clinical Features, and Molecular Characteristics

Circulating strains of Staphylococcus aureus (SA) have changed in the last 30 years including the emergence of community-associated methicillin-resistant SA (MRSA). A report suggested staphylococcal toxic shock syndrome (TSS) was increasing over 2000-2003. The last population-based assessment of TSS was 1986.Population-based active surveillance for TSS meeting the CDC definition using ICD-9 codes was conducted in the Minneapolis-St. Paul area (population 2,642,056) from 2000-2006. Medical records of potential cases were reviewed for case criteria, antimicrobial susceptibility, risk factors, and outcome. Superantigen PCR testing and PFGE were performed on available isolates from probable and confirmed cases.Of 7,491 hospitalizations that received one of the ICD-9 study codes, 61 TSS cases (33 menstrual, 28 non-menstrual) were identified. The average annual incidence per 100,000 of all, menstrual, and non-menstrual TSS was 0.52 (95% CI, 0.32-0.77), 0.69 (0.39-1.16), and 0.32 (0.12-0.67), respectively. Women 13-24 years had the highest incidence at 1.41 (0.63-2.61). No increase in incidence was observed from 2000-2006. MRSA was isolated in 1 menstrual and 3 non-menstrual cases (7% of TSS cases); 1 isolate was USA400. The superantigen gene tst-1 was identified in 20 (80%) of isolates and was more common in menstrual compared to non-menstrual isolates (89% vs. 50%, p = 0.07). Superantigen genes sea, seb and sec were found more frequently among non-menstrual compared to menstrual isolates [100% vs 25% (p = 0.4), 60% vs 0% (p<0.01), and 25% vs 13% (p = 0.5), respectively].TSS incidence remained stable across our surveillance period of 2000-2006 and compared to past population-based estimates in the 1980s. MRSA accounted for a small percentage of TSS cases. tst-1 continues to be the superantigen associated with the majority of menstrual cases. The CDC case definition identifies the most severe cases and has been consistently used but likely results in a substantial underestimation of the total TSS disease burden

Identification and Validation of Novel Cerebrospinal Fluid Biomarkers for Staging Early Alzheimer's Disease

Ideally, disease modifying therapies for Alzheimer disease (AD) will be applied during the 'preclinical' stage (pathology present with cognition intact) before severe neuronal damage occurs, or upon recognizing very mild cognitive impairment. Developing and judiciously administering such therapies will require biomarker panels to identify early AD pathology, classify disease stage, monitor pathological progression, and predict cognitive decline. To discover such biomarkers, we measured AD-associated changes in the cerebrospinal fluid (CSF) proteome.CSF samples from individuals with mild AD (Clinical Dementia Rating [CDR] 1) (n = 24) and cognitively normal controls (CDR 0) (n = 24) were subjected to two-dimensional difference-in-gel electrophoresis. Within 119 differentially-abundant gel features, mass spectrometry (LC-MS/MS) identified 47 proteins. For validation, eleven proteins were re-evaluated by enzyme-linked immunosorbent assays (ELISA). Six of these assays (NrCAM, YKL-40, chromogranin A, carnosinase I, transthyretin, cystatin C) distinguished CDR 1 and CDR 0 groups and were subsequently applied (with tau, p-tau181 and Aβ42 ELISAs) to a larger independent cohort (n = 292) that included individuals with very mild dementia (CDR 0.5). Receiver-operating characteristic curve analyses using stepwise logistic regression yielded optimal biomarker combinations to distinguish CDR 0 from CDR>0 (tau, YKL-40, NrCAM) and CDR 1 from CDR<1 (tau, chromogranin A, carnosinase I) with areas under the curve of 0.90 (0.85-0.94 95% confidence interval [CI]) and 0.88 (0.81-0.94 CI), respectively.Four novel CSF biomarkers for AD (NrCAM, YKL-40, chromogranin A, carnosinase I) can improve the diagnostic accuracy of Aβ42 and tau. Together, these six markers describe six clinicopathological stages from cognitive normalcy to mild dementia, including stages defined by increased risk of cognitive decline. Such a panel might improve clinical trial efficiency by guiding subject enrollment and monitoring disease progression. Further studies will be required to validate this panel and evaluate its potential for distinguishing AD from other dementing conditions

A review of angular leaf spot resistance in common bean.

Angular leaf spot (ALS), caused by Pseudocer-cospora griseola, is one of the most devastating diseases of common bean (Phaseolus vulgarisL.) in tropical and subtropical production areas. Breeding for ALS resistance is difficult due to the extensive virulence diversity of P. griseolaand the recurrent appearance of new virulent races. Five major loci, Phg-1 to Phg-5, confer-ring ALS resistance have been named, and markers tightly linked to these loci have been reported. Quantitative trait loci (QTLs) have also been described, but the validation of some QTLs is still pending. The Phg-1, Phg-4, and Phg-5loci are from common bean cultivars of the Andean gene pool, whereas Phg-2 and Phg-3are from beans of the Mesoamerican gene pool. The reference genome of common bean and high-throughput sequencing technologies are enabling the development of molecular markers closely linked to the Phg loci, more accurate mapping of the resistance loci, and the compar-ison of their genomic positions. The objective of this report is to provide a comprehensive review of ALS resistance in common bean. Further-more, we are reporting three case studies of ALS resistance breeding in Latin America and Africa. This review will serve as a reference for future resistance mapping studies and as a guide for the selection of resistance loci in breeding programs aiming to develop common bean cultivars with durable ALS resistance

Common Bean variety releases in Africa

The Pan Africa Bean Research Alliance is a network of national agricultural research centers (NARS), and private and public sector institutions that work to deliver better beans with consumer and market preferred traits to farmers. The datasets presented here draw from 17 Sub Saharan countries that are members of PABRA. The dataset on released bean varieties is a collection of 357 bean varieties released by NARS and there characteristics. The dataset on bean varieties and the relationship to constraints provides the 357 bean varieties on the basis of resistance to constraints such as fungal, bacterial, viral, diseases and tolerance to abiotic stresses. There is also a dataset of bean varieties that have been released in more than one country, useful for moving seed from one country to another and facilitating regional trade. The dataset on Niche market traits provides the market defined classifications for bean trade in Sub Saharan Africa as well as varieties that fall into these classifications. The datasets are an update to the 2011 discussion on PABRAs achievement in breeding and delivery of bean varieties in Buruchara et. 2011 in pages 236 and 237 here: http://www.ajol.info/index.php/acsj/article/view/74168 . It is also an update to a follow up to this discussion in Muthoni, R. A., Andrade, R. 2015 on the performance of bean improvement programmes in sub-Saharan Africa from the perspectives of varietal output and adoption in chapter 8. here: http://dx.doi.org/10.1079/9781780644011.0148. The data is extracted from the PABRA M&E database available here ( http://database.pabra-africa.org/?location=breeding)

Characterization of the Pseudomonas aeruginosa recA analog and its protein product: rec-102 is a mutant allele of the P. aeruginosa PAO recA gene.

We cloned a 2.3-kilobase-pair fragment of the Pseudomonas aeruginosa PAO chromosome which is capable of complementing recA mutations of Escherichia coli. The recA-complementing activity was further localized to a 1.5-kilobase-pair PvuII-HindIII fragment. Southern blot analysis under conditions of high stringency indicated that DNA sequence homology is shared by the E. coli recA gene and the P. aeruginosa recA analog. The cloned recA analog was shown to restore resistance to methyl methanesulfonate, nitrofurantoin, and UV irradiation to E. coli recA mutants. Upon introduction of the cloned P. aeruginosa gene, these mutants regained recombination proficiency in HfrH-mediated conjugation and the ability to induce lambda prophages and SOS functions (din gene transcription) after exposure to DNA-damaging agents. Lambda prophage carrying a cI ind mutation was not inducible, suggesting that the mechanism of induction of these SOS functions by the P. aeruginosa RecA analog is similar to that by the activated E. coli RecA protein. The product of the recA analog was identified in minicells as a protein of approximately 47,000 daltons. Western blot analysis using anti-E. coli RecA antibody demonstrated that this protein is antigenically cross-reactive with the E. coli recA protein. The recA-containing fragment was cloned into the broad-host-range vector pCP13 and introduced into Rec- strains of P. aeruginosa containing the rec-102 allele. The plasmid was shown to restore recombination proficiency in FP5-mediated conjugations and to restore resistance to UV irradiation and methyl methanesulfonate to these Rec- mutants. It was shown that a wild-type allele of rec-102 is necessary for UV-mediated induction of D3 and F116 prophages. The cloned recA analog restored the UV inducibility of these prophages in rec-102 mutants. These data indicate that rec-102 is a mutant allele of the P. aeruginosa recA gene and suggest that there has been considerable conservation of the recA gene in the evolution of the gram-negative bacteria