Unknown Pathogen Research Articles

First Report of a New Postharvest Rot in Sweet Cherries Caused by Aureobasidium pullulans.

During August to October 2012, several cherry packers in central Washington State reported that a significant volume of sweet cherries (Prunus avium) (cvs. Staccato, Sweetheart, and Lapin) were rotten by an unknown fungal pathogen after packing. Of 14 boxes (9 kg per box) of commercially packed cherries rejected by a retailer, the average incidence of the decay was 68%. Initial symptoms on infected fruit appeared as soft, slippery skin with tan discoloration and later skin cracking, epidermal breakdown, and severe pitting were observed. To isolate the causal agent, decayed fruit were rinsed with water, sprayed with 70% ethanol, and air-dried in a laminar hood. After removing the fruit skin with a sterile scalpel, small fragments of fruit flesh between decayed and healthy tissue were cut and placed on potato dextrose agar (PDA) acidified with 0.1% lactic acid. The plates were incubated at 20°C for 7 days and sub-cultured on PDA to obtain pure cultures. The colonies initially appeared white to cream, yeast-like, and later turned to light yellow to pink or brown with age. Conidia were hyaline, smooth-walled, single-celled, and ellipsoidal with variable shape and size. The fungus was identified as Aureobasidium pullulans (de Bary) G. Arnaud based on its morphology (1). The identity of three representative isolates were further confirmed by analysis of nucleotide sequences of the internal transcribed spacer (ITS) regions amplified using the primers ITS1/ITS4. A BLAST search showed that the sequences had 99% homology (E-value = 0.0) with that of A. pullulans deposited at GenBank (Accession No. JF440584.1). The nucleotide sequence of the isolate, A625, has been assigned GenBank Accession No. KF569512. To test pathogenicity, three single-spore isolates were grown on PDA at 20°C. Cultures grown on 10-day-old PDA were flooded with 20 ml of sterile deionized water, and the resulting conidial suspensions were filtered through two layers of cheesecloth and adjusted to 5 × 105 conidia/ml with a hemacytometer. Organic cherry fruit (cv. Bing for isolate A625 and cv. Sweetheart for isolates A755 and A757) were surface-disinfested in 0.6% sodium hypochlorite solution for 5 min, rinsed twice with deionized water, and air-dried. Ten fruit per replicate, four replications per treatment were inoculated with the conidial suspension using a hand sprayer and placed on sterilized wet paper towel in a plastic container. Control fruit were sprayed with sterile water. All fruit were incubated at 22 ± 1°C for 5 days. The experiments were conducted twice. The same symptoms of skin cracking and epidermal breakdown developed on 73% of the inoculated fruit, while no such symptoms appeared on the control fruit. Koch's postulates were fulfilled by re-isolating the fungus from the symptomatic fruit. A. pullulans, a ubiquitous saprophytic fungus on many fruits, has been reported as a causal agent of melting decay in grapes (2). To the best of our knowledge, this is the first report of postharvest fruit rot in sweet cherries caused by A. pullulans.

The clinical analysis of 60 patients with chronic obstructive pulmonary disease and community-acquired pneumonia

Objective To analyze the pathogens and drug resistance of patients with chronic obstructive pulmonary disease and community-acquired pneumonia,in order to provide the evidence for rational drug use in the future.Methods The sputum specimens of 60 patients with chronic obstructive pulmonary disease and communityacquired pneumonia were detected for pathogens and drug sensitivity.Results 24 patients were infected with pathogens Streptococcus pneumoniae(40％).8 cases were infected with Haemophilus influenza(16.7％).10 patients were infected with Klebsiella pneumonia (13.3％).6 patients were infected with Mycoplasma lung (8.3％).5 patients were infected with alpha-hemolytic streptococcus (6.7％).4 patients were infected with Staphylococcus aureus (3.3％).Two patients were infected with Legionella pneumophila (3.3％).Unknown pathogen was one case (1.67％).Drug sensitive test showed that gram-negative bacteria had high resistance rate.Haemophilus influenzae,Streptococcus pneumonia and Legionella pneumophila had high resistance rate against penicillin.Mycoplasma lung and Klebsiella pneumoniae showed resistance to azithromycin.Staphylococcus aureus and hemolytic streptococcus showed resistance to Cefalotin.Conclusion The patients with chronic obstructive pulmonary disease and community-acquired pneumonia were mainly infected gram-negative bacteria,which had serious antibiotic-resistant.We should choose other drugs according to the results of drug sensitive test in the future,so as to improve the anti-bacteria effect and protect the health of patients. Key words: Pulmonary disease, chronic obstructive ; Community-acquired pneumonia; Gram-negative bacteria; Resistance rate

Escherichia coli O157:H7 LPS O-side chains and pO157 are required for killing Caenorhabditis elegans

As a model host, the nematode Caenorhabditis elegans has been used for studying unknown pathogen–host interactions and identifying novel virulence factors in bacterial pathogens. Among the bacterial pathogens that can induce death of C. elegans is enterohemorrhagic Escherichia coli (EHEC) O157:H7, a major serotype of EHEC that causes hemorrhagic colitis and hemolytic uremic syndrome in humans and animals. However, it is unknown which EHEC O157:H7 factors are required for nematode death. In this study, bacterial ability to kill C. elegans was tested for several EHEC O157:H7 wild-type and mutant strains missing one virulence-associated factor, including Shiga toxins, enterohemolysin, pO157 (a large virulence plasmid in EHEC O157:H7), Type 3 secretion system, LuxS, and lipopolysaccharide (LPS) O-side chains. Our results demonstrate that only mutants lacking either pO157 or LPS O-side chains cause full attenuation in killing C. elegans. The LPS O-side chain-defective ΔperA mutant strain was not able to colonize in the intestine even at 24h post-feeding with C. elegans, while the wild-type strain began to accumulate and colonize in the intestine as early as 3h post-feeding. A simple complementation of the mutant strain with the plasmid carrying the intact perA gene in trans completely restored the production of LPS O-side chains, as well as the ability to kill C. elegans. Our results show that pO157 and PerA are required for EHEC O157:H7 to kill C. elegans.

Infections in Children Treated With Biological Agents

Infections in Children Treated With Biological Agents

Application of proteomics and metabolomics for investigation of food toxins

Fungi, bacteria and other organisms secrete into the extracellular environment numerous compounds that are required for their survival. The secreted proteins and the components of the translocation systems themselves can be scrutinized in-depth by the proteomic and other “omic” tools. Many of these secretion systems are involved in pathogenic processes and indicate mechanisms of pathogenesis and could as well be of great interest for the applications in food technology and biotechnology. Further improvements in existing and developing “omic” strategies and techniques will enable studies of fungal, plant and microorganism secretomes in order to build comprehensive and confident data sets of secreted proteins and other metabolites. Network of these components will lead to the increased understanding of interactions between the host and pathogen. The identification of proteins and small molecules that are produced by a still unknown pathogen will be the first step on the way of detection and further prevention of foodborne diseases.This perspective brings the opportunity to develop new targets in order to ensure food safety that is important for human health as well as for the agriculture, food processing and storage. Ensuring food safety in the future will require new methods for identification, monitoring and assessing of foodborne hazards during production, storage, delivery and consume.In present review the use of proteomics, peptidomics and metabolomics for determination of metabolic pathways and biomarkers of pathogenicity and resistance of biotoxins in the animal and plant food contamination is discussed.

Sero-Epidemiology as a Tool to Screen Populations for Exposure to Mycobacterium ulcerans

BackgroundPrevious analyses of sera from a limited number of Ghanaian Buruli ulcer (BU) patients, their household contacts, individuals living in BU non-endemic regions as well as European controls have indicated that antibody responses to the M. ulcerans 18 kDa small heat shock protein (shsp) reflect exposure to this pathogen. Here, we have investigated to what extent inhabitants of regions in Ghana regarded as non-endemic for BU develop anti-18 kDa shsp antibody titers.Methodology/Principal FindingsFor this purpose we determined anti-18 kDa shsp IgG titers in sera collected from healthy inhabitants of the BU endemic Densu River Valley and the Volta Region, which was so far regarded as BU non-endemic. Significantly more sera from the Densu River Valley contained anti-18 kDa shsp IgG (32% versus 12%, respectively). However, some sera from the Volta Region also showed high titers. When interviewing these sero-responders, it was revealed that the person with the highest titer had a chronic wound, which was clinically diagnosed and laboratory reconfirmed as active BU. After identification of this BU index case, further BU cases were clinically diagnosed by the Volta Region local health authorities and laboratory reconfirmed. Interestingly, there was neither a difference in sero-prevalence nor in IS2404 PCR positivity of environmental samples between BU endemic and non-endemic communities located in the Densu River Valley.ConclusionsThese data indicate that the intensity of exposure to M. ulcerans in endemic and non-endemic communities along the Densu River is comparable and that currently unknown host and/or pathogen factors may determine how frequently exposure is leading to clinical disease. While even high serum titers of anti-18 kDa shsp IgG do not indicate active disease, sero-epidemiological studies can be used to identify new BU endemic areas.

Kawasaki disease: laboratory findings and an immunopathogenesis on the premise of a "protein homeostasis system".

Kawasaki disease (KD) is a self-limited systemic inflammatory illness, and coronary artery lesions (CALs) are a major complication determining the prognosis of the disease. Epidemiologic studies in Asian children suggest that the etiologic agent(s) of KD may be associated with environmental changes. Laboratory findings are useful for the diagnosis of incomplete KD, and they can guide the next-step in treatment of initial intravenous immunoglobulin non-responders. CALs seem to develop in the early stages of the disease before a peak in inflammation. Therefore early treatment, before the peak in inflammation, is mandatory to reduce the risk of CAL progression and severity of CALs. The immunopathogenesis of KD is more likely that of acute rheumatic fever than scarlet fever. A hypothetical pathogenesis of KD is proposed under the premise of a "protein homeostasis system"; where innate and adaptive immune cells control pathogenic proteins that are toxic to host cells at a molecular level. After an infection of unknown KD pathogen(s), the pathogenic proteins produced from an unknown focus, spread and bind to endothelial cells of coronary arteries as main target cells. To control the action of pathogenic proteins and/or substances from the injured cells, immune cells are activated. Initially, non-specific T cells and non-specific antibodies are involved in this reaction, while hyperactivated immune cells produce various cytokines, leading to a cytokine imbalance associated with further endothelial cell injury. After the emergence of specific T cells and specific antibodies against the pathogenic proteins, tissue injury ceases and a repair reaction begins with the immune cells.

Acousto-Optic Tunable Filter Hyperspectral Microscope Imaging Method for Characterizing Spectra from Foodborne Pathogens

A hyperspectral microscope imaging (HMI) method, which provides both spatial and spectral information of bacterial cells, was developed for foodborne pathogen detection. The AOTF-based hyperspectral microscope imaging system can be effective for characterizing spectral properties of biofilms formed by Salmonella enteritidis as well as Escherichia coli. The intensity of spectral images and the pattern of intensity distribution of spectra varied with system parameters (integration time as well as gain) of the HMI system. Preliminary results demonstrated that determination of optimum parameter values of the HMI system and the integration time, which must be no more than 250 ms, are important for quality image acquisition from biofilms formed by S. enteritidis. Among the 89 contiguous spectral images between 450 and 800 nm, the intensity of images at 458, 494, 522, 550, 574, 590, and 670 nm were distinctive for biofilm of S. enteritidis, whereas the intensity of spectral images at 546 nm was distinctive for E. coli with dark-field illumination with a metal halide light source. For more accurate comparison of intensity from spectral images, a calibration protocol of quantitative intensity comparison needs to be developed to standardize image acquisition using neutral-density filters and multiple exposures. For the identification or classification of unknown foodborne pathogen samples, ground truth region-of-interest pixels need to be selected for spectrally pure fingerprints from various foodborne pathogens such as E. coli and Salmonella species.

Assessment of the Microbiota in Microdissected Tissues of Crohn's Disease Patients

The microbiota of the gastrointestinal tract is frequently mentioned as one of the key players in the etiopathogenesis of Crohn's disease (CD). Four hypotheses have been suggested: the single, still unknown bacterial pathogen, an abnormal overall composition of the bowel microbiota (“dysbiosis”), an abnormal immunological reaction to an essentially normally composed microbiota, and increased bacterial translocation. We propose that laser capture microdissection of selected microscopic structures, followed by broad-range 16S rRNA gene sequencing, is an excellent method to assess spatiotemporal alterations in the composition of the bowel microbiota in CD. Using this approach, we demonstrated significant changes of the composition, abundance, and location of the gut microbiome in this disease. Some of these abnormal findings persisted even after macroscopic mucosal healing. Further investigations along these lines may lead to a better understanding of the possible involvement of the bowel bacteria in the development of clinical Crohn's disease.

Initial Experience with Lenalidomide As Consolidation Treatment in Patients with Chronic Lymphocytic Leukemia and Residual Disease After Chemotherapy,

Abstract 3907After treatment with purine analog-based combination chemoimmunotherapy, 40% to 60% of patients with CLL have residual disease. As the extent of the residual disease often correlates with time to progression, eradication of residual disease may improve the duration of remission. Although alemtuzumab has been used as consolidation therapy with improvement of responses in 56% of the patients (pts) (Montillo et al, 2006), its use as been limited by concerns of immunosuppression. Lenalidomide is an oral agent with activity in pts with CLL. Lenalidomide’s easy oral administration and its immunomodulatory properties make it an interesting agent to be evaluated as consolidation therapy. We, therefore, designed a phase II study to evaluate the efficacy and toxicity of lenalidomide for treatment of residual disease after chemotherapy. Pts with stable PR (at two time assessments at least 3 months apart), nodular PR (nPR), or CR with evidence of disease on immunophenotyping were eligible. Pts were required to enroll between 3 and 9 months after completion of combination chemotherapy. Pts received lenalidomide 10mg daily for 12 months (the first 12 pts in this trial received lenalidomide for 3 months, and the study was then amended to allow up to 12 months of therapy). Early discontinuation of treatment was allowed if pts achieved negativity for minimal residual disease (MRD) before 12 months. Responses were evaluated at 4 months and 12 months according to 1996 NCI-WG criteria. Bone marrow biopsy and BM immunophenotyping by multicolor flow cytometry (MFC) with quantification of residual disease were performed at the time of response assessment. The MFC assay used has a sensitivity of 0.02% (20 aberrant cells/100,000 total cells analyzed). Twenty-six pts have been enrolled in this study, and 21 are evaluable for response. Three pts discontinued treatment within the first 28 days (after 2, 7, and 21 days of therapy) and 2 pts are too early for response assessment. The median age is 62 years (range, 41–76), median number of prior treatment was 2 (range, 1–12). Six pts entered the study in CR, 8 pts had nPR and 12 pts were in PR. The outcome of lenalidomide consolidation and duration of therapy are summarized in the table.Pt #Latest chemotherapyResponse at start of lenalidomideDuration of therapyResponse at end of lenalidomide1FCRCR2 daysNot evaluable2OFARCR49 daysProgression3FCRCR21 daysNot evaluable4R-hyperCVADCR12 monthsCR, MRD +5FCRCR5 monthsCR, MRD +6FBRCR10 days +Too early7FCMRnPR3 monthsCR, MRD +8FCRnPR3 monthsnPR9R-CHOPnPR3 monthsCR, MRD −10CFARnPR3 monthsCR, MRD −11R-hyperCVADnPR12 monthsnPR12FCRnPR3 monthsnPR13FCR bevacizumabnPR12 monthsnPR14FCR bevacizumabnPR4 monthsnPR15OFARPR3 monthsCR, MRD −16CFARPR3 monthsPR17PCRPR3 monthsPR18FCRPR3 monthsnPR19FCRPR3 monthsPR20FCRPR6 monthsnPR21FCR bevacizumabPR9 months +CR, MRD +22FCRPR9 months +PR23FCRPR8 months +PR24FCRPR7 daysNot evaluable25FCR bevacizumabPR7 months +PR26FCRPR3 months +Too earlyFor the 6 pts in CR at study initiation: 2 pts had no changes in MRD status, 1 pt had disease progression, 2 pts are not evaluable due to early discontinuation and 1 pt has not had enough time on study. For the 8 pts with an nPR: 3 improved response to CR (2 of them MRD negative) and 5 pts had stable nPR. For the 12 pts with a PR: 2 pts improved to a CR (1 of them MRD negative), 2 pts to a nPR, 5 pts remained in PR, 1 pt is not evaluable due to early discontinuation and 1 pt has not had enough time on study. At a median follow up of 23 months, the median time to progression has not been reached in the 7 pts that improved their response as a result of th, and 5 pts remain in remission between 18 and 35 months after therapy. The most common lenalidomide-related adverse event was myelosuppression: grade 3–4 neutropenia (8 pts, 31%) and grade 3–4 thrombocytopenia (2 pts, 8%). Infections occurred in 5 patients: 3 pneumonia (1 RSV, 1 Pseudomonas and 1 unknown pathogen), 1 vaginal Herpes, 1 sinusitis. One patient experienced a grade 4 PE. Other common grade 1–2 toxicities considered lenalidomide-related were fatigue (8 pts, 31%), rash (8 pts, 31%), constipation (4 pts, 15%), diarrhea (4 pts, 15%), cough (3 pts, 8%) and body aches (3 pts, 8%). Based on our early experience, lenalidomide consolidation after chemotherapy can further improve responses in 27% of patients with CLL. Elimination of MRD was seen in 12% of patients treated. Enrollment to this study is ongoing. Disclosures:Keating:Celgene: Consultancy. O'Brien:Celgene: Consultancy. Ferrajoli:Celgene: Research Funding.

A Comprehensive Evaluation of Colonic Mucosal Isolates of Sutterella wadsworthensis from Inflammatory Bowel Disease

Inflammatory bowel disease (IBD) arises in genetically susceptible individuals as a result of an unidentified environmental trigger, possibly a hitherto unknown bacterial pathogen. Twenty-six clinical isolates of Sutterella wadsworthensis were obtained from 134 adults and 61 pediatric patients undergoing colonoscopy, of whom 69 and 29 respectively had IBD. S. wadsworthensis was initially more frequently isolated from IBD subjects, hence this comprehensive study was undertaken to elucidate its role in IBD. Utilizing these samples, a newly designed PCR was developed, to study the prevalence of this bacterium in adult patients with ulcerative colitis (UC). Sutterella wadsworthensis was detected in 83.8% of adult patients with UC as opposed to 86.1% of control subjects (p = 0.64). Selected strains from IBD cases and controls were studied to elicit morphological, proteomic, genotypic and pathogenic differences. This study reports Scanning Electron Microscopy (SEM) appearances and characteristic MALDI-TOF MS protein profiles of S. wadsworthensis for the very first time. SEM showed that the bacterium is pleomorphic, existing in predominantly two morphological forms, long rods and coccobacilli. No differences were noted in the MALDI-TOF mass spectrometry proteomic analysis. There was no distinct clustering of strains identified from cases and controls on sequence analysis. Cytokine response after monocyte challenge with strains from patients with IBD and controls did not yield any significant differences. Our studies indicate that S. wadsworthensis is unlikely to play a role in the pathogenesis of IBD. Strains from cases of IBD could not be distinguished from those identified from controls.

Pathogen inactivation

Pathogen inactivation

Cutaneous Squamous Cell Carcinoma: A Smoking Gun but Still No Suspects

A viral etiology for cutaneous squamous cell carcinoma (cuSCC) has long been suspected, primarily on the basis of its dramatically increased incidence in immunocompromised individuals. In this issue, Arron and colleagues report a comprehensive hunt for viral gene transcription in cuSCC. Their findings show that it is very unlikely that any currently known virus is commonly responsible for the maintenance of this cancer.

A Sensitive Assay for Virus Discovery in Respiratory Clinical Samples

In 5–40% of respiratory infections in children, the diagnostics remain negative, suggesting that the patients might be infected with a yet unknown pathogen. Virus discovery cDNA-AFLP (VIDISCA) is a virus discovery method based on recognition of restriction enzyme cleavage sites, ligation of adaptors and subsequent amplification by PCR. However, direct discovery of unknown pathogens in nasopharyngeal swabs is difficult due to the high concentration of ribosomal RNA (rRNA) that acts as competitor. In the current study we optimized VIDISCA by adjusting the reverse transcription enzymes and decreasing rRNA amplification in the reverse transcription, using hexamer oligonucleotides that do not anneal to rRNA. Residual cDNA synthesis on rRNA templates was further reduced with oligonucleotides that anneal to rRNA but can not be extended due to 3′-dideoxy-C6-modification. With these modifications >90% reduction of rRNA amplification was established. Further improvement of the VIDISCA sensitivity was obtained by high throughput sequencing (VIDISCA-454). Eighteen nasopharyngeal swabs were analysed, all containing known respiratory viruses. We could identify the proper virus in the majority of samples tested (11/18). The median load in the VIDISCA-454 positive samples was 7.2 E5 viral genome copies/ml (ranging from 1.4 E3–7.7 E6). Our results show that optimization of VIDISCA and subsequent high-throughput-sequencing enhances sensitivity drastically and provides the opportunity to perform virus discovery directly in patient material.

Molecular genetic analysis of off-type plants identified from normal F1 hybrid cultivars of sweet pepper (Capsicum annuum L.)

SummaryOff-type plants occasionally appear when growing F1 hybrid cultivars of sweet pepper (Capsicum annuum L.). In this study, possible genetic factors responsible for the appearance of off-types were evaluated using two off-type sweet peppers selected out of 120 F1 hybrids. The general morphology of off-type plants showed a stunted stature, narrow leaf shape, and small round-shaped fruits. We hypothesised that these off-type plants might have arisen by inadvertent self-pollination of maternal parental lines, since most sweet pepper F1 hybrids are known to be produced by hand-emasculation. Indeed, none of the sweet pepper cultivars analysed in this study contained male-sterile cytoplasm, confirming that cytoplasmic male-sterility was not used during F1 hybrid seed production. If the off-type plants were derived from self-pollination of maternal lines, the genetic make-up of the off-type plants should be different from that of normal F1 hybrids. However, the RAPD and SSR marker amplification profiles of off-type and normal F1 hybrids showed no polymorphism, whereas one RAPD and five polymorphic SSR markers were identified among five other F1 sweet pepper cultivars, indicating that the genetic make-up of the off-type and normal F1 hybrids were almost identical. Furthermore, two SSR markers that showed heterozygosity in both off-type and normal F1 hybrids, segregated in the self-pollinated progenies of both off-type and normal F1 hybrids, indicating that the off-type plants were not maternal inbred lines. Taken together, these results suggest that the off-type F1 sweet pepper plants could have arisen due to other environmental factors or by infection with an unknown pathogen.

Stem Rust Spores Elicit Rapid RPG1 Phosphorylation

Stem rust threatens cereal production worldwide. Understanding the mechanism by which durable resistance genes, such as Rpg1, function is critical. We show that the RPG1 protein is phosphorylated within 5 min by exposure to spores from avirulent but not virulent races of stem rust. Transgenic mutants encoding an RPG1 protein with an in vitro inactive kinase domain fail to phosphorylate RPG1 in vivo and are susceptible to stem rust, demonstrating that phosphorylation is a prerequisite for disease resistance. Protein kinase inhibitors prevent RPG1 phosphorylation and result in susceptibility to stem rust, providing further evidence for the importance of phosphorylation in disease resistance. We conclude that phosphorylation of the RPG1 protein by the kinase activity of the pK2 domain induced by the interaction with an unknown pathogen spore product is required for resistance to the avirulent stem rust races. The pseudokinase pK1 domain is required for disease resistance but not phosphorylation. The very rapid phosphorylation of RPG1 suggests that an effector is already present in or on the stem rust urediniospores when they are placed on the leaf surface. However, spores must be alive, as determined by their ability to germinate, in order to elicit RPG1 phosphorylation.

The cost‐effectiveness of pathogen reduction technology as assessed using a multiple risk reduction model

Pathogen reduction technology (PRT) for labile blood components has the potential to reduce the risk of many adverse events associated with transfusion. Because of the potential broad-spectrum risk reduction capability of PRT, the health economics of PRT could be an important consideration in decision making for this technology. Decision analytic models comparing current blood safety screens and interventions to riboflavin-based whole blood PRT (currently in development) and separately to platelets (PLTs)-and-plasma PRT from the health care system perspective in Canada were used to assess the cost-utility of PRT in reducing the following adverse events: human immunodeficiency virus, hepatitis B virus, hepatitis C virus, human T-lymphotropic virus, syphilis, West Nile virus, bacteria, Chikungunya virus, cytomegalovirus, Trypanosoma cruzi, graft-versus-host disease, febrile nonhemolytic transfusion reactions, and transfusion-related immunomodulation. PRT was modeled as an addition to rather than a replacement for current interventions. The potential of PRT to reduce the risk of an unknown pathogen was not assessed. Whole blood PRT was estimated to have a cost-effectiveness of $1,276,000/quality-adjusted life-year (QALY; 95% confidence interval [CI] approximation, 600,000-3,313,000) compared to current screens and interventions. PLTs-and-plasma PRT was estimated to have a cost-effectiveness of $1,423,000/QALY (95% CI approximation, 834,000-2,818,000) on an all-transfusions basis. Because of the complexity of transfusion risks and practices, the cost-effectiveness of whole blood or PLTs-and-plasma PRT can be modeled provided that assumptions and simplifications are made. Uncertainty remains with respect to the risk reduction that can be achieved for some adverse events. Nevertheless, the results of this cost-effectiveness analysis can be used to inform policy decisions regarding PRT technology in the context of other initiatives designed to improve transfusion safety.

W1899 Dietary Lectins, Altered C. Elegans' Behavior, in the Environmental “Unknown Pathogen” in Parkinson's Disease

W1899 Dietary Lectins, Altered C. Elegans' Behavior, in the Environmental “Unknown Pathogen” in Parkinson's Disease

The H1N1 Outbreak in Mexico

On April 23rd 2009, health authorities in Mexico informed that a new virus was causing an increasing number of severe pneumonia cases in adults with unusually high mortality. After three weeks of intensive clinical and epidemiological research, a new influenza virus was identified as the unknown pathogen in most of the clinical samples sent by Mexico to labs in Winnipeg and Atlanta. The WHO was notified on the night of the 22nd, as soon as the information on etiology was available. At the same time, strict distancing measures were initiated in Mexico City and its suburbs; schools were closed and noncritical activities suspended. The problem was first evident at the Emergency Room of the National Institute of Respiratory Diseases, and confirmed by simultaneous reports received from San Luis Potosi and Oaxaca. We focused our analysis on cases with severe viral pneumonia and thus overestimated the mortality of the virus during the first weeks of the outbreak – the full picture was apparent only afterwards. The initial response was timely as oseltamivir, educational materials, and protective medical equipment were ready to be sent thanks to Mexico's national preparedness plan for a pandemic. 1340 cases fulfilled the case definition during the first month. Mexico's strict social distancing measures had a significant impact on the number of cases but were later relaxed. The epidemic curve shows a sharp increase, followed by a decrease in the number of cases, with growth during June and July due to a high number of cases in the southeast region. More recently, another wave of increased transmission was present in the metropolitan area. A significant feature of this outbreak has been the increased mortality in patients between 15 and 55 years old, some previously healthy, with no increase in the young and the old population. Pregnancy and obesity have also been identified as risk factors for severity. Previous immunity probably plays a role in the severity related to age. Many lessons should be learned from this epidemic: Collaboration, preparedness, transparency, and the importance of being alert towards the unexpected. Abstracts for SupplementInternational Journal of Infectious DiseasesVol. 14Preview Full-Text PDF Open Archive

Necrotising external otitis caused by Aspergillus wentii: a case report

Necrotising external otitis (NEO) is a destructive, potentially fatal, infection usually seen in elderly diabetics or the immunocompromised. The commonest causative organism is Pseudomonas but immunocompromised patients are additionally susceptible to opportunistic infections. Here we describe the first reported case of NEO caused by a previously unknown human pathogen--Aspergillus wentii. A review of the literature reveals that fungal NEO is associated with a high rate of cranial nerve palsies suggesting that infections are not being treated rapidly enough to prevent morbidity. Fungal infection should be considered early in immunocompromised patients and microbiological diagnosis should be obtained wherever possible.