A Piscan Ulcerative Aeromonas Infection

In the immunologic sense, clinical infection is a state of failure of the immune system to combat the pathogenic weapon of the bacteria invading the host. A motile gram negative vibroid organism associated with marked mono and poly nuclear cell responses was traced during the examination of a clinical material from an infected common carp Cyprinus carpio. On primary plate culture, growth was shown to be pure, dense population of an Aeromonas-like colony morphotype. The pure isolate was found to be; Aerobic, facultatively anaerobic, non-halophilic, grew at 0C, and 37C, oxidase positive utilizes glucose through fermentative pathway, resist 0/129 and novobiocin, produces alanine and lysine decarboxylases but non-producing ornithine dehydrolases. Tests for the in vitro determinants of pathogenicity has shown to be; Betahaemolytic onto blood agar, gelatinase, casienase and amylase producer. Three in vivo determinants of pathogenicity were tested as, the lethal dose fifty, the pathogenesis and pathogenicity. It was evident that 0.1 milliliter of the causal bacterial cell suspension of a density 1 x 107 CFU/ml injected intramuscularly into an average of 100gms fish toke five days incubation period, then at the day six morbidity and mortality were initiated. LD50 was recorded at the day 12 post-infection. Use of an LD50 doses to study the pathogenicity, reveals mononuclear and polynuclear cell responses, on examining the stained direct films of the clinical materials from the experimentally infected fish. Re-isolation tests confirm that the reisolant is same. The course of the infection in natural case was shown manifestation of; skin ulceration, haemorrhage and descaling. On evisceration, the internal organs were shown; congestion in the intestines, spleen and, air sacs. The induced infection showed a milder form of these manifestations. The grading of the virulence of this organism was virulent causing chronic course of infections as indicated from the pathogenesis and pathogenicity studies. Thus the infectious bacteria were consistent with Aeromonas hydrophila, and the infection was chronic.

Virulent-GO: Prediction of Virulent Proteins in Bacterial Pathogens Utilizing Gene Ontology Terms

Prediction of bacterial virulent protein sequences can give assistance to identification and characterization of novel virulence-associated factors and discover drug/vaccine targets against proteins indispensable to pathogenicity. Gene Ontology (GO) annotation which describes functions of genes and gene products as a controlled vocabulary of terms has been shown effectively for a variety of tasks such as gene expression study, GO annotation prediction, protein subcellular localization, etc. In this study, we propose a sequence-based method Virulent-GO by mining informative GO terms as features for predicting bacterial virulent proteins. Each protein in the datasets used by the existing method VirulentPred is annotated by using BLAST to obtain its homologies with known accession numbers for retrieving GO terms. After investigating various popular classifiers using the same five-fold cross-validation scheme, Virulent-GO using the single kind of GO term features with an accuracy of 82.5% is slightly better than VirulentPred with 81.8% using five kinds of sequence-based features. For the evaluation of independent test, Virulent-GO also yields better results (82.0%) than VirulentPred (80.7%). When evaluating single kind of feature with SVM, the GO term feature performs much well, compared with each of the five kinds of features.

The Contribution of Growth Rate to the Pathogenicity of Candida spp.

Fungal infections are becoming more common and the range of susceptible individuals has expanded. While Candida albicans remains the most common infective species, other Candida spp. are becoming increasingly significant. In a range of large-scale studies of candidaemia between 1999 and 2006, about 52% of 9717 cases involved C. albicans, about 30% involved either C. glabrata or C. parapsilosis and less than 15% involved C. tropicalis, C. krusei or C. guilliermondii. However, the probability of mortality within 30 days of infection with a particular species was at least 40% for C. tropicalis, C. albicans, C. glabrata and C. krusei and only 22% for C. parapsilopsis. Clinical isolates of Candida spp. grew at rates ranging from 1.65 h-1 to 4.9 h-1. Three species (C. krusei, C. albicans and C. glabrata) had relatively high growth rates (μm > 4 h-1), C. tropicalis and C. dubliniensis grew moderately quickly (Ôëê 3 h-1) and C. parapsilosis and C. guilliermondii grew slowly (< 2 h-1). Based on these data, the log of the odds of mortality within 30 days of diagnosis was linearly related to μm. From this the underlying probability of mortality is 0.13 (95% CI: 0.10-0.17) and it increases by about 0.09 ± 0.02 for each unit increase in μm. Given that the overall crude mortality is about 0.36, the growth of Candida spp. approximately doubles the rate, consistent with the results of larger case-matched studies of candidaemia.