Single Bacterial Infection Research Articles

Culture and Antibiotic Sensitivity of Escherichia coli Isolated from Patients with Urinary Tract Infections (UTI) in Jessore City

Urinary tract infection is caused by the presence and growth of microorganisms in the urinary tract, is perhaps the single commonest bacterial infection of mankind. The present study was carried out to identify Escherichia coli from urinary tract infected patients those come to a community hospital in Jessore city. For the confirmation of the presence of this disease causing agent various cultural and biochemical techniques were performed. A total of 87 clinically suspected patients having urinary tract infection were studied, 50 were found to be culture positive. Among the positive cultures, 30 (60%) isolates were infected with Escherichia coli. The study showed that the most susceptible group for urinary tract infection ranges between 16-45 years of age, as this group comprised of 15(50%) individuals. Antibiotic susceptibility for all 30 isolates was determined against locally available eleven drugs. High resistance rates were observed against most of the antibiotics examined here. Amoxycilin stood to be the most resistant type of antibiotic (90%), followed by nalidixic acid (57%), cephlexin (50%), ciprofloxacin (37%), ceftriaxone (27%), doxycycline (24%) and cefixime (20%). Gentamycin and nitrofurantoin got lower resistance rates at 14% and 3% respectively, but resistance to netilmycine was not found among all 30 isolates. Multidrug resistance pattern of the isolated organism was also observed in this present study.

Immuno-epidemiology of chronic bacterial and helminth co-infections: Observations from the field and evidence from the laboratory

Co-infections can alter the host immune responses and modify the intensity and dynamics of concurrent parasitic species. The extent of this effect depends on the properties of the system and the mechanisms of host–parasite and parasite–parasite interactions. We examined the immuno-epidemiology of a chronic co-infection to reveal the immune mediated relationships between two parasites colonising independent organs, and the within-host molecular processes influencing the dynamics of infection at the host population level. The respiratory bacterium, Bordetella bronchiseptica, and the gastrointestinal helminth, Graphidium strigosum, were studied in the European rabbit (Oryctolagus cuniculus), using long-term field data and a laboratory experiment. We found that 65% of the rabbit population was co-infected with the two parasites; prevalence and intensity of co-infection increased with rabbit age and exhibited a strong seasonal pattern with the lowest values recorded during host breeding (from April to July) and the highest in the winter months. Laboratory infections showed no significant immune-mediated effects of the helminth on bacterial intensity in the lower respiratory tract but a higher abundance was observed in the nasal cavity during the chronic phase of the infection, compared with single bacterial infections. In contrast, B. bronchiseptica enhanced helminth intensity and this was consistent throughout the 4-month trial. These patterns were associated with changes in the immune profiles between singly and co-infected individuals for both parasites. This study confirmed the general observation that co-infections alter the host immune responses but also highlighted the often ignored role of bacterial infection in helminth dynamics. Additionally, we showed that G. strigosum had contrasting effects on B. bronchiseptica colonising different parts of the respiratory tract. At the host population level our findings suggest that B. bronchiseptica facilitates G. strigosum infection, and re-infection with G. strigosum assists in maintaining bacterial infection in the upper respiratory tract and thus long-term persistence.

Synergistic and feedback signaling mechanisms in the regulation of inflammation in respiratory infections

Pneumonia, the most typical and frequent lower respiratory tract infection (LRTI), is a leading cause of health problems in the United States. Bacteria represent the most prevailing cause of pneumonia in both children and adults. Although pneumonia with a single bacterial infection is common, a significant portion of patients with pneumonia is polymicrobial. This infection is often complexed with other physiological factors such as cytokines and growth factors. Nontypeable Haemophilus influenzae (NTHi) is the most frequently recovered Gram-negative bacterial pathogen in the respiratory system and induces strong inflammatory responses. NTHi also synergizes with other respiratory pathogens, such as Streptococcus pneumoniae and respiratory viruses and pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α). It is noteworthy that NTHi not only synergizes with growth factors such as transforming growth factor-beta (TGF-β), but also utilizes growth factor receptors such as TGF-β receptor and epidermal growth factor receptor (EGFR), to enhance inflammatory responses. Although appropriate inflammation is a protective response against invading pathogens, an uncontrolled inflammatory response is often detrimental to the host. Thus, inflammation must be tightly regulated. The human immune system has evolved strategies for controlling overactive inflammatory response. One such important mechanism is via regulation of negative feedback regulators for inflammation. CYLD, a multifunctional deubiquitinase, was originally reported as a tumor suppressor, but was recently identified as a negative regulator for nuclear factor-kappa B (NF-κB) signaling. It is induced by NTHi and TNF-α via a NF-κB-dependent mechanism, thereby serving as an inducible negative feedback regulator for tightly controlling inflammation in NTHi infection.

The multiplicity of divergence mechanisms in a single evolving population

BackgroundEvolutionary divergence is common within bacterial species and populations, even during a single bacterial infection. We use large-scale genomic and phenotypic analysis to identify the extent of diversification in controlled experimental populations and apply these data to differentiate between several potential mechanisms of evolutionary divergence.ResultsWe defined testable differences between five proposed mechanisms and used experimental evolution studies to follow eight glucose-limited Escherichia coli chemostat populations at two growth rates. Simple phenotypic tests identified 11 phenotype combinations evolving under glucose limitation. Each evolved population exhibited 3 to 5 different combinations of the 11 phenotypic clusters. Genome sequencing of a representative of each phenotypic cluster from each population identified 193 mutations in 48 isolates. Only two of the 48 strains had evolved identically. Convergent paths to the same phenotype occurred, but two pleiotropic mutations were unique to slow-growing bacteria, permitting them greater phenotypic variance. Indeed, greater diversity arose in slower-growing, more stressed cultures. Mutation accumulation, hypermutator presence and fitness mechanisms varied between and within populations, with the evolved fitness considerably more uniform with fast growth cultures. Negative frequency-dependent fitness was shown by a subset of isolates.ConclusionsEvolutionary diversity is unlikely to be explained by any one of the available mechanisms. For a large population as used in this study, our results suggest that multiple mechanisms contribute to the mix of phenotypes and evolved fitness types in a diversifying population. Another major conclusion is that the capacity of a population to diversify is a function of growth rate.

Defining the True Sensitivity of Culture for the Diagnosis of Melioidosis Using Bayesian Latent Class Models

BackgroundCulture remains the diagnostic gold standard for many bacterial infections, and the method against which other tests are often evaluated. Specificity of culture is 100% if the pathogenic organism is not found in healthy subjects, but the sensitivity of culture is more difficult to determine and may be low. Here, we apply Bayesian latent class models (LCMs) to data from patients with a single Gram-negative bacterial infection and define the true sensitivity of culture together with the impact of misclassification by culture on the reported accuracy of alternative diagnostic tests.Methods/Principal FindingsData from published studies describing the application of five diagnostic tests (culture and four serological tests) to a patient cohort with suspected melioidosis were re-analysed using several Bayesian LCMs. Sensitivities, specificities, and positive and negative predictive values (PPVs and NPVs) were calculated. Of 320 patients with suspected melioidosis, 119 (37%) had culture confirmed melioidosis. Using the final model (Bayesian LCM with conditional dependence between serological tests), the sensitivity of culture was estimated to be 60.2%. Prediction accuracy of the final model was assessed using a classification tool to grade patients according to the likelihood of melioidosis, which indicated that an estimated disease prevalence of 61.6% was credible. Estimates of sensitivities, specificities, PPVs and NPVs of four serological tests were significantly different from previously published values in which culture was used as the gold standard.Conclusions/SignificanceCulture has low sensitivity and low NPV for the diagnosis of melioidosis and is an imperfect gold standard against which to evaluate alternative tests. Models should be used to support the evaluation of diagnostic tests with an imperfect gold standard. It is likely that the poor sensitivity/specificity of culture is not specific for melioidosis, but rather a generic problem for many bacterial and fungal infections.

Bacterial Models for Tumor Development

The tumor-inducing effects of Agrobacterium, Bartonella and Helicobacter bacterial species are compared step by step. An analogy for the existence of these individual steps is considered in connection with the development of cancer. The transformations of eukaryotic cells occur in particular in the type IV secretion system, i.e. involving the simultaneous transmission of DNA and protein from bacterial cells to eukaryotic cells. Thus, transfected cells facilitate the indefinite growth of tissue cells and additionally produce growth factors, triggering further bacterial multiplication. The higher numbers of bacteria then produce more transfection and the cycle repeats as long as the host lives. The main limiting factor is the frequency of bacterial infection, while the secondary rate-limiting factors are the levels of transforming growth factors and factors triggering bacteria growth. Analogous processes are probably responsible for the tumor induction by the three different bacterial species; however, the critical points for eradication are different. The early eradication or limitation of B. henselae or H. pylori can prevent hemangiomas, stomach cancer and malignant cell proliferation. The crown gall formation by A. tumefaciens can only be avoided by prevention of the transforming activity of a single bacterial infection. Questions arise as to what is common in the three processes, and the nature of the rate-limiting step in the three different models. The frequency of transformation is the rate-limiting step, but the co-transmission of the DNA-protein complex is common in the three systems.

Complex lipid determines tissue-specific replication of Mycobacterium tuberculosis in mice.

Tuberculosis is the leading cause of death in the world resulting from a single bacterial infection. Despite its enormous burden on world health, little is known about the molecular mechanisms of pathogenesis of Mycobacterium tuberculosis. Bacterial multiplication and concomitant tissue damage within an infected host, including experimentally infected mice, occurs primarily in the lungs-the favoured niche of M. tuberculosis. Although it has been proposed that the distinctive cell wall of M. tuberculosis is important for virulence, rigorous genetic proof has been lacking. Here, using signature-tagged mutagenesis, we isolated three attenuated M. tuberculosis mutants that cannot synthesize or transport a complex, cell wall-associated lipid called phthiocerol dimycocerosate (PDIM) which is found only in pathogenic mycobacteria. Two mutants have transposon insertions affecting genes implicated in PDIM synthesis; the third has a disruption in a gene encoding a large transmembrane protein required for proper subcellular localization of PDIM. Synthesis and transport of this complex lipid is only required for growth in the lung; all three mutants are unaffected for growth in the liver and spleen. This clearly shows that a lipid is required for M. tuberculosis virulence.

Phylogenetic relationships of the endosymbionts of mealybugs (Homoptera: Pseudococcidae) based on 165 rDNA sequences

A portion of the gene coding for the 16S ribosomal RNA from the endosymbionts of three species of mealybugs [ Pseudococcus longispinus (Targioni-Tozzetti), Pseudococcus maritimus (Ehrhorn), and Dysmicoccus neobrevipes (Beardsley)] was cloned, sequenced, and compared to a homologous fragment from bacteria representative of aphid endosymbionts as well as major subdivisions of the Proteobacteria. Parsimony analysis of the sequences indicated that the mealybug endosymbionts are related and belong to the γ-subdivision; in contrast, previous studies showed that aphid endosymbionts are part of the -1-subdivision. These findings suggest that the endosymbiosis of mealybugs is a consequence of a single bacterial infection and indicate that this ancestor was different from the ancestor involved in aphid endosymbiosis.