Nosocomial infections are acquired during hospital treatment or in a hospital environment. One such infecting agent, Escherichia coli, harbours many virulence genes that enable it to become pathogenic, causing damage to the host. The mechanism of the E. coli virulence factors provenance to cause infection in host environments is not clearly elucidated. We investigated the virulence and pathogenicity of E. coli affected by the host environment. For this, blood (n = 78) and faecal (n = 83) E. coli isolates were collected from patients with and without sepsis, respectively, who had been admitted to the intensive care unit. The E. coli genomic DNA was isolated; the phylogenetic grouping was conducted by triplex PCR. The occurrence of nine virulence genes among the all the isolates was confirmed by gene-specific PCR. The prevalence of E. coli in blood isolates was more in phylogenetic groups B2 and D compared to groups A and B1. However, in faecal isolates, there was no significant difference. The prevalence of adhesin and toxin (papG, sfa, afa, cnf1, hlyA) genes was higher in blood compared to faecal E. coli isolates. However, the prevalence of aer, traT and PAI was similar as well as higher among both of these groups. These observations indicate a role of external environment (hospital setting) on host susceptibility (development of infection) in the faecal E. coli isolates, thereby making the patient prone to a sepsis condition.
The prevalence of the tcpC in the blood Escherichia coli isolates collected from the sepsis patients admitted to the intensive care unit was investigated for the first time. The blood and faecal samples were collected from sepsis and nonsepsis patients, respectively. The prevalence of the tcpC and phylogroups was confirmed by gene-specific PCR. The occurrence of the tcpC in the blood E. coli isolates from sepsis patients was significantly higher than the faecal isolates. The higher prevalence of blood E. coli isolates among the pathogenic groups (B2, D) compared to the commensal groups (A, B1) suggests tcpC as a prospective new virulence marker for sepsis.
Study Design: Retrospective analysis. Objective: Lumbar disc herniation is one the most common condition responsible for low back and radicular pain. Although the symptoms are not proportional to the size of disc prolapse but massive disc herniation frequently needs surgical management. According to literature, the incidence of low back pain, recurrent disc herniation and segmental instability are more in discectomy whereas incidence of adjacent segment degeneration (ASD) is more after fusion surgery. There are very few studies that directly compare long-term functional outcome of both these procedures. We compared the functional outcome of both the procedures in this study. Methods: All patients of massive disc prolapse, operated at our center between 2011 to 2017, were contacted. All the patients underwent either discectomy or transforaminal lumbar interbody fusion (TLIF). Functional outcomes of all the patients were collected using visual analogue scale (VAS) (back), VAS (leg), modified Oswestry Disability Index (mODI), Sciatica Bothersomeness Index (SBI), and McNab’s criterion. Various complications were also analyzed. Results: There were 144 patients in the discectomy group and 123 patients in the TLIF group. Mean duration of follow-up was 55.07 months and 51.86 months, respectively. Both the groups show no significant difference in VAS. Significant difference was seen in mODI and SBI favoring discectomy. McNab’s criterion showed excellent result in 80% of patients of discectomy compared with 68% patients of TLIF. Overall complication rate in discectomy group was 11% whereas 13% in TLIF group. Conclusion: Both show good functional outcome but better in discectomy. Recurrent herniation and instability were noticed more with discectomy and ASD was more common after fusion surgeries. The choice of procedure should be individualized, and it also depends on surgical expertise, but in developing countries where resources are constrained, discectomy should be preferred.
A 62-year-old man with asthma sought care for intermittent fever, cough with expectoration, breathlessness and orthopnoea with grunting. Computed tomography revealed clusters of centrilobular nodules on both sides with a tree-in-bud appearance and mild diffuse bronchial wall thickening. Sputum sample grew pure colonies of Actinobacillus ureae which was confirmed by MALDI-TOF and 16SrRNA gene sequencing. A. ureae may be an additional bacteriologic causative agent of the tree-in-bud pattern on computed tomographic scan.
Escherichia vulneris is an opportunistic human pathogen. It has been primarily reported in adult patients and invasive infections have been observed in immune-suppressed individuals. This is the first report of E. vulneris causing complicated diarrhoea and sepsis in an infant.Two month old sick infant, born full-term, was admitted to the paediatrics department with loose motions and refusal to feed for four days. E. vulneris was isolated from blood in pure culture. The isolate was characterized for diarrhoeal virulence markers: heat labile and heat stable toxins (LT, ST) and hemolysin (hlyA) by PCR. The presence of LT enterotoxin and hemolysin provides strong evidence of the diarrhoeagenic potential of E. vulneris, further leading to the invasive infection triggering sepsis.As E. vulneris can lead to serious complications, an attempt should be made in clinical laboratories to identify and further characterize this new Escherichia species.
BackgroundHospital acquired infections (HAI) are principal threats to the patients of intensive care units. An increase in the antimicrobial resistance (AMR) observed in gram negative bacteria is a great challenge to deal with. HAI and AMR lead to prolonged hospitalization and additional doses of anti-microbial treatment affecting patient’s fitness and finances. Present study was undertaken to determine the pathotypes, genetic diversity and the antimicrobial resistance of E.coli in isolates from the patients admitted to intensive care unit at a tertiary care hospital in Delhi, India.MethodsE.coli isolates (N = 77) obtained from the blood culture of patients diagnosed with sepsis and the isolates (N = 71) from the stool culture of patients admitted in intensive care unit (ICU) but not diagnosed with sepsis were investigated for their pathotypes, adherence patterns and genetic diversity by Enterobacterial Repeated Intergenic Consensus-polymerase chain reaction (ERIC-PCR). A Kirby-Bauer Disc diffusion test and antimicrobial susceptibility assays were performed according to the Clinical and Laboratory Standards Institute (CLSI) guidelines. Extended-spectrum β-lactamase (ESBL) genes and sequence type 131 (ST131) clone were characterised genotypically by gene-specific PCRs.ResultsPathotypes analysis revealed 46 and 16% of the blood E.coli isolates were ETEC and EAEC respectively, in contrast to the fecal isolates wherein 22% of the isolates were ETEC and 28.5% were EAEC. EPEC, STEC and EIEC pathotypes were not detected in blood or fecal isolates. Of all the isolates studied, more than 90% of the blood and 70% of the fecal isolates were found to be resistant to cephalosporins. On the other hand, 68% of blood and 44% of the fecal isolates were found to be ESBL producers. Interestingly 83% of the blood isolates contained CTX-M15, whereas only 21% of them contained CTX-M9 genes. On the other hand CTX-M15 genes were found in 90% and CTX-M9 genes were found in 63% of the fecal isolates.ConclusionThe antimicrobial resistant profile found in this study is alarming and poses a great threat to public health. Apparently an increased antimicrobial resistance to the extensively used cephalosporins is affecting an optimal drug therapy for patients. In addition, the presence of catheters, prolonged duration of stay in the hospital and poor hygienic conditions due to infrequent urination of the patient can lead to an additional vulnerability. Therefore continuous surveillance and rational use of antibiotics along with effective hygienic measures are urgently recommended in such settings.Electronic supplementary materialThe online version of this article (10.1186/s13756-018-0444-8) contains supplementary material, which is available to authorized users.
Neurodegenerative diseases are a heterogeneous group of disorders among aging populations worldwide characterized by the progressive degeneration of the structure and function of brain cells and the nervous system. Alzheimer's disease and Parkinson's disease are common neurodegenerative diseases (NDs). Classic pathological features of AD are the accumulation of the amyloid betaprotein and aggregates of hyperphosphorylated tau protein around the brain cells. Dopaminergic neuronal death in the midbrain and accumulation of β- synuclein in the neurons are the hallmark of Parkinson’s disease. The pathogenesis is multifactorial, and both neurodegenerative disorders have complex etiology. Oxidative stress closely linked with mitochondrial dysfunction, excitotoxicity, nitric oxide toxicity, and neuro-inflammation, is anticipated to trigger neuronal death. Ample evidence has implicated that oxidative stress and inflammation contribute to the pathology of neurodegeneration in AD and PD. Currently, acetylcholinesterase inhibitors are the main treatment option for AD, while LDOPA is the gold standard therapy for PD. Along with the main therapy, many endogenous antioxidants, like vitamin E, selenium, etc., are also given to the patients to combat oxidative stress. Current treatment for these NDs is limited due to the blood–brain barrier (BBB) that hinders drug targeting towards neurons. In this review, we emphasize adjunct treatment with anti-inflammatory agents that act at the site of the disease and can halt the disease progression by attenuating the effect of ROS triggering neuro-inflammatory response. Polyphenols, either as purified compounds or extracts from various natural plant sources, have been well studied and documented for anti-inflammatory effects, but their use for ND is limited due to their physicochemical attributes. Nanoparticle-mediated drug delivery system exhibits immense potential to overcome these hurdles in drug delivery to the CNS, enabling nanoparticle-based therapies to directly target the inflammation and release bioactive compounds with anti-inflammatory properties to the site of action.
Introduction Even though the increasing incidence of VIM-producing E. coli and K. pneumoniae has been reported worldwide, studies are still lacking in Palestine. The aim of this study was to screen carbapenem-resistant E. coli and K. pneumoniae bacteria in the Gaza Strip, Palestine and further to characterize carbapenemase-producing isolates.Methods A total of 69 E. coli and 27 K. pneumoniae isolates were obtained from three Gaza hospitals and recovered from urine, wound swabs, blood and ear discharge. The screening for metallo-βlactamases (MBLs) was performed by using the imipenem-EDTA disc synergy test. The detection of βlactamases genes, detection of non-β-lactam genes and the characterization of integrons were performed by PCR and sequencing. The clonal relationship among the isolates was determined by pulsed-field gel electrophoresis (PFGE).Results Our study showed that 4 E. coli (5.8%) and 5 K. pneumoniae (18.5%) were positive by the imipenem-EDTA disc synergy test. Bla VIM-4 was detected in six isolates and bla VIM-28 was identified in three isolates. The β-lactamases genes in the VIM-producing K. pneumoniae isolates were bla CTX-M-15 (n=3), bla CTX-M-14 (n=1), bla SHV-1 (n=3), bla SHV-12 (n=1), bla TEM-1 (n=1) and bla OXA-1 (n=1). Aac(6′)-Ib-cr gene was confirmed in four E. coli and in two K. pneumoniae isolates. QnrS1 was identified in two K. pneumoniae isolates. The class 1 integron was identified with the different gene cassette; dfrA17-aadA5, dfrA5, dfrA12-orf-aadA2 and dfrA17-aadA5 were identified. ConclusionsOur study indicated for the first time the emergence of multidrug-resistant VIMcontaining K. pneumoniae and E. coli isolates of clinical origin in Gaza Strip hospitals.
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