Canadian Journal of Infectious Diseases & Medical Microbiology最新文献

Introduction: Hand, foot, and mouth disease (HFMD) is a mild self-limited childhood infectious disease caused by a variety of enteroviruses (EVs). Aim: To investigate the molecular epidemiology of EVs associated with HFMD and their clinical presentation during the HFMD outbreak that occurred in the Jenin district, Palestine, from May to August 2024. Materials and Methods: Forty-four (44) throat and vesicular swabs were tested for enteroviral infections using two RT-PCR assays targeting both the 5'NTR and the VP1-2A regions of the enteroviral genome for the diagnosis and genotyping. Patients' demographic data and clinical history were used to create an epidemiological curve. EpiInfo free software was used to draw a cluster mapping. MEGA-X was used to construct a maximum likelihood (ML) tree. PopArt 1.7 software was used to construct neighbor-joining network. Results: The mean age of the study sample was 2.08 (0.25-12 years) with 95% (42/44) under five years old. The male/female ratio was 0.9. All cases presented with typical HFMD signs and symptoms with variable sites of signs. Of the 44 samples, 36 yield positive RT-PCR targeting the 5'NTR. Seven randomly selected positive RT-PCR-5'NTR samples were sequenced using Sanger sequencing for genotyping. It was shown that all were CV-A16 sub-genogroup B1c. Phylogenetic analysis of VP1-2A region sequences showed that all Palestinian CV-A16 isolates form a pure haplogroup of CV-A16 sub-genotype B1c. Furthermore, although haplotype network analysis showed high variation between the viral sequences, the haplotype analysis supported the ML phylogenetic tree in having them all in one haplogroup. Conclusion: CV-A16, sub-genotype B1c was the virus responsible for the HFMD outbreak in the Jenin district of Palestine in the summer of 2024. Phylogenetic and haplotype analysis showed that CV-A16 strains cluster closely with each other and very close to an Indian isolate (OR437338.1), indicating the monomorphic nature of this strain with low genetic variation and the probability of virus importation.

Long-read sequencing is a valuable technique for high-precision genome analysis. Despite the widespread use of the Mycobacterium tuberculosis H37Rv genome sequence as a reference for genetic variation analysis, its suitability for comparing clinical strains is limited. Therefore, we constructed the first known whole genome of a clinical M. tuberculosis strain, PSNK363, isolated from the Democratic People's Republic of Korea, using high-quality high-fidelity (HiFi) read sequencing and compared its genetic variations to those of H37Rv. PSNK363 was cultured to obtain genomic DNA, which was subjected to de novo whole-genome assembly using PacBio Sequel II with long-read HiFi sequencing. The sequences were compared to the reference genome H37Rv. HiFi long-read sequencing of M. tuberculosis PSNK363, with an accuracy of 99.99%, revealed a single circular chromosome of 4,422,110 bp, which is 10,578 bp longer than the H37Rv chromosome. The assembly had an average G + C content of 65.6%, 4079 protein-coding sequences, 53 tRNA genes, and 3 rRNA genes. Most genes (72.7%) were assigned as putative functions, whereas the remaining 27.3% were annotated as hypothetical. Comparison with H37Rv revealed a large inversion in the PSNK363 genome, which contains most of the deletion and insertion variants. M. tuberculosis PSNK363 had a longer genome sequence, more protein-coding genes, and a larger inversion region than H37Rv. High-accuracy whole-genome sequencing of PSNK363 holds the potential for enriching virulence databases and identifying informative loci for drug resistance analysis in M. tuberculosis isolates in the Democratic People's Republic of Korea.

Coagulase-negative staphylococci (CoNS) are the major pathogen (hospital as well as environmental) and their emerging multidrug-resistant (MDR) strains complicate the treatment process. In this study, we investigated the prevalence and antibiotic resistance of CoNS on frequently touched surfaces in hospital and urban built environments (UBEs) in Vidarbha, Maharashtra, India. A total of 200 isolates screened for Staphylococcus species and 55 methicillin-resistant staphylococci isolates were identified, and among them, 19 were classified as cefoxitin-resistant CoNS. These 19 cefoxitin-resistant CoNS isolates were tested for the presence of the mecA gene by conventional PCR and only nine (47.36%) were found to be mecA-positive. mecA-positive strains were tested to check MIC for various antibiotics and three marker gene characteristics, namely, ß-lactamase, cefoxitin screen, and inducible clindamycin resistance via the VITEK 2 system. These strains were 100% resistant to benzylpenicillin and oxacillin, and approximately 50% were resistant to vancomycin. Amplified mecA gene fragments were sequenced, and SNP analysis was performed alongside a standard sequence from Staphylococcus aureus (Acc no. NG_047938.1). In total, among the 466 nucleotides, 386 sequences were found to be invariable, and 80 polymorphic variables were identified (46 singleton variable sites and 34 parsimony information sites). The spread of antibiotic resistance is very common in both UBEs and hospital environments; thus, our study concluded that a surveillance program is recommended for the Vidarbha region for the assessment of co-occurring CoNS and better infection control of the environment for future reduction in contact infection.

Background: Very few studies have characterized patients with myocardial injury due to Klebsiella pneumoniae bloodstream infections (KP-BSI). Our study aimed to investigate the clinical characteristics, risk factors and outcomes of patients with myocardial injury due to KP-BSI. Methods: A double-center retrospective cohort study of patients with KP-BSI was conducted from January 1, 2013 to December 31, 2022. The clinical data was collected by reviewing electronic medical records. Classification of patients with KP-BSI into myocardial injury and nonmyocardial injury groups based on the levels of high-sensitivity cardiac troponin I (hs-cTnI) after 48 h onset of KP-BSI. Results: Patients with myocardial injury due to KP-BSI were generally younger than those without such injuries, with the former presenting a median age of 60 versus 67 in the latter (p < 0.001). Conditions like chronic cardiac insufficiency and chronic pulmonary disease were more prevalent in the myocardial injury cohort (10.0% and 7.1%, respectively) compared to those without myocardial injury (4.7% and 2.6%, respectively; p values 0.002 and 0.001). However, the nonmyocardial injury group had a higher incidence of solid tumors (15.3% vs. 10.4%, p=0.038). Severity assessments like the acute physiology and chronic health evaluation (APACHE) II, the sequential organ failure assessment (SOFA), and the Charlson Comorbidity Index (CCI) all registered higher for the myocardial injury group (all p < 0.001). Similarly, intensive care unit (ICU) admissions, use of mechanical ventilation, and central venous catheter (CVC) placement were notably more common in this group (all p < 0.001). Regarding infection sources, the myocardial injury group had a higher incidence of pneumonia as the cause for KP-BSI (29.8% vs. 15.9%, p < 0.001), whereas liver and biliary tract infections were less frequent compared to their counterparts. Mortality rates at 7, 14, and 28 days, along with in-hospital mortality, were significantly higher for those with myocardial injury (all p < 0.001). Multivariate analysis identified age > 67 [adjusted odds ratio (aOR), 2.32; 95% confidence interval (CI), 1.59-3.38], SOFA score > 6 (aOR, 3.04; 95% CI, 2.10-4.39), mechanical ventilation (aOR, 1.67; 95% CI, 1.15-2.39), and CVC in place (aOR, 1.50; 95% CI, 0.96-2.02) as independent prognostic factors for myocardial injury in KP-BSI. Conclusions: Older age (> 67 years), higher SOFA score (> 6), mechanical ventilation, and CVC in place were found to be significantly associated with an increased risk of myocardial injury. Clinical physicians should be alert to the potential for myocardial injury in elderly critically ill patients, especially those who are on mechanical ventilation and have indwelling CVC, in the event of KP-BSI.

Diabetes mellitus (DM) is a persistent and steadily progressing metabolic condition distinguished by unregulated high levels of blood glucose. GLP1 receptor agonists have recently gained recognition as first-line therapies in selected instances, as per the updated ADA guidelines, highlighting their efficacy not only in glycemic control but also in their broader health benefits. Nonetheless, the efficacy of GLP-1 is limited by its brief duration of action, rapid clearance from the body, and challenges associated with subcutaneous administration. In this study, we examined the potential diabetes-mitigating effects of a genetically engineered strain of Escherichia coli Nissle 1917 (EcN)-GLP-1, previously developed by our group. We utilized mouse models for both Type 1 diabetes mellitus (T1DM) and Type 2 diabetes mellitus (T2DM) to assess its efficacy. In the case of T1DM mice, the results revealed that EcN-GLP-1 resulted in a notable decrease in blood glucose levels. Furthermore, it exhibited a protective influence on the structural integrity of islet β-cells; downregulated the expressions of key inflammatory markers such as TLR-4, p-NF-κB/NF-κB, and Bax/Bcl-2; promoted the insulin secretion; and reinstated the perturbed diversity of microbial species to a normal state. Similarly, EcN-GLP-1 had a pronounced impact on T2DM mice, manifesting increased presence of islet β-cells, decreased inflammatory response and apoptosis, and regulation of lipid metabolism in the liver. In summary, the genetically modified EcN-GLP-1 strain demonstrates the ability to alleviate diabetes by enhancing the islet β-cell population, mitigating inflammatory reactions and apoptosis, optimizing liver lipid metabolism, and reinstating a balanced microbial diversity. These findings hold promise as a potential avenue for treating DM.

Purpose: To evaluate the pharmacology, pharmacokinetics, pharmacodynamics, antimicrobial activity, efficacy, safety, and the regulatory status of sulbactam-durlobactam. Summary: Sulbactam-durlobactam is a recently approved antimicrobial combination of two β-lactamase inhibitors for the treatment of hospital-acquired bacterial pneumonia (HABP) and ventilator-associated bacterial pneumonia (VABP) associated with Acinetobacter baumannii-calcoaceticus complex (ABC) in patients 18 years and older. Sulbactam is a direct antibacterial activity with high susceptibility to A. baumannii species. Durlobactam, diazabicyclooctane β-lactamase inhibitors possesses a broad-spectrum activity against Ambler class A, C, and D serine β-lactamases. This combination has been studied to overcome resistance to ABC species. Data were obtained from in vitro and preclinical studies as well as phase I, II, and III clinical studies published in English between 200t0 and January 2023. A phase II trial showed similar tolerability and pharmacokinetics parameters of sulbactam-durlobactam in patients with urinary tract infections to placebo. However, no ABC infections were included in the trial. ATTACK, a phase III clinical trial of sulbactam-durlobactam, studied the safety and efficacy of sulbactam-durlobactam in patients with ABC HABP/VABP and showed its noninferiority to colistin. Reported adverse events include anemia, elevated liver enzymes, hyperkalemia, headache, diarrhea, nausea, urticaria, and vascular pain. Sulbactam-durlobactam is a new β-lactamase inhibitors combination active against MDR Gram-negative bacteria including ABC. It is currently approved for the treatment of HABP/VABP caused by susceptible ABC strains.

The monkeypox (Mpox) virus has emerged as a global public health emergency of international concern recently. The virus that was endemic in West and Central Africa has now been reported with chains of global transmission to several countries. A scoping review was carried out from the relevant literature available from PubMed, Scopus and Web of Science. This comprehensive analysis describes the virus epidemiology, pathogenesis, clinical manifestations, complications including secondary bacterial infections, diagnosis, treatment and vaccination. The article underscores the significance of key viral and immune mediators of infection and discusses updated recommendations on therapeutic strategies and vaccination.

Coxiellaburnetii is an airborne bacterial zoonotic pathogen that causes Q fever/coxiellosis in humans and animals. Although dogs are suspected of transmitting Q fever to humans in past outbreaks, the prevalence of C. burnetii in the Indian dog population and risk factors for infection remain unknown. In this study, 452 dogs from pet clinics in three Indian states were screened for coxiellosis using molecular (Trans-PCR, Com 1-PCR) and serological (IFAT) tests. C. burnetii DNA was detected in 0.44% of blood samples using Trans-PCR, and pathogen-specific antibodies were found in 4.20% of sera using IFAT. Contact with stray dogs and ownership by farmers were identified as risk factors for canine coxiellosis. This study appears to be the first systematic assessment of coxiellosis and associated risk factors among dogs in India. A large-scale assessment of canine coxiellosis and its risk factors is warranted among pets and high-risk occupational groups in India.

In December 2022, China classified COVID-19 as a category B infectious disease. This ended 2 years of close epidemiological surveillance of COVID-19. The objective of this questionnaire was to assess the infection status in the COVID-19 pandemic since December in Henan Province, China, and the prevalence of infection in people who were taking ursodeoxycholic acid (UDCA) during this period. We distributed questionnaires to patients attending the gastroenterology clinic at the First Affiliated Hospital of Henan University of Chinese Medicine. The questionnaire lasted for 3 weeks and a total of 660 were collected, of which the number of people taking UDCA was 70. This is the first investigation into the rate of infection among those taking UDCA during the time of the COVID-19 pandemic. Our results showed that the overall infection rate among those taking UDCA was 71.43% (n = 50), with a 10% (n = 7) rate of asymptomatic infections, which was significantly lower than the 85.42% (n = 504) and 6.27% (n = 37) rates among respondents who did not take. The administration of UDCA showed a trend toward reducing the rate of COVID-19 infection, but the difference was not statistically significant when compared to patients with shorter durations of medication use. While less than 30% of participants remained uninfected during the study period, indicating a potential protective effect, it is important to note that complete prevention of SARS-CoV-2 infection by UDCA was not observed.

West Nile Virus (WNV) infection represents a major global public health challenge. Even though most of the patients are asymptomatic, some cases progress to critical condition which may be fatal. Diagnosis traditionally relies on serological methods, but their limitations, including cross-reactivity, highlight the need for alternative approaches. Here, we present the development and validation of a novel RT-qPCR assay for precise and rapid detection of WNV RNA in urine, emerging as a promising specimen due to its noninvasive collection and high viral load. The assay demonstrates high efficiency and sensitivity, with a detection limit comparable to commercially available kits. This study highlights the importance of in-house kit design as a diagnostic tool in regions affected by emerging tropical infections, such as WNV, exemplified Cyprus. It emphasizes the critical role of low-cost, early detection with high sensitivity and specificity in infection control and surveillance efforts.