Jundishapur Journal of Microbiology
Volume:16 Issue: 1, Jan 2023

Carbapenem-resistant Klebsiella pneumoniae (CRKP) strains have been listed as one of the major clinical concerns.

We investigated CPKP isolates from non-tertiary hospitals tofinddisseminated clones and analyze extensive phenotypic and genetic diversity in this study.

In this cohort study, a total of 49 CRKP isolates from 3 hospitals in the same region were collected in 2021. The prevalence and antimicrobial susceptibility patterns were analyzed. Clinical data were retrieved from electronic medical record systems. The molecular types, antimicrobial resistance (AMR) profiles, plasmid replicons, and virulence factors were analyzed. The maximumlikelihood phylogenetic tree and transmission networks were constructed using single-nucleotide polymorphisms (SNPs).

The median age of patients (N = 49) was 66.0 years, and 85.7% were male. The mostcommonCRKP infection was nosocomial pneumonia (75.5%), followed by bacteremia (10.2%). More than 53% of isolates were resistant to ceftazidime-avibactam (CAZ/AVI). Forty-five isolates were successfully sequenced; the predominant carbapenem-resistant gene was blaKPC-2 (93.3%). The 30-day mortality in our cohort was 24.5%. The most dominant sequence type (ST) was ST11 (60.0%), followed by ST15 (13.3%). Whole genome sequencing (WGS) analysis exhibited dissemination of ST11 strain clones, ST420, and ST15 clones, both within and outside the given hospital.

In this surveillance study, several dissemination chains of CRKP were discovered in the hospital and the region, as ST11 was the main epidemic clone. Our findings suggest that effective infection control practices and antimicrobial stewardship are needed in non-tertiary hospitals in China.

Bacterial and viral co-infections are increasingly recognized as the cause of Acute Respiratory Infection (ARI). The role of co-infection in ARI patients with Parainfluenza Virus type 3 (PIV3) infection is unclear.

This study aimed to determine the prevalence of PIV3 co-infections in hospitalized children and assess the co-infections’ role in ARI patients with PIV3 infections.

Between January 2018 and December 2021, children were confirmed to have a PIV3 infection via throat swabs or nasopharyngeal aspirates. Some digital clinical data were analyzed, including demographic, epidemiological, diagnostic, and laboratory data.

During the study period from 2018 to 2021, 2,539 patients were hospitalized with ARI caused by PIV3. Of them, 34.0% had co-infection with other pathogens, and 2.4% had co-infection with more than two pathogens. Mycoplasma pneumoniae was the most common co-infecting pathogen (71.3%), followed by other bacteria (13.3%) and viruses (8.2%). A significantly higher proportion of patients with M. pneumoniae co-infection was found in girls (2 = 19.233, P < 0.001). Co-infections with M. pneumoniae were observed principally in patients aged 1 – 2 years (2 = 202.130, P < 0.001). In contrast, viral (56.3%) and bacterial (66.1%) co-infections occurred mainly in children younger than one year. The diagnosis of PIV3 as a single infection included pneumonia (41.2%), bronchitis (39.9%), upper respiratory tract infections (15.0%), and laryngitis (3.9%), which were distinguished from those with bacterial co-infections (2 = 16.424, P = 0.001) and co-infections with more than two pathogens (2 = 11.687, P = 0.010). Co-infections of PIV3 with any pathogen were not associated with admissions to intensive care units or ventilator support. However, the mean hospitalization was significantly higher in M. pneumoniae co-infections (t = 2.367, P = 0.018), bacterial co-infections (t = 2.402, P = 0.016), and co-infections with more than two pathogens (t = 2.827, P = 0.006) than in single PIV3 infection.

Parainfluenza virus type 3 frequently occurs with other pathogens. The epidemiological and clinical characteristics of co-infections with different pathogens differed. Mycoplasma pneumoniae co-infections, bacterial co-infections, and co-infections with more than two pathogens lengthened the hospitalization. Bacterial co-infections and co-infections with more than two pathogens increased the severity of ARI and worsened the symptoms.

Urinary tract infections (UTIs) are among the most prevalent infections in hospitals and communities worldwide.

Due to the medical importance of UTIs caused by uropathogenic Escherichia coli (UPEC), this study aimed to investigate pathogenicity island (PAI) markers, O-antigen serogroups, andresistance to antibiotic agents associated withUPECisolates obtained from hospitalized patients in Rasht city hospitals.

A total of 110 urine samples were taken from patients with UTI referred to selected hospitals in Rasht, Iran. The doubledisk synergy test (DDST) was used to detect the isolate’s ability to produce extended-spectrum -lactamase (ESBL). Using particular primers, eight PAIs were detected (ie, PAI I536, PAI II536, PAI III536, PAI IV536, PAI ICFT073, PAI IICFT073, PAI IJ96, and PAI IIJ96).

According to the antibiotic susceptibility pattern, a high level of antibiotic resistance was observed against nalidixic acid (81.8%) and co-trimoxazole (78.2%), while the most effective agent was amikacin (85.5%). Double-disk synergy test revealed that the incidence of ESBL-positive strains was 62.7% (69/110). Of the 110 UPEC isolates, 106 (96.4%) carried at least one of the investigated PAI markers. Uropathogenic E. coli isolates with PAI IV536 (81.8%) had the highest prevalence, and PAI J196 (6.4%) had the lowest PAI marker. The most predominant serogroup O was O25 (36.4%), followed by O16 (17.3%), while the O4 and O7 serogroups (0.9%) were the lowest serogroups among UPEC isolates.

The characterization of our strain revealed the co-occurrence of PAI and serogroups, confirming the importance of antibiotic resistance among the distinct serogroups and PAI markers. Our results have potential application for epidemiological studies and designing UTI treatment strategies against UTIs caused by UPEC.

The coronavirus disease 2019 (COVID-19) pandemic has prompted researchers to look for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pathogenicity in depth. Immune system dysregulation was one of the major mechanisms in its pathogenesis. The evidence regarding the levels of interferons (IFNs) and pro- and anti-inflammatory cytokines in COVID-19 patients is not well-established.

This study evaluated the expression level of type-I, II, III IFNs, along with interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-10 (IL-10), and FOXP3 genes in patients with severe COVID-19 to provide additional insights regarding the regulation of these cytokines during COVID-19 infection.

Peripheral blood mononuclear cells were isolated from two groups, including severe COVID-19 patients and healthy controls. Ribonucleic acid was extracted to evaluate the expression level of IFN-a, IFN-b, IFN-g, IFN-la, IL-1, IL-6, IL-10, and FOXP3 genes using real-time polymerase chain reaction. The correlations between the expression levels of these genes were also assessed.

A total of 40 samples were divided into two groups, with each group consisting of 20 samples. When comparing the severe COVID-19 group to the controls, the expression levels of IFN-g, tumor necrosis factor-alpha (TNF-), IL-6, and IL-10 genes were significantly higher in the severe COVID-19 group. The two groups had no significant differences in IFN-a, IFN-b, IFN-la, IL-1, and FOXP3 expression. The correlation analysis revealed a negative correlation between type I and type III IFNs (i.e., IFN-a and IFN-la) and proinflammatory cytokines (i.e., IL-1 and IL-10).

This study suggests the possible upregulation of IFN-g, IL-6, IL-10, and TNF-during SARS-CoV-2 pathogenicity. The preliminary findings of this study and those reported previously show that the levels of IFNs and pro- and anti-inflammatory cytokines are not uniformly expressed among all COVID-19 patients and might differ as the disease progresses to the severe stage.

Bacillus clausii is being studied as a probiotic candidate. There is insufficient information on the antimicrobial and anticancer effects of B. clausii.

The present investigation was designed to evaluate the anti-bacterial, anti-adenoviral, and apoptosis-inducing activity of B. clausii cell-free supernatant (CFS).

First, the supernatant of B. clausii was collected after culture for 24 h. Then, its anti-bacterial impact on several genera of bacteria was assessed through the minimal inhibitory concentration (MIC) and minimal bactericidal concentration (MBC). Adenovirus 5 (Ad5) was exposed to the CFS under four conditions, including pre-treatment: First infecting cells with CFS and then with the virus; pre-incubation: Incubation of the supernatant and virus for 1.5 hours and then adding to the cells; competition: Infection of cells with the simultaneous mixture of the supernatant and virus, and post-treatment: First infecting cells with the virus and then with CFS. The median tissue culture infectious dose (TCID50) technique determined the virus titer. Real-time PCR was performed to assess the E1A expression. After exposure to the CFS, real-time PCR was utilized to measure the expression of MicroRNA-145, BCL-2, and BAX in HeLa cancer cells.

Bacillus clausii supernatant showed an inhibitory effect on Methicillin-resistant Staphylococcus aureus (MRSA), Enterococcus faecalis, S. aureus, Pseudomonas aeruginosa, Escherichia coli, and Acinetobacter baumannii. The Ad5 titers were reduced by about 4.61, 4, 3.9, and 3.1 Log10 TCID50/mL in pre-treatment, pre-incubation, competition, and post-treatment tests (CFS dilution: 1/4), respectively. Similar results of the viral titration were seen when experimental and control E1A expression levels were compared. Also, B. clausii supernatant during 48 h exposure to HeLa cells increased the transcript of the BAX, BCL-2, and miR-145 genes to 9.1, 2.3, and 55 folds, respectively, compared to the untreated condition.

Bacillus clausii can be a potent antimicrobial and anticancer agent. Further research is required to learn about the spectrum of anti-bacterial, antiviral, and anti-cancerous activities of B. clausii.

SARS-CoV-2 progression depends on multiple factors, including the compromised immune system and underlying diseases. HSV-1 reactivation in SARS-CoV-2 infection, more likely in patients with pneumonia and immunodeficiency, may be potentially life-threatening and implicate the prognosis.

We report two COVID-19 cases presenting ocular and neurological manifestations suspicious for HSV-1 encephalitis.

Our study showed HSV-1 ocular manifestation among two COVID-19 cases. So, the recurrence of HSV-1 infection probably is related to immune responses during COVID-19 pathophysiology.