Jundishapur Journal of Microbiology
Volume:16 Issue: 9, Sep 2023

Human rhinovirus (HRV) and human metapneumovirus (hMPV) are common viral causes of pediatric respiratory tract infections. Bacterial co-infections frequently complicate HRV and hMPV illnesses in children, but the interactions between viral and bacterial pathogens and their impacts on disease severity are not well understood.

The present research aimed to analyze and compare the clinical features of HRV and hMPV mono-infections in hospitalized children and to assess the impact of bacterial co-infection on the disease severity of HRV and hMPV infections.

The present retrospective analytical cross-sectional study was conducted to compare the clinical features between HRV and hMPV mono-infections and HRV and hMPV with bacterial co-infections in hospitalized children aged 14 years or younger.

Between January and December 2022, we investigated 1,978 children hospitalized with HRV infection, of which 1,529 had HRV mono-infection and 1,117 hospitalized with hMPV infection, among whom 910 had hMPV mono-infection. Compared to HRV, hMPVmono-infection exhibitedmorepronounced symptoms of fever, cough, and rales in most age groups, whileHRVshowedmore wheezing. Except in patients  6 years old, hMPV was more associated with pneumonia and longer hospitalizations. In contrast to HRV mono-infections, children with bacterial co-infections had a higher proportion of coughs (P < 0.001), pneumonia (P < 0.001), pediatric intensive care unit (PICU) admissions (P < 0.001), and longer hospitalizations (P = 0.003). Demographic characteristics, clinical presentation, diagnosis, and treatments showed no significant differences between patients withhMPVmono-infection and co-infection.

Among hospitalized children, hMPV mono-infection resulted in more severe respiratory illnesses compared to HRV mono-infection. Bacterial co-infections exacerbated disease severity in HRV infections.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection transmits when aerosols or droplets containing the virus are inhaled or come directly into contact, mainly in close contact with an infected person.

This study aimed to evaluate the role of the salivary glands in the secretion of SARS-CoV-2-infected saliva and determine the contagiousness of saliva in asymptomatic coronavirus disease 2019 (COVID-19) patients.

In this cross-sectional analytical study between March 2021 and March 2022, 85 asymptomatic COVID-19 individuals with positive nasopharyngeal/oropharyngeal swabs were recruited. The SARS-CoV-2 cycle threshold (Ct) value was investigated in concomitant nasopharyngeal swabs (NPS), saliva, and pure saliva (collected directly from the salivary duct opening) using Real Time-PCR assay. Statistical analysis was performed using SPSS software (version 23), and a p-value of < 0.05 was considered significant.

The saliva Ct-value was the lowest (the highest viral load) for Delta (29.82 ± 4.66), Omicron (32.75 ± 4.82), and Alpha (36.83 ± 4.8) variants, respectively. Delta-infected saliva and pure saliva revealed the strongest correlation (correlation coefficient = 0.971, P< 0.001). Saliva Ct-value was significantly lower in Delta- (P < 0.001) and Omicron- (P = 0.012) infected patients than in Alpha-infected patients. The pure saliva Ct-value was significantly lower (P = 0.014) in Delta samples (30.13 ± 4.51). Asymptomatic Alpha- and Omicron-infected patients revealed significantly lower NPS Ct-value (30.52 ± 4.02 and 29.44 ± 3.34) than the saliva (36.83 ± 4.8 and 32.75 ± 4.82).

The major salivary glands secrete SARS-CoV-2-infected saliva in nearly all Delta-infected and most Omicron-infected asymptomatic individuals. Although the transmission process is complex, saliva droplets and aerosols seem to have a higher contagiousness potential in individuals infected with the Delta variant.

Listeria monocytogenes (LM) is a facultative intracellular pathogen that causes food-borne infections in humans and animals. To invade and multiply within host cells, LM utilizes various strategies to precisely modulate its gene expression and to adapt to the in vivo environment.

To investigate the regulatory roles of Rli82 sRNA in the motility and pathogenicity of LM EGD-e.

The Rli82 gene knock-out mutant strain, LM-
Rli82, and the complementation strain, LM-
Rli82/Rli82, were constructed using homologous recombination technology, and their motility and virulence, respectively, were determined. Moreover, the potential target mRNA regulated by Rli82 was predicted using TargetRNA2 software, and then the interaction between the target mRNA and Rli82 was verified by the two-plasmid reporter system.

The results showed that the motility of LM-
Rli82 was significantly increased at 25°C, facilitated by the production of more flagella than LM EGD-e and LM-
Rli82/Rli82. Furthermore, LD50 in LM-
Rli82-infected mice was significantly increased as compared to LM EGD-e and LM-
Rli82/Rli82, suggesting that the virulence of LM was weakened when the Rli82 gene was deleted. In addition, the mRNA level of flaA was not significantly elevated, but flaA protein was significantly higher in LM-
Rli82 than in LM EGD-e and LM-
Rli82/Rli82, suggesting that Rli82 might modulate the translation of flaA mRNA at the post-transcriptional level.

Taken together, our findings for the first time revealed that Rli82 sRNA might be involved in the modulation of the expression of flaA protein, thereby influencing the mobility and pathogenicity of LM.

In liver transplant recipients, human Cytomegalovirus (CMV) infection is a significant concern. Ganciclovir is the preferred medication for treating widespread CMV infections. In some cases, patients might require high doses of treatment for CMV infections that are resistant to ganciclovir, although liver transplant patients who have received extended ganciclovir and valganciclovir prophylaxis have reported infrequent cases of ganciclovir-resistant CMV infections. Mutations in the UL54 gene, responsible for encoding deoxyribonucleic acid (DNA) polymerase, can result in resistance.

In this study, the focus was on UL54 mutations and their association with ganciclovir resistance.

In this study, 23 liver transplant recipients who were admitted to the transplant departments of Namazi and Abu Ali Sina hospitals within 2015 and 2017 were examined. Cytomegalovirus infection was then confirmed in them using the quantitative real-time polymerase chain reaction (PCR) method. The UL54 mutations were found after electrophoresis using the nested PCR method, and the PCR products were subsequently sequenced using the Sanger method. Sequence analysis and locating of UL54 mutations were performed using Finch software (version 1.4.0).

After sequencing 52 samples from 23 patients, 25 mutations in the UL54 gene were identified in 9 patients who were CMV-infected, occurring at a median of 32 days after transplant. These mutations, including S655L (10/9, 40%), N685S (8/9, 32%), F669L (4/9, 16%), A688V (2/9, 8%), and the novel AK124703.1: p.V668-G672dup (1/9, 4%), were detected in 9 liver transplant recipients over a median period of 2 years in the UL54 gene. Furthermore, a phylogenetic analysis was conducted to investigate the origins of these mutations in CMV isolated from the Iranian population.

Considering that treatment with the drug ganciclovir has led to resistance mutations, particularly the new AK124703.1:p.V668-G672dup mutation, and inefficiency in treatment, it is necessary to determine drug-resistant CMV strains and closely monitor these patients. This includes determining viral load, assessing response to treatment, and identifying non-response at regular intervals until the viral load is completely eradicated in order to ensure the effectiveness of the treatment.

Drug-resistant hospital-acquired infections (HAIs) are a growing concern in modern medicine throughout the world. Klebsiella pneumoniae is one of the most prominent causative agents of multidrug-resistant nosocomial infections. It is also widely recognized for having a high resistance level to many antibiotic classes, particularly beta-lactams. Carbapenemase-producing K. pneumoniae has been identified as a major global cause of HAIs with adverse clinical outcomes. Therefore, it is of the utmost importance to have an in-depth understanding of the antimicrobial resistance (AMR) genetic determinants of this bacterium to stop the spread of highly resistant K. pneumoniae in healthcare facilities and the resulting patient morbidity and mortality.

This study aimed to investigate the AMR pattern of K. pneumoniae isolates obtained from intensive care units (ICUs), with a focus on extended-spectrum beta-lactamases (ESBLs) genes blaCTX-M, blaGES, and blaIMP.

A total of 105 K. pneumoniae isolates obtained from the sputum samples of ICU patients were identified and confirmed using standard microbiological tests and 16S rRNA polymerase chain reaction (PCR). The antibiotic susceptibility test was performed for all the isolates. The presence of ESBL genes was determined phenotypically and by PCR.

The highest level of resistance was observed against ceftazidime (100%), cefotaxime (99%), and imipenem (93.3%). Approximately 87.6% and 39% of the isolates were sensitive to colistin and gentamicin, respectively. Phenotypic ESBL production was observed in 16 isolates, and the prevalence of blaCTX-M was 86.7%. No blaGES and blaIMP genes were detected.

Periodic investigation of AMR-mediating genes is essential due to the high prevalence of ESBL genes in HAIs. The presence of other ESBL genes needs to be investigated for a more accurate understanding of the AMR status of K. pneumoniae in healthcare settings.

The emergence of resistance to azithromycin complicates the treatment of Neisseria gonorrhoeae, the causative agent of gonorrhea.

The main objective of this study was to investigate the impact of mutations in different sites of the rplD gene on azithromycin resistance (AZM-R) and the molecular characteristics of N. gonorrhoeae. This study aimed to provide evidence for drug resistance and transmission.

A total of 37 isolates of N. gonorrhoeae were collected within January 2018 to December 2020. These isolates were obtained from urine, semen, or vaginal secretions of different patients. Azithromycin resistance was assessed, and genes associated with AZM-R, namely rplD, and rplV, were analyzed using polymerase chain reaction (PCR) and deoxyribonucleic acid (DNA) sequencing. All clinical isolates were characterized through multi-locus sequence typing (MLST).

The study comprised 21 azithromycin-resistant N. gonorrhoeae isolates, with two of them demonstrating high resistance, indicated by a minimum inhibitory concentration (MIC) greater than 256 g/mL. Additionally, 16 sensitive isolates were included in the study. Ten isolates were observed to have rplD point mutations, including mutations such as G70D, G70S, G68D, and A43T. No mutations were detected in rplV. The rate of point mutations in rplD was significantly different between the azithromycin-sensitive (AZM-S) group and the AZM-R group (P < 0.05). Among the 37 isolates studied, 12 distinct MLST types were identified and further grouped into four different MLST goeBURST groups. The two isolates with high-level AZM-R were ST1901 and ST1588, respectively.

The clinical isolates of N. gonorrhoeae from Wenzhou, Eastern China, exhibit significant genetic diversity and a relatively high prevalence of AZM-R. Mutations in the rplD gene were identified, which reduced susceptibility to macrolides and were significantly associated with increased AZM-R.