BackgroundComposition of gut microbiota has recently been suggested as a key factor persuading the pathogenesis of numerous human diseases including hepatic cirrhosis.ObjectiveTo evaluate the potential impact of Lactobacillus acidophilus and Bifidobacterium bifidum microbiota on the progression of hepatic histopathological changes among patients with non-cirrhotic chronic hepatitis C (HCV) infection with different viral load. Additionally, to assess fecal composition of Lactobacillus acidophilus ATCC-4356 and Bifidobacterium bifidum ATCC-11863 microbiota genotypesMaterial and methodsThis study was carried out on 40 non-cirrhotic chronically infected HCV patients, and 10 healthy-controls. Liver biopsy and HCV genomic viral load were assessed for all patients after full clinical examination. Lactobacillus acidophilus ATCC-4356 and Bifidobacterium bifidum ATCC-11863 microbiota were assessed in all fecal samples using PCR assay, after counting total lactic acid bacteria.ResultsThere was a significantly higher difference between the count of both total lactic acid and Lactobacillus acidophilus of healthy controls compared to patients (P-value < 0.001). Though the count of total lactic acid bacteria, and Lactobacillus acidophilus were higher in the cases with early stage of fibrosis (score ≤ 1) compared to those with score > 1, there were no statistically significant differences with both the serum level of hepatitis C viremia (P = 0.850 and 0.977 respectively) and the score of fibrosis (P = 0.246 and 0.260 respectively). Genotypic analysis for the composition of the studied microbiota revealed that diversity was higher in healthy controls compared to patients.ConclusionsThe progression of hepatic fibrosis in HCV chronically infected patients seems to be plausible based on finding the altered Lactobacillus acidophilus and Bifidobacterium bifidum gut microbiota composition. Thus, modulation of these microbiota seems to be a promising target for prevention and control of HCV infection.

BackgroundHelicobacter pylori eradication by the conventional clarithromycin therapy has largely dropped in the recent years possibly due to antimicrobial resistance. Hence, levofloxacin-based regimen has been used as salvage therapy. However, data regarding its effectiveness on eradication are controversial. This study aimed to compare the eradication rate of levofloxacin-based regiment to that of the conventional first-line clarithromycin regimen.MethodsPatients diagnosed with H. pylori infection and treated with levofloxacin triple therapy or clarithromycin-based regimen for 10 or 14 days were included. Patients were excluded if they used antibiotics or proton pump inhibitors within 4 or 2 weeks, respectively, of the H. pylori eradication confirmation test. H. pylori eradication rate was assessed, as well as the impact of diabetes and esophagogastroduodenoscopy (EGD) findings.ResultsOf 245 patients, 145 were in the levofloxacin group and 100 in the clarithromycin group. Most patients in either group received therapy for 14 days vs. 10 days (P = 0.002). Levofloxacin-based treatment was associated with a higher eradication rate compared with clarithromycin-based treatment (74.5 vs. 62%, respectively; P = 0.04). The 14 day levofloxacin-based regimen resulted in the highest eradication rate, followed by the 14 day regimen of clarithromycin (80.9 vs. 66.3%; P = 0.03). The 10 day regimens exhibited 62.7 and 41.2% eradication rates, respectively (P = 0.12). H. pylori eradication was not affected by diabetes or EGD findings (P = 0.98 and 0.3, respectively).ConclusionsResults from this study support the use of a levofloxacin-based regimen as a first-line therapy in the treatment of H. pylori infection for 14 days regardless of diabetes and EGD findings.

BackgroundHelicobacter pylori (H. pylori), Gram negative microaerophilic bacteria, is a well-known pathogen of many gastrointestinal diseases. But several emerging evidences suggest it role in numerous other extra-gastric diseases. The current study investigates the relationship between H. pylori infection and sarcopenia, a clinical condition characterized by the loss of mass and function of skeletal muscle. A total of 3453 eligible participants from the Third National Health and Nutrition Examination Survey (NHANES III), the United States, were enrolled. Based on the serum laboratory results, subjects were categorized into three groups: normal (without evidence of any H. pylori infection), anti-H. pylori IgG positive [H. pylori (+)], and concurrent anti-H. pylori IgG and anti-cytotoxin-associated gene A IgG positive [CagA (+)]. Sarcopenia was determined as having a skeletal muscle index (SMI) value that is more than 1 standard deviation away from the mean value of sex-specific, healthy young adults between 20 and 39 years old. Risk of sarcopenia and its components are compared between subgroups.ResultsOdds ratios (OR) for confirmed diagnosis of sarcopenia were higher in H. pylori (+) (OR = 2.052, 95% CI 1.697–2.481, p < 0.001) and CagA (+) (OR = 1.585, 95% CI 1.278–1.965, p < 0.001) groups. Moreover, negative beta regression coefficient of SMI were shown in H. pylori (+) (β: − 0.023, p < 0.001) and CagA (+) (β: − 0.017, p < 0.001). Sub-analyses which categorized participants by gender revealed that absolute value of beta regression coefficient for SMI were higher in female in H. pylori (+) subgroup (β: − 1.745 in male and − 2.942 in female, p were both < 0.001), and the CagA (+) subgroup (β: − 1.407 in male and − 2.159 in female, p were both < 0.001).ConclusionsPositive serum H. pylori infectious markers including anti-H. pylori antibody and CagA seropositivity are correlated with sarcopenia and low muscle quantity. Therefore, H. pylori eradication therapy may bring benefits to sarcopenia patients with concurrent active H. pylori infection.

A strong and expanding evidence base supports the influence of gut microbiota in human metabolism. Altered glucose homeostasis is associated with altered gut microbiota, and is clearly associated with the development of type 2 diabetes mellitus (T2DM) and associated complications. Understanding the causal association between gut microbiota and metabolic risk has the potential role of identifying susceptible individuals to allow early targeted intervention.

BackgroundCampylobacter jejuni (C. jejuni) is accountable for more than 400 million cases of gastroenteritis each year and is listed as a high-priority gut pathogen by the World Health Organization (WHO). Although the acute infection of C. jejuni (campylobacteriosis) is commonly treated with macrolides and fluoroquinolones, the emergence of antibiotic resistance among C. jejuni warrants the need for an alternative approach to control campylobacteriosis in humans. To this end, vaccines remain a safe, effective, and widely accepted strategy for controlling emerging and re-emerging infectious diseases. In search of a suitable vaccine against campylobacteriosis, recently, we demonstrated the potential of recombinant Haemolysin co-regulated protein (Hcp) of C. jejuni Type VI secretion system (T6SS) in imparting significant immune-protection against cecal colonization of C. jejuni; however, in the avian model. Since clinical features of human campylobacteriosis are more complicated than the avians, we explored the potential of Hcp as a T6SS targeted vaccine in a murine model as a more reliable and reproducible experimental host to study vaccine-induced immune-protection against C. jejuni. Because C. jejuni primarily utilizes the mucosal route for host pathogenesis, we analyzed the immunogenicity of a mucosally deliverable bioengineered Lactic acid bacteria (LAB), Lactococcus lactis (L. lactis), expressing Hcp. Considering the role of Hcp in both structural (membrane-bound) and functional (effector protein) exhibition of C. jejuni T6SS, a head-to-head comparison of two different forms of recombinant LAB vectors (cell wall anchored and secreted form of Hcp) were tested and assessed for the immune phenotypes of each modality in BALB/c mice.ResultsWe show that regardless of the Hcp protein localization, mucosal delivery of bioengineered LAB vector expressing Hcp induced high-level production of antigen-specific neutralizing antibody (sIgA) in the gut with the potential to reduce the cecal load of C. jejuni in mice.ConclusionTogether with the non-commensal nature of L. lactis, short gut transit time in humans, and the ability to express the heterologous protein in the gut, the present study highlights the benefits of bioengineered LAB vectors based mucosal vaccine modality against C. jejuni without the risk of immunotolerance.

BackgroundEven though the incidence of H. pylori infection among Malays in the Malay Peninsula is low, we observed a high H. pylori prevalence in Sumatra, which is the main residence of Indonesian Malays. H. pylori prevalence among Indonesian Malay descendants was investigated.ResultsUsing a combination of five tests, 232 recruited participants were tested for H- pylori and participants were considered positive if at least one test positive. The results showed that the overall H. pylori prevalence was 17.2%. Participants were then categorized into Malay (Aceh, Malay, and Minang), Java (Javanese and Sundanese), Nias, and Bataknese groups. The prevalence of H. pylori was very low among the Malay group (2.8%) and no H. pylori was observed among the Aceh. Similarly, no H. pylori was observed among the Java group. However, the prevalence of H. pylori was high among the Bataknese (52.2%) and moderate among the Nias (6.1%). Multilocus sequence typing showed that H. pylori in Indonesian Malays classified as hpEastAsia with a subpopulation of hspMaori, suggesting that the isolated H. pylori were not a specific Malays H. pylori.ConclusionsEven though the ethnic groups live together as a community, we observed an extremely low H. pylori infection rate among Indonesian Malay descendants with no specific Indonesian Malay H. pylori. The results suggest that H. pylori was not originally among these groups and H. pylori was imported from other ethnic groups.

BackgroundDiarrhea remains the leading cause of childhood illness in China. Better understanding of burden and etiology of diarrheal diseases is important for development of effective prevention measures.MethodsPopulation-based diarrhea surveillance was conducted in Sanjiang (southern China) year-round and Zhengding (northern China) in autumn/winter. Stool specimens were collected from children < 5 years of age experiencing diarrhea. The TaqMan Array Card (TAC), based on multiplex real-time PCR, was applied to detect multiple enteric microbial agents simultaneously. Results using these methods were compared to those derived from conventional PCR assays.ResultsDuring the study period, 6,380 children in Zhengding and 3,581 children in Sanjiang < 5 years of age participated. Three hundred and forty (31.2%) and 279 (22.9%) diarrhea episodes were identified as moderate-to-severe in the two counties, with incidence of 60.4 and 88.3 cases per 1,000 child-years in Zhengding and Sanjiang, respectively. The five most frequently detected bacterial and viral agents in Sanjiang were adenovirus, enterovirus, enteroaggregative Escherichia coli (EAEC), rotavirus, and sapovirus all the year round, while the most common viral agents in Zhengding were rotavirus, followed by astrovirus and adenovirus during the cool season. Compared to conventional PCR assay, the average incremental detection via the TAC method was twofold.ConclusionOur study demonstrated high diversity and prevalence of multiple major bacterial and viral agents, including rotavirus and calicivirus, among children in China. Further studies are needed to define the public health significance of neglected but frequently detected pathogens such as EAEC, enterotoxigenic E. coli, Campylobacter, adenovirus, and enterovirus.

BackgroundPoor self-care skills and personal hygiene resulted from limitations in learning and understanding, put intellectually disabled individuals at greater risk for intestinal parasitic infections (IPIs). Despite several regional reports in Iran, the overall burden on IPIs among intellectually disabled individuals is poorly understood. Hence, the present study aimed to estimate the pooled prevalence of IPIs among intellectually disabled individuals in Iran.MethodsUsing the PRISMA guidelines, we conducted a systematic review and meta-analysis of data retrieved from seven electronic databases (PubMed, Web of Science, Scopus, Embase, and ProQuest for English articles, as well as SID and Magiran for Persian) from their inception up to December 2020. Pooled prevalence was estimated using a random-effects model with a 95% confidence interval (CI) and depicted as a forest plot, while heterogeneity was evaluated using Cochran’s Q-test.ResultsExactly 1263 of the 3004 intellectually disabled individuals examined by 14 studies across 10 provinces of Iran were positive for IPIs. Overall pooled prevalence estimate was 41% (95% CI 29–53%) with a range of 21% (95% CI 10–32%) to 68% (95% CI 55–80%) across sub-groups. Entamoeba coli (16.2%; 95% CI 10.3–22%), Blastocystis spp. (12.2%; 95% CI 7.2–17.2%), and Giardia duodenalis (11.9%; 95% CI 7.4–16.3%) were the most prevalent protozoan species. In terms of helminthic agents, the most prevalent species were Enterobius vermicularis (11.3%; 95% CI 6.3–16.3%) followed by Strongyloides stercoralis (10.9%; 95% CI 5.0–16.9%) and Hymenolepis nana (2.8%; 95% CI 0.4–5.2%)ConclusionIPIs are highly prevalent among intellectually disabled individuals in Iran. Improving the health status and implementing infectious disease prevention strategies in rehabilitation centers, health promotion interventions to improve personal hygiene of intellectually disabled individuals, as well as utilize sensitive diagnostic methods besides routine stool examination techniques, and treatment of infected individuals will help in the control of these infections among intellectually disabled individuals.

Shiga toxin-producing Escherichia coli (STEC) is a pathotype of E. coli that causes enteric and systemic diseases ranging from diarrhoea to severe hemorrhagic colitis (HC) and hemolytic uremic syndrome (HUS). The emergence of multidrug-resistant (MDR) STEC from cattle sources has increased public health risk and limited treatment options. The prevalence of STEC was investigated in 200 raw food samples (milk and beef samples) and 200 diarrheic samples (cattle and human samples) in a matched region. The presence of stx genes (stx1 and stx2), carbapenemase-encoding genes (blaVIM, blaNDM-1, and blaIMP), and extended-spectrum β-lactamase (ESBL)-encoding genes (blaTEM group, blaCTX-M1 group, and blaOXA-1 group) was screened by polymerase chain reaction (PCR). Antibiogram and Enterobacterial repetitive intergenic consensus (ERIC)-PCR were also conducted. STEC isolates were identified in 6.5% (13/200) of food samples [6% (6/100) of milk and 7% (7/100) of beef samples] and in 11% (22/200) of diarrheic cases [12% (12/100) of cattle and 10% (10/100) of human samples]. We found that O26 (4.5%, 18/400) and O111 (1.5%, 6/400) were the most prevalent STEC serovars and were found more commonly in diarrheic samples. STEC strains with both stx genes, stx2 only, and stx1 only genotypes were present in 62.9% (22/35), 20% (7/35), and 17.1% (6/35) of isolates, respectively. Carbapenemase-producing STEC (CP STEC) isolates were found in 1.8% (7/400) of samples [0.5% (1/200) of foods and 3% (6/200) of diarrheic cases]. The blaVIM gene was detected in all CP STEC isolates, and one human isolate carried the blaNDM-1 gene. ESBL-producing STEC strains were detected in 4.3% (17/400) of samples [1.5% (3/200) of food samples and 7% (14/200) of diarrheic cases]. The blaTEM, blaCTX-M1, and blaOXA-1 genes were detected in 42.9% (15/35), 28.6% (10/35), and 2.9% (1/35) of STEC isolates, respectively. Approximately half (51.4%, 18/35) of STEC isolates were MDR STEC; all CP STEC and ESBL-producing STEC were also MDR STEC. The highest antimicrobial resistance rates were found against nalidixic acid (51.4%) and ampicillin (48.6%), whereas the lowest rates were reported against gentamicin (5.7%) and ciprofloxacin (11.4%). MDR STEC strains were 5.3 times more likely to be found in diarrheic cases than in foods (P = 0.009, 95% CI 1.5–18.7). ERIC-PCR was used for genotyping STEC isolates into 27 different ERIC-types (ETs) with a discrimination index of 0.979. Five ETs showed clusters of 2–4 identical isolates that shared the same virulence and antibiotic resistance genetic profile. Human isolates matched food isolates in two of these ET clusters (the O26 CP STEC cluster and the O111 STEC cluster), highlighting the potential cross-species zoonotic transmission of these pathogens and/or their genes in the study region. This is the first detection of CP STEC in milk and diarrheic cattle in Egypt.

The emergence and transmission of the mobile colistin resistance gene (mcr-1) threatened the extensive use of polymyxin antimicrobials. Accumulated evidence showed that the banning of colistin additive in livestock feed efficiently reduce mcr-1 prevalence, not only in animals but also in humans and environments. However, our previous study has revealed that a small proportion of Escherichia coli could continually carry chromosomally-encoded mcr-1. The chromosomally-encoded events, indicated the existence of stabilized heritage of mcr-1 and revealed a potential threat in the antimicrobial stewardship interventions, are yet to be investigated. In this study, we systematically investigated the genetic basis of chromosomally-encoded mcr-1 in prevalence and potential mechanisms of lineage, plasmid, insertion sequence, and phage. Our results demonstrated that the emergence of chromosomally-encoded mcr-1 could originate from multiple mechanisms, but mainly derived through the recombination of ISApl1/Tn6330. We reported a specific transmission mechanism, which is a phage-like region without lysogenic components, could associate with the emergence and stabilization of chromosomally-encoded mcr-1. These results highlighted the potential origin and risks of chromosomally-encoded mcr-1, which could be a heritable repository and thrive again when confronted with new selective pressures. To the best of our knowledge, this is the first study to systematically reveal the genomic basis of chromosomally-encoded mcr-1, and report a specific transmission pattern involved in phage-like region. Overall, we demonstrate the origin mechanisms and risks of chromosomally-encoded mcr-1. It highlights the need of public attention on chromosome-encoded mcr-1 to prevent from its reemergence.