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Foodborne infections cause substantial issues all around the world, hence food safety is a major public health concern. The goal of this research is to provide information to the scientific community on the possible application of two plant essential oil molecules, Carvacrol (CAR) and Cinnamaldehyde (CN), as next-generation antimicrobials in the fight against foodborne pathogens. CAR and CN demonstrated outstanding dose-dependent antibacterial efficacy against 10 foodborne pathogens. Both Gram-positive and Gram-negative bacteria were suitably inhibited by the drugs. Antimicrobial activity of 10% v/v CAR and CN was much higher than that of the conventional antibiotic azithromycin (15g/disc). The study discovered that CAR and CN have very low MIC values (0.08% to 0.31% v/v), indicating that the compounds are efficacious even at very low concentrations. Even at 0.16% concentration, combining CAR and CN with Nisin (a widely available natural preservative) exhibited substantial synergism, with inhibition zones ranging from 8.5- 12.38 mm, decreasing the dose required to produce sufficient antimicrobial action. The findings imply that CAR and CN combined with nisin can be used as a natural antibacterial agent to limit the growth of foodborne pathogens and as a natural food preservative. Bangladesh J Microbiol, Volume 39, Number 1, June 2022, pp 7-14

The emergence of novel coronavirus infectious disease-2019 (COVID-19) in December 2019, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has traumatized the whole world with the ongoing devastating pandemic. After droplet mediated transmission of infectious virus particle, and subsequent tissue tropism through the upper and lower respiratory tract, the acute clinical disease is manifested by severe respiratory illness accompanied by shortness of breath, progressive pneumonia, multi-organ dysfunction and ultimate death in SARS-CoV-2 infected patients. The involvement of other microbial co-infections leading to extortionate ailment in critically ill patients has not been significantly reviewed along with conclusive reporting on underlying molecular mechanisms in COVID-19 patients. Although the incidence of co-infections could be up to 94.2% in laboratory-confirmed COVID-19 cases, the fate of co-infections among SARS-CoV-2 infected hosts often depends on the balance between the host’s protective immunity and immunopathology. The cross-talk between co-pathogens (especially lung microbiomes), SARS-CoV-2 and host is an important factor that ultimately increases the difficulty of diagnosis, treatment, and prognosis of COVID-19, and even increase the symptoms and mortality of the disease. Simultaneously, co-infecting microorganisms may use new strategies to escape host defense mechanisms (by altering both innate and adaptive immune responses) to further aggravate SARS-CoV-2 pathogenesis. This review of literature suggests that clinicians should rule out SARS-CoV-2 infection by ruling in other respiratory co-pathogens, and must have a high index of suspicion for co-infection among COVID-19 patients. Thus, after recognizing the possible pathogens causing co-infection among COVID-19 patients, and the underlying molecular mechanisms of co-infections appropriate curative and preventive interventions can be recommended.

Cancer is considered a major public health concern worldwide and is characterized by an uncontrolled division of abnormal cells. The human immune system recognizes cancerous cells and induces innate immunity to destroy those cells. However, sustained tumors may protect themselves by developing immune escape mechanisms through multiple soluble and cellular mediators. Neutrophils are the most plenteous leukocytes in the human blood and are crucial for immune defense in infection and inflammation. Besides, neutrophils emancipate the antimicrobial contents, secrete different cytokines or chemokines, and interact with other immune cells to combat and successfully kill cancerous cells. Conversely, many clinical and experimental studies signpost that being a polarized and heterogeneous population with plasticity, neutrophils, particularly their subpopulations, act as a modulator of cancer development by promoting tumor metastasis, angiogenesis, and immunosuppression. Studies also suggest that tumor infiltrating macrophages, neutrophils, and other innate immune cells support tumor growth and survival. Additionally, neutrophils promote tumor cell invasion, migration and intravasation, epithelial to mesenchymal transition, survival of cancer cells in the circulation, seeding, and extravasation of tumor cells, and advanced growth and development of cancer cells to form metastases. In this manuscript, we describe and review recent studies on the mechanisms for neutrophil recruitment, activation, and their interplay with different immune cells to promote their pro-tumorigenic functions. Understanding the detailed mechanisms of neutrophil-tumor cell interactions and the concomitant roles of other immune cells will substantially improve the clinical utility of neutrophils in cancer and eventually may aid in the identification of biomarkers for cancer prognosis and the development of novel therapeutic approaches for cancer treatment.

Foot-and-mouth disease (FMD) is an economically devastating disease of the livestock worldwide and caused by the FMD virus (FMDV), which has seven immunologically distinct serotypes (O, A, Asia1, C, and SAT1–SAT3). Studies suggest that VP2 is relatively conserved among three surface-exposed capsid proteins (VP1–VP3) of FMDV, but the level of conservation has not yet been reported. Here we analyzed the comparative evolutionary divergence of VP2 and VP1 to determine the level of conservation in VP2 at different hierarchical levels of three FMDV serotypes (O, A, and Asia1) currently circulating in Asia through an in-depth computational analysis of 14 compiled datasets and designed a consensus VP2 protein that can be used for the development of a serotype-independent FMDV detection tool. The phylogenetic analysis clearly represented a significant level of conservation in VP2 over VP1 at each subgroup level. The protein variability analysis and mutational study showed the presence of 67.4% invariant amino acids in VP2, with the N-terminal end being highly conserved. Nine inter-serotypically conserved fragments located on VP2 have been identified, among which four sites showed promising antigenicity value and surface exposure. The designed 130 amino acid long consensus VP2 protein possessed six surface-exposed B cell epitopes, which suggests the possible potentiality of the protein for the development of a serotype-independent FMDV detection tool in Asia. Conclusively, this is the first study to report the comparative evolutionary divergence between VP2 and VP1, along with proposing the possible potentiality of a designed protein candidate in serotype-independent FMDV detection.

The ongoing mutations in the structural proteins of SARS-CoV-2 is the major impediment for prevention and control of the COVID-19 disease. The envelope (E) protein of SARS-CoV-2 is a structural protein existing in both monomeric and homopentameric forms, associated with a multitude of functions including virus assembly, replication, dissemination, release of virions, infection, pathogenesis, and immune response stimulation. In the present study, 81,818 high quality E protein sequences retrieving from the GISAID were subjected to mutational analyses. Our analysis revealed that only 0.012 % (982/81818) stains possessed amino acid (aa) substitutions in 63 sites of the genome while 58.77% mutations in the primary structure of nucleotides in 134 sites. We found the V25A mutation in the transmembrane domain which is a key factor for the homopentameric conformation of E protein. We also observed a triple cysteine motif harboring mutations (L39M, A41S, A41V, C43F, C43R, C43S, C44Y, N45R) which may hinder the binding of E protein with spike glycoprotein. These results therefore suggest the continuous monitoring of each structural protein of SARS-CoV-2 since the number of genome sequences from across the world are continuously increasing.

Multidrug-resistant (MDR) Escherichia coli has been previously detected in other locations, but not in Chhatak, a diarrhea endemic region of Bangladesh. In this study, 36 E. coli isolated from diarrhea stools of adults and children from Chhatak were investigated for the prevalence of drug resistance, virulence and resistance related genes, genotyping, and other molecular characteristics. Antibiotic resistance profiling was performed by disk diffusion method whereas the presence of virulence genes, mobile genetic elements, plasmids, and resistance-related genes were monitored by PCR assay. Multiple resistance to drugs was observed in 94.4% of the isolates and 24 (66.7%) of the strains were found as enterotoxigenic E. coli (ETEC) pathogroup. Genotyping by ERIC-PCR fingerprinting revealed genetic heterogeneity among the MDR E. coli strains. Overall, 88% of E. coli strains possessed plasmids ranging from 0.6 to 140 MDa. Of the detected integrases (69%), intl1 was predominant (53%). Erythromycin esterase-B (ereB) was present in 8 out of 36 macrolide resistant strains (22%). Of 27 beta-lactam resistant isolates, 70%, 41%, and 33% carried blaCTX-M-1, blaTEM, and blaOXA, respectively. Of 23 tetracycline resistant strains, 13 tetB (57%) and 8 tetA (35%) were detected. All 24 ciprofloxacin resistant strains tested positive for gyrA, but none for qnrA. Sequence analysis of the quinolone resistance-determining regions (QRDR) of gyrA of two ciprofloxacin resistant strains showed two point mutations (S83L, D87N). Computational docking studies revealed a decreased interaction of the drug with the target due to this mutation. In conclusion, high incidence of plasmids and antimicrobial resistance in E. coli carrying virulence genes and resistance markers for antimicrobial drugs in diarrheagenic patients of Bangladesh is alarming as lateral transfer of these virulence and resistance genes in other infectious agents can make them irresistible, and infection control more challenging in the days to come.

The novel coronavirus infectious disease-2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has traumatized the whole world with the ongoing devastating pandemic. A plethora of microbial domains including viruses (other than SARS-CoV-2), bacteria, archaea and fungi have evolved together, and interact in complex molecular pathogenesis along with SARS-CoV-2. However, the involvement of other microbial co-pathogens and underlying molecular mechanisms leading to extortionate ailment in critically ill COVID-19 patients has yet not been extensively reviewed. Although, the incidence of co-infections could be up to 94.2% in laboratory-confirmed COVID-19 cases, the fate of co-infections among SARS-CoV-2 infected hosts often depends on the balance between the host's protective immunity and immunopathology. Predominantly identified co-pathogens of SARS-CoV-2 are bacteria such as Streptococcus pneumoniae, Staphylococcus aureus, Klebsiella pneumoniae, Haemophilus influenzae, Mycoplasma pneumoniae, Acinetobacter baumannii, Legionella pneumophila and Clamydia pneumoniae followed by viruses including influenza, coronavirus, rhinovirus/enterovirus, parainfluenza, metapneumovirus, influenza B virus, and human immunodeficiency virus. The cross-talk between co-pathogens (especially lung microbiomes), SARS-CoV-2 and host is an important factor that ultimately increases the difficulty of diagnosis, treatment, and prognosis of COVID-19. Simultaneously, co-infecting microbiotas may use new strategies to escape host defense mechanisms by altering both innate and adaptive immune responses to further aggravate SARS-CoV-2 pathogenesis. Better understanding of co-infections in COVID-19 is critical for the effective patient management, treatment and containment of SARS-CoV-2. This review therefore necessitates the comprehensive investigation of commonly reported microbial co-pathogens amid COVID-19, their transmission pattern along with the possible mechanism of co-infections and outcomes. Thus, identifying the possible co-pathogens and their underlying molecular mechanisms during SARS-CoV-2 pathogenesis may shed light in developing diagnostics, appropriate curative and preventive interventions for suspected SARS-CoV-2 respiratory infections in the current pandemic.

The ongoing mutations in the structural proteins of SARS-CoV-2 are the major impediment for prevention and control of the COVID-19 disease. Presently we focused on evolution of the envelope (E) protein, one of the most enigmatic and less studied protein among the four structural proteins (S, E, M and N) associated with multitude of immunopathological functions of SARS-CoV-2. In the present study, we comprehensively analyzed 81,818 high quality E protein sequences of SARS-CoV-2 globally available in the GISAID database as of 20 August 2020. Compared to Wuhan reference strain, our mutational analysis explored only 1.2 % (982/81818) mutant strains undergoing a total of 115 unique amino acid (aa) substitutions in the E protein, highlighting the fact that most (98.8 %) of the E protein of SARS-CoV-2 strains are highly conserved. Moreover, we found 58.77 % (134 of 228) nucleotides (nt) positions of SARS-CoV-2 E gene encountering a total of 176 unique nt-level mutations globally, which may affect the efficacy of real time RT-PCR-based molecular detection of COVID-19. Importantly, higher aa variations observed in the C-terminal domain (CTD) of the E protein, particularly at Ser55-Phe56, Arg69 and the C-terminal end (DLLV: 72–75) may alter the binding of SARS-CoV-2 Envelope protein to tight junction-associated PALS1 and thus could play a key role in COVID-19 pathogenesis. Furthermore, this study revealed the V25A mutation in the transmembrane domain which is a key factor for the homopentameric conformation of E protein. Our analysis also observed a triple cysteine motif harboring mutation (L39M, A41S, A41V, C43F, C43R, C43S, C44Y, N45R) which may hinder the binding of E protein with spike glycoprotein. These results therefore suggest the continuous monitoring of the structural proteins including the envelope protein of SARS-CoV-2 since the number of genome sequences from across the world are continuously increasing., Highlights • We found 1.2 % and 58.77% of 81,818 strains possessing amino acid and nucleotide mutations, respectively, in SARS-CoV-2 E protein. • NTD, TMD, and CTD domains of E protein had aa substitutions at 7, 25, and 31 sites, respectively. • A total of 115 unique aa mutations were observed in 63 (84%) sites of the primary structure of E protein.