BM329 Block D

Endospore Forming Bacteria

Bacteria capable of forming endospores, including Bacillus and Clostridium species.

Clostridium difficile

Anaerobic spore-forming bacterium causing hospital-acquired infectious diarrhea, difficult to culture, and producing toxins.

Sporulation

Formation of spores by bacteria as a survival mechanism under unfavorable conditions.

Virulence Factors

Factors possessed by C. difficile enabling it to cause colitis, including toxins, adherence, and mobility factors.

Binary Toxin

Toxin expressed by some hypervirulent C. difficile strains, consisting of CdtA and CdtB proteins.

Gut Microbiome

Microbial community in the human gut, influencing various physiological processes and potentially playing a role in diseases.

Antibiotic-Associated Diarrhea

Diarrhea caused by antibiotics disrupting the normal gut flora, leading to C. difficile overgrowth and toxin production.

Microbiome Mediated Defenses

Defense mechanisms involving the gut microbiota against C. difficile, such as bile acid conversion and sialic acid metabolism.

Pathogenesis

Mechanisms by which C. difficile causes disease, including impaired tight junctions, cell death, and toxin-induced effects.

Prevention

Measures to prevent C. difficile infection, including hygiene practices, isolation of infected individuals, and thorough cleaning protocols.

Shigella Groups

S. flexneri, S. sonnei, S. dysenteriae are the main disease-causing groups with distinct prevalence in different parts of the world.

Salmonella and Shigella Virulence Factors

Key factors include endotoxins, exotoxins, secretion systems, flagella, pilli, and biofilm formation.

Entry into Host Cells

Salmonella and Shigella induce internalization into host cells, subverting host functions and triggering mechanisms for survival and spread.

Type III Secretion

Delivers bacterial effectors into the host cytosol, triggering host cytoskeleton reorganization for bacterial engulfment.

Intracellular Pathogens

Salmonella survive in vacuoles, while Shigella escape into the cytosol, facing challenges like iron acquisition and motility.

Survival in the Host Cell

Salmonella modify phagosomes to avoid lysosome fusion, while Shigella rupture phagosomes to escape into the cytosol.

Salmonella Containing Vacuole

Salmonella adapt to vacuolar environments, preventing maturation and recruiting host proteins for replication.

Shigella in the Host Cell

Shigella escapes phagosomes, spreads in the cytoplasm using actin-based motility, and recruits host proteins for spread.

Actin Based Motility

Bacteria like Shigella use host actin for motility, involving bacterial proteins like IcsA and host factors for spread.

Exotoxins

Enterotoxins like Shiga toxin cause fluid accumulation and diarrhea, affecting eukaryotic ribosomes to stop translation.

Endotoxin and Vi Antigen

Salmonella LPS triggers an inflammatory response, while S. typhi has Vi antigen to mask LPS and avoid immune response.

Disease Transmission

Salmonella and Shigella are transmitted orally via contaminated water or food, with Shigella having a low infectious dose.

Asymptomatic S

Some individuals carry S. typhi asymptomatically, shedding the bacterium intermittently without showing symptoms.

Typhoid Fever Treatment

Antibiotic therapy reduces mortality rates, with fluoroquinolones or cephalosporins being common choices for treatment.

Treatment of Diarrhoeal Diseases

Rehydration therapy is crucial, and antibiotics may be used in severe cases, with specific choices for Salmonella and Shigella infections.

dsRNA Transcription

Occurs in early and late phases, with the negative strand serving as a template for virion core enzymes.

Positive Strand mRNA

Genome has a 5’ methyl guanosine capped, 3’ poly adenylated mRNA leaving the core for translation.

Orthoreovirus

Contains outer capsid proteins associating with the core, virions exit via cell lysis.

Rotavirus Assembly

Process resembles enveloped viruses, replication occurs in the intestine.

Viral Diarrhoea Pathogenesis

Commonly causes infantile diarrhoea, replication in columnar epithelial cells of the small intestine.

VP7 and VP4

Outer capsid proteins used for serotyping, stable virions.

Faecal-Oral Route

Spread mechanism for these viruses, causing serious diarrhoea in children.

Direct Detection

Large quantities of virus in stool allow for direct detection, no specific antiviral therapy available.