Summary
Highlights
Microbial symbiosis is defined as the close association of two dissimilar organisms. Four types are discussed: neutralism (neither affected), mutualism (both benefit, e.g., E. coli producing Vitamin K), commensalism (one benefits, the other is unaffected), and parasitism (one benefits, the other is harmed, e.g., malaria).
The session introduces the microbe-host relationship, focusing on beneficial and harmful interactions, and provides an overview of the human microbiome project and its goals. The project aims to identify a core human microbiome, correlate microbiome changes with health and disease, develop new technologies for data management, and address ethical implications.
Indigenous microbiota (normal flora) includes bacteria, fungi, viruses, and protozoans residing within a person, totaling 100 trillion cells and 500-1000 species, thriving in moist, warm conditions. Transient microbiota are temporary residents picked up from the environment. Dysbiosis, the destruction of balance between host and microorganisms, can lead to superinfections like candidiasis, especially in immunocompromised individuals.
The video details the specific microorganisms found in various body regions: the skin (Staphylococcus epidermidis, Propionibacterium causing pimples), eyes and ears (mostly sterile internally, external parts harbor S. epidermidis, S. aureus), respiratory tract (nasal passages, oropharynx with S. aureus, Corynebacterium, Strep pyogenes), oral cavity (alpha-hemolytic streptococci, S. mutans), and gastrointestinal tract (low in stomach, diverse in colon, e.g., E. coli).
Indigenous microbiota produce useful compounds (vitamins K, B12), stimulate the immune system, and prevent colonization by harmful microbes (antagonistic effect). Opportunistic microorganisms can cause infection when the host's immune system weakens. Biotherapeutic agents (probiotics) like Erceflora restore gut microbiome balance after infection or antibiotic treatment. Fecal transplants are also mentioned for severe infections like C. difficile.
Microbes form complex, persistent communities called biofilms, protected by a glycocalyx membrane. Biofilms are problematic in medical devices as they evade antibiotics and the immune system. Microbial synergism occurs when microbes team up to cause diseases that neither could cause alone, often leading to polymicrobial infections like trench mouth disease.
Infection means colonization and establishment of residence without disease manifestation, while infectious disease involves the appearance of signs and symptoms due to pathogenic factors. The four phases of infectious disease are exposure, incubation, prodromal stage, period of illness, and then convalescence, disability, or death.
Pathogenicity is the ability of a microbial species to cause disease. Virulence is the degree of pathogenicity. A virulence factor is a characteristic that enables a pathogen to cause disease, such as adherence factors (receptors, adhesins, pili), and mechanisms for evading immune function.
Pathogens evade the immune system through various means: intracellular survival (escaping respiratory bursts, possessing protective coatings, inhibiting phagolysosome formation), capsules (anti-phagocytic), flagella (motility), M protein (evades phagocytosis), and protein A (inhibits phagocytosis). Exoenzymes like necrotizing enzymes, coagulases, kinases, hemolysins, and hyaluronidase contribute to tissue damage and evasion.
Exotoxins (gram-positive) are proteins secreted and organ-specific (neurotoxins like botulinum, enterotoxins like cholera toxin, cytotoxins like diphtheria toxin). Endotoxins (gram-negative) are part of the cell wall (lipid A) released upon cell lysis, causing fever and systemic effects. Microbes also use antigenic variation, camouflage, molecular mimicry, and antibody destruction to evade the immune system. Genetic mechanisms like plasmids, transposons, and bacteriophages contribute to pathogenicity and antimicrobial resistance, which is the ability of microbes to resist antibiotics, often via efflux pumps.