Introduction to Host-Microbe Interactions Normal Flora Potential Colonization Sites Types of Pathogens Progression of Disease

Introduction to Host-Microbe Interactions Normal Flora Potential Colonization Sites Types of Pathogens Progression of Disease www.phwiki.com

Introduction to Host-Microbe Interactions Normal Flora Potential Colonization Sites Types of Pathogens Progression of Disease

Manus, Mihio, Managing Editor has reference to this Academic Journal, PHwiki organized this Journal Introduction to Host-Microbe Interactions Normal Flora More bacterial than human cells in the body provide some nutrients (vitamin K) stimulate immune system, immunity can be cross-reactive against certain pathogens Prevent colonization by potential pathogens (antibiotic-associated colitis, Clostridium difficile) Potential Colonization Sites

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Types of Pathogens Primary Pathogens Cause disease upon infection, not normally associated with host Plague (Yersinia pestis), influenza virus Opportunistic Pathogens Cause disease under some circumstances, sometime members of normal flora Pseudomonas, C in addition to ida albicans Progression of Disease Transmission: infectious dose from 10-106 organisms Incubation period: few days (common cold)-weeks (hepatitis A)-months (rabies) Convalescence: Clearing (Strep throat, S. pyogenes) Latency (Chicken pox, tuberculosis, cold sores)

Koch’s Postulates Proposed by Robert Koch Conclude that a microbe causes a particular disease Must fulfill four postulates 1. Microorganism must be present in every case of the disease 2. Organism must be grown in pure culture from disease hosts 3. Produce the same disease from the pure culture 4. Organism recovered from experimentally infected hosts Molecular Postulates Describe virulence factors Four postulates 1. Virulence gene or its product must be present 2. Virulence gene must trans as long as m a non-pathogen into a pathogen 3. Virulence gene must be expressed during disease process 4. Antibodies against gene products are protective Establishing an Infection 1. Encounter: fecal-oral (cholera) human-human (tuberculosis) animal-human (rabies) vector-borne (plague, lyme disease) environmental contact (anthrax)

Establishing an Infection 2. Adherence Prevents early clearance Often bind host tissues via pili Specificity can determine host range of pathogen

Establishing an Infection 3. Colonization: multiplication in addition to maintainance Competition with normal flora Resist: bile stomach acid peristalsis skin secretions IgA (mucosal antibodies) compete with host as long as iron Establishing an Infection 4. Molecule Delivery Affects target cell structure in addition to host response

Invasion:Breaching Anatomical Barriers Find new niche with few competitors Gain access to rich nutrient supply 1. Skin: tough barrier, rely on wounds or insect vectors 2. Crossing mucous membrane (e.g. intestinal epithelial cells) Zippering-model of invasion Tight lig in addition to -receptor interactions direct uptake “one at a time” uptake Ruffling method of invasion General induced cellular response Can lead to co-invasion of other bacteria in close proximity

M cell Invasion M cells are a portal to the immune system Important site of “antigen sampling” Some pathogens use phagocytic nature of M cells to access deeper tissues by transcytosis Avoiding the Host Defenses 1. Hiding within host cells Avoid exposure to host antibodies if remain intracellular Access to rich source of nutrients

Cell-to-cell Spreading Shigella in addition to Listeria species lyse out of vacuole -assemble actin at pole -actin propels them into neighboring cell “convergent evolution” “molecular mimicry” Avoiding the Host Defenses 2. Avoiding complement killing Complement factors in blood serum can assemble into MAC “membrane attach complex” that are bactericidal C3b is first component of complex to bind Some bacteria bind factors that regulate C3b activity, prevent MAC assembly “serum-resistance”

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Avoiding the Host Defenses 3. Avoiding phagocytosis Innate immune cells engulf (phagocytose) in addition to kill microorganisms with degradative enzymes Block signaling molecule production or degrade them after production C5a cleaved by C5a peptidase of Strep pyogenes (strep throat)

Avoiding the Host Defenses 3. Avoiding phagocytosis Capsule production on surface of bacteria: capsule leads to C3b inactivation-”serum resistance” M protein of Streptococcus: also inactivates C3b Fc receptors: bind antibodies in addition to orient dangerous end away from bacteria Found in Streptococcus (Protein G) in addition to Staphylococcus (Protein A) Survival Strategies within Phagocytes A niche without competitors Phagosomal escape: lyse out of vacuole in addition to grow in cytoplasm of host cell Shigella in addition to Listeria

Damage due to the Immune System Inflammation: bacterial meningitis Neisseria meningitis Antigen-Ab complexes Settle in kidney or joints Glomerulonephritis from S. pyogenes Cross-reactive Ab’s Ab’s against pathogen may cross-react with host tissues Accute rheumatic fever, complication of Strep throat

Manus, Mihio Managing Editor

Manus, Mihio is from United States and they belong to Gila River Indian News and they are from  Sacaton, United States got related to this Particular Journal. and Manus, Mihio deal with the subjects like Native American Interest

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