Lectures 28-31 MMG 301

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Two major groups of animals based on gut anatomy Foregut Fermenters - carnivorous animals / complex stomachs Hindgut Fermenters - herbivores and single chamber stomachs
Rumen Contains an anaerobic microbial community that breaks down plant fibers
4 Steps to food digestion in ruminants 1. Food enters rumen & begins digestion 2. Mixture goes to omasum & is concentrated by water adsorption 3. Mixture goes to abomasum (true stomach) - acid kills and digests food & mictobes 4. Food + Microbes go to small intestine
Volatile Fatty Acids Produced in rumen - provide 70% of a ruminants energy supply
dysbiosis Sudden dietary changes that produce significant changes in the makeup of a microbial community
acidosis A buildup of acid that damages the rumen and acidifys blood
Human Microbiome/Human Microbiome Project 1. All the microbes on the site of the body, outnumber human cells 10:1 2. An ongoing study to document microbe populations, diversity and changes at anatomical sites using 16S rRNA gene sequencing
Changes as food goes though the upper&lower gastrointestinal tracts pH - low in stomach, increases to neutral through the tracts Oxygen - decreases through the tracts
Positive effects of intestinal microbes Vitamin Synth.,Glycosidase activity, Steroid Metabolism, Stimulation of immune system, antagonism of pathogens
Transmission of Symbionts 1. Horizontal 2. Vertical 1. Symbiont comes from environment 2. (aka heritable) Symbiotic is passed down from parent
Bacterioicytes Insect host cells for heritable symbionts- i.e. Buchnera bacteria w/ Pea Aphids
Termite source of energy In the hindgut there are symbiots that digest wood fibers, providing nutrients
Hawaiian Bobtail Squid Light emitting bacteria in a specialized light organ that emit light in response to quorum sensing
Rifta Tube endosymbiotic chemolithotropic bacteria in a sponge-like tissue known as a trophosome
Colonization ( and location) -The growth of microbes found at any anatomical site -Commonly occurs on the mucus membrane, outer layer of epithelial cells that are on the surface of many tissues
Skin Communities Containing sebaceous glands (hair growth gland) -skin communities have many examples of bacterial interference - preventing pathogens from colonizing/growing
Anti-Bacterial Enzymes in mouth (2) Lactoperoxidase - Makes a ROS that kills bacteria Lysozyme- enzyme that cleaves peptidoglycan
Oral Microbal Communities -many pollysaccaride-producing bacterial colonies that form a biofilm on the tooth surface & in the gingival crevice
Steps of biofilm formation in dental diseases 1. layer of glycoprotein on clean tooth 2. Colonization of bacteria that form a biofilm 3. Continued growth results in a thicker layer = plaque 4. Plaque calcifys, becomes tartar +Facilitated by surcorse that is used to synth. dextran
Dental Caries Gingivitis 1. anaerobic microbes in an oral biofilm ferment diatary sugars& acids = demineralize tooth enamel 2. Gingivitis - infection of gingival crevice
Heliobacter pylori - often colonized stomach & is associated w/ 80% of stomach ulcers - not an acidophile (urea/blood->Heliobacter->NH4+(alkaline))
Upper Respiratory Tract -normal microfloura antagonize pathogens from growing -in some, pathogenic bacteria are present but do not cause symptons -> hosts are carriers
Lower Respiratory Tract Sterile in healthy individuals
Urogenital Tract -bladder is sterile - in the vagina bacteria like Lactobacillus acidophilus ferment glycogen & produce acid, preventing bacteria growth
Pathogenicity The ability of a microorganism to cause disease
Oppertunistic Pathogen Can cause disease in an already weakened host
Invasion & Infection Invasion is the entry of a pathogen through epithelium layers, and an infection is growth of a pathogen at an anatomical site
ID50 & LD50 ID50 is the amount needed of a pathogen to infect 50% of hosts, LD50 is the amount of a pathogen that kills 50% of hosts
Adherence -Aided by adherence factors -is usually specific - tissue trophism
Adherence Factors Glycocalyx - polymers that aid in biofilm formation (often are slime layers of capsules) Adherence proteins- found on fimbrae and pili
Bacteremia -Bacteria in blood, allows for easy transport to other tissues and organs. Sometimes leads to sepsis in the event of bacteria in the blood or lymph system
Virulence factor - A pathogen-produced substance (protein,enzyme,adherence factor, or toxin) that promotes the establishment & pathogenisis of a disease
Examples of Virulence Factors Hyaluronidase - breaks down polymer that holds cells together Collagenase - breaks down collagen in connecitve tissue Streptokinase - destorys fibrins of blood clots Coagulase - creates a fibrin later around the cell that prevents the immune system from detecting the bacteria
Exotoxin Proteins that are excreted by bacteria and are toxic to host cells -If they affect the small intestine they are known as enterotoxins
Types of Exotoxins 1. Cytotoxins - damage to cell membrance causing host cell lysis and death 2. AB toxins - two subunits; B binds to the surface and A acts as an enzyme to produce host cell damage 3. Superantigens - cause a hyper-stimulated immune response resulting in excessive inflamation and tissue tamage
hemolysins - cytolytic exotozins that can lyse red blood cells -some are phospholipases (break down phospholipids) - others can cause holes in host cell membranes (i.e. Staphylococcas a-toxin)
Diptheria toxin 1 toxin mollecule kills one host cell produced by Corynebacterium Diphtheriae (a URT bacteria) -is an AB toxin, B binds to host cell receptors, A is an enzyme that blocks tRNA from entering the ribosome
Tetanus & Botulism (AB toxins) -similar toxins that elicit opposite effects -block neurotransmitter release from nerve cells that signal muscles -produced by the spore-forming anaerobe Clostridium
Botulism Toxin 7 types, Type A has medical use (Botox) -Results in flaccid paralysis by blocking the release of Acetylcholine which is responsible for muscle contraction
Tetanus toxin Results in spastic paralysis, prevention of an inhibitory interneuron from preventing acetylcholine release
Cholera - Vibrio cholerae -Colonizes small intestinal wall and produces cholera toxin - AB toxin, A acts as an enzyme to stimulate formation of cAMP -increased cAMP alters regulation of ion movment across the epithelium, and osmosis results in large fluid loss (diarrhea)
Effects of endotoxins on humans and animals - Fever - host stimulates to release more endogenous pyrogens which regulate temp -Diarrhea -Inflamaition -Generally less toxic than exotoxins From G- Bacteria lypopollysaccarides
Assay for endotoxins -Limulus amoebocyte assay (LAL) - generates color, uses the cells of Limulus as they are extremely sensitive to endotoxins and lyse easily
Innate Resistance -Physical Barriers ( cilla in nasopharynx, mucus in trachea, etc.) -Chemical Barriers (pH of stomach, etc.) -Normal microfloura (compete with pathogens for colonization & can prevent growth)
Risk Factors for Infections -Age, stress, and overall health - a compromised host is one that is weakened by - Injury, Illness from another pathogens, or being immunocompromised
Innate Immunity A preexisting ability to recognize and destroy pathogens/toxins -carried out by cells known as phagocytes (Specialized blood cells that engulf and kill pathogens)
Adaptive Immunity Relies on previous exposure to a pathogen 3 Main functions -Recognise a pathogen and their toxins -Discriminate for pathogens vs normal cells -Eliminate pathogen/toxin
Antigen Any molecule or portion of a molecule that stimulates a response in immune system; i.e. proteins and pollysaccarides
Phagocyte -Specialized blood cells that engulf and kill pathogens
Macrophage -1st line of defence -Recognize pathogen-associated molecular patterns - structures found on common pathogens -Recognition occurs via pattern recognition receptors on phagocyte -after contact with PAMP, pathogen is destroyed and and pieces of the pathogen are presented on the cells surface
Two Parts of Adaptive Immunity 1.Antibody-Mediated 2.Cell-Mediated
T-Cells T-Cell receptors recognize a specific antigen produced by a phagocyte after pathogen destruction -called the Major histocompatibility complex
T-Cell Subtypes Tc cytotoxic cells - kill host cells infected with virus Th Helper cells (2 types) -T1H - release cytokines to induce inflammation T2H - stimulate antigen-reactive B cells to proliferate and produce antibodies
B cells Antibody Production via. B Cells 1. Antigen-recognizing B cells ingest and degrate antigen 2. Antigen is presented to a T2H cell 3. If the T2H cell recognized the antigen the B cell is stimulated to produce antibodies -Some serve as receptors on B cell surface, some are released to target pathogen for destruction (produced by plasma cells) -Some differentiate into memory B cells for long term protection
Antibodies (immunoglobulins) - 5 major classes based on physical and immunological properties - IgG, IgA, IgM, IgD, IgE -IgG composed of -2 light chains & two heavy chains (Y shape)
epitopes/antigenic determinants The small region of a molecule recognized by T-cells and antibodies
Superantigen bacterial exotoxins that interact indirectly w/ hoest T helper cells and antigen presenting cells, -bing outside the MHC t-Cell receptor binding site -result in the activation of a large number of T-cells and production of cytokines, producing excessive inflammation and tissue damage
Natural Active Immunity After an infection, immunity to a pathogen develops
Artificial Passive Immunity No immune system response involved - individual receives antibodies -i.e. injection of antiserum (antibodies vs. a specific pathogen or toxin) for someone recently exposed to a toxin (i.e. snake bite)
Artificial Active Immunity -uses vaccination to produce response that provides immunity - in some cases boosters are provided for longer immunity
Vaccine Types 1. Toxoid - exotoxin that has been chemically inactivated but is still antigenic 2. Inactivated Pathogen - pathogens are killed w/ reaction of a chemical compound or heat 3. Live attenuated pathogen - a mutated version of the pathogen is used ( can't cause disease but will still allow the immune system to produce immunity)
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