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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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