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Lectures 28-31 MMG 301
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- 1Two major groups of animals based on gut anatomyForegut Fermenters - carnivorous animals / complex stomachs
Hindgut Fermenters - herbivores and single chamber stomachs - 2RumenContains an anaerobic microbial community that breaks down plant fibers
- 34 Steps to food digestion in ruminants1. 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 - 4Volatile Fatty AcidsProduced in rumen - provide 70% of a ruminants energy supply
- 5dysbiosisSudden dietary changes that produce significant changes in the makeup of a microbial community
- 6acidosisA buildup of acid that damages the rumen and acidifys blood
- 7Human Microbiome/Human Microbiome Project1. 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 - 8Changes as food goes though the upper&lower gastrointestinal tractspH - low in stomach, increases to neutral through the tracts
Oxygen - decreases through the tracts - 9Positive effects of intestinal microbesVitamin Synth.,Glycosidase activity, Steroid Metabolism, Stimulation of immune system, antagonism of pathogens
- 10Transmission of Symbionts 1. Horizontal 2. Vertical1. Symbiont comes from environment
2. (aka heritable) Symbiotic is passed down from parent - 11BacterioicytesInsect host cells for heritable symbionts- i.e. Buchnera bacteria w/ Pea Aphids
- 12Termite source of energyIn the hindgut there are symbiots that digest wood fibers, providing nutrients
- 13Hawaiian Bobtail SquidLight emitting bacteria in a specialized light organ that emit light in response to quorum sensing
- 14Rifta Tubeendosymbiotic chemolithotropic bacteria in a sponge-like tissue known as a trophosome
- 15Colonization ( 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 - 16Skin CommunitiesContaining sebaceous glands (hair growth gland)
-skin communities have many examples of bacterial interference - preventing pathogens from colonizing/growing - 17Anti-Bacterial Enzymes in mouth (2)Lactoperoxidase - Makes a ROS that kills bacteria
Lysozyme- enzyme that cleaves peptidoglycan - 18Oral Microbal Communities-many pollysaccaride-producing bacterial colonies that form a biofilm on the tooth surface & in the gingival crevice
- 19Steps of biofilm formation in dental diseases1. 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 - 20Dental Caries Gingivitis1. anaerobic microbes in an oral biofilm ferment diatary sugars& acids = demineralize tooth enamel
2. Gingivitis - infection of gingival crevice - 21Heliobacter pylori- often colonized stomach & is associated w/ 80% of stomach ulcers
- not an acidophile (urea/blood->Heliobacter->NH4+(alkaline)) - 22Upper Respiratory Tract-normal microfloura antagonize pathogens from growing
-in some, pathogenic bacteria are present but do not cause symptons -> hosts are carriers - 23Lower Respiratory TractSterile in healthy individuals
- 24Urogenital Tract-bladder is sterile
- in the vagina bacteria like Lactobacillus acidophilus ferment glycogen & produce acid, preventing bacteria growth - 25PathogenicityThe ability of a microorganism to cause disease
- 26Oppertunistic PathogenCan cause disease in an already weakened host
- 27Invasion & InfectionInvasion is the entry of a pathogen through epithelium layers, and an infection is growth of a pathogen at an anatomical site
- 28ID50 & LD50ID50 is the amount needed of a pathogen to infect 50% of hosts, LD50 is the amount of a pathogen that kills 50% of hosts
- 29Adherence-Aided by adherence factors
-is usually specific - tissue trophism - 30Adherence FactorsGlycocalyx - polymers that aid in biofilm formation (often are slime layers of capsules)
Adherence proteins- found on fimbrae and pili - 31Bacteremia-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
- 32Virulence factor- A pathogen-produced substance (protein,enzyme,adherence factor, or toxin) that promotes the establishment & pathogenisis of a disease
- 33Examples of Virulence FactorsHyaluronidase - 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 - 34ExotoxinProteins that are excreted by bacteria and are toxic to host cells
-If they affect the small intestine they are known as enterotoxins - 35Types of Exotoxins1. 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 - 36hemolysins- 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) - 37Diptheria toxin1 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 - 38Tetanus & 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 - 39Botulism Toxin7 types, Type A has medical use (Botox)
-Results in flaccid paralysis by blocking the release of Acetylcholine which is responsible for muscle contraction - 40Tetanus toxinResults in spastic paralysis, prevention of an inhibitory interneuron from preventing acetylcholine release
- 41Cholera - 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) - 42Effects 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 - 43Assay for endotoxins-Limulus amoebocyte assay (LAL) - generates color, uses the cells of Limulus as they are extremely sensitive to endotoxins and lyse easily
- 44Innate 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) - 45Risk 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 - 46Innate ImmunityA preexisting ability to recognize and destroy pathogens/toxins
-carried out by cells known as phagocytes (Specialized blood cells that engulf and kill pathogens) - 47Adaptive ImmunityRelies on previous exposure to a pathogen
3 Main functions
-Recognise a pathogen and their toxins
-Discriminate for pathogens vs normal cells
-Eliminate pathogen/toxin - 48AntigenAny molecule or portion of a molecule that stimulates a response in immune system; i.e. proteins and pollysaccarides
- 49Phagocyte-Specialized blood cells that engulf and kill pathogens
- 50Macrophage-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 - 51Two Parts of Adaptive Immunity1.Antibody-Mediated
2.Cell-Mediated - 52T-CellsT-Cell receptors recognize a specific antigen produced by a phagocyte after pathogen destruction
-called the Major histocompatibility complex - 53T-Cell SubtypesTc 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 - 54B cellsAntibody 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 - 55Antibodies (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) - 56epitopes/antigenic determinantsThe small region of a molecule recognized by T-cells and antibodies
- 57Superantigenbacterial 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 - 58Natural Active ImmunityAfter an infection, immunity to a pathogen develops
- 59Artificial Passive ImmunityNo 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) - 60Artificial Active Immunity-uses vaccination to produce response that provides immunity
- in some cases boosters are provided for longer immunity - 61Vaccine Types1. 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)