Microbial Mechanisms of Pathogenicity Dr. AckmanSlide 2
Definitions Pathogenicity Ability of a microorganism to bring about ailment by beating the safeguards of a host Virulence The degree or degree of pathogenicitySlide 3
Portals of Entry Pathogens Must access have Adhere to host tissue Penetrate or sidestep have protections Damage have tissueSlide 4
Portals of Entry Portal of Entry Routes microorganisms can infiltrate the body 1-mucous layers 2-skin 3-parenteral courseSlide 5
Mucous film section Mucous layers Respiratory tract Easiest and most regular course of contamination Inhaled through nose or oral depression Duct particles, dampness beads Common cool, pneumonia, tuberculosis, flu and smallpoxSlide 6
Mucous Membrane Entry Mucous layer Gastrointestinal course In sustenance or water Contaminated fingers Most are inactivated by stomach corrosive, proteins, bile Poliomyelitis, hepatitis An, amoeboid diarrhea, choleraSlide 7
Mucous Membrane Entry Mucous layer Genitourinary tract Contracted sexually Intact or broken bodily fluid layers STI (sexually transmitted contaminations) HIV, genital warts, genital herpes, syphilis, and gonorrheaSlide 8
Skin Unbroken skin – boundary to microorganisms Hair follicles and sweat organ pipes Some pathogens infiltrate ordinary skin Hookworm hatchling Some pathogens develop on keratin of skin Ringworm Abscesses, blazesSlide 9
Parenteral Route Parenteral course Microorganisms kept straightforwardly beneath skin Puncture wounds, infusions, nibbles, wounds, and surgery Tetanus, rabies, Hepatitis B, and intestinal sicknessSlide 10
Preferred Portal of passage Some living beings must enter by means of favored course to bring about illness Some life forms may bring about ailment with a wide range of course of sectionSlide 11
Preferred Portal of EntrySlide 12
Numbers of Invading Organisms Disease more probable with more creatures (pathogens) ID 50 - irresistible dosage for half of a specimen populace Measures destructiveness of a microorganism Anthrax Cutaneous (skin) ID 50 10-50 endospores Inhalation ID 50 10,000-20,000 endospores Gastrointestinal ID 50 250,000 – 1,000,000 endosporesSlide 13
Numbers of Invading Microbes LD 50 – deadly measurements for half of an example populace Measures strength of poisons LD 50 Botulinum poison = 0.03 ng/kg Shiga poison = 250 ng/kg Staphylococcal enterotoxin = 1350 ng/kgSlide 14
Adherence of Microorganisms after section into host must hold fast to host Adherence Attachment of microorganisms after passage to host Surface atoms Ligands and adhesins tie particularly for receptors on host cells. Glycocalyx, pili, fimbrae, flagellaSlide 15
Adherence Receptors of host cells Usually a sugar i.e. mannose Altering receptor, adhesin, or both modifies capacity for disease to happenSlide 17
Adherence An illustration Streptococcus mutans appends to teeth by its glycocalyx Actinomyces have fimbrae that cling to glycocalyx of S. mutans Involved in dental caries (holes) E. coli have adhesins on fimbrae, append to particular districts of small digestive systemSlide 18
Biofilms Communities of microorganisms and their extracellular items that join to non-living and living surfaces Algae Dental plaque Medical cathetersSlide 19
How pathogens infiltrate have guards Capsules Impair phagocytosis Prevents phagocytic cell from appending to microorganism Made of glycocalyx Streptococcus pneumoniae Griffith\'s analysis of hereditary changeSlide 20
How pathogens enter have protections Components of Cell Wall M – protein Mediates connection to epithelium Resists phagocytosis Opa Outer layer protein Helps in connection Waxes Resist processing by phagocytes MycobacteriumSlide 21
How pathogens enter have barriers Enzymes Extracellular catalysts (exoenzymes) Dissolve material between cells, shape or disintegrate clumps Coagulase Converts fibrinogen to fibrin cluster Isolates microorganism from host safeguards Kinases Break down fibrin Hyaluronidase Breaks down cell to cell bonds in connective tissue Collagenase Produced by a few Clostridium sp Breaks down protein collagen IgA proteases Destroy antibodiesSlide 22
How pathogens enter have barriers Antigenic variety Pathogens adjust surface proteins Several adaptations of Opa protein New antibodies must be created Gonorrhea Sleeping affliction InfluenzaSlide 23
How pathogens infiltrate have guards Penetration into host cells cytoskeleton Invasins Rearrange actin fibers Facilitates development of microorganism into cellSlide 24
How Pathogens Damage Host Cells 1-use host\'s supplements 2-coordinate harm in prompt region of contamination 3-poison generationSlide 25
How pathogens infiltrate have resistances Using host\'s supplements Siderophores Bind press far from host\'s iron restricting proteins Direct Damage Multiplication of microorganism inside cell Viruses Bacterial ProtozoalSlide 26
Toxins Toxin Poisonous compound delivered by microorganisms Often the pathogenic segment of a microorganism Toxigenicity Ability of a microorganism to create a poison Toxemia Presence of poison inside the bloodSlide 27
Toxins Fever Cardiovascular irregularities Diarrhea Shock Destroy platelets Destroy veins Disrupt sensory systemSlide 28
Exotoxins Produced inside the microbes as a major aspect of development Secreted by the microscopic organisms into encompassing environment Exotoxins are proteins Enzymes that catalyze substance responses Can be utilized again and again Gram – or gram + microscopic organisms Genes carried on plasmid Inhibit certain metabolic capacities Very dangerous Botulinum poison 1 mg murder 1,000,000 individualsSlide 29
Exotoxins Readily diffuse into body liquids and tissue Disease particular Disease brought about by the exotoxin, not the contamination itself Antitoxins Body creation of antibodies against the poison Toxoids Toxin inactivated by warmth or different chemicals (formaldehyde) Still start creation of antibodies Injected into the body (toxoid immunization) Tetanus DiphtheriaSlide 30
Exotoxins 3 sorts of exotoxins 1-A-B Toxins Also called sort III poisons Most exotoxins fall into this class A segment Active catalyst segment B segment Binding segmentSlide 31
Exotoxins A-B poisons A-B poison discharged by microscopic organisms B part ties to receptor of host cell Toxin transported crosswise over film into cell A-B segments isolate A segment hinders protein combination and executes cellSlide 32
Exotoxins 2 – Membrane disturbing poison Type II poisons Causes lysis of cells by upsetting cell film Form protein stations Staphylococcus aureus Disrupt phospholipids Clostridium perfringens Leukocidins Membrane upsetting poisons that slaughter phagocytic WBC\'s Hemolysins Membrane disturbing poisons that murder erythrocyes RBC\'sSlide 33
Exotoxins 3-Superantigens Type I poisons Provoke exceptional insusceptible reaction Protein in nature (antigens) Stimulate T – cells Release cytokines (excessively) Causes fever, queasiness, heaving the runsSlide 34
Exotoxins Neurotoxins Attack nerve cells Cardiotoxins Attack heart cells Hepatotoxins Attack liver cells Enterotoxins Attack coating of GI tract Cytotoxin Attacks wide assortment of cellsSlide 35
Specific Exotoxins Diphtheria poison Cornybacterium diphtheriae Requires lysogenic phage conveying tox quality Cytotoxin restrains protein blend in eukaryotic cells Erythrogenic poisons Streptococcus pyogenes A,B,C poisons harm plasma layers of vessels under skin bringing about rash Scarlet feverSlide 36
Specific Exotoxins Botulinum poison Clostridium botulinum Acts on neuromuscular intersection Prevents nerve drive transmission Inhibits arrival of neurotransmitter acetylcholine Causes flabby loss of motion Tetanus poison Clostridium tetani Tetanospasmin CNS squares inhibitory neurons to skeletal muscle Results in wild muscle withdrawals Lock jawSlide 37
Specific Exotoxins Vibrio enterotoxin Vibrio cholerae Produces cholera poison Sub unit B joins to epithelium of intestinal tract Sub unit A causes cells to emit a lot of electrolytes bringing about the runsSlide 38
Specific Exotoxins Staphylococcal enterotoxin Staphylococcus aureus Similar to cholera poisonSlide 39
Endotoxins Part of the external film Lipopolysaccharides (LPS) Lipid A Released when g-microorganisms experience lysis and duplication Antibiotics?Slide 41
Endotoxins Cause WBC to discharge cytokines Toxic at these levels Cause chills, fever, shortcoming, summed up hurts, stun and demise Can bring about actuation of blood thickening components creating modest blood clusters Disseminated intravascular coagulating (DIC)Slide 42
Endotoxins versus ExotoxinsSlide 44
Plasmids Plasmid qualities may make microorganisms impervious to a few anti-microbials Plasmids may convey other destructiveness variables, for example, poison generation, fimbraeSlide 45
Lysogeny Bacteriophages consolidate DNA into bacterial chromosomes Viruses stay idle inside bacterium, not bringing about lysis May make microscopic organisms with new genome Called lysogenic change Some microbes require disease by bacteriophage to be pathogenic Diphtheria poisonSlide 46
Pathogenic Properties of Viruses Cytopathic impacts of infections Animal infections more often than not bring about death of host cell Accumulation of duplicating infections Alter penetrability of cell layer Inhibit have DNA or RNA Cytopahtic impacts (CPE) Visible impacts of viral contamination cytocidal or noncytocidalSlide 47
CPE\'s 1. Macromolecule combination ended Mitosis repressed (Herpes infection) 2. Arrival of lysosomes inside cell an obliteration of cell substance 3. Consideration bodies Viral parts, nucleic acids Various size and recoloring qualities Eosinophilic, basophilic Negri bodies (Rabies)Slide 48
CPE\'s 4. Syncytium Adjacent contaminated c
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