BIOM 250 1st Edition Lecture 12Outline of Last Lecture I. Controlling MicrobesII. Effective DisinfectionIII. PhenolsIV. HalogensV. AlcoholsVI. Chemical Food PreservativesVII. AldehydesVIII. Hydrogen PeroxideIX. DiseaseX. Normal MicrobiotaXI. Opportunistic PathogensXII. EtiologyOutline of Current LectureI. Disease StagesII. ReservoirIII. Transmission of DiseaseIV. Disease VectorsV. Nosocomial Infection These notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.VI. EpidemiologyVII. Microbial PathogenicityVIII. Adherence IX. InvasionX. ToxinsCurrent LectureI. Disease Stagesa. Incubation stage- interval between infection and the first signs/symptomsi. Depends on host-cell resistance, inoculum, and virulence factorsb. Prodromal- early, mild symptomsc. Illness- period of most severe diseasei. Variable symptoms, immune response is activatedd. Decline- signs/symptoms begin to diminishe. Convalescence- recoveryII. Reservoir- continual sources of infectiona. Human: i. Carriers have the infection but little to no symptomsii. Ex: STDs; hepatitisb. Animal: i. Disease primarily in wild and domestic animalsii. Ex: rabies; lyme diseasec. Nonliving: botulism, tetanus, cholerai. Arise from soil, contaminated water and contaminated foodIII. Transmission of Diseasea. Vehicle transmission:i. May be waterborne, foodborne or airborneii. Airborne can travel longer distances but the agent must remain viable (intact)b. Contact transmission:i. Direct- person to person contactii. Indirect- spread by fomites1. Fomite- an infected non-living object2. Ex: bedding; utensils; medical equipmentiii. Droplet- contaminated droplet nuclei1. Ex: coughing; sneezing; talking2. Travels over a short distanceIV. Disease Vectors- animal disease carriersa. Mostly arthropods—fleas, ticks, mosquitosb. Transmit by two general methods:i. Mechanical transmission- arthropod carries pathogen on its feet1. Ex: flies landing on feces and then landing in your foodii. Biological transmission- pathogen reproduces in vector1. Ex: malaria in mosquitosV. Nosocomial Infectionsa. Infections acquired in the hospitali. Affect 5-15% of all patientsii. Patients typically have weaker immune systems making them more susceptible to these infectionsiii. Transmission chains also play a role—staff to patient; patient to patientiv. Infection control procedures are criticalb. Opportunistic organisms- many of the microbes that cause these infections would not be pathogenic to a healthy individualVI. Epidemiologya. Descriptive- collection and analysis of data from affected individualsi. Retrospective- look at data after outbreakii. Prospective- following healthy subjects forward and charting their diseaseacquisitionb. Analytical- comparison of a diseased group and a healthy groupc. Experimental- controlled experiments (ex: drug trial with a placebo)d. Case reporting- health care workers report specified disease to local, state, and national officese. Notifiable infectious diseases- physicians are required to report occurrence of certain diseasesVII. Microbial Pathogenicitya. Mechanisms of pathogenicity:b. Pathogenicity- ability to cause diseasei. Organism must: enter proper location; stay in that location; cause damage; evade host defensec. Virulence- how damaging a pathogen isi. Many factors play into this: toxins produced; speed of replication; evasionof host defensesd. Entry of pathogens:i. Pathogens may enter through mucous membranes1. Respiratory tract is the most frequent entry point2. Reproductive areas- pathogens may enter through damaged or normal tissue in the mucous membranes of your reproductive areasii. Skin is another common entry point1. Enter through damaged areas, follicles, and places of penetration or growthiii. Parenteral route-1. Enter through penetration or injury2. Through these routes pathogens gain access to their preferred locationsiv. Preferred portal of entry:1. Pathogens must gain access to the correct location in order to produce diseasee. How much of a pathogen you need in order to make you sick:i. ID50: the infections dose necessary for 50% of the test populationii. LD50: lethal dose of a toxin necessary for 50% of the test populationVIII. Adherence a. Adhesin/ligandsi. Glycoproteins and/or lipoproteinsii. Structures used: glycocalyx; fimbriaeb. Adhesins bind to receptors on host cells and form biofilmsc. Biofilms provide resistance to antibiotics and immune attackIX. Invasiona. Capsules around microbes—sugars prevent phagocytosisb. Cell walls provide immunity resistancec. Antigenic variation- antigens change their surface proteins making older antibodies unable to bind to themd. Exoenzymes:i. Coagulases-clot the blood and forms blockage with bacteria insideii. Kinases- dissolve clots by activating the body’s own clot busting proteinsiii. Hyaluronidase- enzyme that digest hyaluronic acid, which is the acid that connects cells in tissues1. This digestion allows bacteria to spreadiv. Collagenase- digests collagen which is part of connective tissue in musclesand organsv. IgA protease- 1. IgA is a secreted antibody usually found in the gut mucous2. Remember: antibodies are immune proteins that bind to foreign substances3. Proteases are enzymes that digest proteins4. Therefore—IgA protease digests the IgA antibodye. Penetration into the host cell:i. Invasins- bacterial surface proteins bind to the target cell1. This induces the cell cytoskeleton to surround and take in the bacteriumii. Siderophores- secreted proteins that bind iron1. Iron is critical to bacterial growth so it is usually limited in the blood stream2. Low iron may induce toxin production to kill cells—which then release ironX. Toxins- microbial poisons; many targets; cause many symptomsa. Exotoxins-i. Part of bacterial metabolismii. Proteins are secreted during infectioniii. Most genes for toxins are carried on plasmids or by phagesiv. Are soluble in fluids and cause damage even in very small amountsv. Can destroy cell components or inhibit functionsvi. Can be inactivated by an antitoxin (antibody)vii. Inactivated endotoxins are used in some vaccines b. A-B toxinsi. Most exotoxins are these, 2-component typesii. Both are polypeptidesiii. The A part is the enzyme and the B part is the binding proteiniv. Process:1. A-B complex is released2. B attaches to target cell receptor3. Plasma membrane invaginates4. Within the target cell A-B