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BMS 212 Week 7

by: Brandon Czowski

BMS 212 Week 7 BMS 212

Brandon Czowski

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About this Document

These notes cover the material from the first week back and the rest of the material that will be covered on the third exam.
Dr. Leonard
Class Notes
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This 4 page Class Notes was uploaded by Brandon Czowski on Friday March 18, 2016. The Class Notes belongs to BMS 212 at Grand Valley State University taught by Dr. Leonard in Winter 2016. Since its upload, it has received 11 views. For similar materials see Microbiology in Biomedical Sciences at Grand Valley State University.

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Date Created: 03/18/16
Ch. 10 cont. Development of Resistant Population o Some populations may have organisms that are naturally partially or completely resistant o Drug resistant oraganisms o Staphylococcus aureus—MRSA o Neisseria gonorrhoeae o Bacteria may acquire resistance via: o Mutations of chromosomal genes o Acquiring resistant genes on R-plasmids (extra-chromosomal pieces of DNA) by horizontal gene transfer (transformation, transduction, conjugation) o Factors contributing to resistance o Natural selection—especially in hospitals o Healthcare missuse by either doctor or patients (over-prescribing or taking inconcsistantly) o Agriculture: used as a preservative to increase profits but extra exposure increases changes of resistance o Avoiding Resistance o Take full prescription to ensure slow growth of infection and allow immune system to catch up o Limit use o Synergism: one drug enhances effects of other § Clavulonic acid/amoxicillin § Trimethoprim/ Sulfamethaxazole § Rifampin/ isoniazid o Research: adding R group to existing drug—designing drugs that target a specific organism o Origins of Resistance o Random Mutations o Horizontal gene transfers o Mechanisms for acquiring resistance o 1: limiting access of the antibiotic by decreasing permeability § Altered porin structure of Gram-negative cells: less drug allowed inside the cell increases the chances of cell survival § Active efflux: pumping antibiotic outside of the cell by using ATP, possible to be multi-drug resistant by pumping any drug outside o 2: Enzymatic inactivation of drug § Beta-lactamase: cleaves beta lactam ring via hydrolysis § Other enzyme: change functional group on drug, inactivating o 3: Modification/protection of target cell structure § rRNA methylation: methyltransferase adds methyl group to RNA at binding site of drug § Point mutation in binding site of targeted enzyme • Quinolones—DNA gyrase • Rifampin—RNA polymerase o 4: Antibiotic tolerance § Microbes in dormant, non-dividing state: not endospores but biofilms allow static state § Multi-drug tolerant § Persister cells in biofilms Chapter 14 • Normal flora: indigenous microorganisms o Transient: obtain and have for a few weeks o Residents: obtained from birth and kept • Mutualism: both members benefit • Commensalism: one benefits while other not affected Infection: entry, establishment, and multiplication within a host Disease: injury to the host True pathogens: cause disease in a healthy host with normal immune defense Opportunistic pathogens: microorganisms that become harmful to the host only if the host’s immune system is compromised Pathogenicity: capacity of microbes to cause disease (chances/likelihood) Virulence: measure of pathogenicity Virulence factors: pathogens ability that allows them to interact with/enter host, adhere to host, gain access to nutrients, and avoid detection by immune system • Normal flora can become opportunistic pathogens… o Introduced to an usual site o Suppressed/weakened immune § Age, genetic defects, immunosuppressant drugs, physical/mental stress, infections, malnutrition o Changes of normal microbiota (antibiotic use): decreases diversity can result in yeast infection, C. diff, or thrush • Portals of entry: o Skin—usually protective barrier o Mucous membranes: lining of body cavities—most common § Respiratory tract § GI tract § Urinary/reproductive § Conjunctiva (eyes) o Placenta: very few able to cross barrier to children o Parenteral routes: breaks in skin (puncture, wounds, cuts, bites) allow abnormal route of entry • Factors affecting virulence 2 o Species o Infectious dose (ID): minimum number of organisms needed to infect host § Varies from 1 to 1 billion § ID 50: # bacterial cells required to establish infection in 50% of test animals o Strength of host immune/defense § Weakened with extreme age § Malnutrition § Genetic/acquired immune defects § Physical/mental stress § Organ transplant—foreign object in body § Cancer/chemotherapy § Hygiene and behavior Adhesion—attachment phase: process microorganisms attach to host cells • Required for successful colonizing on host • Adhesion factors: virulence factors that aid in adherence to epithelial cells of mucous membranes o Special structures: fimbre/pili o Proteins: ligands/adhesions in bacteria—specific and bind to host receptors § Can be on glycocalyces, fimbre, or flagella Virulence factors for invading host • Extracellular enzymes: affect near where active o Hyaluronidase: digests hyaluronic acid—glue of animal cells o Collagenase: breaks collagen—body’s structural protein o Coagulase: causes clotting of blood proteins to protect site of infection from host defense o Kinases: digest blood clots to allow invasion of tissue • Toxins: widespread affects throughout host—harm tissues and trigger host immune response that causes damage o Exotoxins § Usually secreted protein/enzymes § High toxicity: small amounts have certain targets § Very specific and kills in low concentrations • Cytotoxins: toxins kill host cells • Neurotixins: interfere with nerve function • Enterotoxins: affect lining of GI tract o Endotoxins § Lipid A of gram-negative outer membrane that is released when cell dies, much less when cells divide § Low toxicity—fever, inflammation, high doses can cause death/shock • Antiphagocytic factors 3 o Capsule production: makes it more difficult for lysosome to attach during phagocytosis o Anti-phagocytic chemicals: § Chemicals preventing fusion of phagocytic vesicles and lysosomes § Leukocodins: cytotoxins destroy WBCs § M protein: prevent engulfing of bacteria, increasing survival Stages of Infectious Disease • Incubation: very small amounts but can still be contagious • Prodromal • Illness/invasion o Signs—observed by everyone o Symptoms—felt by host • Decline—death Portal of Exit • Shed in large amounts • Respiratory/salivary: coughing, sneezing, breathing • Skin: dead layers shed normal flora and pathogens • Fecal: intestinal pathogens increase inflammation increase activity of bowels • Urogenital: vaginal discharge/semen, urine • Bleeding: released at site of injury, blood draws Source of infection Reservoirs: where pathogens are maintained • Animals • Humans • Non-living: food, soil, water/supply Modes of transmission • Contact: direct contact of formites (inanimate objects), less than a meter • Vehicle transmission: airborne (more than a meter away), water/food borne • Zoonotic vector: living organism carrying disease causing microbes o Biological: microbe growing/diving inside vector o Mechanical: passive carrier 4


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