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BMS 212 Study Guide

by: Brandon Czowski

BMS 212 Study Guide BMS 212

Brandon Czowski

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This study guide has all the newest material we covered in lecture that will be included for the final exam, including all the gram positive/negative species we are responsible for.
Dr. Leonard
Study Guide
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This 8 page Study Guide was uploaded by Brandon Czowski on Saturday April 23, 2016. The Study Guide belongs to BMS 212 at Grand Valley State University taught by Dr. Leonard in Winter 2016. Since its upload, it has received 36 views. For similar materials see Microbiology in Biomedical Sciences at Grand Valley State University.


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Date Created: 04/23/16
Gram Positive Cocci Staphylococcus  Morphology: cocci in grape-like clusters  Tolerance o High salt concentration o pH/temperature changes o desiccation o Disinfectants and antisepsis  Normal flora of skin and mucus membranes Staphylcocccus aureus  Opportunistic  Virulence Factors o Biofilms/capsules: able to survive in host/harsh environment; inhibits chemotaxis and phagocytosis of neutrophils o Protein A: binds to Fc region (stem) of antibody to render it inactive  Exoenzymes o Coagulase: clots blood to allow establishment in host (helps diagnosis sp.) o Staphylokinase: dissolves blood clots, cleaves IgG and C3b— disrupts complement o Hyaluronidase: breakdown the matrix b/w cells to allow access o Lipase: hydrolyze glycerol and fatty acids o Beta-lactams: allows resistant to type of drugs  Exotoxins o Hemolysins: lyse RBCs o Enterotoxin: present in intestines, induces nausea and diarrhea— heat stable  Food poisoning o Exfoliative toxin: desquamation of skin cells, results in flaking  Scaled skin syndrome o Toxic shock syndrome toxin: superantigen that produces massive amounts of cytokines to activate other cells  Infections o Impetigo: pus filled sores around mouth o Folliculitis: localized infection of hair follicle (lipase prod. makes more invasive) o Furuncle: progressed folliculitis into deeper tissue o Carbuncle: spread of multiple furuncles o MRSA: skin infection, hospital acquired more invasive than communal  Systemic infections o Osteomyelitis: invasion of bones o Pneumonia o Endocarditis: heart valves o Meningitis/Bacteremia Staphylcoccus epidermidis  Skin, nose, mucus membranes  Produces capsules & forms biofilms  Not toxigenic/invasive, can cause endocarditis Staph. Saprophyticus  Skin, lower intestine, vagina  Common to cause UTI’s Streptococcus  Non-motile/non-spore forming  Facultative anaerobes—capnophiles (grow in high CO2 levels)  Catalase (-), peroxidase (+)  Classified by hemolysis pattern o Alpha: partial, green color o Beta: complete, yellow o Gamma: no hemolysis  Lancefield Group: separated by surface carbohydrate antigens Streptococcus pyogenes (Group A)  Beta-hemolytic  Virulence Factors o Hyaluronic acid capsule: we use hyaluronic acid to congregate our cells, allowing evasion of phagocytosis o M Protein: destroys C3 convertase (prevents adhesion, stops pathway), resists phagocytosis, stops adherence  Rheumatogenic: autoimmune reacts with heart  Nephritogenic: our antibodies react with kidneys  Exoenzymes o C5a peptidase: neutralizes C5a (chemotactic factor) o Streptokinase: lysis fibrin clot to spread infection o Streptodornase (DNase): prevents bacteria from being trapped in neutrophil extracellular traps (NETS) and digesting the web of DNA  Exotoxins o Streptolysin: degrades RBCs, allowing to acquire nutrients and causes lysosomes to release contents after phagocytosis  Streptolysin O: unstable in presence of oxygen  Streptolysin S: stable in oxygen o Erithrogenic toxin: superantigen on temperate/lysogenic phage, producing rash/fever (scarlet fever)  Infections o Impetigo o Erysipelas: more severe, raised/tough lesions o Necrotizing fasciitis: exoenzymes destroy connective tissue o Streptococcal pharyngitis (strept throat): pyogenic toxin—pus pockets o Scarlet fever: erithrogenic toxin causing rash/strawberry tongue o Rheumatic fever: 3-4 weeks after other infection, infects heart valves, nodules in skin o Acute glomerulonephritis: reaction to M proteins, targeting kidneys leaving permanent damage Strept. agalactiae (Group B)  Forms capsules—sensitive to Tc independent antigens  Normal flora  Infection can be passed from mother-child o Pneumonia, meningitis, sepsis Alpha hemolytic/Viridan groups: lack surface carbohydrates, normal flora (S. mitis) Strept. pneumoniae  Virulence o Capsule: effects complement and phagocytosis; varied surface o Phosphorylcholine: makes cell be taken up, helping with invasion o Pneumolysin (exoenzyme): binds to cholesterol creating pore of ciliated cells causing lysis o IgA protease: destroying antibodies  Disease o Pneumonia: edema, abnormal breathing, productive cough, cyanosis o Otitis media: usually follows viral infection, children likely from narrow ear canals o Meningitis: crosses blood-brain barrier, autolysin production, permanent side effects (deafness, retardation), high fatality rate Acid Fast Mycobacterium  Cell wall composed of mycolic acid (lipid) o Resists digestion in phagolysosome o Resists drying, acids, germicides o Extremely slow growth—resistant to antibiotics  Cord factor (glycolipid) in cell wall o Inhibit migration of neutrophils o Inhibit fusion of phagosome with phagolysosome—lysosome rupture in cell  Tuberculosis o Humans only reservoir o Transmitted through droplet transmission o Stages  Primary: acquired by inhalation, targeting alveolar macrophages (virulence allows replication in macrophages); tubercles form from collagen deposits  Secondary: (reactivated—infectious and spreads easily) early symptoms of rough cough/chest pain, later symptoms of appetite loss, paleness, tiredness  Third (disseminated): becomes systemic, affects kidneys, bones become fragile, meningitis Gram Negative Cocci Neisseria  Diplococcus (pairs) that are non-motile but have twitching motility from pili  Oxidase (+), aerobic, some capnophiles, fastidious (special media to culture) Neisseria gonorrhoeae  Highly asymptomatic, transmitted by sexual intercourse, mother-child from birth  Virulence Factor o Pili: twitching motility, aid attachment, prevent phagocytosis  Antigenic variation: change composition of surface proteins  Phase variation: expression of proteins on/off o Protease: cleaves IgA in mucus membranes o DO NOT have capsules, only certain medias o Lipooligosaccharide (LOS): endotoxin (on outer membrane) causes inflammation  Symptoms o Males: painful urination, pus filled discharge o Females: asymptomatic, painful urination/discharge (similar to UTI); pelvic inflammatory disease could cause infertility  Treatment: cephalosporins; no vaccine Neisseria meningitidis  Human only resivor, spread by droplets  Disease: meningococcal meningitis—fast acting on brain o Early symptoms: fever, headache, stiff neck o Late symptoms: from endotoxin—petechiae (black spots from capillary beds), septic shock, high fever  Virulence Factors o Pili/twitching motility, LOS (inflammation)  Pili specifically for membrane around brain/spinal cord (meninges) o Capsule with serogroups (A, B, C, Y, W135) to protect from complement and neutrophils—we can form vaccine from antigens  Treatment o Cephalosporin—able to cross blood brain barrier o Prophylactic given to prevent spread  Rifampin: target RNA polymerase  Ciprofloxacin: target DNA gyrase o Vaccine: MCV4 for all serotypes except B; very effective Gram Positive Bacilli Bacillus sp.  Environmentalists (endure harsh conditions), saprophytic (dead organic matter)  Aerobic, catalase (+), form endospores  Produces bacitracin Bacillus anthracis  Resides in soil (endospores), zoonotic—passed b/w animals and humans  Virulence o Capsule (when inside host): Poly-D-glutamic acid blocks phagocytosis, resists complement *expressed in animal host o Exotoxins  Edema toxin: potent inflammatory agent—uncontrollable swelling  Lethal toxin: causes cell death—tissue damage, targets macrophages  Disease o Cutaneous anthrax: broken skin exposed to endospores, nodule formation and eschar (black skin) o Pulmonary (inhalation) anthrax: inhaling spores  Prodromal: flu-like  Invasive: rapid multiplying, pulmonary edema, rapid shock; lethal toxin killed macrophages o Gastrointestinal anthrax: ingestion of spores or contaminated meat; necrosis, hemorrhaging of intestines, ascites; high fatality Clostridium  Saprophytic, some commensal with humans, not zoonotic  Strict anaerobes, catalase (-), produces terminal endospores Clostridium botulinum  Resides in soil/water, transmitted through improper preserved food  Virulence Factors o Exotoxin botulin (most potent) that targets neuromuscular junctions, preventing release of acetylcholine causing flaccid paralysis and suffocation  Disease o Foodborne: symptoms within 12-72 hours, progressive paralysis leading to death by asphyxiation o Infant botulism (floppy baby syndrome): non-specific symptoms —fussiness and crying o Wound botulism: germination of spores in wounds, mimic food poisoning  Treatment: passive immunity, respiration/cardiac support for nerve endings to grow Clostridium tetani  Virulence o Tetanosporin: tetanus neurotoxin that causes muscle to stay tense and unable to relax  Progression o Irritability, muscle tightening, irregular heartbeat, inability to relax muscles  Treatment: penicillin, passive immunity from immunoglobulin, active immunity with tetanus toxoid Clostridium difficile  Normal flora of large intestine, opportunistic  Virulence o Toxin A—enterotoxin o Toxin B—cytotoxin o Fimbriae—attachment  Causes persistent diarrhea (pseudomembranous colitis) C. perfringens  Food poisoning, wound infections that are life-threatening Gram Negative (B. pertussis, E. coli) Bordetella pertussis  Coccobacillus (stubby rods), non-motile  Very fastidious, strict aerobe, oxidase (+)  Humans only host  Causative agent for Pertussis o Incubation: 7-10 days o Catarrhal: most infectious, inflamed mucus membrane o Paroxysmal: “violent attack”, mucus impairs cilia, hard cough, and cyanosis  Decrease in # of organisms but worst side effects o Convalescent: 3-4 weeks, possible secondary infections  Transmission: droplets, colonize in trachea/bronchi when inhaled  Virulence Factors o Exotoxins  Pertussis toxin: binds to epithelia cells, blocks cell signaling, blocks chemotaxis  Adenylate cyclase toxin: works w/pertussis toxin to stop chemotaxis, produce more mucus, inhibit death via phagocytosis o Adhesin  Filamentous hemagglutinin (FHA): (used in vaccine) adhesion to ciliated cells, inhibits destruction by neutrophils o Endotoxin  LPS: inflammation  Vaccine: need full series o dTP: diphtheria, tetanus, pertussis killed vaccine (whole cell) o dTaP: (subunit) inactivated pertussis toxin, FHA (membrane protein)  Treatment: macrolides prevent transmission but don’t help with recovery o Erythromycin, azithromycin Enterobacteriaceae  41 genera, 13 associated with humans, involves intestines  Non-spore forming rods, facultative anaerobes, oxidase (-)  Reduce nitrate to nitrite  Fermentative metabolism (all ferment glucose), coliform (lactose fermenter) or non-coliform  Normal flora and disease causing (usually diarrhea disease) Escherichia coli  Most prevalent enteric bacteria, most commensals  Opportunistic pathogen, lactose (+)  Virulence Factors o Fimbriae/pili: attachment o Enterotoxin: exotoxin target large intestine causing more ions in lumen, water follows causing diarrhea o Capsule with K antigen o LPS: inflammation endotoxin o Verotoxin: similar to shigilla (0157:H7 only produces) o Type III secretion: inject protein in mammalian cells to promote infection by reducing host immunity  Serotype antigens: label strains, tested with antibiotics o O antigen: somatic, cell wall o H antigen: flagellar o K antigen: capsule  Disease: Gastroenteritis o ETEC: enterotoxigenic—traveler’s diarrhea (mild case) o EPEC: enteropathogenic—more chronic, still mild and prevents absorption o EIEC: enteroinvasive—diarrheal disease that’s more severe (blood/ulcers) o EHEC: enterohemorrhagic—systemic, damages kidneys  Caused by 0157:H7 (verotoxin/type III secretion system)  Bloody diarrhea, hemolytic uremic syndrome (infects kidneys and could cause death, obtained by contaminated meat; secreting toxins came from transduction) o Urinary tract infections: dominant cause, women more severe than men o Systemic disease: meningitis, endocarditis, septicemia, kidney damage  Treatment o Diarrheal disease:  Rehydration/dialysis if needed  Usually let run course, antibiotics can increase hemolytic uremic syndrome from increased toxin production o Other infections  Cephalosporin, broad-spectrum penicillin, sulfonimides


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