Microbio Exam 3 Review PDF

Exam 3 – Microbiology Review notes Chapter 14 – Infectious diseases 1. Types of interactions (mutualism, commensalism, (slide 2) a. Mutualism b. Commensalism c. Amensalism d. Parasitism 2. What is unique about areas of the body – slide 7 which is axeni...

Exam 3 – Microbiology Review notes Chapter 14 – Infectious diseases 1. Types of interactions (mutualism, commensalism, (slide 2) a. Mutualism b. Commensalism c. Amensalism d. Parasitism 2. What is unique about areas of the body – slide 7 which is axenic, not. a. Skin is salty b. Nose is cooler c. Axenic: alveoli of the lungs, kidneys 3. What area of the body is normal for staph and why (salty) a. Nose, skin (salty) 4. Opportunistic pathogens, true pathogens – slide 13 a. Opportunistic: normal microbiota that cause disease under certain circumstances b. True: cause disease in healthy individuals 5. Match animal reservoirs to diseases (slide 14) a. Rabies, giardia, malaria, many viruses 6. Why diSicult to eradicate? 7. Steps of an infection – slide 20 8. What is LD50, ID50? Slide 21 a. Lethal Dose of 50% of the sample population b. Infectious Dose of 50% of the sample population 9. Main portals of entry – slide 22 a. Skin, mucous membranes, placenta, parental route? 10. Definitions – slide 36 a. Pathology: study of disease b. Etiology: cause of disease c. Infection: invasion/colonization of the body by pathogens d. Disease: an abnormal state in which the body is not performing normal functions e. Morbidity: disease f. Deaths are morality 11. What are signs and symptoms? Slide 37 a. Symptoms: subjective characteristics of disease felt only by the patient b. Signs: objective manifestations of disease observed or measured by others 12. Steps of Koch’s postulates. Slide 42 a. Suspected causative agent must be found in every case of the disease and be absent from healthy hosts b. Agent must be isolated and grown outside the host c. When agent is introduced to a healthy, susceptible host, the host must get the disease d. Same agent must be found in the disease experimental host 13. Categories of diseases. Slide 44 a. Hereditary: caused by errors in genetic code received from parents b. Congenital: anatomical/physiological factors (structural and functional) defects present at both; caused by drugs (legal and illegal); x-ray exposure or infections c. Degenerative: result from aging d. Nutritional: result from lack of some essential nutrients in diet e. Endocrine (hormonal): due to excesses or deficiencies of hormones f. Mental: emotional or psychosomatic g. Immunological: hyperactive or hypoactive immunity h. Neoplastic (tumor): abnormal cell growth i. Infectious: caused by an infectious agent j. Iatrogenic: caused by medical treatment or procedures; are a subgroup of healthcare-associated diseases k. Idiopathic: unknown cause l. Healthcare-associated (nosocomial): disease acquired in health care setting 14. Exceptions to Koch’s postulates. Slide 45 a. Some pathogens can’t be cultured in the lab b. Diseases caused by a combination of pathogens and other cofactors c. Ethical considerations prevent applying Koch’s postulates to pathogens that require a human host 15. Understand virulence factors. Slide 48 a. Know more about this b. Adhesion factors c. Biofilms d. Extracellular enzymes e. Toxins f. Antiphagocytic factors 16. Role of Iron in nutrition of bacteria – slide 50 a. Iron is a good thing for bacteria  b. Required for most pathogenic bacteria but most iron in body is bound to iron transport proteins 17. Examples of extracellular enzymes and what they do. Slide 51 18. DiSerence between exotoxins and endotoxins, what they do slide 53 a. Hyaluronidase b. Collagenase c. Coagulase d. kinases 19. Antiphagocytic factors – slide 62 a. Prevent phagocytosis by the host’s phagocytic cells b. Bacterial capsule: composed of chemicals not recognized as foreign; slippery and diSicult for phagocytes to engulf c. Antiphagocytic chemicals: prevent fusion of lysosome and phagocytic vesicles; leukocidins directly destroy phagocytic white blood cells 20. How are fungi toxic? Slide 69 a. Aflatoxin: carcinogenic toxin produced by Aspergillus (black mold) b. Mycotoxins: produced by mushrooms and are neurotoxic (phalloidin and amanitin) 21. Examples of protozoan pathogens – slide 70 a. Malaria: invades host cells and lyses them b. Toxoplasma: grows in phagocytes c. Giardia: feasts on host material 22. What are helminths? What do they do? Slide 71 a. Worms b. Use host tissue for growth c. Produce large masses; cause cellular damage d. Produce waste products that cause symptoms 23. What do dinoflagellates do? Slide 72 a. Some produce a neurotoxin called saxitoxin (paralytic shellfish poisoning) 24. Stages of infectious disease (Start slide 74) ------ a. Incubation period: infection to first symptoms/signs b. Prodromal period: general, mild symptoms (aches, malaise) c. Illness: most severe, diagnostic signs/symptoms appear d. Decline: peak immune response; if disease doesn’t decline, death e. Convalescence: fully recovered, tissues repaired 25. Portals of entry and exit – slide 79 a. Portals of exit: ear, broken skin, skin, anus, seminal vesicles, urethra, vagina, mammary glands, mouth, nose, eyes 26. What are the types of transmission (manual and automatic? No) slide 80 -91 a. Contact transmission: person to person i. Droplet transmission: spread by mucus ii. Indirect contact transmission: pathogens are spread from host to host by fomites b. Vehicle transmission: air, water, food, and bodily fluids c. Vector transmission: arthropod transmission 27. Types of vectors, examples of each. 80-91 28. Terms slide 96-98 a. Acute disease: symptoms develop rapidly but the disease lasts only a short time b. Chronic disease: symptoms develop slowly c. Subacute disease: intermediate between acute and chronic d. Latent disease: causative agent is inactive for a time but then activates and produces symptoms e. Herd immunity: immunity in most of a population f. Local infection: pathogens are limited to a small area of the body g. Systemic (generalized) infection: an infection throughout the body h. Focal infection: systemic infection that began as a local infection i. Primary infection: acute infection that causes the initial illness j. Secondary infection: opportunistic infection after a primary (predisposing) infection k. Subclinical disease: no noticeable signs/symptoms (inapparent infection) l. Communicable disease: a disease that is spread from one host to another m. Contagious diseases: diseases that are easily and rapidly spread from one host to another n. Noncommunicable disease: a disease that is not spread from one host to another 29. Predisposing factors – make the body more susceptible to disease - Slide 100- a. Gender b. Inherited traits, such as sickle cell gene c. Climate and weather d. Fatigue e. Age f. Lifestyle g. Nutrition h. Chemotherapy 30. Incidence and prevalence of disease – slide 101  a. Incidence: # of new cases of a disease in a given area during a given period of time b. Prevalence: # of total cases of a disease in a given area during a given period of time 31. Terms slide 102 a. Sporadic disease: disease that occurs only occasionally b. Endemic disease: disease constantly present in a population c. Epidemic disease: disease acquired by many people in a given area in a short time d. Pandemic disease: worldwide epidemic e. Emerging infectious disease: diseases that are new, increasing in incidence, or showing potential to increase in the near future (zoonotic, vector-borne) 32. Contributing factors to Hospital acquired infections, how to prevent – slide 116-118 a. Handwashing Chapter 15 – Innate immunity 1. Terms slide 2 a. Immunity: ability to ward oS disease b. Susceptibility: lack of resistance to a disease c. Innate immunity: defenses against any pathogen; rapid, present at birth i. First: barriers to entry; physical and chemical factors ii. Second: leukocytes, inflammation, fever, complement system d. Adaptive immunity: immunity/resistance to a specific pathogen; slower to respond, has memory component 2. Understand the first line of defense – (Skin) slide 6 a. Skin: has chemicals that defend against pathogens b. Perspiration secreted by sweat glands c. Sebum secreted by sebaceous (oil) glands 3. Know the items (salt, lysozyme, etc. where and what they do.) a. Salt inhibits growth of pathogens b. Lysozyme destroys cell wall of bacteria c. Sebum lowers skin pH 4. How does each area of the body do the “first line” of defense? (ex. Slide 13 ) a. Saliva: low pH; uric acid, and IgA that prevents microbial attachment b. Gastric juice: low pH; destroys most bacteria and toxins  c. Vaginal secretions from lactobacillus: low pH; cervical mucous inhibit microbes 5. What is the 2nd line, and all components of it (slide 17) a. Lymphatic system: contains lymph, lymphatic vessels, lymphoid tissue, and red bone marrow b. Lymph carries microbes to lymph nodes where lymphocytes and macrophages destroy the pathogen 6. Types of white blood cells, what they do (slide 22-28) (No Losers May Enter Biology) a. Neutrophils: stain lilac with mix of acidic and basic dyes; phagocytic; work in early stages of infection b. Lymphocytes: most involved in adaptive immunity with T cells and B cells; natural killer lymphocytes c. Monocytes: leave the blood and mature into macrophages; phagocytic cells that devour foreign objects d. Eosinophils: stain red/orange with acidic dye eosin; phagocytic; toxic against parasites and helminths e. Basophils : stain blue with basic dye methylene blue; release histamine; work in allergic responses 7. General ranges of components, where they are after centrifuge (slide 29) a. Neutrophils: 60-70% b. Lymphocytes: 20-25% c. Monocytes: 3-8% d. Eosinophils: 2-4% e. Basophils: 0.5-1% 8. How does phagocytosis work? Slide 30 a. Chemotaxis: chemotactic factors attract WBC (cytokines, complement proteins) b. Adhesion c. Ingestion d. Maturation e. Killing f. Elimination 9. What unique things do various cells do, Eosinophils, Natural Killer cells (NK) slide 34 a. Eosinophilia: often indicative of a helminth infestation or allergies b. Natural killer lymphocytes (NK cells): secrete toxins onto surface of virally infected cells; membrane proteins 10. What does interferon do? Slide 39  a. Interferon: protein molecules released by host cells to nonspecifcally inhibit the spread of viral infections i. Cause many symptoms associated with viral infections (malaise, muscle aches, chills, headache, fever) 11. Complement – what does it do? What is a MAC? Slide 46 a. Complement: set of serum proteins designated numerically according to their order of discovery b. Membrane attack complex (MAC): gram negative bacteria more susceptible due to fewer layers of peptidoglycan 12. 4 Signs of Inflammation Slide 52 --- a. Redness (rubor or erythema) b. Swelling (old – “tumor” – edema) c. Pain (dolor) d. Heat (calor) 13. Example: Swelling is associated with? Vasodilation 14. What is diapedesis? Slide 56 a. Diapedesis: monocyte squeezing through interstitial space 15. What causes fever? Slide 59--- a. When pyrogens trigger the hypothalamus to increase the body’s core temp i. Bacterial toxins ii. Cytoplasmic contents of bacteria released by lysis iii. Antibody-antigen complexes iv. Pyrogens released by phagocytes that have phagocytized bacteria 16. Outcomes of fever? Slide 61--- a. Enhances eSect of interferons b. Inhibits growth of some microbes c. May enhance the activities of phagocytes, cells of specific immunity, and the process of tissue repair d. Death above 108 F – 112 F Slide 16 – Adaptive immunity 1. What is the 3rd line of defense? Slide 2 a. Adaptive immunity: defenses that target a specific pathogen 2. What is diSerent about the 3rd line? Slide 2— a. 3. Five attributes of adaptive immunity – slide 4 – following --- a. Specificity b. Inducibility  c. Clonality d. Unresponsiveness to self e. Memory 4. Natural vs. artificial, active vs. passive and examples – slide 5 ---] a. Natural immunity: acquired as part of normal life experiences b. Artificial: acquired through a medical procedure such as a vaccine c. Active: results when a person is challenged with antigen that stimulates production of antibodies; creates memory, takes time and is lasting d. Passive: preformed antibodies are donated to an individual; does not create memory, acts immediately, and is short term 5. Roles of B and T lymphocytes functions, origins – Slide 7 – a. B lymphocytes (B cells): mature in the bone marrow b. T lymphocytes (T cells): mature in the thymus 6. Antigens – what are they, what type of compounds – slide 16 a. Antigens: molecules the body recognizes as foreign and worthy of attack i. Large foreign macromolecules make the best antigens ii. Proteins of viruses, fungi, and protozoa 7. Types of antigens – slide 18 a. Exogenous: toxins and other components of microbial cell walls, membranes flagella, and pili b. Endogenous: produced by microbes that reproduce inside a body’s cells c. Autoantigens: derived from normal cellular processes d. Haptens: antigens too small to provoke immune responses; attach to carrier molecules and together cause immune response e. Allergens: trigger an allergy response 8. What do MHC 1 and 2 do? -slide 21 a. MHC 1: present on all cells except red blood cells (nucleated cells) b. MHC 2: present on antigen-presenting cells (APCs); include macrophages and dendritic cells 9. Describe the humoral response – Slide 41 --- a. Humoral response: responsible for keeping body’s fluids (humors) clear of pathogens i. Plasma B cells: produce antibodies ii. Memory B cells: remember for future antibody attack 10. What is an antibody? Structure? Epitopes? Slide 41--- a. Antibodies: immunoglobulins similar to BCRs; secreted by activated B cells called plasma cells; have antigen-binding sites and antigen specificity identical to the BCR of the activated B cell  11. How does an antibody recognize an antigen? a. Valence: the number of antigen-binding sites on an antibody b. Google answer: by binding to the surface of the antigen, specifically to amino acids that are brought together in the folded protein 12. Ways that antibodies work. Slide 47 13. Five classes of antibodies – slide 52 a. IgM: first antibody produced b. IgG: most common and longest-lasting antibody c. IgA: associated with body secretions d. IgE: involved in response to parasitic infections and allergies e. IgD: exact function is not known 14. Why are memory cells important? Also Slide 68 – a. Memory response is more eSective than primary response due to increased number of initial cells and quicker activation 15. Describe the cell mediated defenses? Slide 61 a. Cell-mediated immunity requires the direct involvement of T lymphocytes b. T cells act directly against antigen, infected host cells, abnormal host cells, and protozoa c. T cells secrete cytokines that act on other cells d. Sensitized T cells proliferate into long-lasting memory T cells e. Rely on T cell receptors instead of antibodies 16. What do NK cells do? Slide 69 – a. NK cells: granular leukocytes destroy cells that don’t express MHC class I self-antigens 17. What are the primary and secondary responses? Slide 77 a. Primary: small amounts of antibodies produced; may take days to produce enough antibodies to eliminate the antigen from the body b. Secondary: memory cells respond to another exposure to the antigen; much faster than the primary response due to more initial cells and no need for Th activation Chapter 17 – Vaccines 1. History of Immunization - Chinese noticed children who recovered from smallpox did not contract the disease again; they infected children with material from a smallpox scab to induce immunity – variolation 2. Success of vaccines – Slide 3  a. Polio: introduced in the 1950s which decreased a lot and again in 1960s and decreased and remained stagnant b. Measles: introduced in the 1960s and gradually decreased 3. Active and passive immunity – Slide 4, 17-18--- a. Active immunity: administration of antigens so patient actively mounts an adaptive immune response b. Passive immunotherapy: individual acquires immunity through the transfer of antibodies formed by immune individual or animal 4. Questions slide 5--- a. Gives immediate resistance to disease? i. Passive immunity b. Can help after disease is in progress? i. Passive immunity c. Stimulates production of antibodies? i. Active immunity d. Gives lasting protection? i. Active immunity e. Reduces spread of disease, even to people who have no protection? i. Herd immunity 5. Vaccine types Slide 7-10 a. Attenuated (modified live) vaccines: can result in mild infections; can result in disease; provides lasting protection usually without boosters; examples: chickenpox, measles, mumps b. Inactivated (killed) vaccines: called the “killed” virus; considered the safest c. Toxoid vaccines: chemically or thermally modified toxins used to stimulate active immunity Chapter 19 – Gram + bacteria 1. What is diSerent between gram + and gram – organisms? a. Gram positive: thicker layer of peptidoglycan in cell wall and appear purple b. Gram negative: thin peptidoglycan layer surrounded by outer membrane and appears pink 2. Main groups we looked at in this group. a. Low G + C bacteria – firmicutes b. High G + C bacteria – actinobacter 3. Main distinctions of Staphylococcus? Slide 4 S— a. Nonmotile (ALL cocci nonmotile) b. Salt-tolerant  c. Catalase + 4. Two main organisms in groups - Slide 6 a. Staphylococcus aureus: more virulent strain b. Staphylococcus epidermidis: opportunistic infections 5. Why is Staph aureus so pathogenic – Slide 7 --- a. Structures that enable it to evade phagocytosis b. Production of enzymes c. Production of toxins 6. Toxins of staph – Slide 11 a. Cytolytic toxins: disrupt the cytoplasmic membrane of a variety of cells; leucocidin can lyse leukocytes specifically b. Exfoliative toxins: cause skin cells to separate and slough oS by breaking desmosomes c. Toxic-shock syndrome (TSS) toxin: causes TSS d. Enterotoxins: stimulate symptoms associated with food poisoning; heat stable; remain active at 100 degrees C for 30 min 7. Pathogenicity factors – slide 12 a. 8. Know the diseases Staph is associated with, and treatment Slide 14 -21— a. Food poisoning: fasted food poisoning at 4 hours, usually lasts 24 hours b. Scalded skin syndrome, impetigo, folliculitis (infection of hair follicle) c. Toxic-shock syndrome: shock occurs when blood pressure is too low to oxygenate vital organs d. Bacteremia e. Endocarditis f. Pneumonia  g. Osteomyelitis h. Treatment for staph: methicillin; vancomycin used to treat MRSA 9. What are the pathogenicity factors of strep? Slide 24S – a. Hyaluronidase: streptococcus through tissues b. Pyrogenic (erythrogenic) toxins: can stimulate fever, rash, and shock by dilating capillaries c. Streptolysins: lyse red blood cells, white blood cells, and platelets 10. What diseases are associated with Strep? Slide 27S – a. Pharyngitis (strep throat) b. Rheumatic fever: damages the heart valves and muscle c. Scarlet fever: chest rash d. Pyoderma and erysipelas e. Streptococcal TSS: can cause organ failure, shock, and death f. Necrotizing fasciitis (flesh eating bacteria) g. Glomerulonephritis: irreversible kidney damage 11. Treatment for strep – slide 36 – a. Penicillin 12. Diseases associated with various diseases Slide 36 – 41 ---- a. Group B streptococcus: streptococcus agalactiae i. Associated with neonatal bacteremia, meningitis, and pneumonia b. The Viridans Group (streptococcus mutans): opportunistic pathogens; causes dental caries and dental plaques c. Streptococcus pneumoniae: causes disease when it travels to lungs 13. DiSerence between Beta, alpha, gamma hemolysis? a. Beta: complete lysis of RBCs b. Alpha: partial lysis of RBCs c. Gamma: no lysis on RBCs 14. Bacillus, diseases associated with Slide 48 --- a. Bacillus anthracis 15. Characteristics and types of anthrax – a. Transmission: inhalation of spores, inoculation of spores through break in skin, ingestion of spores b. Gastrointestinal anthrax c. Inhalation anthrax (high mortality rate: near 100%) d. Cutaneous anthrax (most common; fatal in 20% of untreated patients) 16. Diseases of Clostridium Slide 56S ---- a. Clostridium perfringens: grows in digestive tract of animals/humans b. Clostridium diSicile  c. Clostridium botulinum: among the deadliest known toxins; 1 kg to kill everyone on earth d. Clostridium tetani 17. Mode of action of various Clostridium diseases. --- a. Clostridium perfringens: i. Treatment: hyperbaric chamber to inject oxygen into tissues to remove anaerobic environment ii. Prevention: proper cleaning of wounds can prevent gas gangrene b. Clostridium diSicile: i. Treatment: discontinue causative antimicrobial drug to resolve minor infections as normal flora return ii. Prevention: proper hygiene to limit nosocomial infections c. Clostridium botulinum: i. Prevention: proper canning of food; infants under 1 year should not consume honey d. Clostridium tetani i. Prevention: immunization with tetanus toxoid 18. How to avoid these! (Identify by pix)---- 70---- 19. Listeria, what is the reservoir? Slide 76-80 a. Humans or animals. Can be found in soil, water, and enters body via contaminated food and drink 20. What is unique about it? a. Can grow at refrigeration temps which allows it to thrive in food that is refrigerated b. Pregnant women can transmit listeria to their fetus 21. What diseases? a. L. monocytogenes is an intracellular pathogen; grows in phagocytes often in the gallbladder 22. Mode of transmission and action? a. Eating contaminated food, mother to fetus, contact with infected birds/animals, contaminated equipment/materials 23. Mycoplasma slide 81- a. What is unique about it? i. Smallest free-living microbes; only a few species cause significant human disease b. Diseases? (Slide 82) i. Mycoplasma pneumoniae: causes primary atypical pneumonia; common in children 5-15 years old 24. Corynebacterium Slide 88 a. Diseases? i. Corynebacterium diphtheriae: causes diphtheria b. Transmission? i. From person to person via respiratory droplets or skin contact c. Signs & Symptoms? i. Diphtheria toxin ii. Inhibits polypeptide synthesis in eukaryotes iii. Bacteria that do not produce the toxin because they are not lysogenized are not pathogenic d. Preventions? i. Immunization with DTaP toxoid vaccine 25. Mycobacterium Slide 94 a. Diseases? (T&L) i. Tuberculosis ii. Leprosy: Hansen’s disease; armadillos are host b. Transmission & reservoirs? --- i. Leprosy: transmitted via person-to-person contact or break in the skin, but patients not quarantined due to low virulence and is fully treatable; main reservoir are armadillos ii. Tuberculosis: transmitted through the air; humans are primary reservoir c. S&S? d. Prevention? i. BCG vaccine e. Speed of growth?--- i. Tuberculosis: slow growth therefore resistant to drugs ii. Leprosy: incubation for years; 12-day generation time 26. Propionibacteria a. Propionibacterium acnes: causes acne b. Many cases require no treatment; antimicrobial drugs help control bacterium