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Microbiology
| Question | Answer |
|---|---|
| Normal Microbiota | Microbes regularly found at an anatomical site |
| How does our skin prevent overgrowth of microorganisms? | Skin prevents microorganism overgrowth by being slightly acidic and salty. |
| How does propionibacterium acnes cause pimples? | P. acnes are normal residents of the skin but when pores become engorged with excess oil and sebum fluid that is secreted by oil glands, it creates an anaerobic environment where P. acnes can live. |
| How does propionibacterium acnes cause body odor? | When oil glands secrete complex lipids, they can be partially degraded by enzymes from certain gram positive bacteria. Secreted lipids then change to unsaturded fatty acids. Some fatty acids are volatile and may be associated with a strong odor. |
| Why is there no normal microbiota in the lower respiratory tract? | We want to avoid getting it into the lungs. |
| What happens if normal microbiota is in the lower respiratory tract? | Can cause pneumonia or TB |
| How do we avoid normal microbiota in the lower respiratory tract? | 1. Ciliated epithetal cells move mucous upward away from the lower part. 2. Phagocytic action of alveolar macrophages (white blood cells); cells catch other cells, eat and kill them. 3. Lysozyme in mucus |
| Streptococcus sobrinus causes | Dental plaque |
| Streptococcus mutans causes | teeth with strands of dextran |
| Why do the stomach and small intestine have a lower number of microorganisms than the large intestine? | In the stomach, most are killed by acidic conditions. In the large intestine, there's a high reproductive rate; mostly anaerobic and facultative anaerobic microbes growing anaerobically. |
| Do kidneys, ureters, or bladders have normal microbiota? | Nope, microbiota free. |
| Do male/female genetalia have normal microbiota? | Female: cmopex microbiota in flux due to menstrual cycle. |
| What bacteria is predominant in female genetalia? | Lactobacilli; it is acid tolerant so it contributes to low vaginal pH. (A high pH leads to a yeast infection) |
| Mutually beneficial effects between normal microbiota: | 1. Prevent pathogen attachment 2. Consume available nutrients so bad things can't eat them. 3. Produce toxic compounds that in hibit other microbes 4. Prime the immune system. |
| Opportunistic pathogen | Organism that exists harmlessly as part of the body's normal environment but becomes a threat when body's immune system fails. |
| Normal microbiota changes because of: | Hormonal changes, type of food consumed, ethnicity, antibiotics. |
| How can a woman get a yeast infection? | If pH gets too high. Or if a woman takes an antibiotic which kills off lactose bacillus, the pH increases in the vagina and a yeast infection is caused. |
| Factors impacting the final outcome of host-pathogen relationships | 1. Number of organisms present 2. Virulence of pathogen 3. Host's defenses and degree of resistance |
| Virulence | Degree or intensity of pathogenicity |
| Virulence is determined by | 1. Infectivity 2. Invasiveness 3. Pathogenic potential |
| Define infectivity | Ability to establish focal point of infection |
| Define invasiveness | Ability to spread to adjacent tissues |
| Define pathogenic potential | Degree to which pathogen can cause damage to host |
| Virulence is measured by | Lethal and infectious dose |
| Define lethal dose | number that kills 50% of experimental host |
| Define infectious dose | number that infects 50% of experimental host |
| Steps of pathogenesis of diseases | 1. Maintain a reservoir 2. Be transported to host 3. Adhere to, colonize and/or invade host 4. Multiply or complete life cycles on or in host 5. Initially evade host defenses 6. Damage host 7. Leave host (Return to reservoir/enter new host) |
| Define reservoir | Place to live before/after causing an infection |
| Reservoirs for human pathogens | Other humans, animals, or the environment |
| How are diseases transported? (Two ways) | Direct or Indirect contact |
| Define direct contact | cough, sneeze, body contact, etc. |
| Define indirect contact | Vehicles: soil, water, food Vectors: living organisms that transmit pathogen Formites: Inanimate objects that harbor/trasmit |
| Define adherence process | Adhesins recognize specific receptors on the host cells surface |
| Define colonization process | Establishment of a site of microbial reproduction on or within a host |
| Invasions can be passive or active, define both | Active: penetration of mucous membrane and epithelium Passive: Entering through skin lesions, wounds |
| When does multiplication in the host occur? | When pathogen finds appropriate environment within the host |
| Define bacteremia | viable bacteria in blood |
| Define Septicemia | bacteria AND toxins in the bloodstream |
| Must occur if microbe is to be perpetuated; and be done by passive mechanisms | Leave the host |
| Virulence genes | Could be in plasmids or lysogenic phages which can be integrated into chromosomes. |
| Most bacteria have a lot or a few clonal types? | A few |
| Define pathogenicity islands | large segments of DNA that carry cirulence genes |
| When are pathogenicity islands acquired? | During evolution of pathogen by horizontal gene transfer |
| What regulates bacterial virulence factors | Environmental factors (control gene expression) |
| What are virulence factors made of? | Proteins with various properties |
| Define Intoxication | disease resulting from entry of a specific preformed toxin into host |
| Define toxin | Specific substance that damages host |
| Define toxemia | Condition caused by toxins in blood of host |
| What is an AB toxin? | 2 cell units bound together on exotoxin. Made up of an A and B subunit. |
| Role of the A subunit | Reponsible for toxic effect; does the damage |
| Role of the B subunit | Binds to the target cell that enables A subunit to enter |
| How do Cytolytic toxins work? | Membrane disrupting |
| Two forms of cytolytic toxins? | Poreforming adn Phospholipase |
| Process of poreforming toxin | Forms a hole in the membrane, Water enters and the cell dies |
| Leukocidins | Kill phagocytic leukocytes |
| Hemoysins | Kill erythrocytes, leukocytes and many others |
| Neurotoxins | Act directly on neurons by interfering with membrane protein and ion channels |
| Endotoxins | Interacts with host molecules and cells, activates host enzymes |
| Systematic effects of endotoxins | Fever, shock, blood coagulation, weakness, diarrhea, inflmmation |
| Barriers of nonspecific resistance | Cells, tissues, chemicals, physical |
| Define nonspecific | Prevent colonization of the host by most pathogens |
| Where do cells involved in immunity originate from? | Stem cells in the bone marrow |
| T & B cells are activated by.. | the innate immune system |
| T cells' job | Perform specific cellular immune responses like assisting B cells and killing foreign cells |
| B cells' job | Differentiate into plasma cells and form antibodies |
| PAMP | Pathogen Associated Molecular Patterns |
| PRR | Patern Recognition Receptors |
| Process of innate immune response | Phagocytes recognize PAMPs via a family of membrane bound PRRs. Phagocytes are activated to produce metabolic products that kill the pathogen and limit its effects |
| Inflammation signs | Pain, swelling, heat, redness |
| First half of Inflammation | 1. Bac/path enter wound 2. Injured tissues/macrophages @ site release chemokines which recruit immune system cells to site |
| Define antigen | molecule on an invader |
| Second half of Inflammation | 3. Mast cells at site secrete factors that constrict blood vessel at wound, dilate blood vessel near wound 4. Neutrophils arrive, remove pathogens by phagocytosis |
| How do dendritic cells start adaptive immune response? | By degrading foreign proteins and presenting them on MHC class II proteins |
| CD8+ cells function | Induce death of cells that are infected with viruses or are damaged. |
| CD4+ cells function | Activate B cells that become plasma cells, which make antibodies |
| Innate immune system: | provides immediate defense against infections and are found in all classes of plant and animal life |
| Anatomical barriers of innate immune system | Skin, gastrointestinal tract, airways, lungs, eyes, nasopharynx |
| Adaptive immune system | Highly specialized; systemic cells and processes to eliminate and prevent pathogenic growth; activated by innate immune system |
| Cells used during adaptive immune system | Lymphocytes T & B cells |
| How do immunological memory cells prevent future disease? | Cells "remember" pathogens by their signature antigen. If the pathogen infects the body more than once, the cells are used to quickly eliminate it. |
| Vaccinations work by: | When a person becomes exposed to a pathogen, use the vaccine to destroy/cut virus into small pieces. Antibodies are produced and find virus cells to gather for macrophages to destroy. |
| Vaccinations use active immunity to: | "turn on" B cell for body to be ready when real sickness comes |
Created by:
rtate17
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