microbiology test 4
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60 terms
Terms | Definitions |
|---|---|
Pathology | study of disease |
Etiology | cause of a disease |
infection | colonization of the body by pathogens |
disease | an abnormal state in which the body is not functioning normally |
Normal Flora | permanently colonize the host |
Transient Flora | may be present for days, weeks, or months |
Microbial Antagonism | competition between microbes: |
Herd immunity | immunity in most of a population |
Predisposing Factors | make the body more susceptible to diseaseex: gender - short urethra in females inherited traits - sickle cell gene climate, fatigue, age, lifestyle, immunosuppression |
Reservoirs of Infection | **Human — AIDS, gonorrhea - Carriers may have inapparent infections or latent diseases**Animal — Rabies, Lyme disease - Some zoonoses (animal diseases) may be transmitted to humans **Nonliving — Botulism, Tetanus - Soil |
Stages of a Disease | ![]() |
Systemic Infection | Infection throughout the whole body |
Toxemia | Toxins in the blood |
types of contact transmission | direct: requires close association between infected person and susceptible hostindirect: spread by fomites (nonliving objects involved in spread of an infection) example: sheets, towels, doorknobs, toys droplet: transmission via airborne dorplets (<1 meter) |
types of vehicle transmission | transmission by an inadequate reservoir-food, water, air and blood |
types of vector transmission | mechanical feet - Arthropod carries pathogen on biological - Pathogen reproduces in arthropod vector |
Sign | A change in a body that can be measured or observed as a result of disease (e.g. fever, swelling) |
Symptom | A change in body function that is felt by a patient as a result of disease (e.g. tiredness, pain) |
Syndrome | A specific group of signs and symptoms that accompany a disease. |
Acute Disease | symptoms develop rapidly, usually short-lived |
Chronic disease | disease develops slowly, longer-lasting |
Nosocomial Disease | Are acquired as a result of a hospital stay*hand-washing is the most important means of preventing the spread of infection |
portals of entry for a pathogen | -mucous membranes (respiratory tract, GI tract)-skin (hair follicles, sweat glands) -Parenteral route (deposited directly under skin - cuts, bites, injections, surgery) -preferred -multiple |
ID 50: | Infectious dose for 50% of the test population; measures virulence |
LD 50: | Lethal dose (of a toxin) for 50% of the test population |
Coagulase | Coagulates blood (fibrinogen -> fibrin clots) |
Kinases | Digest fibrin clots |
Antigenic Variation | Alteration of cell-surface molecules to avoid host's immune system |
Siderophores | Remove iron from host's iron-binding proteins |
portals of exit for a pathogen | *Respiratory tract-Coughing, sneezing*Gastrointestinal tract-Feces, saliva *Genitourinary tract-Urine, vaginal secretions *Skin *Blood-Biting arthropods, syringe needles |
host defenses | ![]() |
Complement System | a group of serum proteins that act in a cascade to destroy invading microbes; these function to keep blood sterile. |
Differential White Cell Count | Percentage of each type of white cell in a sample of 100 white blood cells |
phagocytosis | Ingestion of microbes or particles by a cell, performed by phagocytes. |
Inflammation | 1. vasodilation2. Margination and emigration of WBCs 3.Tissue repair |
Innate immunity | Non-specific defenses against any pathogen |
Acquired (Adaptive) Immunity | **Naturally acquired active immunity: Resulting from infection**Naturally acquired passive immunity: Transplacental or via colostrum **Artificially acquired active immunity: Injection of Ag (vaccination) **Artificially acquired passive immunity: Injection of Ab |
Humoral immunity | Involves Ab production by B cells; mostly against bacteria, toxins, and viruses |
Cell-mediated immunity | Involves T cells; response is against intracellular pathogens and transplanted tissue |
Haptens | Too small to act as antigen alone |
Apoptosis | (programmed cell death)- very clean; phagocytes destroy unused B and T cells |
Necrosis | violent and messy cell death; leads to an inflammatory response |
B Cells | produce antibodies |
Antigen-Antibody Binding | -antibodies protect the host by binding to foreign molecules and tagging them for destruction by phagocytosis or by the complement system |
Affinity | strength of bond between Ag and Ab |
Specificity | Ab recognizes a specific epitope |
Cytotoxic T Cells CD8 | destroy target cells with perforin |
Helper T Cell CD4 | TH1: activate cells related to cell-mediated immunityTH2: activate B cells to produce antibodies |
vaccine | a suspension of organisms or fractions of organisms used to induce immunity |
Inactivated (dead) vaccine | injection of dead virulent form of pathogenexamples: IPV, rabies, flu shot |
Conjugated Vaccines | capsular polysaccharide combined with a protien to make it effective for infants. examples: Hib vaccine to prevent meningitis |
Toxoid vaccines | injection of inactivated toxinsexamples: tetanus toxoid, diphtheria toxoid |
indicator of ELISA | peroxidase enzyme |
direct ELISA | detects antigens |
indirect ELISA | detects antibodies |
Type I (Anaphylactic) Reactions | -Involve IgE antibodies (IgE was made instead of IgG in a previous exposure).-Localized: Hives or asthma from contact or inhaled antigens. -Systemic: Shock from ingested or injected antigens. |
Type II (Cytotoxic) Reactions | -AB reacts to AG on a person's cells-Involve IgG or IgM antibodies and complement activation -Complement activation causes cell lysis (by MAC's) or damage by macrophages that get attracted to the area |
Type III (Immune Complex) Reactions | IgG antibodies and antigens form complexes that lodge in basement membranes. |
Type IV (Cell-Mediated) Reactions | -Delayed-type hypersensitivities due to T-cells.-Cytokines attract macrophages and initiate tissue damage. -Contact dermatitis, transplant rejection |
Autoimmune Diseases | Type I — Cross-reactions with antibodies made against pathogens (Rheumatic fever - anti-Strep-AB's attack heart muscle)Type II — Antibodies react with cell-surface antigens (Myasthenia Gravis - AB's bind at nerve- muscle junction & muscles become progressively weaker) Type III - AB-AG-Complement immune complexes deposit in tissues (Rheumatoid Arthritis -- complexes settle out in joints) Type IV — Mediated by T cells (Multiple Sclerosis -- T-cells attack the myelin sheath) |
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