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104 Cards in this Set
- Front
- Back
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Papilloma virus (papillomavirus) (DNA) |
Found in cervical cancer cells |
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Epstein-Barr Virus (lymphocrytovirus) (DNA) |
Infectious mononucleosis Burkitt's lymphoma, nasapharyngeal Cancer, Hodgkins lymohoma 90% of US population carries EB virus latent stage with no disease. David "bubble boy" 1985 died of cancer following bone marrow transplant contains EBV |
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Herpes simplex virus 2 ( a simplexvirus, HSV 2 or HHV2) (DNA) |
VD and cervical cancer |
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Hepatitis B Virus (HBV, Hepadravirus) (DNA) |
Associated with liver cancer Liver cancer risk is 98 times greater in those with previous HBV infections |
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Which viruses contain DNA containing onconogenic? |
Papilloma virus Epstein-barr virus Herpes simplex virus 2 Hepatitis 2 virus |
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Human T-cell leukemia virus (HTLV1 or HTV2) RNA |
retro viruses Human leukemia and lymphoma (helper) HIV attacks bosses of immune system |
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Latent viral infection |
Virus remains "quietly" in host tissues for many years In lysogenic-like state in host cell. |
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Cold sores |
HSV (HHv1) |
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Shingles (herpes zoster) |
same virus (varicella zoster virus V2V, varicella virus) causes chicken pox (varicella) Caused by reactivation of virus likelihood (10-20%) |
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Pathogenic |
Disease causing balance between: health <-- host resitance--vs. virulence -->disease |
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Host resistance |
Body surface defense, phagocytic cells, specific immune mechanisms (antibodies) |
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Virulence |
Of attacker - degree of disease causing ability host attachment, capsule, enzyme production, toxin production. |
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Pathology |
Study of disease |
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etiology |
Cause of disease (3 major concerns of pathology) |
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Pathogenesis |
Manner of disease development (3 major concerns pathology) |
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Major cause of pathology (3rd) |
structural and functional changes caused. |
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infection |
invasion and growth of microbes in a body. |
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disease |
abnormal state in which part or all of the body is not properly adjusted or is incapable of normal functions morbid process having a charectoristic collection of signs and symptoms difference between HIV infection and AIDS |
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infectious disease |
caused by another organism |
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non infectious disease |
not caused by organism (e.g. inherited, traumatic) |
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normal microbiota |
(normal flora) those microbes normally found in or on certain regions of the body May exhibit microbial antagonism (preventing the overgrowth of harmful microbes) Lactobacillus of vagina maintains a pH of ~4 inhibits growth of Candida effects of antibiotic administration |
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transient microbiota |
organisms temperarily present in or on the body ---> may cause disease |
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Bacteriocin |
Bacteria that kills other bacteria |
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skin |
Propionibacterium acnes, staphylococcus epidermidis, staphlococcus aureus, corynebacterium. |
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Conjunctiva |
Mucous membrane covering inner surface of eyelid and anterior of eyeball up to cornea - staph, epidermidis, S. aureus, diphtheroids Pseudomonas |
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URT (upper resp. Tract) |
S. epidermidis, S. aureus, diphtheroids, hemophilis influenzae, Neisseria meningitidis Streptococcus pneumonie --> most dangerous |
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mouth |
streptococcu, Lactobacillus, Candida, bacteroides, spirochetes, Actinomyces |
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Large intestine |
Bacteroides, Fusobacterium, Lactobacillus, Enterococcus, Escherichia Coli, Enterobacter aerogenes, proteus, + |
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Urethal opening |
S. epidermidis, Enterococcus, enterobacteria, Lactobacillus, + |
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Vagina |
Between pubery and menopause Lactobacillus dominates (acid pH) diphtheroids, streptococcus (group 1) clostridium, + |
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Symbiosis |
2 organisms living together in physical contact with each other |
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commensalism |
One benefited, other inaffected diphtheroids of conjuctiva |
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mutualism |
Both benefit Vitamin K and vitamin B produces bacteria of large intestines |
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parasitism |
One organism benefits (parasite) the other (host) is harmed. |
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Signs |
objective findings that can be observed and/or measured |
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symptoms |
subjective findings, not apparant to observers - pain malaise ( vague feeling of body discomfort) |
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syndrome |
specific group of signs and/or symptoms accompanying a particular disease. |
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communicable disease |
a disease that spreads from on host to another |
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contagious disease |
disease easily spread from one host to another |
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noncommunicable disease |
disease not spread from one host to another |
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Acute disease |
Develops rapidly, last short time -flu (develops in 24-72 hours lasts 2-7 days) -days to weeks. |
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chronic disease |
develops more slowly, longer lasting TB (develops 4-12 weeks, and last 9 months of antitubercular therapy) continual or recurrent, months - years |
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local infection |
limited to small area of body boil, stye |
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system (generalized) infection |
spread throughout the body measles (heart disease) |
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focal infection |
microbes spread to site by blood or lymph e.g. from teeth to tonsils |
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bacteremia |
Bacteria in the blood |
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septicemia |
bacteria in blood and multiplying there |
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viremia, toxemia |
bacteria in blood, condition |
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incubation period |
interval between organism entry and the first appearance of sign and symptoms |
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prodromal period |
early mild symptoms and signs often non specific- malaise, uneasiness short interval |
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period of illness (acute period) |
rapid increase in overt signs and symptoms fever, pain, lymphnode enlargement (hmphadenopathy) change in white blood cells, rash, death |
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period of decline |
signs and symptoms decline vulnerable to secondary infections |
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convalescent period |
regains normal health |
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Nosocomial infection |
hospitals, nursing homes, or other health related facility acquired. CDC 5-15% of all hospital patients In U.S 20,000 die a year. |
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What are 3 principals contributing factors to nosocomial infections? |
microbes in hospitals compromised host chain of transmission |
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What microbes are picked up in a hospital? |
Threat of oppurtunist, special drug resistance (including microbiota of personnel and patients) 40% + Enterobacteria 1% Staph aureus 10% Entercocci - Enterococcus Faecalis 10% fungi (mostly Candida) 9% psuedomonas Aeruginosas |
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What are some compromised host in nosocomial infections? |
Oppurtunist- broken tissue, surpressed immune response, impaired cell activity. Therapeutic and diagnostic procedures tracheotomy, urinary catheters, intravenous, therapy, radiation T and B lymphocyte impairment. |
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What is that chain of transmission in nosocomial infections? |
Hospital staff - patient Patient - patient fomites (something a lot of ppl handle) hospital ventilation system
Legionairres Legioneila Pontiac fever |
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Principal nosocomial infections |
50% urinary tract 25% surgical wound 12% lower RT - high mortality rate 6% bacteremia
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Control of nosocomial infections |
good aspeptic technique hand washing educating personnel and infection control committee. |
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LD ^50 |
Lethal dose (50%) a method of measuring virulence. number of microbes or amount of toxin in a dose that will kill 50% of inoculated test animals. smaller LD^50 - more virulent. |
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ID^50 |
Infectious dose (50%) number of microbes in a dose that will produce infection in 50% of test animals. |
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Direct damage |
At site of invasion - metabolic products cell penetration (phagocytosis - neisseria gonorrheoeae) |
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Toxigenicity |
Ability to produce toxins About 220 known bacterial toxins (40% damage host PM) |
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Cytotoxins |
Specific exotoxins kills cells or inhibit their infection |
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neurotoxin |
specific exotoxin interferes with nerve impulse transmission |
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enterotoxin |
specific exotoxin Affect cells lining G.I.T |
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Toxoid |
Affect cell linings G.I.T chemicals so that it is no longer toxic but still stimulates the production of antibodies. Antibodies called antitoxins A type of vaccine - Diphtheria Vaccine part of (DPT) -Tetanus Vaccine (another part of DPT) |
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Diphtheria exotoxin |
Corynebacterium Diptheriae with lysogenic phage containing toxin gene. Inhibits protein synthesis. (Exotoxin) |
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Erythrogenic toxin |
Streptococcus pyogenes -scarlet fever - damaged capillaries --> rash. |
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Exotoxins |
living cells proteins heat labile (destroyed by heat) specific activity antigenic (lethal) Botulism can kill a guinia pig. |
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Botulinum Toxin |
Clostridium botulinum - neurotoxins - functions at neuromuscular junction inhibits release of acacetylcholine from nerve cell (neurons) --> Flaccid paralysis |
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Tetanus toxin |
Clostridium tetani - neurotoxin binds to nerve cells to CNS that send inhibiting impulses to antagonist muscle -Spasmodic contraction of muscle (spastic paralysis) lockjaw |
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Vibroi enterotoxin |
Choleragen loss of fluid and ions by cell and muscle contractions lead to diarrhea and vomiting |
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Staphylococcal enterotoxin |
staphylococcus aureus affects intestines like choleragen toxin in heat stable. (1 exception)
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Endotoxins |
Gram negative released by dead cells lipid heat stable generalized activity exerts effects upon cell death and lysis may cause worsening S + S following antibiotic administration. Fever, septic shock |
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Types of acquired immunity |
specific defensive response when invaded by foreign organisms or foreign substances Developed during one's lifetime, not inherited. |
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Actively acquired immunity |
An organism exposed to foreign substances (antigens) responds by producing antibodies (ab) or specialized lymphocytes antigen usually destroyed or inactivated long lasting (few years to life-long) protective levels in 10-21 days. |
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Passively acquired immunity |
the transfer of antibodies or specialized lymphocytes from one organism to another short lasting (half-life about 3 wks for AB) immediate protection |
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Naturally acquired active immunity |
as a result of illness and recovery or subclinical infection having mumps or measles. |
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naturally acquired passive immunity |
antibodies transferred from mother to fetus across placental barrier (plancental transfer) antibodies transferred from mother to nursing infant in colostrum |
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Artificially acquired active immunity |
as a result of the administration of antigens (vaccine) process called vacination |
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Kinds of vaccinations agents |
attenuated microbes toxoid - inactivated toxin killed microbes by heat or chemical |
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artificially acquired passive immunity |
administration of antibodies in serum (antiserum) or specialized lymphocytes |
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humoral (antibody-mediated) immunity |
antibodies dissolved in extracellular fluid (serum, plasma, lymph, mucus) - humors special lymphocytes, B cells, exposed to antigen defends against bacteria, bacterial toxin, and viruses in body fluids |
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cell-mediated immunity |
special lymphocytes, T cells, exposed to antigen, antibodies not secreted T cells have antigen receptors on their surface permit t cells to recognize and react to specific antigen defends against bacterial and viruses inside of phagocytic or other infected host cells, fungi, certain protozoans, helmith, foreign grafts, & cancer cells. |
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Antigens (immunogens) |
proteins, nucleoproteins, lipoproteins, glycoproteins, or large polysaccharides components of capsule, CW, flagella, pili, or toxins of bacteria; capsids or envelopes of viruses; cell surfaces, pollen, egg white, serum proteins, blood cells, transplanted tissues molecular weight 10,000 or more |
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antibodies |
immunoglobulins (lg), proteins produced in response to antigen presence bind to and help destroy specific antigen highly specific - generally bind to only 1 kind of antigenic determinant most bivalent, with 2 antigen binding sites result in formation of antigen-antibody (Ag-Ab) complex |
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Antibody basic structure (monomer structure) |
4 polypeptide chains: 2 heavy (H) chains 5 types of C regions: gamma, alpha, mu, delta, epsilon 2 light (L) chains linked by disulfide (-S-S-) bonds |
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regions of antibody molecule |
monomer "Y" or "T" shaped (flexible) variable region (V) parts of H and L chains of arms form antigen bonding sites constant region (C) rest of arms & stem of "Y" relatively invariable in amino acid sequence for Ab type in species Stem of "Y" -Fc portion may bind complement may attach to certain cells (mast cells) |
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lgG |
about 80% of Ab in serum |
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lgA |
10-15% of Ab in serum monomers in serum, dimers in secretion colostrum & breast milk, saliva, mucus, tears |
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lgM |
5-10% of Ab in serum 5 monomers with interlinking disulfide bonds j-chain 10 antigen bonding sites first Ab after initial exposure |
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Immunological Memory anitbody titer |
intensity of humoral response |
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primary response to antigen |
no detectable Ab for several days slow rise in Ab titer (first lgM then lgG) gradual decline in Ab titer |
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secondary response to 2nd exposure to antigen |
involves memory or anamnestic response memory cells can diff. into plasma cells ---> Ab result: must faster and higher rise in Ab titer mainly lgG principle behind booster vaccination tetanus toxoid vaccination series |
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monoclonal antibodies |
Jerne, Kohler & milstein (1975) cultured myeloma cells (cancerous B cells) that are mutants (cant produce antibody) mouse injected with Ag, spleen removed spleen B cells mixed with myeloma cells hybrid cells produced multiply to form clone ( hybridoma) cells transferred to selective media hybridomas producing desired Ab are cultured monoclonal Ab are uniform, highly specific and readily produced in large quantities |
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Uses for monoconal Ab? |
diagnostic kits - chlamydia and strep I.D., pregnancy tests for urine hormone used to destroy T cells involved in transplant rejection specifically attached to cancer cells and poisons it |
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cell-mediated immunity |
immunity based on the activities or certain lymphocytes, particularly T cells release cytokines (60+ known) show different activities under different conditions those that show as communicators between WBC are classified as interleukins (17 known) |
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IL-1 |
released by nucleated cells, especially macrophages; stimulate Th cells in the presence of Ag and attracts phagocytes to infection site |
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IL-2 |
activates Th, b, Tc, and NK cells |
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IL-8 |
attracts macrophages and immune system cells |
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IL-12 |
supports differentiation of T cells |
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-y-IFN- |
inhibits intracellular viral replication, stimulates macrophages against microbes and tumor cells |
