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MedMicroBioFinal
medical micro biofinal - MCPHS
| Question | Answer |
|---|---|
| T and B cells develop from | stem cells in red bone marrow |
| Humoral immunity | B cells mature in bone marrow. Due to antibodies example: Chickens: Bursa of Fabricius |
| Cellular immunity | Due to T cells, they mature in the thymus |
| Antigens are | Molecules recognized by adaptive immune system Proteins are strong antigens while polysaccharides are weak antigens. They have to be enzymatically degraded. |
| After exposure to antigen B cells differentiate into | Antibody-producing plasma cells and Memory cells |
| Clonal deletion eliminates | harmful B cells that would react with your own antigens |
| B cell proliferation | each cell recognizes same antigen, effectors cells-plasma cells= Ig factories, and memory cells- reserve for future recognition (long lived) |
| .Plasma cells | produce antibodies, specific for same antigen epitope, . many antibodies molecules, produced by each B cell |
| The number of antigen-binding sites determines | valence |
| IgA | dimer, 10.15 percent of serum, in secretions, mucosal protection, half life = 6 days |
| IgD | monomer, .2 percent of serum, in blood+ lymph +b cells, on b cells- initate immune response, half life = 3 days |
| IgE | monomer, .002% of serum Abs, on mast cells +basophils + blood, allgerica reactions; lysis of parasitic worms, half life = 2 days |
| T cells mature in | the thymus |
| Thymic selection eliminates | many immature T cells |
| T cells respond to Ag by | T-cell receptors (TCRs) |
| T cells require | antigen-presenting cells (APCs) |
| T Cytotoxic Cells | CD8+ or TC cells, . Target cells are self carrying endogenous antigens |
| Cytotoxic cells are | Activated into cytotoxic T lymphocytes (CTLs) |
| CTLs recognize and induce | Ag + MHC I; apotosis in target cell |
| CTL releases | perforin and granzymes |
| Natural Killer Cells | Granular leukocytes destroy cells that don’t express MHC I, Kill virus-infected and tumor cells and attack parasites |
| igG Antibodies | monomer, 80 percent of serum, in blood+ lymph+ intestine, cross placenta, enhance phagocytosis; neutralize toxins and viruses; protects fetus and new born, half life= 23 days |
| IgM | pentamer, 5.1% of serum, fix complement, in blood + lymph and on B cells, agglutinates microbes- first AB produced in response to infection, half life =5 days. |
| Tooth decay (5 stages) | 1. Healthy tooth with plaque, decay in enamel, advanced decay, decay in dentin and decay in pulp |
| Stages of Periodontal Disease (4) | Healthy ginivae, ginitivities, periodontal pockets, and periodontitis |
| Helicobacter Peptic Ulcer Disease- pathogen | Heliocobacter plylori |
| Helicobacter Peptic Ulcer Disease-symptoms | peptic ulcer |
| Helicobacter Peptic Ulcer Disease- intoxication/infction | infection |
| Helicobacter Peptic Ulcer Disease- diagnosis | urea breath, bacterial culture |
| Helicobacter Peptic Ulcer Disease- treatment | antimicrobial drugs |
| Gastroenteritis (bacterial diseases of lower digestive system) | watery diarrhea, abdominal cramps, nausea or vomiting, and sometimes fever, also dysentery |
| dysentery | inflmation of colon |
| gastroenteritis is usually treated with | fluid and electrolyte replacement. |
| Infection is caused by | growth of a pathogen |
| Incubation is from | 12 hours to 2 weeks. |
| Intoxication caused by | ingestion of toxin |
| Symptoms of intoxication appear | 1 to 48 hours after ingestion |
| Staphylococcus aureus enterotoxin | is a superantigen |
| Problem in foods (staphylococcus) is that | foods are cooked then re handled (food poisoning) |
| Shiga toxin causes | inflammation and bleeding (dysentery) |
| 4 F’s of disease | food, fingers, flies,feces |
| Salmonella enteric serovars such as | S. typhimurium |
| Mortality (<1%) due to | septic shock caused by endotoxin |
| Relationship between Salmonella and | typhoid fever |
| Chloera | Vibrio choleraw |
| Vibrio cholera serotypes produce | cholera toxin |
| Cholera toxin causes | host cells to secrete CL-, HCO- and water |
| Non cholera vibros | usually from contaminated crustaceans or mollusks |
| Escherichia coli- Gastroenteritis | Occurs as traveler's diarrhea and epidemic diarrhea in nurseries. |
| 50% of feedlot cattle may have | enterohemorrhagic strains in their intestines. |
| Enterohemorrhagic strains such as E. coli O157 | H7 Produce Shiga toxin = EHEC (or STEC - Shiga Toxin E. coli) |
| Campylobacter Gastroenteritis | Campylobacter jejuni, Gram – rod, Very common in raw chicken and turkey |
| Yersinia Gastroenteritis | Y. enterocolitica and Y. pseudotuberculosis |
| Yersinia Gastroenteritis | Can reproduce at 4°C, Usually transmitted in meat and milk |
| Yersinia Gastroenteritis- Symptoms | can mimic appendicitis, but appendix is normal |
| Clostridium perfringens Gastroenteritis | Grow in intestinal tract, producing exotoxin |
| Clostridium difficile | associated diarrhea ,Grow following antibiotic therapy , associated with hospitalized patients and nursing home residents |
| Bacillus cerues Gastroenteritis | ingestion of bacterial exotoxin which produces mild symptoms. Fried rice is a common vehicle. |
| Hepatitis | inflammation of the liver, 30 day incubation period |
| Hepatitis A | a commonly food borne (fecal oral) |
| Viral Gastroenteritus- Rotavirus | 1-2 day incubation, 1 week illness, water borne, dangerous to infants and small children |
| Norovirus | 50 percent of US have anti bodies, 3 day illness, cruise ship, treated with rehydration. |
| Mycotoxins | are produced by some fungi |
| Mycotoxins- Claviceps purpurea | grows on grains, produces ergot |
| Ergot | toxin the restricts blood flow to limbs, causes hallucination |
| Local history of Ergot | Witch trials |
| Mycotoxins- Aspergillius Flavus | Grows on grains and peanuts, produces aflatoxin |
| Aflatoxin | Toxin causes liver damage, liver cancer |
| Giardiasis Lamblia | protozoan |
| Giardia Lamblia protozoan | transmitted via contaminated water, (beaver fever), long lasting diarrhea, diagnosed via microscopic examination of stool for ova and trophozoited, treated with metronizdazole |
| Cryptosporidiosis Hominis | transmitted by oocysts in contaminated water, gastroenteritis, treated with oral rehydration |
| Diptheria | Purifies diphtheria toxoid |
| Pertussis | acellular fragments of purified from Bordetella pertussis |
| Tetnus | Purified tetnus toxoid |
| DTaP | diphtheria, pertussis, tetnus |
| Meningococcal meningitis | purified polysaccharide from N. meningitides |
| Haemophilus influenza type b meningitis (Hib vaccine) | polysaccharides conjugated with protein |
| Pneumococcal conjugate vaccine | streptococcus pneumonia antigens conjugated with protein |
| Small pox | live vaccinia virus (not routinely used) |
| Rabies | Inactivatd virus |
| Poliomyletis | inactivated virus |
| Influenza | inactivated or attenuated virus |
| Measels | attenuated virus |
| Mumps | attenuated virus |
| Tubella | Attenuated virus |
| MMR | measles, mumps and rubella- all attenuated virus’ |
| Chicken pox | attenuated virus (herpes zoster= same) |
| Hepatitis A | Inactivated Virus |
| Hepatitis B | Antigenic Fragments (recombinant vaccine) |
| HPV | Ag fragments |
| Protection without developing immunity- Gama globin | Antibodies from pooled serum- human or animal, or general/ special preparations (Hep A exposure) |
| Advantages of passive immunization | protection for immunocompromised, immediate protection and temporary protection while immunity develops |
| Disadvantages of passive immunization | serum sickness (animal preparations), no lasting immunity |
| Naturally Acquired active immunity | disease of normal exposure |
| Naturally acquired passive immunity | placenta/ breast milk |
| Artificially acquired active immunity | vaccine |
| Artificially acquired passive immunity | gamma globulin injection |
| Response to antigens leading to damage, 4 types of reaction | Anaphylactic, cytotoxic, immune complex, cell mediated (or delayed type) |
| Anaphylaxis- Immunization | sensitized to allergen, produce IgE antibody |
| Anaphylaxi- Cellular Response | IgE binds to Fc receptor- mast cells, basophils |
| Anaphylaxis (6) | immunization, cellular response, antigen binds IgE, crosslinking of IgE antibodies, Degranulation, Symptoms |
| Anaphylaxis- Degranulatoin | relase of chemical mediators |
| Anaphylaxis- Symptoms | Smooth muscle contraction (bronchia), vascular permeability, swelling; edema, respiratory disease. |
| Tye II (Cytotoxic) Reactions | involve IgM or IgG antibodies and complement activation => cell lysis or damage by macrophages. |
| Immume Complex Mediated Hypersensitivity- Example- Systemic lupus erythematosus | antibodies to cell nucleus components and deposits in many areas |
| Where does SLE deposit? | Kidneys (most common), skin (cause butterfly rash), joints (arthritis) , brain (mental) |
| Type IV | allergty contact Dermatitis |
| T cell Response to Type IV- Cell Mediated | Delayed (12-48 hrs after exposure), not anti body mediated |
| First exposure of Type IV (t response) | TD cells become sensitized and cells proliferate |
| Second Exposure of Type IV (t response) | TD activated by antigen, release lymphokines, stimulate macrophages, inflammatory response (symptoms) |
| What is the magic Bullet concept? | Bullet kills only selected target (pathogen) and not the innocent by-stander (host) |
| Who was the magic bullet discovered by? | developed by Paul Ehrlich in early 1900s |
| (German organic chemist) - tested 100s of organic arsenic compounds | |
| What cured and how did they test? | #606 cured Trypanosomal infections in mice (test) and then used on syphilis patients, Worked on most (some with miraculous cure) but, treatment killed others |
| Magic Bullet concept now referred to as | selective toxicity. |
| Therapeutic index | The maximum dose that is toxic to patient divided byminimum effective dose against pathogen |
| Toxic dose, effective dose | 10mg/kg Effective dose is 2mg/kg |
| High ratio | = high TI = less toxic to patient |
| Penicillin TI | = >10,000 |
| 1928 | Fleming discovered penicillin, produced by Penicillium. |
| 1940 | Howard Florey and Ernst Chain performed first clinical trials of penicillin. |
| Antibiotic resistance mechanisms- Resistance genes (3) | Antibiotic degrading enzymes, Efflux pump (removes antibiotic from cell before harm occurs and antibiotic altering chemically alters antibiotic |
| Cell mutation event (resistance) (2) | 1. Antibiotic is prevented from entering cell and 2. Target is altered (by mutation) |
| Multiple resistance | plasmid transfer of several genes sets that confer resistances by different mechanisms |
| Gonorrhea- Females | leads to pelvic inflammatory disease (PID)/sterility |
| Gonorrhea endocarditis | heart infection, comes from scarring of fallopian tubes |
| Gonorrhea- infants | can get it in eyes- erythromycin (after birth) used to be silver nitrate |
| Gonorrhea- Symptoms (MEN) | Painful urination and discharge of pus |
| Gonorrhea (Diagnosis) | Gram stain, ELISA, PCR |
| ELISA, PCR | Gram negative dip to coccus |
| Treatment of Gonorrhea | Fluoroquinolones, used to be penicillin, but has resistance- switch to fluoroquinones |
| Pelvic Inflammatory Disease (PID) | Poly microbic- usually N gonnorrhoeae or C. trachomatis |
| Symptoms of PID | Chronic Pelvic Pain |
| Treatment of PID | DOxycycline and cefoxitin |
| Syphilis is caused by | Treponema pallidum |
| In Syphilis- invades | mucosa or through skin breaks |
| Syphilis- Primary Stage | Chancre at site of the infection |
| Syphilis-Secondary stage | Skin and mucosal rashes |
| Syphilils- latent period | no symptoms |
| Syphilis- tertiary stage | Gummas on many organs |
| Treatment of Syphilis | Benzathine penicillin |
| Congential | Neurological Damage |
| Co infection of Syphilis | Chlamydia |
| Chlamydiae | unable to produce ATP in amounts required to sustain metabolism= obligate intracellular parasites of eukaryotic cells |
| Chlamydia is what type of disease | socially transmitted disease (more than medicine to treat) |
| Chlamydia also causes | Trachoma, which is leading cause of blindness world wide |
| Trachoma is transmitted via | a tsetse fly |
| 1983 AIDS | Discover of virus causing loss of immune function |
| In HIV, seroconversion can take up to | 3 months |
| HIV antibodies are detected by | ELISA |
| HIV antigens are detected by | Western blotting |
| HIV | Plasma viral load is determined by |
| How long does HIV survie outside a cell | 6 hours |
| HIV survives ____ inside a cell | less than 1.5 days |
| Infected body fluids transmit HIV via | Sex, breast milk, transplacental infection of fetus, blood contaminated needles, organ transplants, artificial insemination, and blood transfusion |
| How to “slow down” HIV | Combinations of nucleoside reverse transcriptase inhibitors plus- non nucleoside reverse transcriptase inhibitor or protease inhibitor and/or fusion inhibitors |
| Streptococcus pyogenes | GAS ( group A beta-hemolytic streptococcus) |
| Group A | type of polysaccaharide antigen |
| Beta- hemolytic | type of hemolysis of blood agar |
| Clinical syndrome of S p | whitish exuade covering tonsils, inflammation of pharynx, fever |
| Complications of S. pyogenes | scarlet fever, septicemia, rheumatic fever, acute poststreptococcal glomerulonephritis |
| Scarlet fever | toxin kills cells |
| Septicemia | spread in blood stream |
| Rheumatic Fever (auto immune) [3] | Inflammation in organs/ joints, heart valve damage, prevention if strep throat is treated |
| Acute poststreptococcal glomerulonephritis | inflammation in glomeruli in kidneys |
| Pathogenesis (common cold) | replication of epithelial cells, stimulate kinins secretions, immune response clears virus |
| Impetigo | Skin rash, contagious |
| Erysipedas | deeper tissue infection, used to have high death rate before antibiotics |
| Necrotizing fascists- flesh eating disease, strep grows in dead tissue which fools body’s defense | doesn’t kill it. As it continues to grow = more dead tissue. Only cure is to amputate |
| Toxic shock syndrome | rash, organ failure |
| Puerperal fever | Childbed fever |
| Otitis media | child hood ear ache |
| Bacteria, viruses and fungi cause (3) | Bronchitis, bronchiolitis, pneumonia |
| Pertussis | Whopping cough |
| Bordetella pertussis | gram negative coccobacillus |
| In Pertussis | Tracheal cytotoxin damages ciliated cells |
| Mycobacterium tuberculosis | Acid fast rod, transmitted from human to human |
| Tuberculosis is a | facultative intracellular parasite (usually of macrophages) |
| Streptococcus pneumonia | Gram positive encapsulated diplococci |
| When encapsulated b acter excape phagocytosis in lung… | growth leads to inflammation |
| Symptoms of Pneumococcal Pneumonia | Infected alveoli of lung fill with fluids, interferes with oxygen intake |
| Diagnosis of Pneumococcal Pneumonia | Clinical evaluation, serological typing of bacteria |
| Treatment of Pneumococcal Pneumonia | Penicillin, fluoroquinolones |
| Mycoplasmal Pneumonia | walking pneumonia |
| Treatment of Mycoplasmal Pneumonia | tetracyclines |
| Meninges protect | brain and spinal cord |
| Dura mater | outer most layer |
| Arachnoid matter | middle layer |
| Pia mater | Innermost layer |
| Blood Brain barrier | protective layer |
| Bacterial Meningitis | fever, headache, nausea, may progress into coma |
| Bacterial meningitis diagnosed by | gram stain and latex agglutination of CSF (spinal tap) |
| Furious rabies | animals are restless then highly excitable |
| Paralytic rabies | animals seem unaware of surroundings |
| Rabies Virus | virus multiplies in skeletal muscles and then brain cells causing encephalitis |
| Initial symptoms of rabies | muscle spasms of mouth and pharynx => dehydration/ hydrophobia |
| Hydrophobia and rabies | Muscle spasms when drink water,s o one will have a fear of water because of the pain |
| Prevention of rabies (PRE) | pre exposure prophylaxis- injection of human diploid cells vaccine HDCV |
| Prevention of rabies (after) | Vaccine pluse immune globulin |
| Lyme Disease | Borrelia Burgdorferi |
| Reservoir of LD | Deer |
| Vector of LD | Ticks |
| First symptom of Lyme disease | bulls eye rash |
| Second phase of LD | Irregular heart beat, encephalitis |
| Third phase of LD | arthritis |
| Encephalitis | irritation or swelling of the brain due to infections |
Created by:
jenniferigoe
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