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279 Cards in this Set
- Front
- Back
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microbial diseases of the digestive system
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transmitted in food and water
ANP |
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ANP
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long hollow tube-starts at mouth ends at other end
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fecal-oral cycle broken by
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-proper sewage disposal
-disinfection of drinking water -proper food preparation and storage |
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stages of tooth decay
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1. healthy tooth with plaque
2. decay in enamel 3. advanced decay 4. decay in dentin 5. decay in pulp |
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tooth decay
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hole in tooth, starts with biofilm-->plaque-->gets all the way trhough to enamel into dentin-->decay in pulp-->leads to bone/brain even heart and end up with brain or bone infection and abscess
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stages of periodontal disease
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1. healthy gingivae
2.gingivitis 3. periodontal pockets 4. periodontitis |
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periodontal
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category of infectious disease
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heliobacter
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in mucous lining of stomach can even cause inflammatory response when causes tissue damage open sore-->hyperchloric acid
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helicobacter peptic ulcer disease
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pathogen= helicobacter pylori
can be transmitted through soil infection because of microbial aspect antibodies can take care of this |
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helicobacter peptic ulcer disease diagnosis
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urea breath, bacterial culture
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bacterial diseases of lower digestive system
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serious diseases treated with fluids of electrolytes because of loss of fluid
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microbe growing in food leads to a
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toxin
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bacterial diseases of lower digestive systemn symptoms
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usually include gastroenteritis, watery diarrhea, abdominal cramps, nausea or vomiting, and sometimes fever and dystenerty
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dysentery
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inflammation of colon
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infection
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caused by growth of a pathogen
incubation from 12 hours to 2 weeks |
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intoxication
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caused by ingestion of toxin
symptoms appear 1 to 48 hours after ingestion |
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estimated number of food poisoning cases per year in U.S.
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76 million
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estimated death by food poisoning a year in U.S.
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5000
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staphylococcus aureus
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enterotoxin is a superantigen
directly infects intestine |
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staphylococcal food poisoning
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staphylococcus aureus-enterotoxin
problem in foods that are cooken THEN renhandled!!! -staph will grow and produce toxin->reheat it is worse because heat stabilizes toxin-but will kill Staph |
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onset time of staphylococcal food poisoning
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1-6hours
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duration of stayphylococcal food poisoning
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less than 24 hours
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shigellosis
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food infection
shigella toxin causes bleeding in intestines (dysentery) and inflammation 4F disease |
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4F disease
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shigellosis
1. food 2. fingers 3. flies 4. feces |
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salmonellosis
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salmonella enterica serovars such as S. typhinurium
MANY different types effects mostly infants and elderly motality due to septic shock caused by endotoxin |
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cholera
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vibrio cholerae serotypes that produce cholera toxin
toxin causes host cells to secrete Cl-, HCO- and water in Haiti-toxin nmakes water loss in intestine |
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non-cholera Vibrios
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usually from contaminated crustaceans or mollusks
-V. cholerae serotypes other than O:1, O:139, and eltor -V. parahaemolyticus -V. vulnificus |
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V. vulnificus
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non-cholera vibrios
RAW SEAFOOD |
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escheria coli gastroenteritis
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epidemic diahrea
different strain that Traveler's diarhrea -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 |
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e. coli O157:H7 illness has been associated with
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ground beef
apple cider leafy green vegetables day care centers petting zoos macaroni salad |
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campylobacter gastroenteritis
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not common in population
campylobacter jejuni gram- rod very common in raw chicken and turkey |
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yersinia gastroennteritis
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Y. enterocolitica and Y. pseudotuberculosis
can reproduce at 4 degrees celsius->appenditcitis usually transmitted in meat and milk symtpoms can mimic appendicitis but appendix is normal |
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clostridium infections
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associated with diarrhea
fecal-oral clostridiunm perdringens gastroenteritis clostridium difficile |
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clostridium perfringens gastroenteritis
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grow in intestinal tract, producing exotoxin
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clostridium difficile
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associated diarrhea
grow following antibitioc therapy associated with hospitalized patients and nursing home residents |
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baccilus cereus gastroenteritis
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ingestion of bacterial exotoxin produces mild symptoms->cramps/diarrhea
fried rice is common vehicle |
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hepatitis
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inflammation of liver
30 day incubation hepaptis a commonly food-borne (fecal oral) MA 2001 outbreak |
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MA 2001 outbreak of hepatitis
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restaurant worker prepared uncooked foods led to 46 cases in next 2 months
secondary outbreak: victim in 1st outbreak worked in diffnerent restaurant and led to 2nd outbreak |
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viral gastroenteritis
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rotavirus
norovirus treated with rehydration |
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rotavirus
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viral gastroenteritis
3 million cases annually 1-2 day incubation 1 week illness water borne dangerous for infants and small children |
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nnnorovirus
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50% of U.S. adults have antibodies
1-2 day incubation 1-3 day illness cruise ship favorite viral gastroenteritis |
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mycotoxins
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produced by some fungi
claviceps purpurea aspergillus flavus |
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claviceps purpurea
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mycotoxin
grows on frains produces ergot toxin restricts blood flow to limbs; causes hallucination |
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aspergillus flavus
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mycotoxin
grows on grains and peanuts-->PEANUT BUTTER produces aflatoxin -toxin causes liver damage; liver cancer |
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giardiasis
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giardia lamblia protozoan
transmitted by contaminated water beaver fever long lasting diarrhea diagnosed by microscopic examination of stool for ova and trophozoite treated with metronidazole |
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cryptosporidiosis
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cryptosprodium hominis
transmitted by oocysts in contaminated water gastroenteritis treatedn with oraln rehydration milwaukee 1993 |
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milkwaukee 1993 cryptosporidiosis
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403,000 cases
100 deaths from public drinking water |
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how to check for immune response to antigen
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check serum for antibody exposure
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what cells develop from stem cells in red bone marrow
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t and b cells
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humoral immunity
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b cells mature in the bone marrow
first discovered in chickens due to antibodies |
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cellular immunity
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due to T cells
t cells mature in the thymus cell itself is the immunity |
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antigens
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molecules recognized by adaptive immune system
-mostly large molecules (greater than 10,000m. weight) -proteins -nonself 9foreign to body) |
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weak antigens
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polysachharides
ex: lipids, peptidoglycan has to be enzymatically degraded |
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what are shape dependent
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antibodies and antigens
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epitopes
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anyigenic determinants on antigen
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haptens
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exception to antigens that are large
SMALL sixe 300 m. weight or less foreign to host body connects with self carrier molecule |
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activation of b cells
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needs antigen and helper T cell
helper T cell releases cytokines (chemical mediators) plasma cells release antibodies |
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clonal deletion
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eliminates harmful B cells that would react with your own antigens
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clone
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small portion of total B cell population that recognizes specific antigen epitope
-only cells which react with antigen epitope become activated |
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how many different antigens
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100 million antigens
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B cell proliferation
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-each cell recognizes same antigen
-effector cells=plasma cells -memory cells |
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plasma cells
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Ig factories
antibodies -specific for same antigen epitope -many antibodies molecules produced by each B cell |
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memory cells
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reserve for future recognition
long-lived |
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percent of B cells in WBCs
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10-15%
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antibodies
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globular proteins called immunoglobulins
ends of arms on y-shaped antibodies are antigen binding site -antigen binding site matches with epitope -4 peptide bonds -base of y=constant region -->same/identical configuration in different hosts |
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IgG Antibodies
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monomer
80% fix complement in blood, lymph, and intestine cross placenta: only call of antibody able to do this enhance phagocytosis; neutralize toxins and viruses, protects fetus and new born |
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IgG antibodies half-life
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23 days
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IgM Antibodies
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-pentamer
-5-10% fix complement in blood, lymph, and on B cells agglutinates microbes; first Ab produced in response to infection 1st antibody plasma cells make lage molecyle can match up to 10 antigens at one time |
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half life of IgM antibodies
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5 days
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IgA Antibodies
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dimer
10-15% in secretions mucosal protection ends up in tears, mucous, breast milk, saliva, on forefront of portals of entry |
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half-life of IgA
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6 days
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IgD Antibodies
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monomer
.2% in blood, lymph, and on B cells initiates immune response some ppl are missing IgD antibodies |
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half life of IgD antibodies
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3 days
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IgE antibodies
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monomer
.002% on mast cells, on basophils, and in blood allergic reactions; lysis of parasitic worms |
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IgE half life
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2 days
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5 class of antibodies
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IgG
IgM IgA IgD IgE |
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results of antigen and antibodies bonding
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agglutination
activation of complement opsonization antibody-dependent cell-mediated cytotoxicity neutralization |
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agglutination
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reduces number of infectious units to be dealt with
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activation of complement
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causes inflammation and cell lysis
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opsonization
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coating antigen with antibody enhances phagocytosis
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antibody-dependent cell-mediated cytotoxicity
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antibodies attached to target cell cause destruction y macrophages, eosinophils, and NK cells
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neutralization
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blocks adhesion of bacteria and viruses to mucosa
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T-cell receptors
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how T cells respond to Ag
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antigen-presenting cells
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T cells require these
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T cytotoxic cells
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CD8+
target cells are self carrying endogenous antigens activated into cytotoxic t lymphocytes -CTLs recognize antigen and MHC I (presenting cell) -CTL releases perforin and granzymes |
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what triggers T cytotoxic cell
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virus-infected cell
cancer cell |
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natural killer cells
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granular leukocytes destroy cells that dont express MHC I
kill virus-infected and tumor cells attack parasites |
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antibody titer
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amount of antibody in serum
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primary response
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occurs after intitial contact with antigen
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secondary (memory/anamnestic) response
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occurs after second exposure
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principal vaccines used in U.S. to prevent bacterial diseases in humans
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DTaP
Meningococcal meningitis Haemophilus influenzae type b meningitis (Hib vaccine) pneumococcal conjugate vaccine |
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DTaP
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diptheria
pertussis tetanus |
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diptheria vaccine
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purified diptheria toxoid
part of DTaP vaccine |
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pertussis vaccine
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acellular fragments of purified from Bordetella pertussis (around 12 antigens)
no live microorganisms does have microbial antigens |
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tetanus vaccine
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purified tetanus toxoid
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meningococcal meningitis
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purified polysaccharide from Heisseria meningitidis
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haemophilus influenzae type b meningitis
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Hib vaccine
polysaccharides conjugated with protein -common in childhood |
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pneumococcal conjugate vaccine
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Streptococcus pneumoniae antigens conjugated with protein
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smallpox vaccine
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live vaccinia virus (not routinely used)
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rabies vaccine
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inactivated virus
not routine-can be used after exposures |
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poliomyelitis vaccine
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inactivated virus
also attenuated virus version available |
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influenza vaccine
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activated or attenuated virus
use eggs for vaccine |
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principal vaccines in the U.S. to prevent viral diseases
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smallpox
rabies poliomyelitis MMR chickenpox hepatitis A and B HPV influenza |
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measles vaccine
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attenuated virus
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attenuated viruses
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live viruses but weakened
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mumps vaccine
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attenuated virus
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rubella vaccine
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attenuated virus
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MMR vaccine
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trivalent vaccine
measles mumps rubella |
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chickenpox vaccine
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attenuated virus
herpes zoster |
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hepatitis A vaccine
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inactivated virus
can get Hepatitis A from food or water |
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hepatitis B vaccine
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antigenic fragments (recombinant vaccine)
transmitted by blood |
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human papilloma virus vaccine
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HPV
antigen fragments prevents cervical cancer |
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papilloma
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wart
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males get HPV vaccine
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helps against throat, mouth, tongue cancer
which alcoholic smokers can be prone to |
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measles
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can lead to permanent brain damage/death
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MMR vaccine invented in
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1978
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passive immunization
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protection without developing immunity
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gamma globulin
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antibodies from pooled serum
-human/animal general or special preparations |
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passive immunization advantages
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protection for immunocompromised
immediate protection temporary protection while immunity develops |
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passive immunization disadvantages
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serum sickness (animal preparations)
no lasting immunity |
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natural passive immunization
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from mom, crossing placenta or breastmilk
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types of immunity
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naturally acquired active immunity
naturally acquired passive immunity artificially acquired active immunity artificially acquired passive immunity |
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naturally acquired active immunity
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disease or normal exposure
-body makes antibodies -long-lived |
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naturally acquired passive immunity
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protection by somebody else's antibodies
-placenta/breast -short lived |
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artifically acquired active immunity
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vaccine
long-lived but might need booster ex: attenuated microbe |
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artificially acquired passive immunity
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gamma globulin injection
shortlived |
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types of reactions in response to antigens (allergens)
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1. anaphylactic
2. cytotoxic 3. immune complex 4. cell-mediated (or delayed-type) |
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anaphylaxis
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immune system and specialized cells (basophils and mast cells)
*IgE antibodies produced in response to an antigen -->coat mast cells and basophils antigen bridges gap between two adjacent antibody molecules of same specifcity, cell undergoes granulation and releases hitamine and other mediators |
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cells involved in anaphylaxis
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mast and basophils
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when antigen bridges gap between adjacent antibody molecules what happens in anaphylaxis
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cell undergoes degranulation and releases histamine and other mediators
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allergy development
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type 1 anaphylacis
immunization cellular response antigen binds IgE cross-linking of IgE antibodies Degranulation Symptoms |
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allergy development
immunization |
sensitized to allergen
produce IgE antibody |
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allergy development
cellular response |
IgE binds to Fc receptor
-mast cells -basophils |
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allergy development
degranulation |
release of chemical mediators
-histamine -prostaglandins -leukotrienes |
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allergy development
symptoms |
-smooth muscle contraction (bronchia)
-vascular permeability -swelling; edema -respiratory distress -death |
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counter to anaphylaxis
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epinephrine
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cytotoxic reactions
type II |
blood transfusions
involve IgG or IgM antibodies and complement activation->cell lysis or damage by macrophages |
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hemolytic disease of the newborn
Rh factor |
1. Rh+ father
2.Rh- mother carrying her first Rh+ fetrus Rh antigens from the developing fetus can enter the mother's blood during delivery 3. in responses to the fetal Rh antigens, the mother will produce anti-Rh antibodies 4. if the woman becomes pregnant, with another Rh+ fetus, her anti-Rh antibodies, will cross the placenta and damage fetal red blood cells |
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what type of Ig affects the baby's blood
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IgG
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immune complex-mediated hypersensitivity
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systemic lupus erythematosus
rheumatoid arthritis |
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systemic lupus erythematosus
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-antibodies to cell nucleus components
-deposits in many areas ->kidneys-most common ->skin-cause butterfly rash ->joints-arthritis ->brain-mental |
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rheumatoid arthritis
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antibodies to rheumatoid factor
chronic joint inflammation/damage hypersensitive to own tissue |
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type III
immune complex-mediated hypersensitivity |
1. immune complexes are deposited in wall of blood vessel
2. persence of immune complexes activates complement and attracts inflammatory cells such as neutrophiles 3. enzymes released from neutrophils casue damage to endothelial cells of basement membrane |
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type 4
cell mediated |
nickel can act as hapten and contact dermititis
hypersensitivities due to T cells |
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t cell response to cell-mediated reactions
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delayed
first exposure second exposure |
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delayed T cell response
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12-48 hr after exposure
-not antibody mediated |
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first exposure T cell response
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TD cells become sensitized
cell proliferate |
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second exposure T cell response
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TD activated by antigen
release lymphokines stimulate macrophages inflammatory response -->symptoms |
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posion ivy
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type 4 cell mediated
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tuberculin skin test
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-test for EXPOSURE to tuberculosis
-previous TB exposure=sensitized Td cells positive reaction is Type IV hypersensitivity always positive once positive |
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msgic bullet concept
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-bullet kills only selected target (pathogen) and not the innocent by-stander (host)
-developed by Paul EHrlich in early 1900s |
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Paul Ehrlich
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developed magic bullet concept
tested 100s of organic arsenic compounds #606 cured Trypanosomal infections in mice and then used on syphilis patients ->worked on most but killed others |
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Trypanosomal
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first antibitioc discovered by Ehrlich
-syphilis |
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therapeutic index
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maximum dose that is toxic to patient divided by minimum effective dose against pathogen
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high Therapeutic index
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high ratio
less toxic to patient |
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pathogen that needs to be intracellular
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chlmydias
rickettsias |
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streptomycin
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no longer used
adverse side affects not hugely effective |
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Fleming
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discovers penicillin
1928 |
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Howard Florey/Ernst Chain
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1940
performed first clinial trials of penicillin |
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penicillin structure
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beta-lactam ring is key to penicillin
staph. aureus produces penicilinase which cuts bond R group is a benzyl ring |
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actiomycetes
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filamentous bacteria
prokaryotic not fungi streptomyces natural soil organisms |
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action of antimicrobial drugs
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1. inhibition of cell wall synthesis
2. inhibition of protein synthesis 3. inhibition of nucleic acid replication and transcription 4. injury to plasma membrane 5. inhibition of synthesis of essential metabolites: sulfanilaide, trimethoprim |
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resistance genes
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enzymes
1. antibitioc degrading enzymes->penicillinase 2. efflux pump (removes antibiotic from cell before harm ocurs) 3. antibiotic altering-chemialy alters antibiotic |
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cell mutation event
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1. antibiotic is prevented from entering cell
2. target is altered (by mutation) |
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multiple resistance
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plasmid transfer of several genes sets that confer resistances by different mechanisms
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resistance to antibiotics
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1. blocking entry
2. inactivating enzymes 3. alteration of target molecule 4. efflux of antibiotic |
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antiviral drugs
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nucleoside and nucleotide analogs
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protease inhibitors
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indinavir
HIV |
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Enzyme inhibitors
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protease inhibitors
inhibit attachment inhibit uncoating interferons present spread of viruses to new cells |
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lower respiratory system diseases
|
-bronchitis
-bronchiolitis -pneumonia caused by bacteria, viruses, and fungi |
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penuomonia
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clinical diagnosis
no test describe symptoms inflammation on lunfs causes fluid accumulation |
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pertussis
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whooping cough
caused by Bordetella pertussis capsule trachel cytotoxin damages ciliated cells pertussis toxin prevented by DTaP vaccine (aceelular Pertussis cell fragments) |
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Bordetella pertussis
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gram negative
coccobacillus |
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Mycobacterium tuberculosis
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acid-fast rod
transmitted from human to human infects 1.7 billion people= 33% of entire world population 3million deaths a year |
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leading cause of death due to infectious disease
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mycobacterium tuberculosis
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Mycobacterium bovis
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less than 1% U.S. cases
not transmitted from human to human |
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Mycobacterium avium-intracellulare
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complex infects people with late-stage HIV infection
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bacteria that cause different types of Tuberculosis
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Mycobacterium tuberculosis
Mycobacterium bovis Mycobacterium avium-intracellulare |
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treatment of tuberculosis
|
-prolonged multiple antibiotics-isoniazid (6months)
-increase in incidence-->drug resistance -facultative intracellular parasite (usually of macrophages) -acid fast (waxy cell components/mycolic acids/very protective) |
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tuberculosis and macrophages
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facultative intracellular parasite
resistant to phagylosome can grow in macrophage |
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2 options of primary infection of Tuberculosis
|
TB skin test will be positive
90% immune system controls infection. Person remains well can have secondary infection 10% Progressive Primary Infection |
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progressive primary infection of tuberculosis
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immune system fails to control infection
illness or death results fairly soon if person not treated |
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secondary (reactivation) infection
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bacteria escape immune control
hypersensitivity causes tissue damage consumption |
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pneumococcal pneumonia bacteria
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streptococcus pneumoniae
-gram positive encapsulated diplococci normally a secondary infection |
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pneumoccoccal pneumonia
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encapsulated bacteria escape phagocytosis in lung-growth leads to inflammation
symptoms: infected alveoli of lung fill with fluids; interferes iwth oxygen uptake |
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pneumococcal pneumonia diagnosis
|
optochin-inhibition test or bile solubility test
serological typing of bacteria |
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treatment of pneumococcal pneumonia
|
penicillin
fluorquinolones |
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prevention of pneumoccocal pneumonia
|
pneumoccocal vaccine
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mycoplasmal pneumonia
|
primary atypical pneumonia; walking pneumonia
Mycoplasma pneumoniae common in children and young adults |
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walking pneumonia
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persistent cough, not as serious
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Mycoplasma pneumoniae
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causes mycoplasmal pneumonia
pleomorphic wall-less bacteria no peptidoglycan penicillin is inefective |
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mycoplasmal pneumonia symptoms
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mild but persisten respiratory symptoms; low fever, cough, headache
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diagnosis
|
PCR and serological testing
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treatment
|
tetracyclines
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meninges
|
protect brain and spinal cord
dura mater arachnoid mater pia mater |
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dura mater
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outermost layer of meninges
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arachnoid mater
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middle layer of meninges
-subarachnoid space contains cerebrospinal fluid (CSF) |
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pia mater
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innermost layer of meninges
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bacterial meningitis
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initial symptoms of fever, headache, and stuff neck
followed by nausea and vomiting may progress to convulsions and coma diagnosis by Gram stain and latex agglutination of CSF (spinal tap) treament ogf cephalosporins, vancomyocin |
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Spinal tap
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looking for G negatice coccus and WBC (bad to be in spinal tap)
can be used to diagnose bacterial meningitis |
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rabies
|
caused by rabis virus
transmitted by animal bite durios rabies paralytic rabies more likely to get rabies from bat than dog |
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furious rabies
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animals are restless then highly excitable
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paralytic rabies
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animals seem unaware of surroundings
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mortality of rabies
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100%
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pathology of rabies infection
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1. virus enters tissue from saliva of biting animal
2. virus replicates in muscle near bite 3. virus moves up peripheral nervous system to CNS 4. virus ascends spinal cord 5. virus reaches brain and causes fatal encapbhilitis 6. virus enters salivary glands and other organs of victim |
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hydrophobia
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fear of water
seeing water can cause muscle spasms occurs when infected with rabies |
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annual deaths of rabies in world
|
50,000-100,000
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rabies virus
|
virus multiplies in skeletal muscles then brain cells, causing encephalitis
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initial symptoms of rabies
|
muscle spasms of the mouth, pharynx
hydrophobia |
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animal diagnosis of rabies
|
tissue examines: brain
diagnosis: Negri bodies (black granules, rabies positive) |
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prevention of rabies
|
preexposure prphylaxis
postexposure treatment |
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preexposure prophylaxis
|
injection of human diploid cells vaccine
-Pastueur aged rabbit spinal cords -->no longer inject rabies viruses |
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postexposure treatment
|
vaccine plus ratbies immunoglobulin
antigen and antibodies rabies has long incubation periof enabling us to vaccine after exposure |
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Lyme disease
|
causative agent: Borrelia burgdorfi (spiral)
reservoir: deer vector: ticks, deer mouse first symptom: bulls-eye rash second phase: irregular heartbeat, encephalitis third phase: arthtritis |
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malaria
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protozoan: plasmodium
vector: mosquito prophylaxis treatment: artemisinartesmia and arlendtor -tonic and gin control: bed nets |
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prophylaxis
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chloroquome
malaronatonquine proguanil mefloquine |
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sexually transmitted infections (STIs) increased in 1960s because
|
antibiotic resistance
newly recognized pathogens multiple sexual partners |
|
|
chlamydia
|
dangerous STI
usually no symptoms |
|
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gonorrhea
|
one of most frequently reported STI
|
|
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hepatitis B
|
vaccine exists, but there's no cure; can cause cancer of the liver
|
|
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herpes
|
painful and episodic
can be treated but theres no cure |
|
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HIV/AIDS
|
first recognized in 1984, AIDS is the sixth leading cause of death among young men and women
|
|
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human paplloma virus (HPV) and genital warts
|
the most common STI, 33% of all women have this virus, can cause cervical or penile cancer and genital pain
implicated in oral/throat cancer |
|
|
syphilis
|
untreated, can lead to serious damage of the brain or heart
|
|
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Neisseria gonorrhoeae
|
causes gonorrhea
|
|
|
gonorrhea
|
sexually transmitted disease
through urethra (epithelial attachment) 300,000 cases/yr in US- 60% age 15-24 potential for systemic infection |
|
|
gonorhhea potential for systemic infection
|
gonorrheal endocarditis-heart infection
gonorrheal meningitis gonorrheal arthritis |
|
|
male gonorrhea
|
80% have symptoms
painful urination/discharfe |
|
|
female gonorrhea
|
usually asymptomatic
-leads to pelvic inflammatory disease (PID)/sterility sterility-caused by scarring of felopian tubes |
|
|
infant gonorrhea
|
ophthalmia neonatorum
-gonorrhea in eyes possible when born use to treat with silver nitrate |
|
|
diagnosis of gonorrhea
|
gram stain
ELISA PCR |
|
|
treatmne tof gonorrhea
|
fluoroqinolones
|
|
|
pelvic inflammatory disease
|
polymicrobic usually
-N. gonorrhoeae -C. trachomatis salpingitis (infection of uterine tubes) symptoms: chronic abdominal pain treatment: doxycycline and cefoxitin |
|
|
syphilis cause
|
Treponema pallidum-spiral
invades mucosa or through skin breaks |
|
|
primary stage of syphilis
|
chancre at site of infection
|
|
|
secondary stage of syphilis
|
skin and mucosal rashes
|
|
|
latent period of syphilis
|
no symptoms
|
|
|
tertiary stage of syphilis
|
gummas on many organs
|
|
|
treatment of syphilis
|
benzathine penicillin
|
|
|
congenital syphilis
|
neuological damage
|
|
|
chlamydia
|
most prevalent sexually transmitted disease in the U.S. (usually co-infection with gonorrhea)
-chlamydia trachomatis (bacterium) STD that needs more than medicine to treat 75%women and 25% men do not show symptoms can cause Trachoma |
|
|
cause of chlamydia
|
chlamydia trachomatis
-four million cases annualy, 24 billion a year -most occuring in mean and women under 25 -bacterium unable to produce ATP in amount required to sustain metabolism= obligate intracellular parasites of eukaryotic cells |
|
|
trachoma
|
can be caused by clamydia
leading cause of blindness worldwide transmitted by the testse fly |
|
|
worldwide deaths caused by TB, malaria,HIV
|
7 million
|
|
|
prevalence of TB, malaria, and HIV
|
300 million
|
|
|
Acquired Immunodeficiency Syndrome Retrovirus
|
unstable increase in mutations because of RNA
makes DNA from RNA=backwards! retrovirus |
|
|
reverse transcriptase enzyme
|
only active in host cell
associated with AIDS |
|
|
origin of AIDS
|
crosses species barrier into humans in Africa in 1930s
patient who dies in 1959 in COngo is oldest known case spread in Africa as a result of urbanization spread world-wide through modern transportation and unsafe sexual practices |
|
|
first known case in Western world of AIDS
|
norwegian sailor died in 1976
|
|
|
HIV infection
|
virus destroys helper T cells
can't respond to pathogens of other antigens virus binds to CD4 receptor |
|
|
Stages of HIV infection
|
1. 1-2 month following initial infection, the population of HIV in blood peaks at about 10,000,000/ml
2. 1-2 months following initial infectionm poulation of CD4 T cells plunges 3. Seroconversion 4. HIV in blood stabilizes at steady state of 1000 to 10000/ml 5 CD$ T cell population declines steadily 6. huge but infedinite number of HIV in lymphoid tissue, in latent or proviral form. 100 billion HIV generated each day for years, mostly by infected T cells 7. clinical AIDS 8. rise of HI in blood as immune system breaks down |
|
|
seroconversion
|
antibodies against HIV appear
HIV population ib blood crashes stage 3 of HIV infection |
|
|
Clinical AIDS
|
CD4 T cell population at 200/mm3
|
|
|
HIV diagnosis
|
serconversion-takes up to three months for antibodies to build up
HIV antibodies dereced by ELISA HIV antigens detected by Western blotting Plasma ciral load determined by PCR or nucleic acid hybridization |
|
|
How are HIV antibodies detected
|
ELISA
|
|
|
How are HIV antigens detected
|
Western blotting
|
|
|
how is HIV plasma viral load determined
|
PCR or nucleic acid hybridization
|
|
|
HIV transmission
|
HIV survives 6 hours outside a cell
HIV survives less than 1.5 days inside a cell infected body fluids transmit HIV |
|
|
Body fluid that can transmit HIV
|
sexual contact
breast milk transplacental infection of fetus blood-contaminated needles organ transplants artificial inseminaion blood transfusion **NO SALIVA |
|
|
prevention of AIDS
|
use of condoms and sterile needles
healthcare workers use Universal Precautions |
|
|
universal precautions
|
wear floves, fowns, masks, and goggles
-do not recap needles risk of infection from infected needlestick injury is .3% |
|
|
high active antiretroviral therapy (HAART)
|
treatment for AIDS
-combination of nucleoside reverse transcriptase inhibitors plus -->non-nucleoside reverse transcriptase inhibitor or protease inhibitor or fusion inhbitiors |
|
|
upper respiratory system diseases
|
pharyngitis
laryngitis tonsilitis sinusitis epiglottitis (Hib) |
|
|
epiglottitis
|
H. influenzae type b
dangerous for children blocks airway Hib infective vaccine |
|
|
streptococcal pharyngitis
|
strep throat
streptococcus pyogenes group A beta-hemolytic streptococcus (GAS) clinical syndrome |
|
|
clinical syndrome of strep throat
|
witish exudate covering tonsils
inflammation of pharynx fecer |
|
|
group A beta-hemolytic streptoccus
|
GAS
group A-type of polysaccharide antigen beta-hemolytic-type of hemolysis of blood agar |
|
|
diagnosing strep throat
|
throat culture-->blood agar (24hrs)
latex agglutination detect antigens-rapid Strep A test (minutes) |
|
|
complications of S. pyogenes
|
scarlet fever
septicemia rheumatic fever acute poststreptococcal glomerulonephritis |
|
|
scarlet fever
|
complication of S. pyogenes
toxin kills cells |
|
|
septicemia
|
spread in the bloodstream
beta-hemolytic-->destroys red blood cells |
|
|
rheumatic fever
|
auto-immune
occurs 3 weeks after strep throat inflammation in organs/joints heart calve damage (IgG cross with heart tissue) prevention if Strep throat is treated |
|
|
Acute poststreptococcal glomerulonephritis
|
inflammation in glomeruli in kidneys
|
|
|
permanent penicillin
|
prescribed to people to avoid strep throat sometimes
|
|
|
common cold
|
rhinoviruses and other ciruses (coranoviruses, adenoviruses)
|
|
|
coranoviruses
|
SARS
|
|
|
rhinoviruses
|
25-50% of common colds
100 plus serotypes transmission by respiratory droplets (eye, nose entry) +mainly touch of finger restoration of epithelium-months 500 million cases a year |
|
|
pathogenesis of rhinoviruses
|
replication in epithelial cells
stimulate kinins-secretions immune response clears virus |
|
|
otitis media
|
earache
S. pneumoniae H. influenzar M. catarrhalis S. pyogenes S. aureus incidence of S. pneumoniae and H. influenzae |
