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109 Cards in this Set
- Front
- Back
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Type I (IgE) hypersensitivity |
-IgE mediated -Allergen induced - IgE attaches to mast cells and basophils during sensitization - 30 minutes or less -histamine, serotonin, leukotrienes, prostaglandins, cytokines - ex: hay fever, asthma, anaphylaxis |
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Type II (ctyotoxic) hypersensitivity |
- IgG mediated - Macrophages, B lymphocytes - 5-8 hours -complement -ex transfusion reactions, hemolytic disease of the newborn, rheumatic fever |
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Type III (immune complex) hypersensitivity |
-Caused by aggregates of IgG -Deposition of complexes in host tissue cells - 2-8 hours -ex serum sickness, arthus phenomenon, SLE, rheumatoid arthritis, haptins(penicillin), hashimoto's thyroiditis, myasthenia gravis |
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Type IV cellular (delayed) |
exaggeration of cell mediated immunity. delayed rxn characterized by thickening and drying of skin tissue and surrounded by erythema - T lymphocytes - no antibodies - 1-3 days - contact dermatitis, infection allergy transplant rejection - cytokine release |
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Gram + |
Stains purple, lipoteichoic acid in cell wall |
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Gram - |
Stains pink red, LPS in cell wall, produce endotoxin lipid A |
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Spherical |
Cocci |
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Rod |
bacilli |
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Curved |
spirilla |
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sulfanilamide |
-disrupt folic acid synthesis by competitive inhibition.
- prevents nucleic acid synthesis and DNA replication |
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inhibits cell wall synthesis |
isoniazid: interferes with cell wall synthesis in mycobacterium vancomycin: same mechanism. effective against all gram+ but lactobacillus. Last resort in MRSA tx. damages kidneys and ears. IV only. consider VRE. |
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penicillin |
beta lactam. effective against many gram +and some gram -. inhibits enzyme transpeptidase. can cause anaphylaxis in some. penicillin resistant bacteria produce beta lactamase. |
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cephalosporins |
beta lactam. aka keflex. broader spectrum than penicillin. use 1st gen (weaker class) first, then move up. |
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monobactam |
beta lactam. only against aerobic, gram negative, rods |
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carbapenems |
beta lactam. broad spectrum ex. imipenem, meropenem, doripnem, ertapenem |
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bacitricin |
affects cell membrane. interferes with transport of cell wall precursors through the membrane. pokes holes in membrane. only topical |
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polymyxins/ polymyxin b / colystin |
affects cell membrane. increases membrane permeabilility of gram-negative rods. pokes holes in membrane of gram -. hydrophobic |
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daptomycin |
affects cell membrane. only against gram positive |
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aminoglyycosides |
30s ribosome inhibition =. attached to ribosomes, blocking transcription. ex. streptomycin (sometimes tb), gentamycin (gram - uti), tobramycin, amakacin, neomycin (GI infections and as ointment), kanamycin (against gram - wounds) gentamycin -> amakacin (strength) |
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tetracyclines |
30s ribosome inhibition similar antimicrobial range to chloramphenicol; benzene ring formation, can stain teeth and destroy gut flora. |
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chloramphenicol |
50s ribosome inhibition. -used against a wide variety of bacteria (meningitis, choldera, typhoid, RMSF) and some rickettsiae and fungi; -reserved for serious infection due to side effects like aplastic anemia and gray syndrome. |
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macrolides |
50s ribosome inhibition. erythro (against gram postive) /azithro/clarithro mysins -used against gram + |
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clindamycin |
50s ribosome inhibition. mostly against gram +. semisynthetic drug used against penicillin resistant bacteria. can cause c-diff, leading to psuedomembranous colitis |
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stretogramins |
50 s ribosome inhibition. -effective against gram + |
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oxazolidinones |
aka linezolid. effective against gram + bacteria, including MRSA |
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rifampin |
inhibit nucleic acid synthesis. interfers with RNA synthesis. used against TB, leprosy, meningits. can caues liver damage |
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quinilinones |
inhibit nucleic acid synthesis. aka cipro. treatment for anthrax. blocks DNA synthesis and transcription |
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koch's postulates |
identifies a specific organism to a disease 1. same organism is present in every disease 2. isolate the organism and prepare a culture 3. inoculate a healthy specimen and reproduce the disease 4. recultivate the same organism from the infected specimen. not all ogranisms can be grow. ex. syphillis. proved germ theory. |
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pili |
conjugation or sex pili, transfer genetic materials between cells
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fimbriae |
attach to cell walls and help from biofilms |
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glycocalyx |
sugar coat around cell that helps protect from phagocytosis and dehydration. maintains nutrients and helps with attachment. |
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virulence |
degree of pathogenicity |
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pathogenecity |
microbes ability to enter a host and cause disease |
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coagulase |
forms clots that protect bacteria |
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streptokinase |
enzyme that breaks up clots |
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hyaluronidase |
enzyme that breaks down connective tissue, enhancing pathogen penetration. allows further spread. |
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superantigens |
antigen that causes an exaggerated immune response |
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botulism tx |
AB neurotoxin. B binds to the receptor. A gets into the cell. Cuts SNARE proteins that cause vesicle to bind to cell membrane and release ACH. Flaccid paralysis because ACH not released into synaptic cleft |
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pertussis tx |
AB toxin. A causes paralysis of cilia lining throat |
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tetanus tx |
AB toxin. blocks inhibitory interneuron. No GABA NTs or glycine. Continued ACH release causing constant contraction. |
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cholera tx |
enterotoxin. increases cAMP in cell, causing ions to flow out. Where sodium goes, water flows. Results in sever dehydration and water loss. |
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diphtheria tx |
AB toxin. some strains produce diphtheria toxin, which inhibits protein synthesis, causing cell death. |
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leukocidins |
kill leuokocytes |
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hemolysins |
kill RBCs |
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AB mechanism |
B binds to receptor on the cell membraine. A binds to B, activating A and allow A to cross cell membrane. A subunit effects cell.
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microbiome |
microbes that reside in the body without causing disease |
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mutualism |
moth host and microbe benefit. ex e coli producing vitamin k |
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commensalism |
bacteria benefits, but host is unaffected |
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exogenous infection |
pathogen breaches host defenses |
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endogenous infection |
normal flora enter sterile tissue |
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opportunistic infection |
commensals take advantage of a change that favors microbe ( immunosupression, HIV, etc.) |
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naturally acquired active immunity |
comes from exposures to antigens. usually follows disease. |
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naturally acquired passive immunity |
passage of IgG across placenta from maternal to fetal circulation ex. antibodies passed from mom to fetus. antibodies passed in mother's milk |
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artifically acquired active immunity |
from vaccination |
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artificially acquired passive immunity |
induced by transfer of antibodies taken from circulation from an animal or another person. ex. injection of immune serum ( gamma globulin) |
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whole agent vaccines |
contain weakened or inactivated antigens
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live attenutated: |
whole agent. weakened microbes that multiply only low levels, inducing a strong immune response. may provide lifelong immunity. can revert to virulent form and cause disease. may affect those not inoculated nearby. can combine single doses for x diseases. ie MMR |
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inactivated vaccine |
whole agent. contain killed pathogens. induces weaker response. booster require dot maintain immunity. does not cause disease directly, safer than live attenuated. ex salk polio |
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toxoid vaccine |
contain inactivated toxins with formalin product. inactivated, boosters required. ex. TDaP, tetanus, diphtheria toxoids, acellular pertussis |
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subunit vaccine |
contain only parts of antigen that stimulte a strong response. created with recombinant DNA tech. Cannot cause disease. ex hep b vaccine |
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conjugate vaccine |
created by attaching bacterial capsule polysaccharides to a toxoid. elicit a strong immune response. ex haemophilus influenzas b |
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DNA vaccine |
depend on ability of some cells to 1. take up and translate foreign DNA and 2. display resulting proteins, inducing a strong immune response. naked DNA vaccines contain engineered plasmid that contains a gene from a a pathogen. not infective and do not replicate, cannot cause disease ex. West NIle vius for horses. |
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atopic disease |
IgE. most common season allergy, or year round allergy due to chronic exposure. |
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sensitization |
in type I hyper sensitivity, this is the first exposure to an antigen. IgE attaches to mast cells and basophils, produce histamine. |
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anaphylaxis |
whole-body reaction. type I |
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serum sickness |
IgG produced against residual proteins in a serum from non-human source. Can cause kidney damage, rash, hematuria, shock. Similar rxn to type I, but Type III hypersensitivity rxn. |
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autograft |
graft taken from one part of the body and transplanted to another part of the same body |
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isograft |
graft from an identical twin to another identical twin. |
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allograft |
grafts between genetically different members fo the same species. |
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xenograft |
graft between members of different species. rarely successful (bovine heart valves) |
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Bruton's agammaglobilinemia |
primary immunodeficiency (genetic abnormality). X linked congental immunodeficiency. B cells fail to develop properly, patients lack mature B cells, plasma cells, and antibodies. Sex linked trait. More common in males than females |
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Chediak-Hagashi |
phagocyte abnormality. lysosomes within phagocytes cannot release contents to kill microbes |
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SCIDS |
severed combined immunodeficiency disease involving lymph nodes deficient in B and cells. One form caused by enzyme (adenosine deaminase, ADA) deficiency that can be corrected using gene therapy. ADA activity is highest in thymus and other lymphoid tissue. dATP buildup ix toxic to T and B cells. accumulation of dATP inhibits ribonucleotide reductase and prevents DNA synthesis so cells cannot divide. T and B cells are very mitotically active and are highly susceptible. "bubble boy" |
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stretococcal pharyngitis (strep throat) |
Streptococcus pyogenes common in kids 5-15. symptoms: fever, chills, red, sore throat that may have white patches that are not common with viruses. pain when swallowing, swollen tender neck glands. common complication - otitis media, abscesses, septicemia, systemic spread. treatment: penicillin, amoxicillin |
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scarlet fever |
streptococcus pyogenes -strep throat with accompanying skin rash -significant of erythrogenic toxin: capillary damage - virulence: caused by a prophage which coes for erythrogenic toxin. not all strain of s. pyogenes have this. rare -antitoxin (antibody) producation can lead to life long immunity |
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rheumatic fever |
streptococcus pyogenes
most common in school age children. fever, join pain, inflammation of small blood vessels symptoms in joints and heart -permanent scarring and distortion of heart can lead to rheumatic heart disease. type II hypersensitivity. autoantibodies against M protein attack connective tissue and possibly cardiac myofiber protein. |
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acute glomerulonephritis |
streptococcus pyogenes inflammation of glomeruli or small blood vessels in kidney caused by deposition of immune complexes. (too many to filter) |
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erysipelas |
streptococcus pyogenes open wounds or skin abrasions, deep red inflammation of skin and mucous membranes |
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peurperal sepsis |
streptococcus pyogenes infected uterus tissue "childbed fever" occurs 1-10 days after childbirth |
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bacteremia |
streptococcus pyogenes bacteria in blood |
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septicemia |
streptococcus pyogenes bacteria and their toxins in blood |
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necrotizing fasciatis |
streptococcus pyogenes fascia destruction by phage encoded toxins -some strains have acquired new virulence factors and code for exotoxins and hemolysins -new exotoxins encoded by prophage include a protease that degrades host cell proteins and a superantigen that causes healthy cells to commit suicide. can also be caused by staphylococcus aureus, clostridium perfringrens, bacteroides fragilis, aeromonas hydrophila Type I: polymicrobial due to a number of different organisms (more common) Type II: monomicrobial due to a single infective orgnism (less common 25-45%) |
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diphtheria |
corynebacterium diphtheria life threatening gram positive rod. -local throat infection. - diphtheria bacilli remain in clumps after multiplying, forming a palisade layer -produce an exotoxin that inhibits protein synthesis through AB mechanism. causes accumulation of peusomembrane on tonsils or pharynx -toxin can circulate to neck (bull neck), damage heart, damage fatty shearth around nerves, swell epiglottis to black trachea -not all c diphtheria strain cause disease toxin produced from prophage DTaP/TDaP; vaccine for diphtheria, tetanus, pertussis -antibiotics: penicillin, amoxicillin |
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meningococcemia (sepsis) and meningococcal meningitis |
Neisseria meningitidis
gram negative cocci -major cause of disease and mortality in infants -90% occur in africa's meningitis belt 13 serogroups important A, B, CY, -W-135 |
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meningococcemia (sepsis)
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rapid onset. toxins can cause death in 2 hours symptoms: stiff arched neck, bright rad patches and blue black spots due to broken capillaries -spinal tap to diagnose. Gram stain and culture of CSF -complications: brain damage, hearing loss, learning disability, kidney failure, death -grade school classrooms, camps |
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complications of meningococcal disease and treatment |
complication: waterhouse-friderschen syndrome - lesions in adrenal glands and hormone imbalances; hypersensitivity reactions. -vaccine: meningococcal conjugate vaccine is routinely recommended at 11-12 years. booster at 16 -treatment: Penicillin G, chloramphenicol, 3rd gen cephalosporin ( cefotaxime, ceftriaxone) |
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Haemophilus meningitis |
haemophilus influenza type b (HIB)
gram-negative coccobacilli, non-motile, encapsulated -passage: repiarotry tract to blood to nervous system; usually as "secondary infection" - symptoms: stiff neck, headaches, neurologic abnormalities -immunization with acellular components: HiB vaccine ( capsular polysaccharides); tetramune: dTaP - Hib - can cause meningitis but has fewer symptoms. no skin rash. more rare. occurs usually in young children with lower mortality rate than meningococcal meningitis. |
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pertussis |
Bordatella pertussis - highly contagious - pertussis toxin: AB toxin. A toxin paralyzes cilia and promotes lymphocytosis; causing inflammation, enhances insulin secretion: ADP-ribosylation treatment: erythromycin |
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Bordatella parapertussis |
has silent copy of pertussis toxin gene. an cuase subclinical disease |
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Bordatella bronchioseptica |
canines "kennel cough", rabbits "snuffles," swine atrophic rhinitis (chronic inflammation of nouse; cause infrequent respiratory tract infection in humans. |
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mycobacteria facts |
-rod shaped - asporogenic -contain mycolic acid in cell wall - resist decolorization with acid alcohol; sstain avid fast positive -called acid fast bacilli "gram positive" - slow growing to rapid grower (can have 6 week culture time) -pigmented and non-pigmented -cause various diseases in humans |
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mycobacteria symptoms |
-cough > 3 weeks fever, night swearts > 3 weeks -weight loss -breathing pain -hemoptysis -apical (esp. cavitary) lesions in lung |
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progression of TB |
1. inhaled as droplets or dried sputum. carried to alveolar space 2. bacilli phagocytosed by alveolar macrophages as more monocytes are attracted to the site. 3. macrophages become infected and can't clear infection. uninfected macrophages in developing granuloma differentiate into multinucleate cells and foamy (lipid containing) cells. lymphocytes organize around the perpihery of the granuloma as fibrous collagen sheath walls off the infection 4. granulomas usually remain steady in this state. Reactivation or secondary infection breaks structure and bacilli are free into alveolar airways and into lung. cough can now spread to other people. |
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ghon complex |
gohn focus + lymphatic involvement |
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ranke's complex |
fibrosis and calcification of gohn complex |
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spread of TB |
-initial infection: spread from foci via lymphatics to regional lymph nodes - miliary (hematogenous or disseminated spread: distributes Mtb to all organs discharge of caseating tubercule from veins into the bronchi can swallowed, causing TB in GI tract
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TB diagnosis |
-Acid fast stain or auramin-rhodamine stain, and culture - bactet blood culture -skin test: tuberculin or mantoux test; PPD; erythema > 10 mm - positive -CXR - TB cavitatations -may need several sputum specimens over several days to get positive; serpentine coding is a good indicator -quantiferon gold: used to detect latent TB; amount of interferon-gamma (IFN-gamma) is meaured. in infected, WBCs will release IFN gamma in response to contact with TB antigens |
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TB prevention |
BCG vaccine. -live attenuated avirulent M. bovis strain -Only 60-80% effective. -Not used in US because it doesn't circumvent disease reactivation in those already exposed. -may complicate skin test result |
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mycobacterium avium complex (MAC) and M intracellulare |
-MAC is the typical mycobacterium most commonly associated with human disease -MAC is primarily a pulmonary pathogen that affects immunocompromised (AIDS, leukemia, etc) -M avium is the Isolate in more than 95% of AIDS patients who develop MAC infections - very resistant to antibiotics, 70-90% mortality within 4 months |
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mycobacterium marinum |
-free living bacterium, causes opportunistic infections in human -causes rare disease known as aquarium granuloma. typically affects those who work with fish or home aquariums |
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mycoplasma penumonia |
-pleomorphic. no cell wall. no gram reaction. beta-lactam insensitive -transmitted byh droplets, water -symptoms: fever, fatigue, dry-hacking cough --no septicemia. doesn't thrive in bloodstream -crowded conditions contribute to epidemic -diagnosis: colonial characteristics "fried egg". cold agglutination screening test positive test: Patient SERUM agglutinate type O RBC at 4 C but not 37 C. for of autoimmune hemolytic anemia which annitbodies (usually IgM) only bind to RBS at low body temps, 28-31C -prevention: sextreme cleaning, disinfecting water systems |
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legionella pneumophillia |
legionnaire's disease -gram negative rod, motile -similar to pontiac fever, milder form of pneumonia -related to water collecttion systems: lakes, pools, AC units -becomes airborne by winds and breezes -can live within waterborne protozoans -prevention: extreme cleaning, disinfecnting water systems -hard to culture. use DFA stain |
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Q fever |
results from breathing airborne particles Coxiella burnetti gram- bacillus -similar to rickettsiae -small bacteria, 0.45 microns, unable to be sseen with light microscopy -no flagella, pili, or capsule -obligate intracellular parasite prevalent in livestock: cows, sheep, goats -transmission: inhaling particles, handling infected animals -symptoms: severe headches, fever, dry cough -diagnostic: PCR, serology, culture -prevention: vaccine for high risk population -treatment: doxycycline |
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chlamydia psitacci |
causes psittacosis -zoonotic disease. can be caught from psittacine bird and their droppings (parrots, parakeets, canaries, turkeyk, seagulls) |
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chlamydia pneumoniae |
zoonotic disease, causes chlamydial pneumonia treatment: tetracyclline: erythromycin |
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Lancefield Classifications |
Group A: Streptococcus pyogenes (beta) Group B: Streptococcus agalactiae (beta) Group C/G: Streptococcus dysgalatiae (beta) Group F: Streptococcus anginosus (beta) |
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Haemophilus influenza type B |
gram - coccobacillinon-motile, encapsulated, passage: respiratory tract to blood to nervous system usually as a secondary infection6mo- 2 yearssymptoms: stiff neck, headaches, neurologic abnormaliltiestreatment: ceftriaxone, cefotaxime
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Klebsiella pneumoniae |
Gram negative bacilli primary disease, sudden onset reddish brown sputum secondary - nosocomial treatment: cephalosporins, aminoglycosides, tetracycline, resistant to penicillins |
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Serratia pneumoniae |
S. marcescens Gram negative bacillus respiratory disease in compromised, pneumonia, conjunctivitis. treatment: cephalosporins, aminoglycosides, tetracylcline, resistant to penicillins. |
