Chapter 18

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Chapter 18
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2011-11-13 13:17:47
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Cocci
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  1. Gram- and Gram positive cocci
    • Most significant infectious agent in humans
    • in Skin, normal flora,oral cavity, intestine
    • Pyogenic-pus
  2. Most common organisms in cocci that cause infections:
    Staphylococcus,Streptococcus,Enterococcus,Neisseria
  3. Staphylococci characteristics:
    • Spherical
    • Irregular clusters
    • Gram possitive
    • Common in skin and mucous membranes
    • Not spore forming, no flagella
    • MAY have capsule
    • 31 species
  4. Most Imp staph. human pathogens:
    • Staph aureus
    • Staph epidermis
    • Staph saprophyticus
    • STAPH AUREUS most serious pathogen!!!
  5. Staph Aureus:
    • large, round,opaque colonies-gold, yellow
    • optimum growth temp-37%
    • facultative anaerobe-grows w/out oxy-but better in oxy and carbon dioxide
    • most resistant of the non-spore forming pathogens
    • Produces many virulent factors
    • does not mind high salt,ph, temp
  6. Enzymes of Staph Aureus:
    • Cagulase:clots blood, plasma-in 97% of humans,prescence found w diagnosis
    • Hyaluronidase:digest hyualronic acid-blocking binding of conn tissue-PROMOTES INVASION BY BACTERIA
    • Staphylokinas:digest blood clots(would give heart attack victim
    • DNAse:digests DNA-enables transformation
    • Lipases:help bacteria colonize skin
    • Penicillinase:inactivates penicillin-has other enzymes may deactivate othet antibiotics
  7. Toxins of Staph Aureus:
    • 1Hmolysins: disrupts membranes of RBS-causes to lyse
    • alpha hemolysin:partial lysis green zone on blood agar around colonies
    • beta hemolysin: complete lysis of R BC clear zone
    • gamma hemolysin:no lysis
  8. 2 alpha toxin:
    • most damaging effcets-sign.conrt. to disease process
    • damages and lysis-RBC, leukocytes, skeletal muscles, heart muscle, kidney tissue
  9. 3-Leukocidin:
    lysis macrophages and neutrophils
  10. 4-Enterotoxins:
    causes food posioning
  11. 5-Exfoliative toxin:
    causes SSSS (staphylococcus scalded skin syndrome)
  12. 6-Toxic shock syndrome-
    Above abb-TSST
  13. StaphAureus:
    • Common in humans
    • 20-60% healthy humans are carriers
    • often in anterior nares, skin, nasopharynx, and intestines
  14. Diseases caused by Staph Auerus
    lcalized and systemic
  15. Localized:
    • Abscess-large, inflammed pustule
    • Folliculitis-MOST COMMON-infalmmation of hair follicle
    • Furuncle-Hair follicle blows up-known as boil
    • Carbuncle-large, deep lesion-group of furuncles
    • Impetigo-bubble like swelling, breaks and peels-VERY CONTAGIOUS!!!
  16. Systemic:
    • Osteomyelistis-pathogen in the bone
    • Bacteremia-bacteria in bloodstream -taken to organs
    • Endocarditis-bacteria in heart-CAN CAUSE DESTRUCTION OF HEART VALVES
  17. Toxigenic Disease:
    • Food Poisoning:Toxin not inactivated by heat. Sick within 2-6 hrs-recovery 24 hours
    • SSSS (Staphylococcal Scalded Skin Syndrome)-Toxin cause separation of epidermis from dermis -skin peels away-usually in infants and children under 4
    • TSS (Toxic Shock Syndrome)-seen in menstruating women-don't change vety absorbent tampons enough
  18. Coagulase negative Staphylococcal (CNS)-account for large population of nosocomial and oppurtunistic infections in immunocompromised patients
    • Staph Epidermis-on skin, mucous membranes-causes bacteremia, UTI, endocarditis
    • Staph Hominis-on skin and apocrine sweat glands
    • Staph Capitis-on face, scalp, external ear
    • ALL three may cause wound infection
    • Staph Saprophyticus-(less understood)-primary cause UTI-on skin, lower intestine, vagina
  19. Clinical concerns:
    • 95% Staph Aureus produce penicillinase-resitant to penicillin and ampicillin
    • Abcesses must be surgically opened cleared of pus in order to respond to therapy
    • Systemic infections require intensive, lengthy therapy
  20. As long as humans
    there will be pathogenic staphylococci and infections
  21. Streptococci:large varied group
    • some normal flora, some pathogenic
    • gram positive, seen in chains
    • spherical-no spores
    • not usually motile but can have flagellated strains
    • form capsules and slime layers
    • facultatative anaerobe-ferments a variety of sugars
    • no catalase but has peroxidase to inactivate hydrogen peroxide-can survive in prescence of oxy
    • MOST parasitic forms are afstidious and require enriched medium(blood agar)
    • colonies small, pinpiointed, glistening
    • SENSITIVE to heat, disinfectants, drying -BUT some are drug resistant bacteria-(pneumococci and enterococci)
    • 25 species
    • no cat
  22. Classification:
    Traditional method-SYSTEM developed by Rebecca Lancefield uses cell wall carbohydrate antigens-these antigens stimulate formation of antibodies with differing species-14 kinds
    SECOND METHOD-reaction of the organisims on blood agar-used in clinical labs
  23. The streptococci that PRODUCE BETTA HEMOLYSIS (CLEAR-LYSIS ALL RBC)-ARE MEMBERS OF LANCEFIELD GROUPS A,B,C G, AND CETRAIN STRANDS OF D
    STREPTOCOCCUS PNEUMONIA PRODUCES ALPHA HEMOLYSIS-green zobe, partial lysis,-called VIRADINS STREPTOCOCCI-latin for green
  24. CAPSULE-FOOLS host immune system (does not cause immune response in host)-made of HYALURONIC ACID-made by most Streptococcus pyogens
    next
  25. Extracelullar toxins:
    • Streptolysins-found in group a, 2 types, STREPTOLYSIN O AND STREPTOLYSIN S-CAUSES BETTA HEMOLYSIS ON BLOOD AGAR -RAPIDLY INJURES MANY CELL TYPES AND TISSUES
    • PYROGENIC- called ERYTHROGENIC TOXIN-key toxin in dev SCARLET FEVER
    • only found in STRAINS OF STREPTOCOCCUS THAT CONTAIN GENES FROM A TEMPERATE BACTERIOPHAGE
  26. extracelullar enzymes:
    • STREPTOKINASE-like staphylokinase-helps break down fibrin clots-play role in invasion
    • HYALURODINASE-breaks down acid in conn tissue, helps spread of pathogen
    • STREPTODORNASE(DNAse)liquifies discharges by hyrdrolzying DNA
  27. Clinically SiGNIFICGANT SPECIES:
    human disease most closely ass with Strept. pyogenes (strep throat), Strep. agalactiae, Strep.pneumoniae, Enterococcus faecalis, and VIRADANS streptococci
    MOST SERIOUS IS STREP, PYOGENES-IN LANCEFILED GROUP A
  28. STREPTOCOCCUS PYOGENES:
    • STRICT PARASITE; in throat, nasopharynx, skin
    • LINKED W BROAD SPECTRUM OF DISEASE AND INFECTION-RHEUMATIC FEVER AND PUERPERAL SEPSIS9infection after childbirth)-has diminished in last 40 years
    • HUMANS ARE ONLY SIGN. RESERVOIR-5-15% carries through virulent strains though they aren't sick
    • TRANSMITTED THROUGH DIRECT CONTACT, DROPLETS, AND OCCASIONALLY FOOD OR FOMITES
    • skin infections occur during summer, fall, pharyngeal in winter
  29. Diseases caused by Strep pyogenes:
    • Impetigo:PYODERMA-ass w/ insect bites, poor hygiene, crowded places and schools-burning itching papules-contagious yellow crust
    • Erysipelas: more invasive-enters through small wound on face or extremities, spraeds to dermis and subcutaneous tissue, can be superficial or fatal
    • Streptococcal pharyngitis:strep throat-bacteria multiplies in tonsils and pharyngeal mucous membranes-causes redness, swelling, hard to swallow-symptoms are headache, nausea, abd pain, and a purulent exudates(pus) over tonsils,swollen lymph nodes and sometimes tonsils
    • Scarlet fever:SCARLATINA caused by strep pyo strain that carries a prophage coding for pyrogenic toxin TOXIN is produced and SPREADS VIA BLOODSTREAM AND RESULTS IN HIGH FEVER, BRIGHT RED DIFFUSE RASH ON FACE,TRUNK,INNER ARMS AND LEGS AND TONGUE. Usually diss withinn 10 days-epidermis may slogh off
    • NECTORIZING FASCIITIS: begins like impetigo but more serious, ENZYMES released and TOXINS that digest conn tissue and poison epidermal and dermal tissue. Flesh dies, sloughs off-allows bacteria deeper access to tissue and muscle-may result in amputations and loss of face too.
    • FORTUNATLY-all strains of strep pyo not drug resistant!
  30. Possible sequela to infection w/ strep:
    • Rheumatic fever:delayed inflammatory condition of joints,heart,and subcutaneous tissue
    • Acute Glomerulonephritis: disease of kidney glomeruls and tubular epithelia

    Both may be to invasion of tissue or action of toxins-don't really know
  31. Theory:
    Autoimmune theory that antibodies formed against streptococcal cell wall and membranes cross-react with the molecules in the host tissue that are similiar
  32. Streptococcus agalactiae:
    can cause prob in new borns, found in vagina, pharynx and large intestine-rep of LANCEFILED GROUP B strep
  33. Strep Agalactiae Diseases:
    • In newborns, immunocomprimesd people-increased infection
    • because in vagina GROUP B CAN BE TRANSFERRED TO NEWBORN DURING DELIVERY. EARLY ONSET INFECTION BEGINS FEW DAYS AFTER BIRTH LEADS TO SEPSIS AND PNEMONIA-HIGH MORTALITY RATE
    • LATER COMPLIACTION:2-6 weeks SYMPTOMS OF MENINGITIS -fever, vomiting, diarhea-20% of infected babies have neurological damage
    • This pathogen MOST PREVALANT CAUSE OF NEONATAL PNEOMONIA, SEPSIS,MENINGITIS in Europe and US
    • PREGNANT WOMEN SHOULD BE SCREENED FOR COLONIZATION IN THIRD SEMESTER and immunized
  34. Viradan Streptococci:(mostly normal flora)
    • large, complex group
    • MOST NUMEROUS AND WIDEPSREAD OF ORAL CAVITY-also in nasopharynx, genital tract, skin
    • NOT HIGHLY INVASIVE -enter tissue through oral surgery-CONSTANT INHABITANTS OF GUMS AND TEETH-even chewing candy or brushing teeth can cause entry
  35. Diseases of Viradans Strep:
    • Dental proc. can lead to BACTEREMIA, TOOTH ABSCESSES, EVEN MENINGITIS AND ABDOMINAL INFECTION
    • SUBACUTE ENDOCARDITIS:most inportant of all viridan strep infections-BACTERIA COLONIZE SURFACE OF HEART LINING AND VALVES that have beem injured by rheumatic fever, valve surgey, etc
    • Form thick layers of bacteria and fibrin called VEGETATIONS- as dis. inc. these increase in size and can release bacteria into blood-masses can travel to brain and lungs causing damage
  36. People with pre-existing heart conditions:
    • at high risk for these diseases! usually given prophylactic antibiotics prior to dental and surgical proc
    • DENTAL CARIES-DENTAL CAVITIES-common dental disaese in this group
    • In prescence of sugar(carbs)-Strep. Mutans produce slime layers that adhere to teeth -BASIS FOR PLAQUE-a heterogenous group of bacteria in a biofilm
  37. Strep. Pneumoniae:
    • SIGNIFICANT HUMAN PATHOGEN-ALSO CALLED PNEUMOCOCCUS-causes 60-70% ALL BACTERIA PNEMONIAS
    • small, gram positive-LANCET SHAPED CELLS ARRANGED IN PAIRS AND SHORT CHAINS
    • REQUIRES COMPLEX MEDIA, like blood or chocolate, EXHIBIT A HEMOLYSIS
    • culture dies in presc of oxy-improved by 5-10% CO2-does not have peroxidase or catalse
    • Pathogenic strains form LARGE CAPSULES -MAJOR VIRULNECE FACTOR -rough strains do not have capsules and are avirulnet-so far 90 diff capsular types
  38. Diseases of Strep. Pneumoniae:
    • Ititis Media-middle ear infection-3rd most common childhood disease
    • Pneumonia-occurs when mucous containing abcteria inhaled from pharynx into lungs in immunocompromised people. Multiplies inducing overwhelming inflammatory response causes release of fluid intro lungs-LOBAR PNEUMONIA
    • fluid acc. in alveoli w/ red and white blood cells-patient can drwon in own fluids
  39. Meningitis:
    • imflammtion of meninges of brain-can be fatal if not detected early-SITUATION IS A MEDICAL EMERGENCY! can cause influx of WBC into brain causing build up of pressure in skull end death as brain stem is crushed
    • Prevention_this is only strep. disease which effective vacc. available-active immunity!
  40. 2 vaccines:
    • Capsular antigens: from 23 most encountered strains-older vaccine good for adults and high risk patient-effective 5 years in 60-70% who recieve
    • Conjugate vaccine: newer, for kids 2-23 months-effective against oititis media
  41. Enterococcus faecalis: called enterococci because is normal flora of colon
    • usually in elderly undergoing surgery, affect urinary tract, wounds, blood, endocardium, blood, appendix
    • ENTEROCOCCI EMERGING AS SERIOUS NOSOCOMIAL OPPURTUNISTS- because of rising multi-drug resistant strains-VRE-VANCOMYCIN -RESISTANT ENTEROCOCCI-and the exceptional ease transfrerrd from one person to another
  42. Family Neisseria
    • GRAM NEGATIVE, BEAN SHAPED,MORPHOLOGY, FOUND I N PAIRS
    • no spores-PATHOGENIC SPECIES HAVE CAPSULES
    • outer membrane as well as cell wall
    • have sex pili
    • STRICT PARASITES-DON'T SURVIVE LONG OUTSIDE HOST
    • AEROBIC OR MICROAEROPHILIC-HAVE OXIDATIVE METABOLISM, PRODUCE CATALASE AND ENZYMES
    • identified by producing enzyme cytochrome c oxidase
    • PATHOGENIC SPECIES REQUIRE RICH COMPLEX MEDIA
    • grow best in increased CO2
  43. Neisseria gonorrhoae:
    • causes GONORRHEA-GONOCOCCUS
    • VIRULENECE DUE TO PILI WHICH SLOW PHAGOCYTOSIS by macrophages and neutrophils
    • PROTEASE BINDS TO IgA - prevents from binding to the bacteria
    • DOES NOT SURVIVE MORE THAT 1-2 HRS ON FOMITES, MOST INFECTIOUS WHN TRANSFERRED TO MUCOUS MEMBRANE
    • INFECTION IS ASYMPTOMATIC IN 10% MALES AND 50% FEMALES
  44. GONNORHEA CONT:
    • STRICTLT HUMAN DISAESE-AMONG TOP 5 SEXUALLY TRANSMITTED DISAESE
    • infectious dose range from 100-1000 COLONY FORMING UNITS
  45. IN MALES:
    • INFECTION OF URETHA CAUSING URETHRITIS-painful urination, yelolowish discharge,
    • SCAR TISSUE IN SPERMATIC DUCTS CAN CAUSE INFERTILITY
  46. IN FEMALES:
    • PURULENT OR BLOODY DISCAHRGE IN HALF THE CASES
    • SALPINGITIS-PELVIC INFLAMMATORY DISAES(PID)
    • BUILDUP SCAR TISSUE BLOCK FALLOPIAN TUBES CAUSING STERILTY AND ETOPIC PREGNANCIES
  47. GONNORHEA:
    VERY RARELY GONOCOCCAMAL BACTEREMIA LEADS TO MENINGITIS AND ENDOCARDITIS
  48. IN NEWBORNS:
    • can pass on to baby when passing through birth canal
    • GONOCOCCAL EYE INFECTIONS: van cause blindness in newborns
    • GONORRHEA IN CHILDREN OTHER THAN NEWBORNS STRONG EVIDENCE OF SEXUAL ABUSE
  49. Neisseria meningitidis:
    • MENINGOCOCCUS-ass w/ EPIDEMIC CEROBROSPINAL MENINGITIS
    • VIRULENCE FACTORS ARE POLYSACCHARIDE CAPSULE, ADHESISVE PILI,IgA PROTEASEENDOTOXIN (LPS) RELEASED FROM CELL WALL WHEN LYSED
    • TYPES A,B,C RESPONSIBLE MOST CASES OF INFECTIONS
    • HUMANS ARE RESERVOIRS
    • AQUIRED THROUGH CLOSE CONTACT OR DROPLETS
  50. MENINGITIS:
    • IN VULNERABLE People-BACTERIA ENGULFED BY EPITHELAIL CELLS, PENETRATE BLOOD VESSELS-MOVE RAPIDLY TO BRAIN AND PRODUCE SIGNS OF MENINGITIS
    • PETECHIA-lesions on trunk
  51. in small 3 of cases FULMINATE DISEASE produced
    • high mortality rate-HIGH FEVER, CHILLS, DELIRIUM, SHOCK AND COMA
    • GENEARLIZED INTRAVASCULAR CLOTTING, CARDIAC FAILURE, DAMAGE TO ADRENAL GLANDS AND DEATH can occur in few hours
  52. THIS IS MEDICAL EMERGENCY:
    • TREATMENT-PENICILLIN G-given intravenously in high doses
    • if allergic to penicillin GIVE CHLORAMPHENICOL OR THIRD GENERATION CEPHALORSPORIN
    • EVN TREAED IT HAS A HIGH MORTALITY RATE OF 15=%
  53. VACCINES:
    • specific PURIFIED CAPSULAR ANTIGENS
    • GROUP A VACCINES PROTECT ALL AGES-ONLY FOR PEEPS 2 AND OLDER
    • SO FAR NO VACCINE FOR GROUP B
  54. GRAM POSITIVE BACILLI OF MEDICAL IMPORTANCE:
    • 3 general shapes
    • based on prsecnce or absence of endospores and the charateristics of being acid fast
  55. GENUS BACILLUS:
    • gram + FORM ENDOSPORES
    • saprobic, mobile-none fastidious
    • USEFUL AS DECOMPSOERS AND BIOREMEDIATORS
    • PRIMARY HABITAT IS SOIL
    • some produce antibiotics-BACILLUS SUBTILUS-BACITRACIN
    • ONLY TWO MEDICALLY IMP-BACILLUS ANTHRACIS, BACILLUS CEREUS
  56. BACILLUS ANTHRACIS:
    • causes anthrax-LRG BLOCK SHAPED RODS, AMONG LARGEST PATHOGENIC BACTERIAL PATHOGEN
    • whn produces spores-CENTRALLY LOCATED-NO SPORSE IN A LIVING BODY
    • ZOONOTIC DISAESE
    • disease model used by ROBERTH KOCH FOR DEVELOPING HIS POSTULATES
  57. 3 TYPES OF ANTHRAX:
    • CUTANEOUS:FORMS BLACK SORE CALLED ESCHAR-LEAST DANGEROUS FORM
    • PULMONARY:(INHALATION)-SPOERS INHALED IN LUNGS-ALSO CALLED WOOLSORTER'S DISEASE-100% LETHAL IF NOT TREATED
    • GASTROINTESTINAL:INGSETION OF SPORES, RARE BUT DANGEROUS-20-60% DIE IF UNTRAETED
  58. MORE INFO
    • macrophages pick up the endospores but the endosporse kill them using (PA) PROTECTIVE ANTIGEN TOXIN, EDEMA TOXIN, AND LETHAL TOXIN
    • none effective alone-ANTIGEN MUST EB COMBINED WITH EITHER EDEMA OR LETHAL TOXIN
    • TRAETED WITH PENICILLIN, TETRACYCLIN,OR LAST RESORT CIPROFLOCIN(CIPRO)
  59. Anthrax:
    there is a VACCINE-IT IS A TOXOID PREP administered 6 timesover 18 minths with annula boosters
  60. Clostridium:
    • GRAM POSITIVE
    • 120 SPECIES IN NATURE
    • SPORES PRODUCED ONLY UNDER ANEROBIC CONDITIONS
    • SYNTHESIZE ORGANIC ACIDS AND ALCOHOLS-ALLOWS THEM TO DECOMPOSE ALOT OF THINGS
    • MOST OF THEIR DISEASES DUE TO RELAESE OF POTENT EXOTOXINS
  61. Clostridium perfingens:
    • CAUSES MAJORITY SOFT TISSUE DEATH AND WOUND INFECTIONS
    • CAUSES GAS GANGRENE
    • MYONECROSIS-muscle cell death
  62. Clostridium perfingens virulence factors:
    • TOXINS:14 SO FAR-contributes to METABOLISM OF HOST MUSCLE TISSUE, bacteria FERMENTS MUSCLE CARBS,PRODUCES LARGE AMOUNTS OF GAS, CUTTING OFF BLOOD FLOW-NECROSIS
    • ALPHA TOXIN:MOST IMP-CAUSES HEMOLYSIS
    • HYALURODINASE:allows bacteria to move between cells
    • HEMOLYSIN-destroys rbc
    • NEUROTOXIN:damage nervous system
  63. treatment:
    • DISEASE CAN SPREAD THROUGH ENTIRE LIMB AND REQUIRE AMPUTATION TO STOP SPREAD OF NECROSIS
    • AFFECTED PART IS EXPOSED TO HIGH CONCENTRATIONS OF OXYGEN
  64. Clostridium difficle:
    • NORMAL FLORA OF TH E COLON-in small numbers
    • CAUSES NOSOCOMIAL IN FECTIONS
    • 2ND MOST COMMON INTESTINAL INFECTION AFTER SALMONELLOSIS
    • CAUSES ANTIBIOTIC -ASS PSEUDOMEMBRANEOUS COLITIS
    • MAJOR CAUSE OF DIARHEA IN HOSPITALS
    • ca
  65. TREATMENTS:
    VANCOMYCIN, METRONIDAZE
  66. Clostridium tetani:
    • FOUND IN SOIL AND GI TRACTS OF ANIMALS
    • LARGE BACILLI WITH TERMINAL SPORE-LOOKS LIKE DRUMSTICK OR TENNIS RAQUET
    • also called LOCKJAW-brought on by production of TETANOSPASMIN- neurotoxin CAUSES SPASTIC PARALYSIS
  67. tETANUS:
    • INCIDENCE LOW IN NORTH AMERICA
    • NEONATAL TETANUS DUE TO INFECTION OF UMBILICAL CORD STUMP OR INFECTION AFTER CIRCUMCISION
  68. FIRST SYMPTOMS:
    • CLENCHING OF JAW
    • ARCHING OF BACK
    • FLEXION OF ARMS
    • EXTENSION OF LEGS
    • DIAPHRAM CAN'T RELAX, PATIENT CAN'T BREATHE-RESULTS IN DEATH
  69. TREATMENT AND PREVENTION:
    • IMMEDIATE IS ADMINISTER TETANUS IMMUNE GLOBULIN
    • PENICILLIN WILL KILL BACTERIA BUT WONT STOP TOXIN FROM DAMAGING PATIENT
    • VACCINE-DTaP-given at 2 months-BOOSTER MUST BE EVERY 10 YEARS
  70. Clostridium botulinim:
    • MOST POTENT TOXIN IN THE WORLD
    • BOTULINUM TOXIN
    • 1 OUNCE WOULD KILL whole world
    • INHIBITS RELEASE OF ACETYLCHOLINE-CAUSES FLACCID PARALYSIS
  71. Disease it produces:
    • called botulism
    • Fodder disaese-livestock graze on contaminated food
    • LIMBERNECK DISAESE-waterfolw get cuz can't hold their heads out of the water
  72. 3 Forms of Botulism:
    • FOOD POISONING:if sporse not cooked out-germinate in can and produce BOTULINUM TOXIN-LETHAL IF ABSORBED IN BLOODSTREAM
    • MOST OFTEN ASS W LOW ACID FOODS-corn, green beans-onset is 12-72 hours
    • INFANT BOTULISM:RAW HONEY HAS BEEN IMPICATED
    • WOUND BOTULISM:primarily in p[eople using black tar heroin
  73. treatment:
    • GIVE A ANTITOXIN AND LIFE SUPPORT
    • 7 TYPES-A,B,E CAUSE MOST HUMAN DISEASES
    • ANTITOXIN MUST BE SPECIFIC
    • TOXIN IS DESTROYED BY HEATING FOOD TO 90%C FOR 10 MIN-BOILING TEMP 100%C
  74. uses for botulinim:
    • RELAXATION OF CONTRACTED MUSCLES LIKE STRABISMUS(CROOSED EYE)AND BLEPHAROSPASM(CLENCHED EYELID)
    • COSMETICALLY-PREVENT FOREHEAD AND CROWS FEET WRINKLES
  75. Listeria monocytogenes:
    GRAM POSITIVE NON-SPOREFORMEING ROD

    • MOTILE-CAN LOOK LIKE LONG FILAMENTS OR COCCOBACILLI
    • RESISTANT TO COLD,HEAT,SALT,EXTREME PH, BILE
    • disaese called LITERIOSIS-IN IMMUNOCOMPROMISEDPATIENTS,FETUSES, AND NEONATES-BRAIN AND MENINGES SERIOUSLY DAMAGED CAN CAUSE DEATH
    • MOST CASES-ASS WITH INGESTION OF CONTAMINATED POULTRY, MEAT DAIRY PRODUCTS
    • PREGNANT WOMEN SHOULD NOT EAT UNCOOKED FOOD
  76. Corynebacteria diptheria:
    • most human diseases ass with this species
    • GRAM POSITIVE ARRANGED IN PALISADES
    • AEROBIC PRODUCE CATALASE
    • CELL WALL DIFF-CONTAINS MYCOLIC ACID AND UNIQUE TYPE OF PEPTIDOGLYCAN
    • DISAESE CAUSED BY IS DIPTHERIA-POTENTIAL FOR INFECTION ALWAYS PRESENT
  77. 2 STAGES OF DISEASE:
    • LOCAL INFLAMMATORY RAECTION:mostly in upper respiratory trcat
    • TOXEMIA:due to productiojn of DIPTHEROTOXIN-affects heart and nerves, can be irreversible, but can cause death by asphyxiation
    • ASPHYXIATION-due to prescence of PSEUDOMEMBRANE-greenish gray film develops from solidification of fluid expressed due to inflammation
  78. TOIXN IS PRODUCED ONLY IN STRAINS TAHT HAVE AQUIRED GENE for toxin from BACTERIOPHAGES during transduction
    TREATMENT:dat-diptheria antitoxin, derived from horses
  79. DIPTHERIA:
    • EASILY PREVENTED BY VACCINATIONS-DTaP given to infants 6-8 weeks-booster 15 months
    • adults can be immunized against toxin 2 doses of diptheria-tetanus Td
  80. PROPIONIBACTERIUM ACNES:
    • GRAM + RESEMBLES CORNEYBACTERIUM-DIFF IN AEROTOLERANT OR ANEOROBIC AND NON-TOXGENIC
    • FOUND IN SEBACEOS GLANDS
    • ASS W ACNE, EYE INFECTIONS,ARTIFIAL JOINTS
  81. MYCOBACTERIUM-GRAM =IRREGULAR BACILLUS-
    • HIGH MOLECULAR WEIGHT MYCOLIC ACIDS AND WAXES IN CELL WALL
    • high lipid content-ACID FAST
    • STRICT AEROBIC, PRODUCE CATALASE
    • NO FLAGELLA
    • DON'T FORM SPORES CAPSULES
    • GROW SLOWLY
    • 2 SPECIES CAUSE IMP DISEASE
    • MYCOBACTERIUM TUBERCULOSIS
    • MYCOBACTERIUM LEPRAE
  82. MYCOBACTERIUM TUBERCULOSIS:
    • TUBERCLE BACILLUS
    • CAUSES TUBERCULOSIS OR TB
    • thin rods grow in CORDS
    • CORD FACTOR
    • WHITE PLAGUE
    • TRANSMITTED AIRBORNE RESPIRATORY DROPLETS
    • VERY RESISTANT
    • CAN SURVIVE 8 MONTHS IN FINE AEROSOL PARTICLES
    • UNTREATED TB PROGRESSES SLOWLY
  83. CLINICAL TB divided in 3 groups:
    • primary TB
    • secondary (reactivation or reinfection)TB
    • disseminated TB
  84. PRIMARY TB:
    • MINIMUM INFECTIOUS DOSE OF TUBERCLE BACILLUS IS 10 ORGANISMS
    • after becomes bad-3-4 weeks,immune system mounts and forms TUBERCLES-granulomas consist of central core contain bacilli and enlarge macrophage
    • the attack stops spread of infection, BUT carries potential damage to lungs since CENTER OF THE TUBERCLES BREAK DOWN INTO NECROTIC CASEOUS LESIONS THAT HEAL BY CALCIFICATION
    • -NORMAL LUNG TISSUE REPLACED BY CALCIUM DEPOSITS
  85. TUBERCULIN REACTION:
    • THE t cell response to the proteins is seen in yhis reaction
    • also the diagnostic tool used to test for exposure and potential infection
  86. SECONDARY TB:
    • REACTIVATION of bacilli occurs in weeks, months, or years later. Tunbercles expand and drain into bronchial tubes and URT
    • patient experiences severe symptoms
    • gradula wasting of body accounts for older name-CONSUMPTION
    • UNTREATED-secondary disease has a MORTALITY RATE OF ABOUT 60%
  87. EXTRAPULMONARY TB:
    • during secondary bacteria the BACILLI CAN disseminate to regional lymph nodes, kidneys, long bones
    • complications VERY SERIOUS
    • RENAT TB-causes necrosis scarring of kidneys,uterers,bladder
    • GENITAL TB in males:damages prostrate gland, epididymis, testi
    • GENITAL TB IN FEMALES:damge to fallopian tubes, ovaries, uterus
    • TB IN BONE AND JOINTS-can result in paralysis and sensory loss
    • TB IN THE BRAIN (MENINGITIS) ALWAYS FATAL IF NOT TREEATED
  88. TREATMENT OF TB:treatment requires drugs within good amount of time
    usually from 6 months-2 years

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