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9 cocci

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cocci

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9 cocci

  1. 1. CocciCocci
  2. 2. Gram positive and negative cocciGram positive and negative cocci
  3. 3. Classification G+ : Staphylococcus Streptococcus Pneumococcus G- : Meningococcus Gonococcus
  4. 4. §1 Staphylococcus I. Morphology II. Culture III. Antigenic structure IV. Resistance Biological characters
  5. 5. MorphologyMorphology ※※ Gram positiveGram positive ※※ Grape like-clustersGrape like-clusters
  6. 6. Culture characteristics S.SaprophyticusS.EpidermidisS.Aureas ※※ Facultative anaerobesFacultative anaerobes ※ Low nutritional required and grow rapidly ※ Colonies : circular, 2-3 mm in diameter with a smooth, shiny opaque surface; ※ Pigments : golden 、 grayish white or lemon ※ Hemolysis on sheep blood agar plate
  7. 7. Important properties ※ Mannitol fermentation ※ Produce catalase H2O2 →O2 + H2O ( hydrogen peroxide ) ※ Coagulase : S aureus, can clot citrated plasma (-) (+)
  8. 8. Antigenic StructureAntigenic Structure
  9. 9. ★★ Staphylococcus protein AStaphylococcus protein A ,, SPASPA Binds to the Fc portion of IgG at the complementBinds to the Fc portion of IgG at the complement binding sitebinding site SignificanceSignificance ※※ Preventing the activation of complementPreventing the activation of complement ※※ anti-phagocytosisanti-phagocytosis ※※ coagglutinationcoagglutination
  10. 10. PHAGOCYTEPHAGOCYTE Fc receptorFc receptor Protein AProtein A immunoglobulinimmunoglobulin Bacterium, etc. immunoglobulinimmunoglobulin Bacterium, etc.
  11. 11. Staphylococcus protein AStaphylococcus protein A ,, SPASPA Binds to the Fc portion of IgG at the complementBinds to the Fc portion of IgG at the complement binding sitebinding site SignificanceSignificance ※※ Preventing the activation of complementPreventing the activation of complement ※※ anti-phagocytosisanti-phagocytosis ※※ coagglutinationcoagglutination
  12. 12. Antigen+antibody+SPA→compound with High molecular weight
  13. 13. Resistance Thermotolerance : 60 1h or 80 30min℃ ℃ Salt tolerance : can grow in 10-15% sodium chloride solution. resistant to common disinfectants Antibiotics resistance : multidrug resistant MRSA (methicillin resistant staphylococcus aureus)
  14. 14. ▲ Catalase ▲ Coagulase and clumping factor ▲ Hyaluronidase and Lipaseipase ▲ Hemolysin or sphingomyelinase Csphingomyelinase C ▲ Leukocidin ▲ Exfoliative Toxin (superantigen) ▲ Toxic Shock Syndrome Toxin (superantigen) ▲ Enterotoxins (superantigen) PathogenesisPathogenesis
  15. 15. PathogenesisPathogenesis
  16. 16. H2O2 →O2 + H2O ▲ Destruction of the bactericidal activity of hydrogen peroxide ▲ Differentiate the staphylococci from the streptococci ※ catalase
  17. 17. ▲ Coagulase: an enzyme-like protein that clots citrated Coagulase prothrombin + Enzymatically active(thrombin-like)→fibrin polymerization Free coagulase ※ Coagulase and clumping factor Coagulase= ↓
  18. 18. ☆ Coagulase can deposit fibrin on the surface of the agent, altering their ingestion by phagocytic cells and their destruction within such cells, so coagulase production is considered synonymous with invasive pathogenic potential. ▲ Clumping factor: a surface compound of S.aureus and adherence of the agents to fibrinogen and fibrin S.aureus(clumping factor) + plasma Clumps forms BoundBound coagulase ※ Coagulase and clumping factor Coagulase=
  19. 19. ※ Hemolysin Hemolysin is a exotoxin that cause lysis of red blood cells, white blood cells, platelet and macrophages in vitro and in vivo. Alpha-hemolysin, a transmembrane heptamer αhemolysin: a broad spectrum of eukaryotic cells βhemolysin: a broad spectrum of eukaryotic cells γhemolysin: white blood cells δhemolysin: play a role in S.aureus diarrheal diseases. Can increase cation permeability
  20. 20. ※ Leukocidin Leukocidin: a pore forming toxin, so it can form pores in white blood cell membrane especially the neutrophil and increase cation permeability. This toxin may be an inportant virulence factor in community associated methicillin resistant S. aureus infection.
  21. 21. ※ Exfoliative toxins Epidermolytic toxins= Dsg-1:desmoglein 1; Dsg-3:desmoglein 3 Responsible for staphylococcal scalded skin syndrome (SSSS), a disease predominantly affecting infants and characterized by the loss of superficial skin layers, dehydration, and secondary infections Superantigen
  22. 22. ※ Toxin shock syndrome toxin-1 Toxic shock syndrome toxin (TSST) is a superantigen with a size of 22 KDa produced by 5 to 25% of Staphylococcus aureus isolates. It causes toxic shock syndrome (TSS) by stimulating the release of large amounts of interleukin-1, interleukin-2 and tumor necrosis factor. In general, the toxin is not produced by bacteria growing in the blood; rather, it is produced at the local site of an infection, and then enters the blood stream. Superantigen TSST-1 binds to MHC- molecules, yielding T cellⅡ stimulation, which promotes the protean manifestations of the toxic shock syndrome.
  23. 23. ※ Enterotoxins Superantigen Staphylococcal enterotoxin is an enterotoxin produced by Staphylococcus aureus. It is a common cause of food poisoning, with severe diarrhea, nausea and intestinal cramping often starting within a few hours of ingestion. Being quite stable, the toxin may remain active even after the contaminating bacteria are killed. It can withstand boiling at 100 for a about 30℃ minutes. Gastroenteritis occurs because the toxin is a superantigen, causing the immune system to release a large amount of cytokines that lead to significant inflammation.
  24. 24. ※ Enterotoxins Superantigen The emetic effect of enterotoxin is probably the result of central nervous system stimulation (vomiting center) after the toxin acts on neural receptors in the gut.
  25. 25. Formation conditions of staphylococcal enterotoxin Storage Temperature: below 37 , the higher of the℃ temperature, the shorter of the time of toxin production; Storage location: easy form enterotoxin in environment of poorly ventilated, low partial pressure of oxygen. Types of food: rich in carbohydrate and protein Physicochemical properties : Low molecular weight proteins, heat-resistant, protease-resistant.
  26. 26. Formation conditions of staphylococcal enterotoxin Mechanism of action : ▲ Acting on the gastrointestinal mucosa, result in inflammatory changes such as congestion, edema, erosion and metabolic disturbance of electrolyte and eventually diarrhea. ▲ stimulate the visceral ['v sərəl] branch of the vagusɪ nerve, and result in reflex vomiting
  27. 27. Pathogenesis of staphylococcal infectionsPathogenesis of staphylococcal infections
  28. 28. Skin (local) infectionSkin (local) infection ※※ Furuncle:Furuncle:Protein A, Leukocidin, HemolysinProtein A, Leukocidin, Hemolysin ※※ Stye:Stye: lipaselipase ※※ Impetigo:Impetigo:contagiouscontagious ※※ Epidermal necrolysisEpidermal necrolysis ※※ Exfoliative Dermatitis:Exfoliative Dermatitis: Exfoliative toxinExfoliative toxin ※※ MastitisMastitis ※※ Abscess (deep tissue); granulation:Abscess (deep tissue); granulation: coagulase, hyaluronidasecoagulase, hyaluronidase (burn, wound)(burn, wound) Systemic infectionSystemic infection Bactermia (from abscess, wound, burn)Bactermia (from abscess, wound, burn) ,, Osteomyelitis (tibiaOsteomyelitis (tibia ['t biə])ɪ['t biə])ɪ ,, PneumoniaPneumonia Clinical findings Invasive infections
  29. 29. Food poisoningFood poisoning Toxic shock syndromeToxic shock syndrome scalded skin syndrome Babiesscalded skin syndrome Babies ExfoliatinExfoliatin feverfever scarlatiniformscarlatiniform rashrash desquamationdesquamation vomitingvomiting diarrheadiarrhea myalgiasmyalgias not a human infectionnot a human infection food contaminated from humansfood contaminated from humans - growth- growth - enterotoxin- enterotoxin onset and recovery both occur within few hoursonset and recovery both occur within few hours VomitingVomiting// nauseanausea// diarrheadiarrhea// abdominalabdominal //painpain Toxic diseases
  30. 30. ※※ Cause vomiting and watery, nonbloody diarrheaCause vomiting and watery, nonbloody diarrhea ※※ SuperantigenSuperantigen ※※ Heat-resistant (100 30min)℃Heat-resistant (100 30min)℃ EnterotoxinEnterotoxin
  31. 31. Food poisoningFood poisoning Toxic shock syndromeToxic shock syndrome scalded skin syndrome Babiesscalded skin syndrome Babies ExfoliatinExfoliatin feverfever scarlatiniformscarlatiniform rashrash desquamationdesquamation vomitingvomiting diarrheadiarrhea myalgiasmyalgias not a human infectionnot a human infection food contaminated from humansfood contaminated from humans - growth- growth - enterotoxin- enterotoxin onset and recovery both occur within few hoursonset and recovery both occur within few hours VomitingVomiting// nauseanausea// diarrheadiarrhea// abdominalabdominal //painpain No feverNo fever
  32. 32. Toxic shock syndrome toxin 1Toxic shock syndrome toxin 1 ※※ Cause toxic shockCause toxic shock ◆◆ Tampon['tæmp n]ɑːTampon['tæmp n]ɑː 止血棉塞止血棉塞–– usingusing menstruating womenmenstruating women ◆◆ Individuals with wound infectionIndividuals with wound infection ◆◆ Patients with nasal packing used to stop bleedingPatients with nasal packing used to stop bleeding from the nosefrom the nose ※※ SuperantigenSuperantigen
  33. 33. Food poisoningFood poisoning Toxic shock syndromeToxic shock syndrome scalded skin syndromescalded skin syndrome BabiesBabies ExfoliatinExfoliatin feverfever scarlatiniformscarlatiniform rashrash desquamationdesquamation vomitingvomiting diarrheadiarrhea myalgiasmyalgias not a human infectionnot a human infection food contaminated from humansfood contaminated from humans - growth- growth - enterotoxin- enterotoxin onset and recovery both occur within few hoursonset and recovery both occur within few hours VomitingVomiting// nauseanausea// diarrheadiarrhea// abdominalabdominal //painpain
  34. 34. ExfoliatinExfoliatin ※※ Cause scalded skin syndrome in young childrenCause scalded skin syndrome in young children ※※ Acts as protease that cleavesActs as protease that cleaves desmosomedesmosome ,, leadingleading to the separation of the epidermis at the granularto the separation of the epidermis at the granular cell layercell layer
  35. 35. §2 Streptococcus§2 Streptococcus
  36. 36. MorphologyMorphology Gram-positive, spherical or ovoid, arrange inGram-positive, spherical or ovoid, arrange in chainschains, no spore and flagella; in very young cultures, the capsules are noticeable.
  37. 37. ※※ Facultative anaerobeFacultative anaerobe ※※ Much higher nutritional requirement, growMuch higher nutritional requirement, grow well on enriched media.well on enriched media. ※※ colonies: 1-2 mm in diametercolonies: 1-2 mm in diameter with a smooth, shiny opaque surface, different hemolytic zone, different hemolytic zone around the colonies.around the colonies. Culture and typical biochemical reaction CatalaseCatalase negativenegative (staphylococci are catalase positive)(staphylococci are catalase positive)
  38. 38.  α-hemolytic streptococcus Incomplete hemolysis, green zone around colonies * Opportunistic pathogens ClasssificationClasssification (1) According to the Hemolytic activity:(1) According to the Hemolytic activity:
  39. 39.  β-hemolytic/pyogenic streptococcus Complete hemolysis, clear zone around colonies *major human pathogens
  40. 40.  γ-streptococcus No hemolyzation, no pathogenicity.
  41. 41. ( 2 ) According to the antigenic structure Group-specific cell wall antigen: on the basis of this antigen, streptococci can be classified in to A-H and K-U groups. Chemical property: carbohydrate, the serologic specificity of this antigen is determined by an amino sugar. M protein: ▲ The foundation of subtype within groups. ▲ Major virulence factor of group A S.pyogenes. Group A : more than 100 serotypes Group B: 4 serotypes Group C : 13 serotypes
  42. 42. Pathogenesis Virulence factors exotoxin Invasive enzyme Hyaluronidase Streptokinase DNAases Streptolysin (O, S) Pyrogenic exotoxin LTA M protein Attachment
  43. 43. (1) Attachment: Surface structure * LTA (lipoteichoic acid) : Adhere to sensitive cell * M-protein : ◆ Anti-phagocytotic ◆ Common antigen -- heart muscle cell, glomerular basement membrane cells, etc. ◆ M Ag-Ab complex: type Ⅲ hypersensitivity Such as: poststreptococcal acute glomerulonephritis, rheumatic fever, rheumatic heart disease. There is common antigenicity between M protein and Myocardial cells, glomerular [ 'l mrj lə] basement membrane cells, so theɡ ɒ ʊ antibody just against M protein can also combine with these cells, activate complements and result type Ⅱ hypersensitivity
  44. 44. ▲ Hyaluronidase : Destroy the polysaccharide (hyaluronic acid) that holds animal cells together, making it easier for the pathogen to spread through the tissues of the host organism. (2) Invasive enzyme ▲ Streptokinase (SK) = fibrinolysin [ fa brə'n l s n]ˌ ɪ ɒ ɪ ɪ ▲ Streptodornase (SD): an enzyme produced by hemolytic streptococci that catalyzes the depolymerization of deoxyribonucleic [di ksi ra bə nu 'kli k] acidːˌɒ ː ɪ ʊ ː ːɪ (DNA). a protein secreted by several species of streptococci which can bind and activate human plasminogen [plæz'm nəd ən]ɪ ʒ 血浆酶原 plasminogen Streptokinase plasmin digest Fibrin and other proteins Spreading factorSpreading factor
  45. 45. (3) exotoxin: (i) Pyrogenic exotoxins (erythrogenic toxin) ▲ Coded by lysogenic phage. ▲ superantigen ▲ Low molecular weight proteins, heat-resistant. Biological activity ▲ Pyrogenic ▲ increased the permeability of blood-brain barrier ▲ cytotoxicity: have cytotoxic activity to spleen cells and macrophages cultured in vitro ▲ Increase the sensitivity of Animal to endotoxin
  46. 46. (ii)hemolysins Streptolysin S – alters membrane permeability; lyses RBCs, leukocytes, and other cells containing sterols in membrane Streptolysin O – forms membrane penetrating channels (porin) leading to membrane defects and cell lysis Streptococcus can produce two hemolysins: △ Cytotoxic to RBCs and many tissue cells, particularly cardiotoxic △ Antigenic - anti-streptolysin O (ASO) antibody used to diagnose recent infection property Streptolysin S has no antigenicity
  47. 47. Pathogenesis of S. pyogenes infections. [ er 's p l s]ˌ ə ɪ ə ə
  48. 48. Invasive disease Clinical findings pharyngitis Pyoderma Dermatocellulitis necrotizing fascitis erysipelas puerperal fever …… ▲ systemic infection septicemia ▲ local purulent infections:
  49. 49. Scarlet fever Toxin-Mediated diseases Caused by Hemolytic streptococcus B group A, Acute respiratory infectious disease. Clinical features: fever, pharyngitis, genernal diffused fresh red eruption and obvious desquamation Complication: heart, kidney and joints diseases
  50. 50. Scarlet fever is characterized by: ▲ Sore throat ▲ Fever ▲ Bright red tongue with a "strawberry" appearance ▲ Forchheimer spots (fleeting small, red spots on the soft palate) may occur ▲ spares the face (although some circumoral [ s kəm'o rəl] pallorˌ ɜː ʊ 口周苍 白 is characteristic) ▲ Characteristic rash: △ fine, red and rough-textured △ blanches upon pressure △ Pastia lines (where the rash runs together in the armpits and groin) appear and can persist after the rash is gone. Strawberry tongue Pastia lines 帕斯蒂亚
  51. 51. (1) acute glomerulonephritis ( group A) [glə merj lə nef'ra t s]ʊ ʊ ʊ ɪ ɪ (2) Rheumatic fever (3) rheumatic heart disease poststerptococcal diseases (hypersensitive disease)
  52. 52. Prevention & treatmentPrevention & treatment ※※ Treat the pharyngitis and tonsillitis in time,Treat the pharyngitis and tonsillitis in time, avoid the post streptococcal diseases.avoid the post streptococcal diseases. ※※ Antibiotics and chemical agents: penicillin G forAntibiotics and chemical agents: penicillin G for the first choicethe first choice
  53. 53. Gram stain of pure culture Urethral exudate §3 Neisseria§3 Neisseria
  54. 54. ※※ Gram negative cocci, usuallyGram negative cocci, usually arranged in pairs and the flat orarranged in pairs and the flat or concave sides are adjacent.concave sides are adjacent. ※※ Some are normal inhabitants inSome are normal inhabitants in respiratory tract. Others arerespiratory tract. Others are human pathogenshuman pathogens
  55. 55. ※※ Gram negative cocci, kidney-shaped, in pairs haveGram negative cocci, kidney-shaped, in pairs have capsules and pilicapsules and pili ※※ Need enriched mediaNeed enriched media :: grow best on mediagrow best on media containing complex organic substances such ascontaining complex organic substances such as heated blood, hemin and in an atmosphereheated blood, hemin and in an atmosphere containing 5% COcontaining 5% CO2.2. Common biological characteristicsCommon biological characteristics
  56. 56. Gonococci and meningococci are the main pathogens in neisseriae, and they are closely related, with 70% DNA homology. The main differences between these two agents △ Meningococci have polysaccharide capsules, but gonococci do not. △ Meningococci rarely have plasmids whereas most gonococci do. △ Meningococci cause meningitis, whereas gonococci cause genital infections.
  57. 57. ※※ Resistance: relativelyResistance: relatively fragilefragile organism, susceptibleorganism, susceptible toto temperature changes, drying, uv light,temperature changes, drying, uv light, andand other environmental conditions.other environmental conditions. ※ They are rapidly killed by drying, sunlight, moist heat and many disinfectants. ※ produce autolytic enzymes that result in rapid swelling and lysis in vitro at 25℃
  58. 58. gonococci and their coloniesgonococci and their colonies Neisseria gonococciNeisseria gonococci GonoGonococcal colonies on chocolate agar plate: grayish white, round, convex, smooth, opaque.
  59. 59. 1. Pili 2. Por proteins 3. Opa 4. Rmp 5. Lipooligosaccharide (LOS): Antigenic structure N. gonorrhoeae is capable of changing its surface antigens (particularly pilin) rapidly to avoid host defenses. N. gonorrhoeae (Gonococcus)
  60. 60. Pathogenicity and immunityPathogenicity and immunity 1. Pathogenicity: (1) Human is the only natural host. (2) Virulence factor: ※ Pili — key factor in anchorage of organisms to mucosal epithelium. Nonpiliated gonococci are avirulent ※ Capsule-antiphagocytosis ※ Endotoxin (lipooligosaccharide: LOS)-main pathogenic substance ※ IgA1 protease: can split and inactivate secretory IgA1, a major mucosal immunoglobulin of human. Has no long O-antigen side chains
  61. 61. ▲ Porin proteins (Por) : form porins and mediate resistance to neutrophil and serum killing, allow intracellular survival of the bacteria[ also called protein I]. ▲ Opacity proteins (Opa) : associated with opaque colonies; an outer membrane protein functioning in attachment to host cells[ also called protein Ⅱ]. ▲ Reduction-modifiable proteins (Rmp) : stimulates antibodies that block serum bactericidal activity [also called protein Ⅲ]. ※※ Outer membrane proteins (OMPs):Outer membrane proteins (OMPs):
  62. 62. Pathogenesis Attachment to mucosal cells (requires pili) →Invade into the cells and multiply (Opa mediates tighter association with and invasion of host cells; Por inhibits phagolysosome fusion) →Pass through the cells into the subepithelial space →Establish infection (LOS stimulates inflammatory response; Rmp blocks bactericidal activity) Establishment of infection
  63. 63. Pathogenesis and Pathology Gonococci attack mucous membrane of the genitourinary tract, eye, rectum, and throat, producing acute suppuration that lead to tissue invasion; this is followed by chronic inflammation and fibrosis.
  64. 64. △ Gonorrhea occurs only in humans. △ Gonorrhea is transmitted by sexual contact △ 95% infected men and 50% infected women have acute symptoms. So, asymptomatic carriage is more common in women than in men. △ Rectal and pharyngeal infections are more commonly asymptomatic than genital infections. Epidemiology
  65. 65. ※ Gonorrhea (sexually transmitted disease STD) in male: acute urethritis in female: pelvic inflammatory ※ Ophthalmia [ f'θælm ə]ɒ ɪ neonatorum [ni næ't r m]ːɒ ɔː ʌ →blindness
  66. 66. Symptoms 1. Male: urethritis with yellow, creamy pus and painful urination. The process may extend to the epididymis [ epə'd dəm s]ˌ ɪ ɪ . As suppuration subsides in untreated infection, fibrosis occurs, sometimes leading to urethral strictures (sterility).
  67. 67. 2. Female: infection starts from the endocervix, and results in vagina discharge, dysuria, and abdominal pain. Uterine ['ju təra n]ː ɪ tubes may be involved, causing salpingitis , fibrosis, and obliteration of the tubes (20% may become infertile). When gonococcal cervicitis is either asymptomatic or unrecognized, the patient may progress to pelvic inflammatory disease (PID).
  68. 68. 3. Gonococcal ophthalmia neonatorum : bilateral conjunctivitis often follows vaginal delivery from an infected mother. The symptoms are eye pain, redness, and a purulent discharge. The organism can cause permanent injury to the eye in a very short time; prompt recognition and treatment are essential to avoid blindness. prevention: tetracycline, erythromycin or silver nitrate.
  69. 69. 4. Gonococcal bacteremia (1-3% of infected women and much lower percent of infected men) can lead to fever, pustular rash over the extremities, tenosynovitis [ teno s nə'va t s]ˌ ʊˌ ɪ ɪ ɪ 腱鞘炎 and suppurative arthritis.
  70. 70. ※ Specimen: purulent secretion of genitourinary tract *note: “fragile” →bed-side inoculation ※ Isolation and identification: direct smear, isolation and culture, biochemical tests, antigen detection, etc. Laboratory diagnosisLaboratory diagnosis
  71. 71. Prevention and treatment Penicillin, Spectinomycin 奇霉素 , Ceftriaxone[seftra' æksn]ɪ 头孢三嗪 , and so on ※ Treatment △ neonatorum ophthalmia - silver nitrate △ Strengthen health education and prohibit dirty sex △ No vaccine ※ Prevention
  72. 72. Infection rate can be reduced by: 1. avoiding multiple sexual partners; 2. early diagnosis and treatment; 3. finding cases and contacts through education and screening of population at high risk. 4. combined with doxycycline 强力霉素 or azithromycin [e z θrə'ma s n]ɪ ɪ ɪ ɪ 阿奇霉素 for dual infections with Chlamydia ※ Prevention
  73. 73. meningococci and their coloniesmeningococci and their colonies Neisseria meningococciNeisseria meningococci Meningococcal colonies on chocolate agar plate: Colorless, round, convex, smooth, transparent and just like Dew drops.
  74. 74. 1. Capsular polysaccharide: more than 13 serogroups have been identified (serogroups A, B, C, X, Y, and W135 are most commonly isolated). 2. Pili (allow bacterial colonization of nasopharynx). 3. Outer membrane proteins: these are analogues to the Por and Opa proteins of gonococci. 4. Lipooligosaccharide (LOS): responsible for diffuse vascular damage in meningococcal infections. Antigenic structure
  75. 75. 1. Pathogenicity: (1) Meningococci are pathogenic only for humans under natural conditions. Child: susceptible (2) virulence factor: *Pili– attach to nasopharyngeal mucosa *capsule – antiphagocytosis *endotoxin – main pathogenic substance →capillary, small blood vessel *IgA1 protease: can split and inactivate IgA1, a major mucosal immunoglobulin of human. Pathogenicity and immunity
  76. 76. Symptoms: begins suddenly, with intense headache, vomiting, and stiff neck, and progress to coma within a few hours. Mortality: nearly 100% if untreated; <10% in patients treated promptly with appropriate antibiotics. Neurologic sequelae: uncommon; hearing deficit, Intellectual impairment
  77. 77. Pathogenesis Like gonococci, meningococci are able to invade the epithelial cells. The capsule of meningococci protects the bacteria from phagocytic destruction.
  78. 78. 2. Pathogenesis:2. Pathogenesis: Epidemic cerebrospinal meningitisEpidemic cerebrospinal meningitis Clinical typing: common, outbreak, septicemic typeClinical typing: common, outbreak, septicemic type (1) Organisms(1) Organisms →→ attach to epithelial cells of nasoparynxnasoparynx with the aid of pili ( nasopharyngeal infection : asymptomatic , most are carriers,( nasopharyngeal infection : asymptomatic , most are carriers, only 2~3% go to next stage )only 2~3% go to next stage ) (2) Blood stream <fever, skin ecchymosis[ ekə'mo s s] >ˌ ʊ ɪ(2) Blood stream <fever, skin ecchymosis[ ekə'mo s s] >ˌ ʊ ɪ →→cross the braincross the brain barrier <severe headache ,vomitting, stiff neck > (meningococcemia.barrier <severe headache ,vomitting, stiff neck > (meningococcemia. bacteremia or septicemia. blood contain cocci )bacteremia or septicemia. blood contain cocci ) (3) Meninges [mə'n nd i z] (meningitis. meninges pyogenic inflammation.ɪ ʒ ː(3) Meninges [mə'n nd i z] (meningitis. meninges pyogenic inflammation.ɪ ʒ ː spinal fluid contain cocci )spinal fluid contain cocci ) Clinical cause: 3 stagesClinical cause: 3 stages
  79. 79. ※※ Immunity:Immunity: Group-specific antibody(subclinicalGroup-specific antibody(subclinical and symptomaticsymptomatic infection).infection). ※※ Prevention and treatmentPrevention and treatment 1. Polysaccharide vaccine (group A, C)1. Polysaccharide vaccine (group A, C) 2. Penicillin; cefotaxime [sefə 'tæksa m]ʊ ɪ2. Penicillin; cefotaxime [sefə 'tæksa m]ʊ ɪ 头孢噻肟头孢噻肟 ; chloramphenicol; chloramphenicol
  80. 80. Exercises:Exercises: Staphylococcus protein A , SPA Coagulase Toxin shock syndrome toxin-1 Streptolysin O Lipooligosaccharide (LOS) Streptokinase (SK) Streptodornase (SD) 1.The pathogenic substances and pathogenicity of cocci? 2.The main pathogenic substances and pathogenicity of strptococci?
  81. 81. THANKS

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