Staphylococci: S.aureus : pathogen

1. Staphylococci: • S.aureus : pathogen • S.epidermidis : oppotunistic pathogen, are members of the normal flora of human skin and respiratory. • S.sarophytius : non-pathogen

3. S aureus • Pathogenic substances

4. A)Coagulase: • a)free coagulase; b) bound coagulase (clumping factor) Deposit fibrin on the surface of staphylococci: altering their ingestion by phagocytic cells or their destruction within such cells

5. Clumping factor • A surface S aureus compound that is responsible for adherence of the organisms to fibrinogen and fibrin • Because of these two kinds of meterial. When mixed with plasma, S aureas forms clumps or thrombus, • Cause local infection not systemic infection.

6. B) toxins

7. a) α-toxin 1,broad spectrum of eukaryotic cell membranes, it disrupts biologic membranes 2, the toxin is a potent hemolysin. Can lyses red blood cells 3,The α-toxin degrades sphingomyelin and therefore is a toxic for many kinds of cells, including red blood cells.

8. b) leukocidin • Kill white blood cells, two components,they act synergistically on white blood cell membraneto form pores and increase cation permeability, and the dead white blood cell formed purulent (pyic/pyoid) clump

9. c) exfoliative • Also called epidemolytic toxin, desquamation of the staphylococcal scalded skin syndrome. • d)toxic shock syndrome toxin associated with fever, shock, and multisystem involvement including a desquamative skin rash

10. Clinical finding

11. 1. Invasive and pyogenic infection Furuncle and carbuncle: a superficial skin infection that develops in hair follicle, sebaceous gland or sweat gland. 2. Toxic shock syndrome: this disease is characterized by high fever, vomiting diarrhea, sore throat, musle pain, within 48 hours, it may progress to severe shock with evidence of renal and hepatic damage, a skin rash may develop followed by desquamation at palm and bottom of feet

12. 3. toxin-mediated disease 1)Scaled skin syndrone: the disease result from the production of exfoliation larger blisters, from there S aureus cannot be isolated, easily broken by hurt, then superficial skin drop off. 2).Food poisoning Food contaminated by staphylococcal entertoxin,results in acute vomiting and diarrhea within 1 to 5 hours, but usually no fever, few severe patient may prostration or shock recovery is rapid 1—2days. Usually happen in summer and autumn

13. lab diagnosis produce deep yellow pigment Hemolysis: complete lysis of erythrocyte ferment mannitol 甘露醇 catalase test : positive coagulase test : positive

14. Treatment and control: 1.Ubiquitous human parasites 2.reinfection: pathogenic organisms are commonly spread from one lesion to other areas of the skin by fingers and clothing,so scrupulous local antisepsis is important to control recurrent furunculosis 3.75% of S.epidermidis are nafcillin resistant 4.90% of S.aureus are penicillin resistant, do drug susceptible test, help us to choose correct medicine, and prevent the drug-resistant bacteria from spreading.

15. streptococcus

16. Biological characterization 1.shape. Liquid media long chain 2.cell wall antigen: divided into serologic groups (A-H, K-V), majority of human pathogenic streptococci are group A(90%) 3.hemolysis:α: incomplete lysis of erythrocyte with formation green pigment β: complete disruption of erythrocytes with release of hemoglobin γ: non-hemelysis α: opportunistic pathogen β: pathogenγnon pathogen 4.Transmitted by coughing, sneezing and wound infection.

17. pathogenesis

18. 1.SK a.transform the plasminogen(纤维蛋白溶酶原) of human plasma into plasmin b. digesting fibrin c. help the bacteria spread in human body 2.SD also called DNA enzyme, depolymerizes DNA, decrease viscosity DNA in purulent exudates（渗出物）.

19. 3.hyaluronidase Splits hyaluronic acid, an important portant component of the ground substance of connective tissue, thus, hyaluronidase aids in spreading infecting microorganisms (spreading factor) 4.Pyrogenic exotoxins elaborated by group A streptococci, can cause scarlet fever.

20. 5. M protein, F protein, LTA( lipoteichoic acid) All three appear to be involved in mediating attachment to the epithelial cell surface

21. Clinical findings 1. streptococcal sore throat Little fever, thin serious discharge 2.Erysipelas丹毒: this characterized by a spreading area of erythema红斑and edema浮肿水肿with rapidly advancing, well-demarcated划分edges, pain and systemic manifestations including fever and lymphadenopathy淋巴结病 3.Shock syndrome and scarlet fever

22. 4. acute rheumatic fever (ARF) Both streptococci and heart tissue have same or similar antigens. Bacteria entered human body can stimulate immune system to produce antistreptococci antibodis, and this kind of antibody also react with heart tissue, then cause the disease. 5. Acute glomerulonephritis caused by deposition in the glomerulus of antigen-antibody complexes with complement activation and consequent inflammation, M protein of some nephritogenic strains have been shown to share antigenic determinants with glomeruli, similar to rheumatic fever

23. Control or treatment: 1.Because the bac can be transmitted by coughing and sneezing, cure patient or carrier as soon as possible, aids to contron infection source. 2.air, medicine device, dressing must be aseptic. 3.Prevent rheum(感冒)，avoid streptococci infection 4..Usually use penicillin G. all β-hemolytic group A are sensitive to penicillin G and most are sensitive to erythromycin, some are resistant to tetracycline5.In acute streptococcal infections, every effort must be made to rapidly eradicate streptococci from the patient, eliminate the antigenic stimulus and thus prevent poststreptococcal disease (ARF& Acute glomerulonephritis ) 6.Antimicrobial drugs have no effect on established ARF and glomerulonephritis, but it very useful in preventing reinfection with β-hemolytic group A streptococci in rheumatic fever patient

24. Streptococcus pneumoniae • Gram positive • Pairs or in chains • Can produce autolysis( can damage the bacteria cell wall,on solid media small round colony, at first domeshaped and later developing a central plateau with an elevated rim. Lysis of pneumococci occurs in a few minutes when ox bile is added to a broth culture) • α-hemolytic on blood agar

25. Pathogenesis 1. capsule: anti phagocytic cells 2.pneumolysin O:lyse red blood cell Clinical findings 1. pneumococcal pneumonia shaking chill, high fever, cough with production of sputum pink to rusty in color 2.Pneumococcal meningitis Treatment Penicillin . Penicillin resistant chains:erythromycin, vancomycin or quinolones

26. neisseria • Gram negative • In pairs • neisseria gonorrhoeae(gonococci) and neisseria menigitidis(meningococci )are pathogenic for humans Different capsule: Meningococci have polysaccharide capsules whereas gonococci do not Plasmid:Meningococci rarely have plasmid where as most gonocicci do Disease: Meningococci typically are found in the upper respiratory tract and cause meningitis, while gonococci cause genital infections

27. meningococci Pathgenisis Capsule, pili, IgA1 protease Transmitted by coughing and sneezing Infection source: carrier and patient Clinical findings: meningitis Treatment vaccines are currently used to protect human largedose penicillin G, either chloramphenicol or a third-generation cephalosporin such as cefotaxime or ceftriaxone is used in persons allergic to penicillins

28. gonococci Transmitted by sexual contact Infection source: women and men with asymptomatic infection Pathogenisis: 1.pili: adhere cannot wash away by urine 2.outermembrane protein: PⅠinsert into cell membrane ,PⅡadhere, PⅢ prevent antibody from killing bacteria 3.IgA1 protease damage SIgA(mucous), bac also can adhere to mucous

29. Treatment and control • Worldwide spreading, the infection rate can be reduced by avoiding multiple sexual partners • How to use antimicrobials page 125