1. COCCI OF MEDICAL IMPORTANCE 1 Chapter 18

2. COCCI Spherical shaped Both Gram+ and Gram- species Most significant infectious agents of humans Most are “pyogenic” –they stimulate pus formation 2

3. STAPHYLOCOCCI Spherical cells arranged in irregular clusters, divides on three planes Gram positive Common inhabitant of the skin & mucous membranes (nose, mouth and throat) Lack spores and flagella May have capsules 31 species 3

4. STAPHYLOCOCCUS AUREUS grows in large, round, opaque colonies optimum temperature of 37 o C (10-46) facultative anaerobe withstands high salt, extremes in pH, high temperatures, drying, disinfectants produces many virulence factors Most resistant of all non-spore-forming bacteria “Staph” infections @ 80,000 deaths in U.S. each year 4

5. S. AUREUS 5

6. ENZYMES PRODUCED BY S. AUREUS coagulase – coagulates plasma and blood; produced by 97% of human isolates-- #1 diagnostic tool Hyaluronidase – breaks apart “glue” that holds tissues together Staphylokinase –digests blood clots Dnase – digests DNA Lipases –help colonize on oily skin Penicillinase – inactivate penicillin 6

7. TOXINS PRODUCED BY S. AUREUS Hemolysins Alpha-toxin lyse red blood cells and other damage (heart, kidney, bones) Leukocidin Lyse neutrophils and macrophages Enterotoxins Induce nausea, vomiting and diarrhea Exfoliative toxin Desquamation of skin (SSSS) Toxic shock syndrome toxin (TSST) Induces fever, vomiting, rash, organ damage 7

8. S. AUREUS 8

9. Present in most environments frequented by humans Readily isolated from fomites Carriage rate for healthy adults is 20-60% Carriage is mostly in anterior nares, skin, nasopharynx, intestine Infection caused by: Poor hygiene Poor nutrition Tissue injury Infections Diabetes Immunodeficiency diseases 9

10. S. AUREUS DISEASES Ranges from localized to systemic localized -abscessfolliculitis, furuncle, carbuncle, impetigo systemic – osteomyelitis, bacteremia, endocarditis, pyoarthritis, pneumonia, meningitis toxigenic disease – food intoxication, scalded skin syndrome, toxic shock syndrome (magnesium ions) 10

11. S. AUREUS 11

12. S. AUREUS 12

13. S. AUREUS 13

14. IMPETI GO 14

15. CLINICAL CONCERNS 95% have penicillinase & are resistant to penicillin & ampicillin MRSA – methicillin-resistant S. aureus – carry multiple resistance HA – Hospital-acquired CA – Community-acquired 94,000 new cases a year (19,000 deaths) Abscesses have to be surgically perforated Systemic infections require intensive lengthy therapy 15

16. OTHER STAPHYLOCOCCI S. epidermidis – lives on skin & mucous membranes--endocarditis, bacteremia, UTI (catheters, shunts, prosthetics S. hominis – lives around apocrine sweat glands S. capitis – live on scalp, face, external ear All 3 may cause wound infections S. saprophyticus – infrequently lives on skin, intestine, vagina –UTI 16

17. TREATMENT Skin infection: use a topical antibiotic Most S. aureus resistant to Penicillin and ampicillin (MRSA) Use cephalexin, tetracyclines, vancomycin (VRSA- synercid), teicoplanin, linezolid and daptomycin Use a combination of two drugs Vaccines are being developed 17

18. CONTROL Nosocomial prevention Carriers, handwashing, proper disposal, isolation, catheters and needles Good personal hygiene Do not eat, smoke, cough or sneeze in food prep areas Food should be handled as little as possible (gloves) Hot food kept at 140 o F Refrigerated food stored at 40 o F or below 18

19. STREPTOCOCCI Gram-positive spherical/ovoid cocci arranged in long chains Non-spore-forming, nonmotile Can form capsules & slime layers Facultative anaerobes Most parasitic forms are fastidious & require enriched media Small, non-pigmented colonies Sensitive to drying, heat & disinfectants 25 species 19

20. STREPTOCOCCUS 20

21. STREPTOCOCCI Lancefield classification system based on cell wall Ag – 17 groups (A,B,C,….) Another classification system is based on hemolysis reactions  -hemolysis – A,B,C,G & some D strains  –hemolysis – S. pneumoniae & others collectively called viridans 21

22. S. PYOGENES Lancefield Group A,  -hemolytic Most serious streptococcal pathogen Strict parasite Inhabits throat, nasopharynx, occasionally skin Live on domestic animals 22

23. S. PYOGENES Produces C-carbohydrates (protects from lysozyme M-protein fimbriae (phagocytosis) hemolysins DNase, pyrogenic toxin (erythrogenic) 23

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25. S. PYOGENES Humans only reservoir 5-15% subclinical carriers Transmission – contact, droplets, food, fomites Skin infections –pyoderma, impetigo, erysipelas Warm weather Systemic infections – strep throat, pharyngitis, scarlet fever, septicemia, pneumonia, Streptococcal toxic shock syndrome Cold weather Sequelae – rheumatic fever (joints), acute glomerulonephritis (kidneys) 25

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29. S. AGALACTIAE  - hemolytic, Lancefield B,C, and D Regularly resides in human vagina, pharynx & large intestine can be transferred to infant during delivery & cause severe infection Most prevalent cause of neonatal pneumonia, sepsis, & meningitis 15,000 infections & 5,000 deaths in US Pregnant women should be screened & treated wound and skin infections endocarditis in debilitated people 29

30. STREPTOCOCCAL TESTS 30

31. VIRIDANS GROUP  -hemolytic Large complex group Most numerous & widespread residents of the oral cavity & also found in nasopharynx, genital tract, skin Not very invasive, usually a dental or surgical procedure facilitates entrance 31

32. VIRIDANS GROUP Bacteremia, meningitis, abdominal infection, tooth abscesses Most serious infection – subacute endocarditis – blood-borne bacteria settle & grow on heart lining or valves Persons with preexisting heart disease are at high risk & receive prophylactic antibiotics before surgery or dental procedures 32

33. VIRIDANS GROUP S. mutans produces slime layers that adhere to teeth, basis for plaque Likes smooth surface with pits involved in dental caries (“rotten”) Buildup of plaque mixture of protein, polysaccharide and enormous amount of bacteria Carbohydrates (especially sucrose) Acidogenic plaque bacteria The bacteria produce acid that breaks down the calcium phosphate salts in the enamel 33

34. S. MUTANS 34

35. S. PNEUMONIAE Causes 60-70% of all bacterial pneumonias small, lancet-shaped cells arranged in pairs and short chains Culture requires blood or chocolate agar Growth improved with 5-10% CO 2 Cultures die in O 2 35

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37. S. PNEUMONIAE 5-50% of all people carry it as normal flora in pharynx Very delicate, does not survive long outside of its habitat All pathogenic strains form large capsules – major virulence factor 84 capsular types have been identified using the Quellung test or capsular swelling reaction (immunity to each) Pneumonia occurs when cells are aspirated into the lungs of susceptible individuals 37

38. S. PNEUMONIAE 38

39. S. PNEUMONIAE Pneumococci multiply & induce an overwhelming inflammatory response Symptoms and signs... High fever, sharp chest pains, difficulty breathing, rust colored sputum Walking (lobar) or double pneumonia Earache, otitis media, high temps (deafness) young children @300,000 cases a year, 40,000 deaths Vaccine available for high risk people 1983 (1989 – 40,000 deaths) Treated with penicillin, tetracycline, cephalosporin 39

40. FAMILY NEISSERIACEAE Gram-negative cocci Residents of mucous membranes of warm- blooded animals Genera include Neisseria, Moraxella, Acinetobacter 2 primary human pathogens Neisseria gonorrhoeae Neisseria meningitidis 40

41. NEISSERIA Gram-negative, bean-shaped, diplococci Do not develop flagella or spores capsules on pathogens pili slows macrophages Strict parasites, do not survive long outside of the host Aerobic or microaerophilic Pathogenic species require enriched complex media and CO 2 41

42. NEISSERIA 42

43. NEISSERIA GONORRHOEAE Causes gonorrhea (Clap), an STD Albert Neisser (1879) Virulence factors: pili, other surface molecules, IgA protease (cleaves IgA) Strictly a human infection In top 5 STDs Infectious dose 100-1,000 Does not survive more than 1-2 hours on fomites Infection is asymptomatic in 10% of males and 50% of females 43

44. GONORRHEA Males – urethritis, yellowish discharge, scarring & infertility Females – vaginitis, urethritis, salpingitis (PID) mixed anaerobic abdominal infection, common cause of sterility & ectopic tubal pregnancies Extragenital infections – anal, pharygeal, conjunctivitis, septicemia, arthritis Treated with penicillin until PPNG Cephalosporins used now No immunity, no vaccine 44

45. NEISSERIA GONORRHOEAE 45

46. GONORRHEA IN NEWBORNS Infected as they pass through birth canal Eye inflammation, blindness Prevented by prophylaxis after birth 46

47. GONORRHEA DIAGNOSIS 47

48. NEISSERIA MENINGITIDIS Virulence factors: Capsule pili IgA protease 12 strains: serotypes A, B, C, cause most cases One of the most prevalent cause of meningitis Beginning symptoms and signs: Fever Headache (Meningism) Stiff neck Vomiting Myalgia Malaise 48

49. Transmitted through saliva Disease begins when bacteria enter bloodstream, pass into cranial circulation, multiply in meninges; very rapid onset; endotoxin causes hemorrhage and shock; can be fatal petechea Ecchmycoses – large lesions Shock Coma Death (within 24 hours) Treated with penicillin, chloramphenicol Vaccines exist for group A (anyone) and C (2 and up) 49

50. NEISSERIA MENINGITIDIS 50

51. NEISSERIA MENINGITIDIS 51