1. Foundations in Microbiology
PowerPoint to accompany
Foundations in Microbiology
Fifth Edition
Talaro
Chapter 18
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2. Cocci of Medical Importance
Chapter 18

3. Cocci of Medical Importance
Gram + and gram - are among most significant infectious agents of humans. Also prevalent members of the normal flora of skin, oral cavity, and intestine.
Pyogenic cocci- infections with these bacteria tend to stimulate pus formation.
Most common infectious species belong to 4 genera: Staphylococcus, Streptococcus, Enterococcus, and Neisseria

4. General characteristics of the Staphylococci
Spherical cells arranged in irregular clusters
Gram positive
Common inhabitant of the skin & mucous membranes
Lack spores and flagella
May have capsules
31 species
Most important human pathogens are: S. aureus*, S. epidermidis (and close relatives, S. capitis, and S. hominis) and S. saprophyticus.

5. Staphylococcus aureus
grows in large, round, opaque colonies
optimum temperature of 37oC
facultative anaerobe
withstands high salt, extremes in pH, & high temperatures
produces many virulence factors
Implicated in nearly 80,000 deaths nationwide.

6. Staphylococcus aureus
This genus owes its name to the grapelike clusters it forms.

7. Major Virulence Factors of S. aureus - Enzymes
coagulase – coagulates plasma and blood; produced by 97% of human isolates; diagnostic
Hyaluronidase- digests connective tissue of the host
Staphylokinase- digest blood clots
Dnase- breaks down DNA
Lipases- digests oils, allowing bacteria to more easily colonize skin
Penicillinase- inactivates penicillin

8. Major Virulence Factors of S. aureus - Toxins
Hemolysins (a, b, g– lyse RBCs
Leukocidin- lyses neutrophils and macrophages
Enterotoxins- induce, nausea, vomiting and diarrhea
exfoliative toxin- causes desquamation of the skin
toxic shock syndrome toxin- induces fever, vomitting, rash, and organ damage
Virulence factor- any characteristic or structure of the microbe that contributes to the disease state

9. S. aureus
Blood agar plate growing Staphylococcus aureus

10. S. aureus Present in most environments frequented by humans
Readily isolated from fomites (an inanimate object)
Carriage rate for healthy adults is 20-60%
Carriage is mostly in anterior nares, skin, nasopharynx, intestine

11. S. aureus diseases Ranges from localized to systemic
localized infections- abscess, folliculitis (inflammation of hair follicles), furuncle (boil), carbuncle (deeper lesion, aggregation of furuncles cluster)
Systemic infections:
osteomyelitis- pathogen establishes in the highly vascular part of the bone
Bacteremia- bacteria that escaped infection site and are transported to kidneys, liver, spleen and heart lining
toxigenic diseases – food intoxication, scalded skin syndrome (SSS), toxic shock syndrome

12. S. aureus skin infections
A furuncle
Sectional view of boil or furuncle
A carbuncle

13. S. Aureus osteomyelitis in a long bone
Important systemic infections:
S. Aureus osteomyelitis in a long bone

14. Effects of S. Aureus toxins on the skin
Staphylococcal scalded skin syndrome (SSSS) results when exfoliative toxin produced by local infections
Segment of skin affected by SSSS

15. Other Staphylococci
S. epidermidis – lives on skin & mucous membranes; endocarditis, bacteremia, UTI
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. Staphylococcus aureus test
Other Staphylococcus species
S. aureus present
S. aureus present

17. Fig. 18.7 Identifies Staphylococcus isolates-can separate 19 species
PHS= phosphatase production, URE= urea hydrolysis, GLS= glucosidase production, MNE= mannose fermentation, MAN= mannitol fermentation, TRE= trehalose fermentation, SAL= Salicin fermentation, GLC= glucuronidase production, ARG= arginine hydrolysis, NGP= galactosidase production

18. Table 18.1

19. Clinical concerns of Staph
95% have penicillinase & are resistant to penicillin & ampicillin
MRSA – methicillin-resistant S. aureus – carry multiple resistance
Abscesses have to be surgically perforated
Systemic infections require intensive lengthy therapy

20. General Characteristics of the Streptococci
Gram-positive spherical/ovoid cocci arranged in long chains
Non-spore-forming, nonmotile
Can form capsules & slime layers
Facultative anaerobes
Do not form catalase, but have a peroxidase system
Most parasitic forms are fastidious & require enriched media
Small, nonpigmented colonies
Sensitive to drying, heat & disinfectants
25 species

21. Streptococcus
Characteristic long intertwining chains

22. Streptococci
Lancefield classification system based on cell wall Antigens – 14 groups (A,B,C,….)
Another classification system is based on hemolysis reactions
b-hemolysis – A,B,C,G & some D strains
a-hemolysis – S. pneumoniae & others collectively called viridans
Antigen- any cell particle or chemical that induces a specific immune response by B cells or T cells

23. Hemolysis patterns on blood agar may be used to separate streptococci into major subgroups
Streptococcus pneumoniae displaying -hemolysis

24. Table 18.2

25. Human streptococcal pathogens
S. pyogenes- primary pathogen of group A, has a variety of virulence factors, including surface antigens, toxins, and enzymes
S. agalactiae- neonatal and wound infections
viridans streptococci- - hemolytic
S. pneumoniae- bacterial pneumonia
Enterococcus faecalis- endocarditis and UTI

26. b-hemolytic S. pyogenes
Main representative of group A
Most serious streptococcal pathogen
Strict parasite
Inhabits throat, nasopharynx, occasionally skin
Produces cell surface antigens and virulence factors C-carbohydrates, M-protein (fimbrae), streptokinase, hyaluronidase, DNase, hemolysins (SLO, SLS), pyogenic toxin

27. b-hemolytic S. pyogenes
Antigens:
C-carbohydrates- specialized polysaccarides or teichoic acids found on cell wall surface, protect bacterium from being dissolved by the lysozyme defense of host
M-protein (fimbrae)-spiky surface projection, resist phagocytosis and improves adherence
Enzymes and extracellular toxins:
Streptokinase-digests clots
Hyaluronidase- digests binding substance in connective tissue
DNase- digists DNA
hemolysins (SLO, SLS)- streptolysins that cause -hemolysis and damage cells and tissues
pyogenic toxin-key toxin in dev of scarlet fever, causes bright red rash and fever by effecting temperature regulating center

28. Cutaway view of group A Streptococcus

29. S. pyogenes Humans only reservoir- 5-15% of population carriers
Transmission – contact, droplets, food, fomites
Skin infections –pyoderma, impetigo, erysipelas
Systemic infections – strep throat, pharyngitis, scarlet fever
Sequelae -rheumatic fever, glomerulonephritis

30. Streptococcal skin infections
Streptococcal impetigo, or pyoderma
Streptococcal erysipelas

31. Streptococcal pharyngitis or strep throat
The appearance of the throat in pharyngitis and tonsillitis-pharynx and tonsils become bright red and swollen, pus nodules on tonsils

32. Heart disease due to Rheumatic Fever-group A streptococcal infection can extend to the heart

33. Invasive Group A Streps and “flesh-eating” syndrome or necrotizing fasciitis
Caused by virulent strains of Streptococcus pyogenes

34. Group B: S. agalactiae
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

35. Group D, C and G: Enterococci Enterococcus faecalis, & E. faecium
Normal colonists of human large intestine
Cause opportunistic urinary, wound, and skin infections, particularly in debilitated persons

36. Streptococcal tests
Bacitracin disc test- only Streptococcus pyogenes is sensitive to minute bactiracin conc.
Group A streptococci are negative for SXT sensitivity and the CAMP test
Rapid, direct test kit for diagnosis of group A infections, throat swab introduced to latex beads and monoclonal antibodies
Positive-the C-carbohydrate on group A streptococci causes clumping
Negative-milky smooth reaction

37. Group A & B are treated with penicillin
Sensitivity testing needed for enterococci
No vaccines available

38. Viridans streptococci group
a-hemolytic
Large complex group
Most numerous & widespread residents of the oral cavity & also found in nasopharynx, genital tract, skin
Not very invasive, dental or surgical procedures facilitate entrance

39. Viridans streptococci 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

40. Effects of stretococcal colonization on the heart
Valve leaflet
Nodular vegetations on the surface constantly release bacteria into the circulation

41. Viridans streptococci group
S. mutans produces slime layers that adhere to teeth, basis for plaque
involved in dental caries

42. Streptococcus 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 by 5-10% CO2
Lack catalase & peroxidases – cultures die in O2

43. Diagnosing Steptococcus pneumoniae
Small diplococci
Gram stain of sputum from a pneumonia patient

44. S. pneumoniae
All pathogenic strains form large capsules – major virulence factor
Specific soluble substance (SSS) varies among types
84 capsular types have been identified using Quellung test or capsular swelling reaction
Causes pneumonia & otitis media
Vaccine available for high risk people

45. S. pneumoniae 5-50% of all people carry it as normal flora in pharynx
Very delicate, does not survive long outside of its habitat
Pneumonia occurs when cells are aspirated into the lungs of susceptible individuals
Pneumococci multiply & induce an overwhelming inflammatory response
Treated with penicillin

46. The course of bacterial pneumonia

47. Pneumococcal otis media

48. 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

49. Neisseria Gram-negative, bean-shaped, diplococci
Reside in the mucous membrane of humans and animals
none develop flagella or spores
capsules on pathogens
pili
Strict parasites, do not survive long outside of the host
Aerobic or microaerophilic
Oxidative metabolism
produce catalase & cytochrome oxidase
Pathogenic species require enriched complex media and CO2

50. Neisseria

51. Neisseria gonorrhoeae
Causes gonorrhea, an STD
Virulence factors: pili, other surface molecules, IgA protease
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

52. Neisseria gonorrhoeae

53. 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

54. Gonorrheal damage to the male reproductive tract

55. Gonorrheal damage to the female reproductive tract

56. Gonorrhea in newborns Infected as they pass through birth canal
Eye inflammation, blindness
Prevented by prophylaxis after birth

57. Gonorrhea diagnosis
Gram stain of urethral pus from a patient with gonorrhea

58. Neisseria meningitidis
Virulence factors – capsule, pili, IgA protease
12 strains; serotypes A, B, C, cause most cases
Prevalent cause of meningitis
Disease begins when bacteria enter bloodstream, pass into cranial circulation, multiply in meninges; very rapid onset; endotoxin causes hemorrhage and shock; can be fatal
Treated with penicillin, chloramphenicol
Vaccines exist for group A and C

59. Neisseria meningitidis
Dissemination of the meningococcus from a nasopharyngeal infection

60. Neisseria meningitidis
One clinical sign of meningococcemia

61. Table 18.4