1. Cocci

2. Cocci 5 pathogenic cocci/ pyogenic cocci - G+: staphylococcus
S. aureus
streptococcus
S. pyogenes, S. pneumoniae
- G-: Neisseria
N. meningitidis, N. gonorrhea

3. (I) Staphylococcus

4. Staphylococcus Primary reservoir >30 species
-Human carriers
-Nasopharynx, throat, skin
>30 species
- main bacteria in the nosocomial infection
- S. aureus: the most virulent species
- S. epidermidis: opportunistic pathogen
- S. saprophyticus: rarely cause human diseases

5. Thermostable nuclease
Comparison
Properties
S. Aureus
S. Epidermidis
S. saprophyticus
Pigment
Golden yellow
white
citrine
Coagulase + -
Mannitol
Thermostable nuclease
Hemolysin
SPA
pathogenicity
strong
weak

6. Biological characteristics
Grape like-clusters, no capsule
Facultative anaerobes
Liposoluble pigments
Hemolysis
Resistance

7. Pathogenicity (S. aureus)
Virulence factors
invasiveness
- surface structure
SPA
- invasive enzymes
coagulase
Toxin---exotoxins
- hemolysins/ Staphylolysin
- leukocidin
- Staphylococcal enterotoxin
- toxic shock syndrome toxin-1, TSST-1
- exfoliative toxin/
epidemolytic toxin

8. SPA inhibits phagocytosis
IgG
Fc receptor
PHAGOCYTE
BACTERIUM
Fab Fc
Free protein A binds to Fc of IgG, blocking Fc receptors and is thus anti-phagocytic.

9. Pathogenicity (S. aureus)
Disease
Invasive infection/ pyogenic infection
- local infection: lesion is limited in local area
- organ infection: pneumonia, meningitis
- systemic infection: septicemia, pyemia
Bactermia (from abscess, wound, burn) , Osteomyelitis (tibia) ,Pneumonia

10. folliculitis
Boil/ furuncle

11. Impetigo---staph skin infection, multiple pustules (small skin abscesses)
carbuncle

12. Pseudomembranous Enteritis, PME Pseudomembranous Colitis

13. Pathogenicity (S. aureus)
Disease
Toxin-associated diseases
- food poisoning (enterotoxin)
- TSS (TSST-1)
sudden high fever, shock, kidney failure, red skin rash
- SSSS (exfoliative toxin)
staphylococcal scalded skin syndrome
- staphylococcal enterocolitis- dysbacteriosis

14. Staphylococcal scalded skin syndrome (SSSS)
- most often occurs in infants and young children Low mortality rate
Skin blister---denudation (like scald)

15. Laboratory diagnosis Direct examination: Gram Stain Primary media: BAP
Differential Tests.
Mannitol Salts
Coagulase
DNase
Enterotoxin
Antibiotic Sensitivity (plasmid, B lactamase) : penicillin /methicillin/vancomycin
API STAPH Kit

16. Staphylococcus epidermidis
coagulase negative staphylococci
Staphylococcus epidermidis
Major component skin flora
Opportunistic infections (less common than S.aureus)
urinary tract infection (UTl)
septicemia
wound infection
Nosocomial infections
bacterial endocarditis
Identification
Non-hemolytic (sheep blood agar)
Does not ferment mannitol
Coagulase-negative
Staphylococcus saprophyticus
urinary tract infections

17. (II) Streptococcus Widely exist: Diseases:
-water, air, feces, human nasopharynx
Diseases:
-pyogenic infection
- scarlet fever
-streptococcal hypersensitive disease
- rheumativ fever

18. - G+, arranged in chains (II) Streptococcus
- Nutrient requirement: high
*fastidious (flesh-eating bacteria)
- Facultative/ obligate anaerobe
- On blood agar:
*different hemolysis
- Catalase negative (staphylococci +)

19. Classificaton based on hemolytic activity - α-hemolytic strep
incomplete hemolysis
opportunistic pathogens
- β-hemolytic strep
complete hemolysis
main human pathogens
-γ-hemolytic strep
no hemolysis
no pathogenicity

20. Hemolysis
alpha
beta
gamma

21. Classificaton Antigenic structure - polysaccharide antigens (C Ag)
* group-specific antigen
* 20 groups (A-H, K-V)
* group A main human pathogens
- surface protein antigens (M Ag)
* type-specific antigen
* group A>80 serotypes

22. Pathogenicity (Step. Group A)
Virulence factors
Surface structure
- LTA: adhere to host cells
- M- protein
- Peptidoglycan

23. Lipoteichoic Acid and F-protein
fibronectin
epithelial cells

24. M protein IMMUNE Complement IgG M protein NON-IMMUNE peptidoglycan
fibrinogen r

25. Pathogenicity (Step. Group A)
Virulence factors
Invasive enzymes
- hyaluronidase (spreading factor)
- streptokinase (SK)
- streptodornase (SD)
Toxins---exotoxins
- streptolysin (hemolysin)
- erythrogenic toxin
Erythrogenic toxins
---pyrogenic exotoxin
scarlet fever toxin
- protein
- serotype A, B, C
- scarlet fever

26. streptolysins Properties Streptolysin O (SLO) Streptolysin S (SLS) O2
Oxygen-labile
Oxygen-stable
Antigenicity
Strong (ASO test)
weak
Biological
Destroy WBC, platelet virulence of Mφ, NC
Destroy WBC virulence of many tissues
Chemical
Protein (MW )
Polypeptide (28 aa)

27. Anti-SLO test (ASO test)
A neutralization test between the toxin (SLO) and its specific anti-toxin (ASO) which is used to diagnose or monitor rheumatic fever caused by group A strep.

28. Pathogenicity (Strep. Group A)
Disease
3 types of infections
- pyogenic infection:
skin & subcutaneous infection, impetigo,
lymphangitis, septicemia
- toxin-associated diseases
pharyngitis--scarlet fever
- hypersensitive disease
acute glomerulonephritis, rheumatic fever

29. pyogenic infection Acute tonsillitis--- Erysipelas
Abscess with surrounding cellulitis
Erysipelas
Acute tonsillitis---
There is a risk of developing rheumatic fever
Erysipelas on the cheek

30. toxin-associated diseases
Strawberry tongue
Paly around mouth
Red rash

31. Diseases caused by other streptococci
Group B strep.
- neonatal infection
- adult infections: endometritis, pneumonia, meningitis, endocarditis
Group C strep.
- epidemic sore throat, acute glomerulonephritis
Group G strep.
- sore throat, cellulitis, erysipelas
Group D strep.
- nosocomial infection, urinary infection, biliary tract infection, peritonitis

32. Laboratory diagnosis Direct examination: Gram Stain Primary culture
ASO Tests.

33. Prevention and treatment
Treat the pharyngitis and tonsillitis in time
Antibiotics: penicillin for the first choice

34. (III) Pneumococcus

35. Characteristics Morphology & cultivation properties
- G+, arranged in pairs, bullet shape
- capsule: polysaccharide
- blood agar or chocolate blood agar, festidious
- α-hemolysis
- autolysis
- bile solubility test: +
*distinguish from other α-hemolytic strep.
- ferment inulin

36. Pathogenicity Virulence factors - capsule
- pneumolysin & neuraminidase
- Surface protein adhesin and secretory IgA protease.
- Teichoic acid and the Peptidoglycan fragment,
phosphorylchorine .

37. Pathogenicity Main disease - pneumonia *particularly young and old
*after damage to upper respiratory tract
e.g. following viral infection
- bacteremia
- meningitis
- middle ear infections (otitis media)

38. Laboratory diagnosis + -
Differentiate S. pneumoniae from other α-hemolytic strep.
- bile solubility test
- optochin sensitivity test
-capsule swollen reaction
- animal test + -

39. Treatment & prevention
(S. pneumoniae)
Sensitive to a wide range of antimicrobial agents, but resistance is common:
penicllin, erythromycin, chloramphenicol, sulphonamides, clindamycin, vancmycin
Prevention
polysaccharide vaccine
14 capsule types mixed vaccine

41. Not optochin sensitive
Bile solubility test
Not optochin sensitive
optochin sensitive
Streptex antiserum
Quellung reaction
using antisera
capsule "fixed"
visible microscopically
Latex agglutination - streptococci

42. (IV) Neisseria Genus Neisseria > 10 species N. Meningitidis
- meningitis
- low prevalence but high mortality
N. Gonorrhoeae
- human gonorrhea
- high prevalence but low mortality

43. Biological characteristics
G-, coffee bean-shaped or kidney-shaped, in pairs
Capsules and pili
Fastidious
Resistance: very low
Polymorphonuclear cells

44. Biological characteristics
Oxidase positive
Culture: 5-10% CO2
Thayer Martin.
selective
chocolate agar
heated blood

45. Pathogenesis--meningococcus
Virulence factors
-pili: attach to nasopharyngeal mucosa
-capsule
-endotoxin: damage capillary blood vessel
Transmission
-respiratory droplets
Disease
- epidemic cerebrospinal meningitis

46. Pathogenesis--gonococcus
Virulence factors
-pili
-IgA, protease
-outer membrane protein (OMP)
-LPS
Transmission
-sexual contact
-indirect contact (basin, towel, etc)
Disease
- gonorrhea

47. X LPS PILI Capsule N. meningitidis N. gonorrhoeae Virulence Factors
Similar, but –
Differences
in utilization
LPS
LPS
IgA protease
Capsule
PILI
Opacity (OPA) proteins
Outer Membrane Proteins
Hemolysin
IgA protease
PILI
Opacity (OPA) proteins
Outer Membrane Proteins X
NO capsule
NO hemolysin

48. Neisseria gonorrhoeae
After 2-14 days
Found only in man
Gonorrhea: second most common venereal disease
Using the Gram stain in patient specimens, the organisms are most often observed in polymorphonuclear leukocytes
Gram stain of pure culture Urethral exudate

49. Neisseria gonorrhoeae
adults
-transmission: STD (sexually tranmitted disease)
-clinical dsease: genitourinary tranct infection
urethritis, prostatitis, epididymitis (male)
cervix inflammatin (female)
infertility
newborns
-ophthalmia neonatorum

50. Neisseria gonorrhoeae
Pili = key in anchorage of organisms
to mucosal epithelium.
Nonpiliated gonococci are avirulent
OUTER MEMBRANE PROTEINS
Porin proteins (Por) = prevent phagolysosome fusion & allow intracellular survival [ also called protein I]
Opacity proteins (Opa) = binding of organisms to epithelium
[also called protein II]
Reduction-modifiable proteins (Rmp) = protection against bactericidal antibodies [ also called protein III]

51. Bartholin’s Duct
Urethritis

52. Disseminated gonococcal infection (DGI).
Fever, polyarthritis
(or monoarticular septic arthritis),
and/or dermatitis
(pustules on a hemorrhagic base).
Purulent conjunctivitis/Ophthalmia neonatorum Infection in newborns during vaginal delivery

53. Smear Antibiotic therapy polymorphonuclear cell
G- cocci, many in cells
Culture
Antibiotic therapy
lactamase-resistant cephalosporin
e.g. ceftriaxone
resistant strains
common
produce lactamases
destroy penicillin

54. Prevention and treatment
penicillin
1% silver nitrate--- ophthalmia neonatorum

55. Neisseria meningitidis
Meningococcal meninigitis
Neisseria meningitidis
resides in man only
usually sporadic cases
mostly young children
outbreaks
adults
crowded conditions
e.g. army barracks
1-4 days
Second most common meningitis
pneumococcus, most common
Fatal if untreated
Responds well to antibiotic therapy
penicillin
Upper respiratory tract infection
adhesion pili
Bloodstream
Brain

56. Diagnosis spinal fluid Gram negative diplococci
within polymorphonuclear cells
meningococcal antigens
Culture
Thayer Martin agar

57. Prevention capsule inhibit phagocytosis anti-capsular antibodies
stop infection
antigenic variation
serogroups
vaccine
multiple serogroups

58. Pseudomonas aeruginosa

59. Pseudomonas aeruginosa
Widely distributed in nature
Frequently present in small numbers in the normal intestinal flora and on the skin
Commonly present in moist environments in hospitals
It is primarily a nosocomial pathogen

60. Typical Organisms Gram- rod
Unipolar flagellum (1~3) ---- actively mobile
Occurs as single bacteria, in pairs, and occasionally in short chain
Capsule
Pili in strains obtained from clinical specimens

61. Culture Grow readily on many types of culture media
Smooth and round colonies
Multiple colony types in one culture
Fluorescent greenish color
Sometimes produce a sweet or grape-like or corn taco-like odor

62. Culture Obligate aerobic Grow well at 37~42℃and no growth at 4℃
Produce water-soluble pigments
Pyocyanin; Pyoverdin; Pyorubin; Pyomelanin
Produce hemolysin
Oxidase-positive
Ferment glucose but not other carbohydrates

63. Diverse sites of infection by P aeruginosa

64. Who are at risk? People with cystic fibrosis Burn victims
Individuals with cancer
Patients requiring extensive stays in intensive care units

65. Control and Treatment
The spread of Pseudomonas is best controlled by cleaning and disinfecting medical equipment.
In burn patients, topical therapy of the burn with antimicrobial agents such as silver sulfadiazine, coupled with surgical debridement, has markedly reduced sepsis.
Susceptibility testing is essential.
The combination of gentamicin and carbenicillin can be very effective in patients with acute P aeruginosa infections.

66. Summary Concepts -Pathogenic/ pyogenic cocci
-ASO test
Pathogenicity of 5 pathogenic cocci