1. Dept. Microbiology-PIFM School of Medicine-UAG
Bacterial Infection of the Skin and Soft Tissue
Dept. Microbiology-PIFM
School of Medicine-UAG

3. A.- General Characteristics
1.- Skin is relatively resistant to infection.
2.- Microflora inhibits harmful organism.
3.- Skin infections occur when protective
mechanism fall.

4. A.- General Characteristics
Entry
1) Skin (pores, hair follicles).
2) Wounds (scratches, cuts, burns).
3) Insect & animal bites.

5. A.- General Characteristics
Diseases
Localized infections with local and/or systemic effect.
Systemic infections.
Multiplication
Extracellular.
Intracellular (??).
Damage
Toxin.
Host immune response.

6. A.- General Characteristics
Defense
Dry
Usual infection sites are wet areas, skin folds, armpit, groin
Acidic (pH 5.0)
Temperature less than 37oC
Some pathogens grow best <37oC
Lysozyme and toxic lipids (pore, hair follicles, sweat gland)
Resident microflora (mainly Gram positives)
Skin-associated lymphoid tissue (SALT)

7. B.- Skin and Soft Tissue Infections
1.- Impetigo: Initially a vesicular infection
that rapidly evolves into pustules that
rupture, with the dried discharge forming
honey-colored crust on an erythematous base.

8. 2.- Ecthyma(Pustules): Begin as vesicles
that rupture, creating circular erythematous
lesions with adherent crusts.
3.- Folliculitis: Inflammation at the opening
of the hair follicle that causes erythematous
papules and pustules surrounding
individual hairs.
4.- Furuncle: Deep-seated inflammatory
nodule with a pustular center that develops
around a hair follicle.
(painful, localized, abscess).

9. 5.- Carbuncle: Involvement of several adjacent
follicles, with pus discharging from multiple
follicular orifices.
6.- Cutaneous abscesses: Painful, fluctuant, red,
tender swelling, on which may rest a pustule.
7.- Erysipelas: Erythema and swelling of the
cutaneous surface, involves the superficial
dermis (redness-lymphangitis).

10. 8.- Cellulitis: Erythematous, hot, swollen skin
with irregular edge.
(affects the deeper dermis and subcutaneous fat.)
9.- Acne: Infection of sebaceous follicles
with plugs of keratin blocking the
sebaceous canal, resulting in
“blackheads”.

11. 10.- Necrotizing fasciitis: Rapidly spreading cellulitis
with necrosis (skin and deeper fascia; may
involve muscle).
Begin with fever, systemic toxicity, severe pain
in the development of a painful, red swelling that
rapidly progress to necrosis of the subcutaneous
tissue and overlying skin.

12. Dept. Microbiology-PIFM School of Medicine-UAG
Staphylococcus
Dept. Microbiology-PIFM
School of Medicine-UAG

13. Family Micrococcaceae Genera: Micrococcus Planococcus Stomatococcus
Staphylococcus
Saprophyte

14. Family Micrococcaceae Genera: Staphylococcus
The name staphylococcus is derived
from the Greek term sthapylé meaning
“ a bunch of grapes”.

15. Family Micrococcaceae Genera: Staphylococcus
May occur singly, in pairs, or clusters,
this arrangement is due to tendency of
the organism to divide in different
planes.

16. Clinically important species of staphylococci
1.- Staphylococcus aureus
2.- Staphylococcus epidermidis
3.- Staphylococcus saprophyticus

17. Clinically important species of staphylococci
1.- Staphylococcus aureus (Coagulase +)
2.- Staphylococcus epidermidis
3.- Staphylococcus saprophyticus

18. Clinically important species of staphylococci
S. Aureus classically has a golden or
yellow pigmentation, but many clinical
isolates have a creamy or white pigmentation.

19. Morphology and Physiology
1.- Gram positive cocci, usually arranged in
clusters.
2.- Non-motile, non-sporeforming.
3.- Grow over a wide temperature range
(10-42° C), optimum of 37° C
4.- Aerobic and facultatively anaerobic.
5.- Grow on simple media
6.- Catalase positive.

20. Morphology and Physiology
Gram positive cocci which may lose the ability to retain their gram positive staining characteristics with age.
Capsule: a loose – fitting, polysaccharide layer ( slime layer) is only ocasionally found on staphylococci cultured in vitro.
Eleven capsular serotypes have been indentified in S. aureus, with serotypes 5 and 7 associated with the mayority of infections.
Half of the cell wall by weight is peptidoglycan, a feature common to G+.

21. Morphology and Physiology
The peptidoglycan consists of layers of glycan chains built with 10 to 12 alternting subunits N- acetylmuramic acid and
N- acetylglucosamine.
The peptidoglycan has endotoxin – like activity, stimulating the production of endogenous pyrogens, activation of complement and the production of IL- 1 from monocytes.

22. Morphology and Physiology
Teichoic Acids are species – specific, ribitol teichoic acid with N- acetylglucosamine residues (polysaccharide A) is present in
S. aureus.
Glycerol teichoic acid with glucosyl residues
(polysaccharide B) is present in S. epidermidis.
The outer surface of most strains of S. aureus
contains clumping factor ( bound coagulase)

23. Characteristics of Staphylococcus aureus
1.- Colonial morphology: Colonies are grey
to golden yellow and produces hemolysins
(beta hemolysis on Blood Agar).
2.- Enzymes:
a) Coagulase, which acts on plasma to
form a clot.
b) Deoxyribonuclease (DNAase)
3.- Protein A, cell-wall antigen
4.- Halophilic (tolerate high concentrations of salt)
and ferments mannitol

25. Epidemiology 1.- Reservoir: Nasal carriage (30-50% of healthy
adults), fecal carriage (20%), skin carriage in
5-20% of healthy individuals.
2.- Transmission:
a) Via droplets (sneezing) and skin scales
(hands)
b) Direct contamination of surgical wounds
c) Contaminated foods: Ham, canned meats,
custard pastries, and potato salad.

26. Epidemiology Major defenses against S. aureus
C3b
Activated by Staph cell wall fragments.
Opsonizes the bacteria.
Enhances phagocytosis.
1) Chemotaxis – attracts neutrophils.
2)Neutrophils – engulf the bacteria.
3) Intracellular killing by O2 radicals.

27. Epidemiology Conditions predispose to Staph infections
1) C3 hypercatabolism
2) Chemotherapy–induced neutropenia
3) Cyclic neutropenia
4) Chronic granulomatous disease (reduced
H2O2 production)
5) “Lazy leukocyte” (chemotaxis deficiency)

28. 3.- Predisposing Factors:
a) Skin trauma: Break or surgery, surgical.
packing foreign bodies; e.g. Tampons.
b) Neutropenia: < 500/μL Cystic fibrosis.
c) IV drug abuse.
d) Chronic granulomatous disease.

29. E.- Virulence Factors: 1) Coagulase: convert fibrinogen to a
fibrin deposition which interferes with
phagocytosis and increases the invasion of
tissue.
2) Hemolysins and Leucocidin: cytolytic exotoxin
a) α-Toxin: lyses erythrocytes and damage
platelets (pore-forming toxin in
cell membrane)
b) β-Toxin: degrades sphingomyelin and is
toxic for erythrocytes.
c) Leucocidin: lyses WBC.

30. 3) Protein A: inhibit phagocytosis, binds Fc of
IgG (prevent Complement activation).
4) Exfoliatins: causes desquamation of the
skin (Scalded skin syndrome), formation
of bullae.

31. 5) Toxic shock syndrome toxin(TSST-1):
desquamation of skin, shock.
Superantigen: activates large numbers of
CD4 T cells with induction of cytokines
production.
6) Staphylokinase: fibrinolysis
7) Hyaluronidase: dissolves hyaline
8) Lipase: solubilize lipids
9) EnteroToxins: A-E, soluble, heat stable
at °C for 10min; resistant GI enzymes,
acts 2-6 h, vomiting.

32. F.- Clinical Manifestations:
1) Folliculitis, Furuncles, Carbuncles,
Abscess.
Mechanism: Coagulase, cytolitic exotoxins.

33. Suppuration (pus production) is a hallmark of these
Infections.

34. 2) Impetigo: Erythematous papules to bullae.
Mechanism: Coagulase, exfoliatins
3) Staphylococcal Scalded Skin
Syndrome(SSSS)
Mechanism: Exfoliatins
*Ritter’s disease: Infants, bullous exfoliative
dermatitis. From localized perioral erythema
to entire body (2 days).
*Bullous impetigo.
Negative Nikolsky’s sign. Erythema limited to
localized blisters (contains bacteria).

39. 4) Staphylococcal Food Poisoning:
Mechanism: Preformed Enterotoxin A-E
Onset is abrupt and rapid (4 h). Severe vomiting,
diarrhea, and abdominal pain or nausea.
Sweating and headache may occur, but not fever.
Watery, non-bloody diarrhea.
5) Toxic Shock Syndrome: Mechanism: TSST-1
Localized growth of toxigenic strains in vagina
or wound. Start abruptly, fever, hypotension,
and diffuse macular erythematous rash. Multiple
organs and systems are involved, entire body skin
desquamates.

42. 6) Bacteremia and Endocarditis:
Mechanism: Cytolytic toxins, Fibrin-platele mesh.
Nosocomial use of contaminated intravascular
catheter or IV drug abusers.
Nonspecific influenza-like symptoms, disruption
of cardiac output and septic embolization.
7) Pneumonia and Empyema:
Mechanism: Cytotoxins and enzymes
Aspiration or hematogenous pneumonia:
Patchy infiltrates with consolidation or abscesses.

44. 8) Osteomyelitis and Septic Arthritis:
Hematogenous dissemination or secondary
infection from trauma.
In adults: Vertebral. Intense back pain with
Fever. Brodie’s abscess.
In children: Metaphyseal area of long bones.
Localized pain, fever.
Septic arthritis: Young children and adults
who are receiving intraarticular injections or
have abnormal joints. Painful, erythematous
joints, purulent exudates(shoulder, knee, hip).

46. Laboratory diagnosis 1.- Clinical specimen: Scrapes the base of
the abscess with a swabs.
Gram stain: Gram (+) cocci in clusters
2.- Culture: Blood Agar, Mannitol Salt Agar
Identification: Coagulase (+), heat-stable
nuclease (+), and mannitol fermentation
On blood agar S. aureus produces beta hemolysis.
Other Staph. species produce alpha or gamma
hemolysis.

47. Laboratory diagnosis
2.- Mannitol salts agar (MSA) – high salt(7.5) inhibits the grow most ohtrer organisms, S. aureus ferments mannitol,
the acid produce turns the colonies yellow and S. epidermidis does not.

48. Laboratory diagnosis
2.- Coagulase (+).
2.- Catalasa (+).

49. Laboratory diagnosis 2.- Bacitracina (+). 2.- Novobiocin
S. epidermidis is sensitive
S. sprophyticus is resistant
2.- Bacitracina (+).

50. S. Epidermidis
1.- Endocarditis.
2.- Catheter and shunt infections.
3.- Prosthetic Joint Infections.
Urinary Tract Infections.

51. TREATMENT:
1.- Methicillin (Nafcillin), Mupirocin to reduce
nasal colonization.
2.- Vancomycin and Fusidic acid.

52. Streptococcus pyogenes
Streptococcal toxic shock-like syndrome. (STSS)
Skin or wound infection develop into blood stream infection, produce Spe which cause fever, rash and shock (death rate 30%)
Scarlet fever
Toxin released from “strep throat” or impetigo

53. Streptococcus pyogenes Impetigo - epidermis
Erysipelas - dermal lymphatics
Cellulitis - subcutaneous fat layer
Necrotizing fasciitis (flesh-eating
bacterium)
Pyogenic exotoxin (Spe) – super Ag
Dnase A-D