skin and soft tissue infections by streptococcus and staphylococcus and its treatment , also covers carriage and its suppression and treatment

1. JAI KUMAR PILLAI
KIMS, BANGALORE
STAPHYLOCOCCAL &
STREPTOCOCCAL INFECTIONS
1

2. Staphylococci
2
 Common inhabitant of the skin
and mucous membranes
 Spherical cells arranged in
irregular clusters
 Gram-positive
 Lack spores and flagella
 May have capsules
 31 species

3. STAPHYLOCOCCI
 Classified into 2 major groups
 Coagulase-pos & Coagulase-
neg

 Staph aureus S. epidermidis
S. hominis
S. capitis
S.
saprophyticus
3

4. SPECIES HABITAT DISEASES
S.epidermidis Skin & mucous
membrane
Endocarditis,
UTI
S.hominis Apocrine sweat
glands
Wound
infections
S.capitis Scalp, face &
external ear
Wound
infections
S.saprophyticus Intestine,
vagina
UTI
CONS in nosocomial infections
4

5. STAPHYLOCOCCUS AUREUS
 It is distinguished from other species of
staph by a +ve test for coagulase
 Important causes of skin infections &
serious systemic diseases.
 The wide use of antibiotics results in
selective survival of resistant strains.
5

6. CARRIAGE
 Anterior nares -35%
 Perineum -20%
 Axillae - 5-10%
 Toe webs – 5-10%
 In neonates- nose and
umblical stump.
 High rates of nasal carriage in
atopic eczema
 Intestinal carriage common in
hospitalized patients6

7. Supression of carriage
 Nasal carriage: physiological and is not itself an
indication for Rx.
 Indications: where staphylococcal dispersal a
significant hazard to others( operating theater
and neonatal nursery staff)
 Wegeners granulomatosisrelapse more
frequently in those with nasal carriage of
S.aureus.
7

8. Components of Staph.aureus
resposible for binding
 Techoic acid
 Lipotechoic acid
 Fibronectin-binding proteins
 Type 5 and 8 capsular
polysaccharides
8

9. Biologically active substances
produced by s.aureus
Toxins
 Exfoliative or epidermolytic toxin(ET-A & ET-B)
 Toxic shock syndrome toxin(TSST-1)
 Staphylococcal erythrogenic toxin (staph
scarlatina)
9

10. Enzymes
 Coagulase – coagulates plasma and blood;
diagnostic
 Hyaluronidase – digests connective tissue
 Staphylokinase – digests blood clots
 DNAase – digests DNA
 Lipases – digest oils; enhances colonization on
skin
10

11. 11

12. Diseases caused by Staph
Direct infection of
skin and adjacent
tissue
Secondary infection Due to effect of
toxin
Impetigo Eczema SSSS
Ecthyma Infestations TSS
Folliculitis Ulcers Staphylococcal
scarlitina
Furunculosis Recurrent
perineal erythema
Carbuncle
Sycosis
Cellulitis
12

13. Resistance to Staph infection
 Main host defense- ingestion & killing by
phagocytes
 in pts with uncontrolled DM, renal
insufficiency, malignancies, alcoholism ,
corticosteroid therapy
 AIDS folliculitis, facial impetigo are common
 Chediak higashi syn & chronic granulomatous
diseasestrong predisposition to Staph. Infections
 Wiskott-aldrich syn  recurrent pyoderma &
13

14. Antibiotic resistance
 Due to application of antibiotics to skin
 Gentamycin resistance-could be transferred
between strains of S.aureus
 MRSAdue to gene mecAencodes for altered
penicillin binding protein (PBP2a)
14

15. Streptococci
15
 Gram-positive
spherical/ovoid cocci
arranged in long chains
 Non-spore-forming,
nonmotile
 Can form capsules and
slime layers
 Facultative anaerobes
 Do not form catalase
 Most parasitic forms are
fastidious and require
enriched media
 Small, non-pigmented

16. Streptococci
16
 Lancefield classification
system based on cell
wall Ag – 18 groups (A,
B, C,…R)
 Another classification
system is based on
hemolysis reactions
b-hemolysis – A, B, C,
G and some D strains
a – hemolysis – S.
pneumoniae and others
collectively called
viridans

17. Major species of streptococci
Species Lancefiel
d group
Hemolysi
s
Habitat Diseases
S.pyogen
es
A Beta Throat Throat inf
S.agalacti
ae
B Beta Vagina Neonatal
inf
Enterococ
cus
Faecalis
D Alpha
,beta
Intestine Endocardi
tis,
UTI
S.sanguis H alpha Oral
cavity
Endocardi
tis
S.mutans none none Oral
cavity
Dental
caries17

18. Virulence Factors of b-Hemolytic
S. Pyogenes
18
Produces surface
antigens:
 C-carbohydrates –
protect against
lysozyme
 Fimbriae – adherence
 M-protein – contributes
to resistance to
phagocytosis
 Hyaluronic acid
capsule – provokes no
immune response
 C5a peptidase hinders

19. Carriage
 It is carried in throat by about 10% of the normal
population.
 Transient skin carriage found in 0.5 to 1%
 Carriage rates are higher after clinical infection
 Strep.pyogenes is broadly divided into throat and skin
serotypes.
 Rheumatic fever – complication of strept. pharyngitis19

20. Diseases caused by Strep.
Pyogenes
Superficial
pyoderms
Invasive
infections
Toxin
associated
syndrome
Provoked by
strept
Impetigo Acute
Lymphangiti
s
Scarlet fever Guttate
psoriasis
Ecthyma Erysipelas Streptococc
al TSS
Kawasaki
dis
Blistering
distal
dactylitis
Cellulitis Scleredema
of bushke
Perianal
Cellulitis
Necrotizing
fascitis
Vulvovaginiti
s
septicemia
20

21. IMPETIGO
 ‘To attack’
 DEF: It is a contagious
superficial pyogenic
infection of the skin.
 Bullous and non- bullous
forms
 Non bullous impetigo aka
‘impetigo contagiosa of
Tilbury fox’21

22.  Conditions disturbing integrity of epidermis
 Insect bites
 Dermatophytoses
 Herpes simplex
 Varicella
 Abrasions , lacerations
 Provide a portal of entry of impetiginization
22

23. Cutaneous lesions
Non-bullous impetigo
A transient vesicle/pustuleevolves into honey
coloured crusted plaque
Gradual, irregular,peripheral extension occurs
without central clearing
Regional lymphadenopathy present
23

24. Bullous Impetigo
 More common in newborns and
infants
 Rapid progression of vesicles to
flaccid bullae
 Bullae initially contains clear
fluiddark yellow & turbid
 Central healing & peripheral
extension give rise to circinate
lesions
 Bullous varicella represents24

25.  Bullous impetigo may
occur in neonates
forming widespread
bullae called as
pemphigus
neonatorum
 Thorn pricks,
arthropod bites, minor
abrasions sec
infectionwhich
forms crusting it is
25

26. FEATURES Bullous impetigo Non bullous impetigo
Causative organism Staph.aureus Stap.aureus and/or strep
pyogenes
Age Neonates and infants but
can occur at any age
Commonly in preschool
and primary school
children
Bullae Thick walled ; lasts for 2 to
3 days
Thin walled and transient
Base Very little or no erythema.
Forms varnish colored
crusts
Erythematous .
Forms honey colored
crusts
Extension May extend peripherally
with central clearing
May extend peripherally
without central clearing
Regioinal adenitis rare common
Complications rare Cellulitis, post
streptococcal
AGN(S.pyogenes M-type
49)26

27. ECTHYMA
 Caused by both staphylococci and streptococci
 It is a pyogenic infection of skin characterized by the
formation of adherent crusts, beneath which ulceration
occurs.
 It is a deeper variant of impetigo
 Poor hygiene, malnutrition and repeated trauma are
predisposing factors27

28. Clinical features of ecthyma
 Common on buttocks, thighs and
legs.
 Small bullae or pustules on an
erythematous base are soon
surmounted by a hard crust of dried
exudate which appears in chocolate
color.
 Base becomes indurated
 On removal of the crust a purulent
irregular ulcer is present.
 Healing occurs after few weeks with
scarring.
28

29. Impetigo
(staph.aureus and
strep.pyogenes)
Ecthyma
(strep pyogenes)
superficial deep
Honey or varnish color crusting Chocolate color crusting
Crust is loosely adherent Crust is tightly adherent
No ulcer on removal of crust Ulcer on removal of crust
Common site: face Common site: lower limbs
Heals without scarring Heals with scarring
29

30. CELLULITIS
 It is an infection of dermis &
subcutaneous fat
 Caused mainly
strept.pyogenes and
staph.aureus
 Factors that increase the
chance of cellulitis
 Local breach of skin barrier
function
 AD, psoriasis, trauma, toe web
intertrigo, arthropod bites,
surgical procedures
 Immunocompromised ( AIDS,30

31. Clinical features of cellulitis
 Erythema, warmth , swelling
and pain or tenderness are
constant features.
 Borders are indistinct
 Severe cellulitis may show
bullae and can progress to
dermal necrosis and
uncommonly to fascitis or
myositis.31

32. ERYSIPELAS (St.Anthonys’s fire)
 It is a bacterial infection, of the
dermis and upper
subcutaneous tissue, its
hallmark is a well-defined,
raised edge reflecting the more
superficial involvement.
 Caused by streptococcus group
A (also G, B and C)
 Rarely by staph.aureus.
32

33. Clinical features
 The edge of the lesion is well
demarcated and raised.
 Skin becomes brawny ,
edematous , indurated (peau d’
orange appearance ) and
spreads peripherally
 Blistering is common , and there
may be superficial haemorrhage
33

34.  Classical erysipelas starts
abruptly and systemic
symptoms may be acute
and severe, but the
response to the treatment is
more rapid
 Lymphangitis and
lymphadenopathy are
frequent.
 In recurrent cases there
may be defect in the
34

35. erysipelas cellulitis
Caused by strep.pyogenes Caused by strep.pyogenes and rarely
by staph.aureus.
Involves upper subcutaneous tissue
and lymphatic vessels
Invoves deeper subcutaneous tissue
History antecedent throat infection An intertrigo or deep fissures( definite
portal of entry)
Common site: face with bridge of nose
and cheeks
Common site: legs
Well defined margins( peau d orange
appearnace)
Indistinct margins
vesicle or bulla formation. bulla formation in severe
Self limiting If untreated necrosis can supervene
35

36. Superficial Folliculitis (Bockhart
impetigo)
 It is an infection of follicular
ostium with S.areus.
 Common in scalps of children
& in beard area
 Heals without scar formation
 Use of topical steroids, is a
predisposing factor.
36

37. Clinical features
 Presents as dome shaped ,
yellow pustule, sometimes
with a narrow, red areola.
 Pustules develop in crops
and may heal within 7-10
days
 Chronic folliculitis of the legs
has been described mainly
in young adult males37

38. Pseudofolliculitis
 Penetration into skin ,
sharp tips of shaved hairs
 Hair may curve
backwards, to penetrate
adjacent skin
Folliculitis keloidalis
 Chronic perifollicular
inflammation- nape of
neck
 Males afetr puberty38

39. Deep Folliculitis (Sycosis)
 ‘small fig’
 It is a subacute or chronic
pyogenic infection involving the
whole depth of hair follicle.
 If the follicles are destroyed with
clinically evident scarring the term
lupoid sycosis is used.
 It occurs mostly in males after
puberty, and commonly involves
the follicle of the beard (sycosis
barbae)
 The infecting organism is
S.aureus.
 Predisposing factors: seborrheic
dermatitis, trauma produced by
39

40. Pathology
 The affected follicle is packed with PMNLs, which inflitrate
its wall.
 Around the follicle there is a chronic granulomatous
infiltrate in which lymphocytes, plasma cells, histiocytes
and foreign-body giant cells are conspicous.
 The sebaceous gland, or the whole follicle , may be
destroyed and replaced by scar tissue.
40

41. Clinical features
 Presents as an oedematous, red,
follicular papule or pustule
centred on a hair.
 The individual papules remain
discrete & if neighbouring follicles
are involved the perifollicular
oedema coalesce to produce
the raised plaques studded with
pustules (ripe fig)
 In lupoid sycosis , the follicles are
destroyed by scarring,
 Granulomatous inflammatory
41

42. Furuncle (boil)
 ‘Petty theft’
 A furuncle is an acute,
usually necrotic , infection
of a hair follicle with
S.aureus.
 Neck, face, axillae &
buttocks
 Predisposing factors:
 Mechanical damage to the
skin( friction of collar and
belt)
 Malnutrition42

43. Pathology
 A furuncle is an abscess of hair
follicle usually of vellus type.
 The perifollicular abscess is
followed by necrosis with
destruction of the follicle.
 Cytotoxin( PVL) produced may
play role in the development of
lesions.
43

44. Clinical features:
 It presents as a hard, tender,
folliculocentric nodule pustular
necrotic healing after
discharge of the necrotic core
violaceous macule
permanent scar.
 Development of necrosis occur
within 2d to 3 weeks
 Single or multiple.
 On the upperlip and
cheekcavernous sinus44

45. Carbuncle
 ‘a small piece of fiery coal’
 Deep infection of a group of
contiguous follicles with
S.aureus, a/w intense
inflammatory changes in the
surrounding and underlying
connective tissues including
the subcutaneous fat.
 Predisposing factors:
 Diabetes
 Malnutrition
 Cardiac failure
 Drug addiction
 Prolonged steroid therapy45

46. Clinical features
 Common sites: nape of the
neck, the shoulders or the hips
and thighs
 Initial stage of
infectionpainful, hard, red,
lump which is dome-shaped
and acutely tender.
 It increases in size for a few
days to reach a diameter of 3-
10cm
 After 5 to 7 days Suppuration
begins and pus is discharged
from multiple follicular orifices.
 Necrosis of the intervening skin
leaves a yellow slough46

47. Botryomycosis
 Purulent chronic, subcutaneous
infection by S.aureus
 Predisposing factors
 Immunosuppresion(HIV)
 Chronic alcoholism
 DM
 Presents as solitary lesion, often in
genital area
 HPE: Splendor-hoeppli phenomenon47

48. Staphylococcal Paronychia
 Predisposition
 Hand trauma
 Chronic moisture
 C/f : skin of proximal &
lateral nail fold are red, hot &
tender
 If untreated leads to abscess
formation
48

49. Staphylococcal whitlow(Felon)
 Purulent infection of bulbous
distal end of finger
 Portal of entry injury or
extension of paronychia
 Finger bulb is red, hot, tender
& edematous
49

50. Hidradenitis suppurativa
 It is a chronic suppurative
inflammatory disease of apocrine
glands and surrounding tissues,
terminating in a sinus formation
and scarring.
 The disease begins after puberty .
 Apocrine poral occlusion
associated with bacterial infection;
commonest S.aureus.
 Predisposing factors: obesity ,
severe acne, wearing tight clothes.
50

51. Clinical features
 Initially there is a tender,
inflammatory firm to soft swelling
of about 1cm
 Abscess is formed which grows
in size and perforates overlying
skin producing multiple sinuses
purulent and seropurulent
discharge.
 It is often associated with cystic51

52. Intertrigo
 It is the term used for
inflammation of the opposed
skin surface.
 Heat , moisture, friction and
sweat retention induces
maceration and
inflammation of these areas.
 Strep.pyogenes is the
commenest offender.
 Chronic bacterial or52

53. Clinical features
 Initially the skin is red and
slightly macerated.
 The folds when seperated, show
erythema of contiguous surfaces,
covered by a macerated horny
layer
 Itching, burning , exudation and
offensive odour are common
symptoms.
 Brevibacteria add to damage by
their proteolytic action which
53

54. Necrotizing fascitis
 This condition usually occurs in
diabetics or those with arterial
insufficiency.
 Strep.pyogenes is the commonest
organism followed by S.aureus
 The infection is associated with
excessive collagenase production
leading to dissolution of
connective tissue.
54

55. Clinical features
 It is a very painful condition and has a high mortality
 Diffuse swelling of an arm or leg, followed by
appearance of a clear bulla that rapidly turns
violaceous.
 extensive induration, dusky central discoloration and
rapidy developing cutaneous necrosis.
 There is rapid progression to frank gangrene and
myonecrosis supervenes with eventual shock and
organ failure.
55

56. Progressive bacterial synergistic
gangrene
 It is a mixed bacterial infection due to synergistic
action of microaerophilic streptococci and S.aureus.
 The disease presents as a tender erthematous
swelling after 1 to 2 weeks after an operation.
 A small superficial ulcer develops and enlarges with a
gangrenous margin surrounded by a zone of purple
erythema blending peripherally with a pink edematous
area.
56

57. Staphylococcal scalded skin syndrome
 It is an exfoliative dermatosis in
which most of the body surface
becomes erythematous and
necrotic superficial epidermis
strips off.
 S.aureus group II phage type 71’
 It occurs mainly in infants and
children under the age of 5 yrs
 Renal failure, malignancy,
immunosuppression or alcohol57

58. Pathology
 Histologically, there is
splitting of the epidermis
at or below granular layer
 A few lymphocytes
surround the superficial
blood vessels.
 The disease is caused by
one or more exfoliative
toxins (A and B) which
cause distruption of
58

59. Clinical features
 The initial event is usually a
localized staph infection.
 A few days later, the patient
develop fever, irritability and
skin tenderness.
 A widespread erythematous
eruption follows, which
progresses rapidly to blister
formation.
 painful erosions appear when
blisters rupture or when
erythematous sheets of skin
59

60.  Mucous membrane other
than lips are usually
spared.
 Condition usually heals in
7 to 14 days.
 Mortality rate is 2 to 3% in
untreated cases
60

61. Toxic shock syndrome
 Mediated by toxin TSST-1 of
S.aureus
 Feverrashdesquamation after
1-3wkscirculatory shockmulti
organ failure
 Staph infection of any
site/severity/age/sex can cause
TSS
 TSST1 belongs to superantigens
family which stimulate T cell
proliferation in non-antigenic
manner
61

62. Clinical features
 The onset is acute with fever
and rash.
 A widespread macular
erythema, sometimes faint, and
clearing within 3days.
 Vomiting and diarrhoea are
common early features
 Then muscle, liver, kidneys CNS
involves
 Marked oedema of hands & feet
 Circulatory shock may be severe
and the mortality rate is 7%
62

63.  Generalized mucous
membrane erythema. Oral,
oesophageal, vaginal and
bladder mucosae may ulcerate.
 Towards 2nd wk pts develop
widespread, itchy,
maculopapular rash
 Desquamtion occurs by 10-2163

64. Scarlet fever (Scarlatina)
 Acute infection caused by strains of
strep.pyogenes
 Producing pyrogenic
toxin(erythrogenic toxin or
erythrotoxin)
 Pathology: The toxin is reponsible
for cutaneous vasodilatation
 a/w oedema and perivascular
cellular infiltrate.64

65. Clinical features
 IP 2 to 5 days
 Fever, anorexia , nausea
and vomiting.
 Acute follicular or
membranous tonsillitis ,
with painful
lymphadenopathy .
 The rash which appears
on the second day, first on
the trunk , is a finely
punctate erythema which
resembles sunburn with
goose pimples.( sand
paper rash)
 It generalizes within a few65

66.  Transverse red streaks in the
skin folds due to capillary
fragility are known as pastia
lines.
 After 7 to 10 days the rash is
succeeded by desquamation.
 The oral mucous membranes
are bright red and there may
be deeper red puncta on the
palate.
 Tongue is heavily coated first
(white strawberry tongue)
and when the epithelium is
shed , the tongue becomes
smooth and dark red ( red
strawberry tongue)
66

67. Other Staph & Strept infections
Blistering distal dactylitis
 Large blister containing
thin seropurulent fluid
forms on distal phalanx
 An URTI is sometimes
present
Toxin mediated perineal
erythema
 After sore throat pts
develop eruption in
perineal area
 Resembles erysipelas67

68. Management of staph and strep skin
infections
 General principles:
 Local hygiene
 Elimination or control of predisposing
factors like diabetes, malnutrition,
steroid therapy, insect bites etc.
 Carrier sites and carriers should be
treated.
 In case of crusted lesions crusts
should be removed
68

69. Methods for reducing carriage
 Long term application of chlorhexidine cream-to
carriage sites
 Use of antiseptics : povidone-iodine
 Intranasal mupirocin
 Haemodialysis pts: oral rifampicin 600mg daily
for 7-10d
 Bacterial interference: nasal inoculation of
S.aureus strain 502A, achieves bacterial
69

70. Topical treatement
 Bacitracin ,polymyxin B , neomycin ,
mupirocin, 2%sodium fusidate are
useful for superificial skin infections.
They should be applied 3 to 4 times a
day.
 1% gentian violet or 1% chlorhexidine
can be used in patients who cannot
70

71. Systemic treatment
 The most common type of resistance is due to
pencillinase production.
 Methicillin , naficillin and isoxazolyl pencillins (cloxacillin
and dicloxacillin) may be used.
 Cloxacillin resistance among S.aureus is rare. Adult
dose: 250-500mg qid for 5-7d
 Erythromycin 30-50mg/kg/d q6h for children; 250-500mg
q6h for adults (if allergic to penicillin)71

72.  Azithromycin 500mg once daily can be tried in adults
 Cephalexin – 500mg twice daily useful for SSTI
 In adults quinolones like ciprofloxacin in a dose of 500mg
twice a day can also be tried.
 MRSA infections- Vancomycin 1gm i/v twice daily
Linezolid 600mg oral twice daily
Quinipristine/dalfopristin
Daptomycin (4mg/kg/d), tigecycline
5th gen cephalosporin- ceftaroline & ceftobiprole
72

73. REFERENCES
 ROOKS 8th edition
 FITZPATRICKS 8th edition
 BOLOGNIA 3rd edition
 IADVL 4th edition
 WOLVERTON 3rd edition
73

74. THANK YOU
74