In this lecture, I talked about everything concerning bacterial skin infection and its management from dermatological aspect.

1. Bacterial skin
infection
Jaber Manasia
5th year medical student
Mutah University-Jordan
Jaber.manasia@gmail.com

2. Bacterial Skin infections
Intact
skin is one of the body’s defences
against infection
Normal flora (resident organisms) exist on
the skin
Normal flora become pathogenic when
transported to alternate locations
Break in the normal skin barrier
Uncomplicated skin infections usually
involve 1 or 2 pathogens
Predominant organisms for skin infection
are Staphylococcus and Streptococcus spp
2

3. Normal Skin Flora
Gram Positive
 Staphylococcus
 Micrococcus
 Coryneforms
- Corynebacterium
- Propionibacteria
- Dermobacter
- Brevibacterium

Gram Negative
 Acinetobacter

3

4. A. Staphylococcus Aureus &
Streptococcal Infections



S. aureus does not normally reside on
the skin, but may be present transiently,
inoculated from colonized sites such as
the nares (30%), also axillae & vagina.
Colonization is usually intermittent; 10 to
20% of individuals have persistent
colonization
Frequent hand washing reduces the risk
of person-to-person transmission of
cutaneous pathogens.
4

5. 






Folliculitis
Pseudofolliculitis
Boils
Carbuncles
Impetigo
Infected eczema
Ecthyma
5

6. Folliculitis
•
Folliculitis is a superficial infection of the hair
follicles characterized by erythematous,
follicular-based papules and pustules.
S. aureus is the usual pathogen, although
exposure to Pseudomonas aeruginosa in hot
tubs or swimming pools can lead to folliculitis.
usually in scalp of children
also in beard, axilla, extremities, buttocks

Causes:

Bacteria (staph.)
Yeasts (pityrosporum)
Chemical or physical injury
•
•
•


6

7. Hot tubs Folliculitis
Folliculitis
7

8. DDx:
Pseudofolliculitis
oTreatment:
Mild
folliculitis can be treated with a
topical antibacterial agent, but if it is
extensive a systemic antibiotic may be
required.
8

9. Pseudofolliculitis:
Also called “sycosis barbae”.
Deeper folliculitis of the hair follicles of the beard area in
males due to shaving.
Often the lesions are sterile & poorly respond to antibiotics.
9

10. 10

11. Furuncle ( Boils )
•
It is an acute, necrotic infection/abscess of a hair
follicle (usually vellus).
•
causative agent: Staphylococcus aureus
firm, red and tender papule that becomes painful
and fluctuant pustule
developed from preceding folliculitis
deep seated
occur in areas that are subject to friction and
perspiration and contain hair follicles (vellus)
(neck, face, axillae, buttocks)
•
•
•
•
11

12. 






Precipitating factors:
Poor hygiene
Stress
DM
It may recur at intervals for no apparent cause.
Such patients are carriers to the staph in the nose,
axillae & groins between the attacks.
Carriers may be treated with topical antibacterial
applied to nostrils.
They may also be helped by an antibacterial bath
additives, & a prolonged course of flucloxacillin
12

13. Furuncle

Furuncle: S.
aureus Soft-tissue
swelling of the
forehead with
central abscess
formation, nearing
rupture.
13

14. 14

15. Carbuncle
•
•
•
•
•
•
•
causative agent: Staphylococcus aureus
extend into the subcutaneous fat in areas
covered by thick inelastic skin
more severe and painful than furuncles
multiple pustules
with fever and malaise
usually located at the nape, neck, back and
thigh
blood stream invasion may occur usually as a
result of manipulation causing osteomyelitis,
endocarditis or other metastatic foci
15

16. Carbuncle
•
Carbuncle: S.
aureus A very large,
inflammatory plaque
studded with
pustules, draining
pus, on the nape of
the neck. Infection
extends down to the
fascia and has
formed from a
confluence of many
furuncles.
16

17. 17

18. Treatment:
Moist heat, compresses
Dicloxacillin, Clindamycin, Erythromycin
Bed rest
Immobilize involved area
Hand washing
Need systemic flucloxacillin
Incision of abscess
18

19. Impetigo



Worldwide distribution
More frequent among economically
disadvantaged children in tropical or
subtropical regions
Also prevalent in northern climates in
summer months
19

20. Impetigo





Peak incidence aged 2-5 years
Older children and adults also afflicted
M=F
All races susceptible
Nearly always caused by B-haemolytic
streptococci and / or S. aureus
20

21. Impetigo
•
•
•
•
•
Contagious Superficial infection of the epidermis
Discrete purulent lesions
Occurs on exposed areas, well localised,
frequently multiple, bullous or non bullous in
appearance initially→characteristic thick yellow
brown crusts
Deeply ulcerated form (extend into the dermis ) =
ecthyma
Systemic symptoms usually absent
21

22. Differential Diagnosis for impetigo & ecthyma
 Erosion ± Crust/Scale-Crust
Excoriation, perioral dermatitis, seborrheic dermatitis, allergic
contact dermatitis, herpes simplex, epidermal
dermatophytosis, scabies.
 Intact Bulla(e)
Allergic contact dermatitis, insect bites, thermal burns, herpes
simplex, herpes zoster, bullous pemphigoid, porphyria
cutanea tarda (PCT) (dorsa of hands), pseudo-porphyria.
 Ulcer ± Crust/Scale-Crust
Chronic herpetic ulcers, excoriated insect bites, neurotic
excoriations, cutaneous diphtheria, PCT, venous (stasis) and
atherosclerotic ulcers (legs).
22

23. 


Non-bullous impetigo is caused by
S.aureus,
streptococci, or both organisms together.
In the nonbullous form the initial lesion is a
small pustule which ruptures to leave an
extending area of exudation and crusting.
The crusts eventually separate to leave
areas of erythema, which fade without
scarring.
23

24. Non bullous Impetigo

Crusted
erythematous
erosions becoming
confluent on the
nose, cheek, lips,
and chin in a child
with nasal carriage
of S. aureus and
mild facial eczema
24

25. 25

26. 26

27. 27

28. Bullous Impetigo
Scattered, discrete,
intact thin-walled
blisters on the thigh
of a child;
 Caused by strains of
S. aureus that
produce exotoxin
causing cleavage in
the superficial skin
layer

28

29. Impetigo: Treatment

topical & systemic antibiotics.
flucloxacillin or 1st gen cephalosporins are
preferred (eg cephalexin, cephradine)
29

30. Staph Scalded Skin Syndome ((lyell’s
disease):
SSSS


Is a toxin mediated epidermolytic
disease characterized initially by painful
tender erythematous skin followed by
widespread detachment of the
superficial layer of the skin
It occurs mainly in newborns and infants
<2 years, and is rare in adults.
30

31. 
Etiology
Staph aureus phage group II (types 71 and
55) which produce exfoliatin toxins that
disseminates systemically.
The site of infection and production of the
toxins is remote (Not in the skin). (purulent
conjunctivitis, otitis media, omphalitis).
31

32. •
Course and prognosis
– With adequate antibiotic treatment the
superficially denuded skin heals in 3-5 days
with no scarring.
– Without therapy, death occurs due to fluid
and electrolyte loss and Sepsis
– Treatment:
– Hospitalization with IV fluid replacement and
systemic antibiotics ( Flucloxacillin or 1st
generation cephalosporins)
32

33. SSSS
•
Staphylococcal
scalded-skin
syndrome In this
infant, painful, tender,
diffuse erythema was
followed by
generalized epidermal
sloughing and
erosions. S. aureus
had colonized the
nares with perioral
impetigo, the site of
exotoxin production.
33

34. 34

35. Ecthyma





lesion of neglect—develops in
excoriations; insect bites; minor trauma
in diabetics, elderly patients, soldiers,
and alcoholics. ( more common in
debiliated patients ).
Caused by strep.pyogenicus & staph
Usually on upper posterior thighs or
buttocks
Vesiculopustule -erosion-ulcer covered
by a crust
Treatment (topical or Oral Abx)
35

36. Ecthyma


A large,
circumscribed
chronic ulcer with
surrounding
erythema in the
pretibial region
Heals with scar
36

37. DDx:
Impetigo
Cellulitis
leshmaniasis
37

38. 38

39. Infected eczema :
Eczema with exudates, crusts & inflammation.
The cause is due to persistent scratching & using
topical steroids.
Cause: staph & strept.
Treatment: weaker topical steroids & topical
antibiotics, systemic antibiotics if necessary.
Commonly in atopic eczema.
39

40. 40

41. Erysipelas
•
•
•
•
•
Diffuse spreading skin infection without
underlying suppurative foci
Red tender lesions raised above level of
surrounding skin, clear line of demarcation
of involved tissue.
Usually involves lower extremities,
classically butterfly area of face
The patient looks ill & feverish.
Cavernous sinus thrombosis is an
important complication on face
involvement.
41

42. Erysipelas




More common among infants, young
children, and older adults
Almost always caused by B-haemolytic
strep (usually Group A, but can be
caused by serogroups C or G)
Rarely Group B streptococci or S.
aureus be involved, also H.influenzae
type b
An area of broken skin forming portal of
entry, may be found ( ex. Tenea pedis )
42

43. Erysipelas
•
Erysipelas of face:
group A
streptococcus
Painful, well-defined,
shiny, erythematous,
edematous plaques
involving eyelids,
cheeks, and the nose
of an elderly febrile
male. On palpation the
skin is hot and tender.
Portal of entry was
conjunctivitis
43

44. Erysipelas
•
Erysipelas of leg: S.
aureus The lower leg
is red, hot, tender,
and edematous.
Erythematous plaque
is well defined. The
infection is recurrent
with interdigital tinea
pedis as the portal of
entry.
44

45. Erysipelas: Treatment

Penicillin or erythromycin
45

46. 46

47. Cellulitis


Also a diffuse spreading skin infections
without underlying suppurative foci
Extends more deeply than erysipelas to
involve subcutaneous tissues and lacks
distinctive anatomical features as
erysipelas
47

48. Cellulitis


Manifests clinically as erythema,
oedema, heat+/- lymphangitis, peau
d’orange, vesicles, bullae,
petechiae/ecchymoses
Systemic: fever, tachycardia, confusion,
hypotension, leucocytosis
48

49. Cellulitis


Usually due to Beta Hemolytic
streptococcus (commonly Gp A, less
commonly from B, C or G) , also
H.influenzae type b in childern
S. aureus less frequently, often result
from penetrating trauma including
injection sites
49

50. Cellulitis
•
Cellulitis of cheek:
H. influenzae
Erythema and edema
of the cheek of a
young child,
associated with fever
and malaise. H.
influenzae was
isolated on culture of
the nasopharynx
50

51. Cellulitis
•
Cellulitis of arm: S.
aureus Cellulitis with
abscess formation
and blistering
occurred as a
puncture wound
infection in a
construction-site
worker. The lower
arm had to be
debrided down to the
facia and grafted.
51

52. Cellulitis: Investigation &
Management


Blood cultures: low yield unless very severe
Needle aspirations / skin biopsies unnecessary in
typical cases

D.DX: Acute dermatitis, gout, herpes zoster,
acute lipodermatosclerosis

Therapy: targeted at streptococci +/- S. Aureus

Flucloxacillin, clindamycin, erythromycin all
suitable unless resistance common in community
Severely ill pts: flucloxacillin, 1st gen cephalosporin
Penicillin allergy: Clindamycin or vancomycin. In
uncomplicated cases, treat for 5 days


52

53. Necrotizing Fasciitis

a rare subcutaneous infection that tracks along
fascial planes and extends well beyond superficial
signs of infection
53

54. Necrotizing Fasciitis





Caused by: S. pyogenes, S.aureus, and
anaerobic streptococci
Community acquired
Present in the limbs
Underlying cause: diabetes, arteriosclerotic
disease, venous insufficiency
Mortality is high: 50-70% in pts with
hypotension and organ failure
54

55. Necrotizing Fasciitis
55

56. Necrotizing Fasciitis: Diagnosis








Suspect when there is:
Failure to respond to initial antibiotic
therapy
Hard wooden feel of subcutaneous
tissues
Systemic toxicity
Bullous lesions
Skin necrosis or ecchymosis
Appearance of tissue at operation,
samples for culture best obtained from
deep tissues
Blood culture results
56

57. Necrotizing fasciitis: Treatment




Surgical intervention: major therapeutic
modality
Usually returns 24-36 hrs after first
debridement, daily thereafter till no need
for further debridement
Aggressive fluid administration
Antimicrobial therapy until operative
procedures no longer needed, obvious
clinical improvement and fever absent for
48-72 hours
57

58. Scarlet Fever
Scarlet fever (SF) is an acute infection of the tonsils, skin, or other
sites by an exotoxin-producing strain of Streptococcus
pyogenes, associated with a characteristic toxigenic
exanthem.
Epidemiology and Etiology
 Age of Onset
Children.
 Incidence
Much less than in the past.
 Etiology
Usually group A -hemolytic S. pyogenes (GAS). Uncommonly
S. aureus.
58

59. History
• Incubation Period
Rash appears 1 to 3 days after onset of
infection.
• Exposure
Household member(s) may be a
streptococcal carrier
• Site of Infection
Pharyngitis; tonsillitis. Infected surgical or
other wound. Impetiginous skin lesion.
59

60. Physical Examination / Skin Lesions
exanthem Finely punctated erythema
has become confluent
(scarlatiniform);
petechiae can occur and have a
linear configuration within the
exanthem in body folds (Pastia's
line).
Desquamation: Exanthem fades
within 4 to 5 days and is followed
by browny desquamation on the
body and extremities and by
sheetlike exfoliation on the palms
and soles
60

61. Physical Examination / Mucous Membranes

white and red strawberry
tongue Bright red tongue
with prominent papillae on
the fifth day after onset of
group A streptococcal
pharyngitis in a child. The
white patches at the back
of the tongue represent
residuals of the initial white
strawberry tongue.
61

62. Management

Symptomatic Therapy
Aspirin or acetaminophen for fever and/or pain.

Systemic Antimicrobial Therapy
Penicillin is the drug of choice because of its
efficacy in prevention of rheumatic fever. Goal is to
eradicate throat carriage.
For penicillin-allergic patients:
Erythromycin
Azithromycin
Clarithromycin

Follow-Up
Reculture of throat recommended for individuals with
history of rheumatic fever or if a family member has
history of rheumatic fever.
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