Bacterial skin infections

(Last Updated On: 26 February 2020)

I- Introduction:

  • The majority of bacterial skin infections are caused by cocci Gram: Streptococcus A, golden staph. These infections are self-inoculable and non-immune.
  • They are favoured by local factors (plagues, pre-existing dermatoses, skin maceration…).
  • Staphylococcus infections often reflect chronic personal and/or family contact.
  • The diagnosis of these common skin infections is mostly clinical.
  • Complications are rare but potentially serious, justifying the usual use of general antibiotic therapy.
  • The prevention of recidivism is based on:

– Treatment of entrance doors (intertrigo to dermatophytes in erysipelas..);

– Detection and decontamination of deposits in the event of boils.

II- Skin Infection Control Mechanisms:




Integrity of the corneal layer Renewal of the corneal layer




Skin acidity

Lipid inhibitor (free fatty acids, sphingolipids) Antibiotic peptides secreted by keratinocytes




Humoral Immunity Cellular Immunity


Competition between microorganisms


Substances secreted by microorganisms:

Bacteriolytic enzymes

Surface lipid lipolysis in free fatty acids – Antibiotic, antifungal and bacteriocin

"Occupation" of the land


III- Factors that promote skin infection:

  • Local factors:

Promiscuity and poor hygiene


Skin alteration

Local Corticotherapy

  • General factors:

Congenital or acquired immune deficits

Unbalanced diabetes

General Corticotherapy


  • Finally, the weakening of the host's defenses.

IV- Impetigo:

A- Etiology:

  • Impotigo is a superficial skin infection (under the corneal layer of the epidermis) with group A beta-hemolytic streptococcus and/or golden staph.
  • Autoinoculable and non-immunizing,
  • Especially reaches the child.
  • Contagious with small family epidemics or school-friendly communities.
  • In adults, imptigo almost always shows pre-existing skin lesions.

B- Diagnosis:

  • The child's usual form:
  • The elemental lesion is a superficial, under-horny bubble. Very fragile at a glance
  • Rapidly evolves into an erosion covered with yellowish crusts ("melices" i.e. honey color) with centrifugal extension.
  • Often peripherial start, to broadcast on the face and super limbs.
  • No general signs (especially no fever).
  • Bubble impetigo:

This is the characteristic form of the newborn, especially staphylococcal.

  • LE: Bubbles sometimes large
  • Complication: Staphylococcal epidermolysis syndrome (or SSSS for staphylococcal scalded skin syndrome): Diffuse Erythema and superficial epidermal detachment begin around a sometimes minimal infectious focus (nasal, umbilical or perineal) and  spread rapidly into a febrile picture that can become complicated by dehydration. Nikolski's sign is positive. This is due to a cleavage induced by a staphylococcal exfoliating toxin (exfoliatin)
  • Differential diagnosis: toxic epidermal necrolysis
  • Ecthyma:

It is a digging form of impetigo usually located in the lower limbs.

  • Impetiginization:

This is the appearance on a dermatosis (the most svt pruriginous) of pustules or melicer crusts.

C- Positive diagnosis:

It's clinical.

  • Bacteriology: is not useful in common practice. The germs involved are either streptococci, or golden staph, or the combination of the two.
  • Histology, rarely necessary, – subcornated pustule.

D- Evolution:

  • It is quickly favorable.
  • Very rarely impetigo can be the gateway to a severe general streptococcus or staph infection.
  • The exceptional risk of post-streptococcal glomerutonephritis warranted the search for proteinuria 3 weeks after the infectious episode.

E- Treatment:

  • Local treatment may suffice in small forms:

– Antiseptics (chlorhexidine);

– Topical antibiotics (fusidic acid…).

  • General antibiotic treatment is most often prescribed.
  • Indication:
  • Numerous injuries (up to 5) and/or several territories,
  • Failure of local TTTs,
  • Aggravating factors (particularly immune deficiency). Cloxacillin, Amoxicillin – Clavulanic Acid, Cephalusin, Pristinamycin, Fusidic Acid.
  • Additional measures:

– School eviction for a few days;

– Treatment of siblings;

V- Boil:

A- Etiology:

  • It is a deep infection of the pilo-sebaceous follicle caused by golden staph.
  • It is favoured by manual porting from staphylococcal deposits.

B- Diagnosis:

  • Boil:

– The beginning is a simple folliculitis, then

– Quickly appears

  • an undurable, red, warm area, centered by a pustule,
  • The sometimes intense pain,
  • adenopathy and fever,

– Within a few days, the bulge is removed from a depressed scar.

– Seat: stt back, shoulders, thighs or buttocks (role of friction).

– Irritation or manipulation of the boil at the outbreak of infection.

  • Anthrax

It is an agglomerate of boils, producing a hyperalgic inflammatory closet dotted with pustules. Its elective seat is the neck or upper back.

  • Furonculosis:

It is the repetition of episodes of boils, with passage to chronicity over periods of several months.

It should have a contributing factor and a staphylococcal (s) outbreak sought:

– Narinaire

– Retroatrial,

– Interfessier,

– Scars of old boils.

C- Positive diagnosis:

  • It is primarily clinical.
  • Search for Staph in the lodges in case of furonculosis.

D- Differential diagnosis:

  • Superficial folliculitis:

Papulo-pustules centered by a hair (taking the name sycosis for the damage to the beard).

It is most often a golden staph infection, but other organisms may be involved (particularly yeasts).

  • Suppurated hidrosafenite:

Inflammatory, recurrent and debilitating skin follicular disease that usually appears after puberty with painful and inflammatory lesions deep in the body areas carrying apocrine glands , most often the axillary, inguinal and anogenital regions.

  • Acne:

Confusion is common, although acne is distinguished from boils by its lesionic polymorphism (comedons, cysts, papulo-pustules).

E- Evolution:

The most common complication is the transition to chronicity (or chronic furonculosis). Sepsis and other visceral golden staph complications remain very rare.

Malignant staphylococcia of the face with cavernous sinus thrombophlebitis is exceptional. It is feared in the presence of a manipulated centrofacial boil becoming hyperalgic with a marked infectious syndrome and an important centro-facial edema.

F- Treatment:

  • Isolated boil:

– 1st flare-up without signs of gravity, simple treatment:


Don't manipulate the lesions,

Local antiseptic.

– Centrofacial injury, extension of lesion and/or onset of fever inAntibitherapy

(oral penicillin M, pristinamycin, fusidic acid).

  • Furonculosis:

– Strict hygiene;

– Per bone antibiotic therapy;

– Prolonged local treatment of lodges with antiseptics or antibiotics; – The collection and treatment of lodgings for the whole family.

VI- Erysipelas:

A- Definition:

Most svt-streptococal acute dermo-hypodermitis A

B- Epidemiology:

Location to the leg in more than 80% of cases

Frequent and the first dgc to evoke in front of a large red leg acute and febrile

Average age of onset around 60 years.

C- Factors favouring:

CVI and/or lymphatic.


Intertrigo inter-toe front door, leg ulcer

Generals (obesity).

D- Clinic:

Usual picture of "big febrile acute red leg" unilateral

  • Start is brutal
  • SG: high fever (39 to 40 degrees Celsius) – chills,
  • Inflammatory skin placard:



Circumscribed, A peripheral bulge is rarely observed

Painful to palpation.

superficial bubble peelings or purpura,

  • Homolateral inflammatory ADPs are frequently associated.
  • A trail of homolateral lymphangitis is present in a quarter of cases.

E- A front door:

Clinically detectable in 2/3 of cases.

Minimal: inter-toe intertrigo, puncture, traumatic erosion

Obvious (leg ulcer).

F- No further examination is required.

Hyperleucocytosis at PNN is common

Biological inflammatory syndrome is important (CRP often – 100 mg/L).

Hemocultures are of low profitability;

G- Evolution:

Favorable in 8 to 10 days on antibiotic treatment.

Apyrexia in 48 to 72 hours;

Local signs in one week.

H- Less typical tables:

1- Atypical Erysipele:

  • Subacute forms, where fever and hyperleucocytosis are moderate or absent. Dgc mentioned before:

The clinical traits of the inflammatory skin closet

Regression with anti-treptococcal antibiotic therapy.

2- Erysipele in diabetics:

  • Classic shape, or
  • Subacute dermo-hypodermitis, torpid, foot and lower leg third:

– Skin inflammation appears deeper,

– Placard less well limited,

– Moderate pain,

– Fever sometimes absent.

  • The front door is often a plantar perforating pain.
  • The germs involved: Staphylococcus aureus, Pseudomonas aeruginosa, anaerobic.
  • Systematic results: underlying osteitis/decompensation of diabetes.
  • Evolution is less favourable
  • If a bad response to anti-infective surgical gesture treatment.

3- Dermo-infectious hypodermites of immunosuppressed:

Clinical presentation is often misleading (few inflammatory signs) to underestimate the severity and in particular the possibility of deep necrosis.

4- Other acute bacterial dermo-hypodermitis:

  • An animal-primed pasteurellosis (cat, dog);
  • Pork mullt: erythematous wound with an oedematic rim, extremely painful after being wounded by a pig, sheep, fish bones or crustacean bone.

I- Treatment:

  • If hospitalization: penicillin G IV at least until apyrexia then relay per bone (penicillin V, amoxicillin). Total time: 10 to 20 days.
  • If maintaining at home: amoxicillin per bone for about 15 days.
  • Pristinamycin (or clindamycin) in case of allergy to lactamines.
  • Preventing recidivism:

– Processing a front door

– Support for favourable factors

VII- Dermo-hypodermitis necrotizing:

"necrotizing fasciitis," gas gangrene, necrotizing dermo-hypodermitis,

  • Signs of sepsis:

– Fever – 39oC or hypothermia

– AEG / collapsus

  • Local signs:

– dr – or hypoesthesia

– Diffuse induration

– Cyanosis / necrosis

– A crackle

  • The germs responsible: streptococcus, golden staph, Gram-negative bacillus, anaerobics.
  • Surgical emergency.

Professor AS. CHEHAD

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