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BACTERIAL INFECTION

IMPETIGO

INTRODUCTION

  • Contagious superficial Pyogenic infection of the skin.


Two main clinical form are
  • Non – Bullous impetigo ( or Impetigo contagiosa of Tilbury Fox)

Causative organism – Staph. aureus, Streptococcus or both

  • Bullous Impetigo

Causative organism – Mainly Staph disease but rarely can be due to streptococci


Pathology 

Bullous impetigo 

  • Epidermis split just below the granular layer to form large blister


  • Neutrophils migrate through spongiotic epidermis to blisters cavity, which may also contain bacilli


  • Occasionally acanthotic cells may be seen


  • Dermis contains inflammatory infiltrate of Neutrophils and lymphocytes



Non – Bullous impetigo

  • Histology is similar except that blister formation is slight and transient 



Clinical Feature

  • In non-bullous impetigo, the initial lesion is a very thin-walled vesicle on an erythematous base. 
  • The vesicle ruptures so rapidly that it is seldom seen as such.
  • The exuding serum dries to form yellowish brown crusts.
  • The crusts eventually dry and separate to leave erythema, which fades without scarring.
  • The face, especially around the nose and mouth, and the limbs are the sites most commonly affected,



Non-bullous impetigo

  • In bullous impetigo, the bullae are less rapidly ruptured and become much larger;, and persist for 2 or 3 days.
  • After rupture thin, flat, brownish crusts are formed. Central healing and peripheral extension may give rise to circinate lesions.


  • Although the face is often affected, the lesions may occur anywhere.



Bullous impetigo
Treatment

  • Topical:

    Mupirocin or fusidic acid is active against both    organism.
    Washing with soap and water.
  • Oral:

    Antibiotics like Flucloxacillin or Erythromycinin severe cases.
  • Proper education


Complication 

  • Infective complication are uncommon in the absence of systemic disease or malnutrition


  • Cellulitis occasionally follow streptococcal disease


  • Post streptococcal glomerulonephritis 

Specially following S. pyogens infection

  • Scarlet fever, Urticaria and Erythema multiforme



Ecthyma 

Introduction 

Pyogenic infection of the skin characterized by the formation of adherent crusts, beneath which ulceration occur.

Aetiology 

Bacteriological status – Similar to Impetigo

  • Predisposing factors 

Poor hygiene 
Malnutrition 
Minor injuries 
Other skin condition, like scabies
IV drug abusers

Clinical Feature 

  • Small bullae or pustules on an erythematous base


  • Soon surmounted by hard crust of dried exudate, which increase in size by peripheral accretion.


  • The base may become indurated and a red edematous areola is often present.


  • Crust is removed with difficulty , to reveal a purulent irregular scar.




Ecthyema enduratum of Bazin


  • Healing occur after few weeks, with scarring


  • Common sites 

Buttocks, Thighs and Legs


Treatment 

  • Antibiotics' active against both staph. and streptococcus


  • Improve hygiene and nutrition 


  • Topical therapy either with sulconazole or miconazole clears lesions satisfactorily over 1 week.


  • Treatment of underlying disease – e.g.. Scabies



Erythrasma

  • Erythrasma is a mild, chronic, localized superficial infection of the skin caused by bacteria, known as C. minutissimum.


  • Clinical infection may occur at any age but is more common among adults than children.


  • Detected by Wood’s light examination- pink fluorescence


Clinical features

  • Asymptomatic or mild itch.


  • Erythrasma involves the toe clefts more frequently than any other site. 


  • As clinically manifest lesions it occurs most commonly in the groins, axillae and the intergluteal and submammary flexures. 





Treatment

  • Topical azole cream- cotrimazole, miconazole.
  • Topical antibiotics
  • Extensive cases: oral erythromycin

Cellulitis and Erysipelas 

Introduction 

  • Cellulitis is an inflammation of subcutaneous tissue which is usually infective.

  • Erysipelas is a bacterial infection of the dermis and upper subcutaneous tissue
  • Well defined, raised edge, reflecting more superficial (dermal) involvement (clinical hallmark)
  • It can sometime penetrate deep dermis and subcutaneous tissue to form cellulitis.

Bacteriology 

Group A beta hemolytic streptococci most of the time

Other organisms 
Group C or G streptococci
Group B streptococci in new borne
Staph aureus 



Predisposing factors:
DM
Vericose leg ulcer
        Tinea pedis

Clinical Features 


Erythema, heat swelling and pain.
In erysipelas, the edge of the lesion is well-demarcated and raised, but in cellulitis it is diffuse.
Blistering occur in both conditions.
Site
Cellulitis:
Legs
Erysipelas:
Lower extremities 
Face  - may spread to eyelids but orbital complications are rare



Cellulitis



Erysipelas

Dx

  • Specimens for bacteriological examination should be
  • taken from vesicle fluid or eroded or ulcerated surfaces, in addition to blood cultures.

Treatment
  • Antistreptococcal agent:
Phenoxymethylpenicillin
Erythromycin/ciprofloxacin- in case of penicillin sensitivity
          I.V antibiotics- in severe cases.

Folliculitis

Circumscribed infectious process that originate in the hair follicle and is defined by its anatomic features.

Mainly of two types
Superficial 
Located superficially

Deep 
It extend more deeply to produce perifollicular inflammation

Superficial folliculitis 
  • Subacute or chronic inflammation confined to ostium or extend slightly below it
  • Common condition which heals without scarring



Common causes

  • Staphylococcus auerus and coagulase negative staph


Physical 
  • Traumatic epilation
  • Adhesive plaster and dressing


Chemical injury 
  • Contact with mineral oils
  • Exposure to tar products
Sites 

  • Commom in children and common sites being scalp and limbs.


Lesion 

  • Present as small follicular papules or pin head pustules, which are rarely painful


  • Pus culture is sterile most of time and rarely coagulase negative staph can be isolated




Follicular impetigo of Bockhart

  • Variant of superficial folliculitis caused by staph. aureus 

  • Common in childhood age

Treatment 

  • Removal of causative agent in case of physical and chemical factors suspected

  • Mild staphylococcus
Self limiting 
Cleansing and local antiseptic

  • Severe
Topical and systemic antibiotics

  • Recurrent and persistent cases
Prophylaxis against staph in carriage sites


Deep folliculitis

Furuncle
  • A furuncle is an acute, usually necrotic, infection of a hair follicle with S. aureus.


  • Site:

Any site and common site are neck, buttocks and anogenital area.

  • Aetiology

S.aureus
M>F
Most common in adolescence and early adult life.
Tight clothes predisposes
The infecting strain of Staphylococcus is usually also present in the nares or the perineum

Clinical features

  • A furuncle first presents as a small, follicular, inflammatory nodule, soon becoming pustular and then necrotic and healing after discharge of a necrotic core to leave a violaceous macule and, ultimately, a permanent scar.


  • Occasionally, there may be fever and mild constitutional symptoms.





Treatment

  • Antistaphylococcal antibiotics.

Carbuncle
  • A carbuncle is a deep infection of a group of contiguous follicles with S. aureus, accompanied by intense inflammatory changes in the surrounding and underlying connective tissues, including the subcutaneous fat.


  • Aetiology

S.aerues
Common in men (middle or old age)
They may be seen in the apparently healthy but are more common in the presence of diabetes, malnutrition, cardiac failure, drug addiction or severe generalized dermatoses, such as exfoliative dermatitis or pemphigus, and during prolonged steroid therapy.


Clinical features

  • Very tender nodule associated with severe constitutional symptoms.


  • May be upto 10cm in size and discharge in several days.


  • Site: neck, shoulders and hips.





Treatment
  • Antistaphylococcal antibiotics

  • Diabetes and other possible underlying conditions should be sought.

Staphylococcal scalded skin syndrome
  • SSSS is an exfoliative dermatosis in which most of the body surface becomes erythematous and the necrotic superficial epidermis strips off.


  • Occurs predominantly in childern (esp. neonates)


Etiology

  • Staph. Aereus
  • Due to protease like effect of exfoliative toxins
  • Two of the toxins (A and B) cause disruption of the desmosomes by cleaving desmoglein-1 in the most superficial epidermis and also cause the split beneath the stratum corneum which leads to peeling of skin.



Clinical features

  • The initial event is usually a localized staphylococcal infection. This may be in the skin or at a distant or ‘occult’ site.
  • A few days later, patients develop fever, irritability and skin tenderness.
  • A widespread erythematous eruption follows, which progresses rapidly to blister formation.
  • The tender skin becomes gathered into folds and, as it shrinks, leaves raw areas which are extremely painful.
  • The condition usually heals within 7–14 days
  • Swabs and cultures of blister fluids do not usually grow the staphylococci, as the blisters are mediated by the toxins which are disseminated haematogenously. The staphylococci may be isolated from the original septic site.





Treatment


  • Systemic antibiotic:

Flucloxacillin

  • Supportive measures
  • Bacterial swabs from carrier sites- to exclude satph. Carrriage.