RECOMMENDED READING

1. Jones RO. Lichen simplex chronicus. Clin Pediatr Med Surg 1996;13:47­54.

Pyodermas are the infections of the skin and/or its adnexa by pus producing microorga nisms.

They are fairly common in hot and humid season and account for bulk of dermatology outpatients. They may affect any individual;

however, the children are its most common victims. Hot and humid climate, poor hygeine, uncleanliness, circumstances which lower the standard of sanitation and malnutrition predis­

pose to pyo derma.

Pyoderma may manifest as either primary or secondary pyoderma. Primary pyodermas arise in the normal skin, have a characteristic morpho logy, and are usually caused by a single micro organism. Secondary pyodermas arise over as dermatoses and/or damaged skin as super imposed condition.

Coagulase positive staphylococci (Staphylo­

coccus aureus) and betahemolytic Streptococcus (Streptococcus pyogenes) are responsible for most of the primary as well as secondary pyodermas.

However, the already affected skin may also be colonized by gram­negative microorganisms like Proteus, Klebsiella, Pseu do monas aeruginosa and Escherichia coli.

Primary Pyodermas

Impetigo:    It  is  classified  into  impetigo  conta­

giosa and impetigo bullosa. Impetigo conta­

giosa is caused by either Staphylococcus aureus

11 ^Pyodermas

or Streptococcus pyogenes. Both the microorgan­

isms may be simultaneously isolated from the lesion. It begins as a small, reddish macule which may soon turn into a vesicle. The vesicle has a thin roof that ruptures, leaving a raw, ooz­

ing area. The fluid oozing out dries to form a  crust, which is thick and honey colored, and has a ‘stuck­on’ appearance (Figs 11.1A to C). There is a slight erosion under it. The lesion has a pre­

dilection for the face and the extremi ties. Its morphological variants in the form of impetigo circinata, annu laris, and follicularis may also be encountered.

Impetigo bullosa is caused by Staphylococcus aureus (phage group II type 71). It starts as a vesicle which enlarges to form bulla. The fluid  inside the bulla is at first clear, and later turns  turbid. The roof of the bulla collapses, collecting the fluid into folds. The fluid then dries to form  a thin crust.

Folliculitis: It is an infection of the hair follicle that may manifest either as superficial or deep  folliculitis.

Superficial folliculitis: It is caused most often by coagulase­positive staphylococci (Staphylo coc cus aureus). It starts as a small dome­shaped pustule situated at the mouth of the hair follicle. The pustules rupture, and the pus dries to form small crust. Hair growth is not impaired. Face and the extremities are the sites of predilection (Fig. 11.2).

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Textbook of Clinical Dermatology

Deep folliculitis: The infection extends deeply in and around the hair follicle, the resulting perifol­

liculitis is resposible for marked inflam matory 

response. Furuncles, carbuncles, sycosis barbae, stye, and perforating folliculitis of the nose are its morphological variants.

Furuncle or a boil arises in relation to a hair follicle as a deep seated nodule, which is red and painful. It remains tense for a day or two and subsequently softens. A yellowish point forms at the summit of the nodule. It may rup­

ture, with the discharge at the core of necrotic tissue. Furuncles usually arise over hairy areas, exposed to fricion and/or maceration. The buttocks, neck, face and axillae are most often involved by furunculosis (Fig. 11.3).

Figures 11.1a to C: Ecthyma—shallow ulcer, after removal of heaped up ‘crust’

Figure 11.2: Multiple dome-shaped papules situated at the mouth of hair follicle(s)

Figure 11.3: Furuncle a deep seated nodule in and around the hair follicle

a B C

47

Pyodermas Carbuncle is a deep­necrotizing infection which involves several adjacent, hair follicles.

In fact, it may be regarded as an aggregation of furuncles. It drains through a number of sinuses (usually hair follicles) to the surface. Diabetes mellitus predisposes to carbuncles. The patient affected by carbuncle may be toxic and unless properly managed, it may prove fatal.

Sycosis barbae: It presents as follicular pus tu­

les. The pustules may rupture leading to impe­

tiginization and crust formation. The con di tion is often persistent and chronic as the individual tends to harbor the patho genic microoganism (usually Staphylococcus aureus) in the nose.

Ecthyma: It is initiated by beta­hemolyic strep­

tococci, and begins as a vesicle which arises over an inflamed base. It is followed by formation of  dry hard and firmly adherent crust. A shallow  ulcer is revealed on removal of the heaped up crust (Fig. 11.4). Healing occurs with scar

formation. It affects children and lesions develop on the exposed, trauma prone sites. It is to be differentiated from impe tigo in which the crus­

ting is less and there is no ulceration under it.

Cellulitis and erysipelas: Cellulitis is the infec­

tion of the subcutaneous tissue, caused by streptococci. The affected area is red, warm and edematous. However, the borders are flat and  not sharply circumscribed. Vesicles or bullae, may appear over the area affected by cellulitis.

Systemic toxicity may be its accompaniment.

  Erysipelas is a type of superficial cellulitis in  which there is development of an edematous, brawny,  infiltrated,  sharply  circumscribed  plaque that spreads peripherally. The borders are well­circumscribed and distinct. Face and scalp are the favored sites for erysipelas. The hands and genitalia are also frequently invol­

ved. The patient may have constitutional symptoms in the form of fever, malaise, and appear toxic.

seCondary Pyodermas

Infection may complicate any pre­existing cuta neous lesion such as an abrasion, wound, eczematous lesion, ulcer, fungal infection, and scabietic lesions. The morphologic features of the primary lesion may be masked by the super­

imposed infection.

Infectious eczematoid dermatitis: It is a fre­

quently encountered condition. The patient has a primary lesion which is productive of infec­

tious exudate. This may be in the form of a rup­

tured furuncle, an ulcer or an infected wound.

The exudate seeps over the surrounding skin, which becomes sensitized to the exudate and its components. This is followed by the appearance of erythema, edema, and vesicle along the path of  flow  of  discharged  exudate.  Oozing  and  crusting appear. Autoinoculation is its hallmark.

Figure 11.4: Ecthyma

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Textbook of Clinical Dermatology diagnosis

Laboratory investigations are of limited value.

Hemogram may reveal polymorphonuclear leuko cytosis. Urine examination is essential in children as they may develop poststrepto coccal glomerulonephritis. Culture sensitivity is requi­

red only if the patient fails to respond to an apparently adequate treatment.

TreaTmenT

Cleansing and degerming of the skin is of para­

mount importance. Removal of the bacteria lad­

en crust and debris is essential. Saline or potas­

sium permanganate compresses are effec tive.

Topical therapy is adequate for milder infec­

tions. Various topical antibiotics which may be used are as follows:

•  Hydroxyquinolines like iodochlorohydroxy­

quin which exerts broad spectrum antibac­

terial action

•  Neomycin  in  combination  with  bacitracin  and polymyxin B. Bacitracin is effective against gram­positive organism and poly­

myxin B against gram­negative orga nism

•  Gentamicin

•  Sisomicin (Ensamycin)

•  Framycetin (Soframycin)

•  Fusidic acid (Fucidin leo skin cream)

•  Nitrofurazone (Furacin).

Systemic therapy: It is required when:

•  There are systemic signs

•  The infection is widespread

•  Epidemics of pyoderma

•  The  patients  fail  to  respond  to  topical  therapy

•  The children are managed better with syste­

mic therapy.

Staphylococci are usually resistant to penici­

l lin and tetracycline. Betalactamase resistant penicillins, macrolide group of antibiotics,

Table 11.1: Treatment of pyodermas Clinical variant Treatments

Impetigo contagiosa 8 to 10 lac units of procaine penicillin, intramuscular, after test dose, daily for a requisite and bullosa period, or

250 to 500 mg of ampicillin (Campicillin) four times a day for a requisite period, or 250 to 500 mg of cloxacillin (Klox) four times a day for a requisite period, or

250 to 500 mg of erythromycin (Erythrocin, Thromycin) four times a day for a requisite period, or

250 to 500 mg of cephalexin (Phexin, Sporidex, Ceff) four times a day for a requisite period.

Superficial folliculitis —do—

Furuncles —do—

Ecthyma —do—

Periporitis —do—

carbuncle 500 mg of cloxacillin, intramuscular or intravenous, four times a day for a few days followed by 500 mg of cloxacillin (Klox) orally four times a day for a requisite period.

Diabetes should be monitored if present.

Sycosis barbae 250 to 500 mg of cloxacillin (Klox) four times a day till clinical improvement, followed by 1.2 to 2.4 mega units of benzathine penicillin (Penidure LA) intramuscular, after test dose, once a month.

Infectious eczemetoid 250 to 500 mg of cloxacillin (Klox) four times a day for a requisite period and 30 to 40 dermatitis (IED) mg of prednisolone (Wysolone) every day.

Erysipelas and Admit the patient.

cellulitis 1 to 2 million units of crystalline penicillin G, intravenous, after test dose, every four hours, for 2 to 3 days followed by 8 to 10 lacs of procaine penicillin, intramuscular, daily for a requisite period.

49

Pyodermas cep ha losporins  and  fluoroquinolones  are  effective against staphylococci. Beta­hemolytic strepto cocci are sensitive to penicillin (Table 11.1).

reCommended reading

1. Feingold DS. Bacterial infections of the skin. J Am Acad Dermatol 1989;20:469­475.

  2.  Sadick NS. Current aspects of bacterial infections  of the skin. Dermatol Clin 1997;15:341­349.

ScabieS

Scabies, a common cause of itching, is produced by infestation with the mite Sarcoptes scabiei var hominis. Poor hygeinic conditions and over­

crow d ing, permitting close body contact, favor the transmission of the disease.

Acarus scabiei has four pairs of legs. The female measures 400 µ by 300 µ in size (Fig. 12.1).

The male is appreciably smaller. Acarus scabiei undergoes its life cycle on the skin surface. The

In document VN Shegal - Textbook of Clinical Dermatology, 5th Edition (Page 55-61)