CHAPTER 6 

BACTERIAL SKIN INECTIONS

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DERMATITIS GANGRENOSA

Gangrene of the skin is a serious skin problem.

Predisposing factors

Devitalization of tissues due to loss of blood supply

Trauma or lacerations to the skin.

Certain viral skin disease in infants or children that are followed by bacterial invasion.


Fig. 35b. Skin Gangrene

Etiology

Different bacterial strains can cause skin gangrene. These include hemolytic streptococci, non-hemolytic and clostridium species causing gas gangrene.


Fig. 36a. Dermatitis Gangrenosa

 

Fig. 35a. Skin gangrene

Clinical manifestations

General manifestations:

Severe constitutional symptoms, which may lead to a fulminating course endangering life especially in young children.

Skin manifestations

Skin lesions may show bullae, pustules or abscesses followed by lymphangitis and lymphadenitis. After few days the skin at the inflamed site becomes dark in color, necrotic and may show extensive ulceration.

 

DERMATITIS GANGRENOSA INFANTUM

Dermatitis gangrenosa infantum is a special type of skin gangrene that occurs in infants and young children.

Two types of skin gangrene may occur in infants:

  • Primary skin gangrene - this begins as an ulcerating skin lesion surrounded by an inflammatory zone due to invasion of bacteria such as Staph. Pyogenes or hemolytic streptococci.

  • Secondary skin gangrene - this begins following varicella or measles infections.

Fig.35 b,c,d,e  Skin gangrene due to Chicken pox

Treatment

Surgical debridement and cleaning of the lesion.

Cases due to Clostridium species are given gas gangrene anti serum.

Wet oozing lesions can be dried by using Potassium permanganate compresses 1: 9000 followed by topical antibacterial cream as Mupricine (Bactropan).

High doses of antibiotics may be needed in the beginning to control severe infection.

 

ERYTHRASMA

Erythrasma is bacterial skin infection of the intertriginous areas caused by Mycobacterium minutismus.

Clinical features

 

The crural and intertriginous areas are the most common sites involved. The lesions are sharply defined erythematous patches and are usually unilateral with minimal scaling. Itching is not a prominent feature while excessive sweating and irritation of the crural area may cause mild itching.


Fig. 39. Erythrasma


Fig. 38. Erythrasma


Fig. 37. Erythrasma

Characteristically, erythrasma gives a coral red fluorescence as seen under Wood‘s Light. That differentiates the condition from other crural skin diseases such as T. cruris.

Treatment

Mild cases can be treated by topical erythrocin lotion (Eryderm), Tolniftate, and antibacterial soap as Cidal soap. These usually can help in rapid clearance of the skin lesion.

Erythrocin may be given orally for two weeks in extensive cases.

 

ANGULAR CHEILITIS
(Perleche)

Perleche or angular cheilitis is a low-grade inflammation at the angles of the mouth.

Predisposing Factors

Angular stomatitis has been attributed to different factors:

  • Staphylococcal infection or Candidiasis.

  • Avitaminosis of the B complex group.

  • The condition is usually aggravated and perpetuated by constant licking of the lips especially in children.

  • Bottle-feeding may lead to accumulation of remnants of irritating debris and sugar on the angle of the mouth predisposing to infection.

  • Certain food or beverages such as orange juice may increase the inflammatory changes.


Fig. 41. Angular cheilitis


Fig. 40. Angular cheilitis

  • Problems of the teeth as malocclusion may play also an important role.

    Clinical features

    The lips become macerated and fissured, and may bleed in severe cases. The condition may become exceedingly chronic, and in many patients all local treatments may be of no value.


Fig. 42. Chronic Actinic Cheilitis

Treatment

Treatment of angular cheilitis is directed to the causative factor.

Topical antifungal or anti bacterial preparations may cure some cases.

Correction of the avitaminosis.

Mothers should be instructed to prevent their children from licking their lips.

Perfumes and perfumed soaps should be avoided.

Proper mouth hygiene of the child.

Pufexamac Cream or Ointment (Flogocid, Parfenac) may give good results.

 

Erythema Neonatorum Exfoliativa
(Ritter‘s Disease)

This is a rare staphylococcal and streptococcal infection of the breast-fed infants. The disease occurs during the first weeks of life and is characterized by a fulminating course.

The lesions show extensive bullous eruption with easily detached epidermis leaving red oozing areas. The condition is caused by the bacterial exotoxins.

A similar condition occurs in adults known as "Lylle Disease" or epidermolysis acuta toxica.

Clinical features

Skin lesion presents with red macules that begin around the mouth. These change into vesicles and pustules that rupture leaving a yellowish crust. The condition may spread eccentrically to the face and other parts of the body. The skin later becomes scalded, scarlet red empetiginized, covered by vesicles and bullae.

Complications

Stomatitis, rhinitis and corneal ulceration.

Differential diagnosis

Toxic epidermal necrolysis: may simulate Ritter‘s disease.

Leiner‘s disease: Leiner‘s disease shows branny greasy scales while in Ritter‘s disease there are large bullae, which peel off, in large sheets.

Treatment

  • Improving the general condition of the infant is very important.

  • Proper hygiene of both the mouth and nose.

  • Mild antiseptic soaks as potassium permanganate 1:10000.

  • Topical anti bacterial cream and a septic sterile dressings.

  • Systemic antibiotics according to the culture and sensitivity results.

  • Treatment of the complications such as corneal ulcers and others.

 

TOXIC SHOCK SYNDROME

Toxic shock syndrome is a serious problem affecting infants and other age groups due to staphylococcal toxins.

The disease is characterized by fever, multisystem involvement, circulatory shock, widespread erythema and desquamation.

Clinical features

The onset of the disease is acute with fever and skin rash.

Constitutional manifestations: fever, vomiting, diarrhea, purpura, thrombocytopenia, alopecia and nail destruction.

Systemic manifestations

Involvement of muscles, liver, kidneys and central nervous system may follow. Dizziness and shock are important manifestations of the syndrome.

Skin manifestations

The rash may develop within the first day in the form of widespread macular erythema, papulopustular eruption or scarlatiniform that may clear within 3 days.

Desquamation of the affected skin is highly characteristic.

Edema of hands and feet may be marked.

Towards the end of the second week the majority of patients develop a widespread, itchy, maculopapular or urticarial rash, which simulate drug reaction.

Occasionally vesicles and bullae may be formed.

Purpura due to thrombocytopenia may be another manifestation.

Alopecia and nail changes as transverse ridging and nail loss.

Mucous membrane manifestations:

There is generalized mucous membrane erythema, especially intense in the conjunctiva under which there may be hemorrhage.

Oral, esophageal, vaginal and bladder mucosa may ulcerate.

Diagnosis

The diagnosis is primarily clinical. Fever, rash, and later desquamation.

Staphylococcal organisms detection from the skin or mucous membrane lesions.

Bacterial culture from the primary site, not from the scalded skin, and frozen section of peeled skin may show the causative organism.

Shock is a marked feature in the fully developed disease, but postural dizziness may be sufficient for the diagnosis in mild cases.

Differential diagnosis

  1. Erythema multiform.

  2. Drug reaction.

  3. Kawasaki disease may simulate toxic shock syndrome. The diseases have features in common but prolonged fever, cardiac involvement, generalized lymphadenopathy and absence of peripheral shock can usually differentiate Kawasaki disease.

  4. Staphylococcal Scarlatina may represent milder cases of toxic shock syndrome.

Treatment

  • Hospitalization of severe cases and intensive care may be needed especially in young age groups.

  • Appropriate systemic antibiotic therapy should be given.

  • Intensive general supportive measures are essential.

  • Treatment and care of skin lesions.

 

TOXIC EPIDERMAL NECROLYSIS

This is a serious skin problem that may be fatal especially in infants and young children.

Etiology

  1. Staphylococcal infection toxins:
    The skin of children may be more susceptible to staphylococcal toxins or the renal clearance of the toxin is slower in children.

  2. Drug reaction:
    Different drugs that can cause this syndrome are: Tetracycline, Sulfa, Penicillin, antihistamines, Phenolphthalein, antipyretics, Boric acid powder, Salicylates, Phenylbutazone, Barbiturates, Aminopyrine and others.


Fig. 43. Toxic Epidermal Necrolysis


Fig. 44. Toxic Epidermal Necrolysis


Fig. 45. Toxic Epidermal Necrolysis 
(Drug Reaction)

Fig. 45b. Exfoliative dermatitis

  1. Vaccines:
    Such as polio vaccine and diphtheria inoculation.

Clinical features

Generalized skin eruption appears suddenly in infants and children following Staphylococcal infections of the upper respiratory tract.

The skin shows flaccid blistering which later becomes red, scalded, tender mainly on the trunk, perioral and the peri-genital areas .The tender skin becomes gathered into folds and may separate into sheets leaving raw areas which are extremely painful.

Differential diagnosis

Toxic shock syndrome.

Staphylococcal scalded skin syndrome.

Erythema multiform and Stevens-Johnson‘s syndrome have the same clinical manifestations.

Treatment

Symptomatic to relieve pain and discomfort by using analgesic. Care should be taken to select an analgesic not causing drug reaction.

Care of the scalded areas of skin: Potassium permanganate compresses 1:9000 and topical anti bacterial cream.

Topical and systemic steroids for cases due to drug reaction.

Antibiotics - culture and sensitivity to detect any causative bacteria and to be treated by the proper antibiotic (Tetracycline, Sulfa and Penicillin should be avoided because of the possibility of drug reaction.

 

SCARET FEVER
(Scarlatina)

Scarlet fever is an acute infection affecting mainly children, caused by strains of Strep. Pyogenes.

Modes of Infection

Droplet infection from the infected upper respiratory tract.

Infected belongings of patients.

From infected milk.

Clinical features

The incubation period is usually from 2-5 days.

Constitutional symptoms

Fever, which may be high, anorexia, vomiting, and sore throat.

The patient is delirious or comatosed.

Other serious manifestations such as myocarditis may complicate certain cases.

Skin manifestations:

The skin lesion appears on the second day on the upper trunk in the form of punctate erythema that becomes generalized.

There is flushing of the face with pallor around the mouth, which is one of the characteristic signs of scarlet fever.

Desquamation of the rash, with branny lamellar scales mainly on palms and soles.

In its severe toxic form, the eruption is very intense and may be purpuric.

Pastia‘s lines - Transverse red streaks appear on the skin folds due to capillary fragility.

Mucous membrane manifestations:

The oral mucous membranes are bright red and there may be deeper red puncta on the palate.

Strawberry tongue

First, the tongue becomes heavily coated. By the second or third day scattered, swollen, red papillae give the "white strawberry tongue" appearance. As the epithelium is shed the tongue becomes smooth and dark red ("red strawberry tongue").

In the septic forms the local pharyngeal lesions are severe and there may be extensive edema. Otitis media and peritonsillar abscesses are frequent. The rash may be slight.

Diagnosis

  • Typical clinical picture associated with tonsillitis.

  • Culture and detection of hemolytic streptococcus.

  • Antistreptolysin-O titter is high.

  • Schultz-Charlton test is positive.

  • Polymorphonuclear leukocytosis.

Differential diagnosis

  • Rubella

  • The early stage of smallpox.

  • Drug reactions can simulate scarlet fever. The lack of pharyngeal lesions and the distribution of the exanthema will usually enable the diagnosis to be established.

Treatment

Penicillin should be given in full dose as soon as the diagnosis is suspected. Management of the complications and renal damage should be taken into consideration.

 

MENINGOCOCCAL INFECTIONS

Meningococcal infection is an acute inflammation of the meninges accompanied by other systemic manifestations and skin rash.

Clinical features

Acute meningococcal septicemia and meningitis may present with fulminating course.

Purpura follows in nearly all cases.

Skin manifestations

The skin eruption may be very helpful for the early diagnosis.

Early skin lesions are discrete pink macules or small papular lesions that may be hemorrhagic, appearing on palms and soles. Some lesions are erythematous, morbilliform or urticarial.

A purpuric eruption is characteristic, and occurs mainly on trunk and limbs. The petechiae are usually small and scanty, but vary in size and number.

In severe cases larger purpuric lesions may occur including extensive ecchymoses and necrotic ulceration. The condition may be associated with a high mortality.

Vasculitis may occur during the acute illness, beginning 5 -9 days after the onset even if adequate antibiotic treatment has been given. Arteritis and episcleritis may be associated with some cases.

 

PSEUDOMONAS INFECTIONS

This is a serious skin infection caused by Pseudomonas aeruginosa organisms, which is common in infants.

Clinical features

Skin lesions may be localized or extensive.

  1. Localized lesions

    Local infections in infants or patients with debilitating illnesses should be regarded as potentially dangerous.

    Periumbilical lesions: The lesions may manifest with spreading erythema, a foul-smelling and bluish-green discharge. Necrotic ulcers may develop.

    Nail involvement - paronychial pustules may be accompanied by green discoloration of the nails.

    Lips and cheeks may become gangrenous.

    Superficial wounds and burns may be secondarily infected. Secondarily infected burns show discoloration of the sloughs with extensive surrounding edema.

  2. Extensive lesions

    Extensive lesions may present as:

  • Extensive necrosis develops around a local erosion.

  • Non-specific tender erythema, purpura, or a cellulitis-like picture. Bullae may form, particularly in moist areas, such as the axillae, perineum and the buttocks. These may rupture rapidly to give necrotic ulcers.

Complications

The prognosis of systemic infections is always grave, even with early treatment.

Fever and shock may supervene.

High mortality rate especially in infants and young age due to septicemia is common.

 

SWIMMING POOL RASH

This type of skin infection may be due to Pseudomonas aerogynosa organisms. Pseudomonas usually of serotype O type II, which may be cultured from the skin and the infected water.

Clinical features

Skin manifestations include macular, papular or pustular lesions. Some are urticarial suggesting insect bites. Any part of the body that has been immersed in water may be affected but often the worst areas are those in contact with bathing costumes. Hot tubs and whirlpools even if chlorinated may act as a source of infection.

 

TROPICAL IMMERSION FOOT

This is a distinctive infection of the toe webs caused by pseudomonas organisms. Sharply demarcated macerated areas, sometimes tinged with green patches, characterize the lesions. The devitalized tissues are invaded by Candida albicans.

 

PERIPORITIS

Periporitis is the term applied to pustular lesions appearing in the neonatal skin as a result of secondary infection of sweat glands by staphylococcus aureus.

The commonest sites involved are the buttocks, upper part of the trunk and the scalp. The lesion affects mainly malnourished infants and young children. Skin lesions may progress to sweat gland abscesses.

Sweat gland abscesses are clinically distinguished from furuncles by a lack of any tendency to "point", "coldness" and absence of tenderness.

Clinical manifestations

Erythematous deep seated infiltrating nodules, which may be single or multiple, small or big size. The inflammation becomes localized and soften where it ruptures exuding thick, creamy pus and later on heals leaving a scar.

Differential diagnosis from furuncles can be confirmed by that furuncles arise in relation to hair follicles and have yellow center, where it points to the surface and ruptures later.

Treatment

Treatment is directed towards improving the nutrition and general condition of infants as well as young children.

Preventing sweat retention by aeration of the crural area and minimizing sweating.

Appropriate topical antibiotic may be enough to control periporitis.

Oral antibiotics may be needed, especially when there are multiple abscesses.

 

NECROTIZING FASCITIS

Etiology

  • In neonates: narcotizing fascitis may arise spontaneously.

  • Following complication of physical birth trauma, omphalitis or circumcision.

  • Secondary infection from infected genital tract of the mother.

The organisms responsible for the infection are Streptococci group A, but also group B Streptococci, Staphylococcus aureus and Escherichia coli can cause the infection.

Clinical features

Skin manifestations

The early skin manifestations are cellulitis, which become very indurated and extend progressively. Purpura, and occasionally bullae, may appear in the center of the indurated area, often followed by frank necrosis.

Systemic manifestations

The child becomes toxic.

Local cutaneous anesthesia due to destruction of superficial nerves.

Pneumonia.

Treatment

Antibiotic therapy appears to be of limited value in this potentially lethal situation.

Early surgical excision of necrotic tissue is the most important aspect of treatment.

 

OMPHALITIS

The umbilical cord may become colonized by a variety of potentially pathogenic bacteria mainly Staph, Streptococci and E. coli. Occasionally infection of the umbilical cord becomes disseminated, either by blood stream or by direct spread via the umbilical vessels to the peritoneal cavity. Tetanus, diphtheria and necrotizing fasciitis may also occur as complications of umbilical infection.

Such infections are still responsible for a high proportion of deaths in the neonatal period in developing countries.

 

CLINICAL FEATURES

Skin manifestations

The skin lesion presents with cellulitis where the skin around the umbilical area becomes indurated.

Bullae may appear in the center of the indurated area followed by necrosis.

Purpura: Purpuric reactions are common manifestations of omphalitis and may be related to bacterial toxins.

 

TREATMENT

The most important aspect of treatment is early surgical excision of necrotic tissue.

The use of Hexachlorophene as an antiseptic was popular until it became apparent that this could lead to serious neurotoxicity, particularly in the preterm infant. The best substitute may be Chlorhexidine that can be applied as a dusting powder rather than as an alcoholic solution.

Antibiotics are of limited value.

 

PARONYCHIA

Paronychia is an inflammation of the folds of the skin surrounding the nail. Infection usually extends to the adjacent soft tissue causing painful tender swelling around the nail.

Paronychia may be bacterial or fungal.

Pyogenic paronychia

Infection is due to Staphylococci, pseudomonas aeruginosa and less frequently to streptococci.

Fungal paronychia

Candida albicans is the commonest fungi causing paronychia. Dermatophytes and saprophytic fungi may be responsible for some cases of paronychia.

Predisposing Factors

  • Trauma to the nails such as in using tight footwear.

  • Continuous emersion of the nails in water.

  • Certain chronic diseases such as diabetes predispose to invasion of the nails by bacterial or fungi.

 

CLINICAL MANIFESTATIONS

The infection is characterized by an acute or chronic purulent, tender and painful swelling of the tissue around the nail. Horizontal ridges appear at the base of the nail in chronic conditions. The moist groove of the nail and the nail fold becomes inflamed.

Fig. 47b.Bacterial paronychia & Ingrowing nail

Fig.47c Bacterial Paronychia

 


Fig. 46. Candidal paronychia


Fig. 47. Bacterial paronychia

Candidal paronychia

The manifestations are less severe than the bacterial paronychia. Candida paronychia is usually chronic. The finger becomes swollen, tender and beads of pus characteristically can be squeezed from the lesion.

 

TREATMENT

This is directed to correct the predisposing factors as preventing trauma to the fingers or toes and to keep these areas in normal dry conditions.

Pyogenic paronychia

Topical antibacterial and oral antibiotic besides dressing of the inflamed areas. If an abscess is formed incision and drainage is indicated.

Fungal paronychia

Topical and oral anti fungal medications such as Itraconazole, Ketoconazole or Fluconazole are effective. These medications should be used for a long period extending from 3-6 months.

 

ACTINOMYCOSIS

Actinomycosis is a chronic bacterial skin infection caused by Actinomyces Israeli, characterized by suppurative granulomatous lesions with draining sinuses.

 

CLINICAL FEATURES

The commonest sites involved are the jaw and to less extent the trunk.

The lesions present with dusky red, firm, fluctuating swellings with multiple sinuses exuding yellowish granules known as "sulfur granules" which are pathogonomonic for Actinomycosis. The underlying jaw shows periosteitis and even osteomylitis.

Actinomycosis is usually classified into three main types according to the areas involved.

  • Cervico-facial (Lump jaw)

  • Thoracic

  • Abdominal.

 

DIAGNOSIS

Examination of the granules from the draining sinuses is a characteristic of the disease. These show lobulated bodies consisting of delicate branching and intertwining filaments resembling sunrays.

Gram stain of the crushed sulfur granules will show gram-positive mycelia.

 

TREATMENT

High doses of penicillin are effective.

Erythromycin and tetracycline are also  effective medications.

 

CUTANEOUS DIPHTHERIA

Cutaneous diphtheria is a skin infection caused by "Corynebacterium Diphtheria." Carriers have the organism in the throat. The disease occurs in non-immunized persons with the diphtheria toxoid mainly in the tropical areas or in poor communities with poor hygiene.

  

CLINICAL FEATURES

Different clinical pictures may be seen during the course of the disease:

  1. Diphtheric Ulcer - occur mainly on the extremities but other sites may be involved. It leaves a scar after healing.
    Clinically the ulcer is shallow, well demarcated with rolled firm borders. There is a brownish gray or gray membrane covering the ulcer that can be easily removed leaving a clean surface. Later on a black brownish adherent leathery sloughs or eschar appears on the ulcer surface. The eschar is removed with difficulty leaving an unhealthy base.

  2. Bulla - this is very characteristic to cutaneous diphtheria when present. The bulla extends about 2 cm beyond the ulcer. Repeated formation of bulla on the scar is an important sign for diagnosis.

  3. Anesthesia around the ulcer, 2-5 weeks after infection. This sign is diagnostic to diphtheria ulcer. This is due to destruction of cutaneous nerves by diphtheria bacilli toxins.

  4. Non-specific lesions - sometimes the cutaneous diphtheria lesion is non-specific simulating skin abrasion, insect bite or eczematous lesion where the lesion can‘t be easily diagnosed.  

 

DIAGNOSIS

Diagnosis depends on the following:

  • Clinical picture

    Repeated formation of bulla on healed scars may be diagnostic

    Culture - isolation of the gram-positive Corynebacterium. This is not a always possible especially in chronic old lesions

  

TREATMENT

Combination of diphtheria antitoxin and appropriate antibiotic.

Intramuscular injection of 20,000-40,000 units of anti toxin.

General measures as good supportive care, bed rest, immunization of the contacts.

It should be noted that immunity requires several weeks to develop after the injection of diphtheria toxoid

 

RAT BITE FEVER

Rats or other animals such as cats, or squirrels may cause cutaneous and systemic manifestations after biting human beings.

Different organisms may cause different syndromes

Sodoku is a clinical type caused by Spirillium minus.

Haverhill Fever Septicemia caused by Sterptobacillus moniliformis due to rat bite or in some cases due to contaminated milk by the Sterptobacillus moniliformis.

 

CLINICAL FEATURES

The clinical picture of Sodoku and Haverhill are the same and differentiation is only by the different isolated microorganism.

  • The skin lesion is a wound at the site of biting. After healing of the wound, an inflamed edematous lesion appears associated by lymphangitis and constitutional symptoms such as fever, malaise, pain in the joints and relapsing fever.

  • Rose spot macular eruption develops on the abdomen and spreads to the face. The lesions enlarge and form purplish red indurated plaques.

 

DIAGNOSIS

Blood culture or fluid aspirated from the joints has the characteristic causative organism.

Animal inoculation: Spirillium minus can be demonstrated.

Blood picture - the disease is accompanied by leucocytosis and sometimes eosinophilia.

 

TREATMENT

Penicillin is an effective antibiotic for treatment of rat bite fever.

Cauterization of the wound by nitric acid may prevent spread of the disease when this is applied early after the bite.

 

CAT SCRATCH DISEASE

Cat scratch disease is caused by Gram-negative rods, which are part of the normal bacterial flora of cats, dogs and some other animals.

Most of the patients are children playing with cats, dogs that are a vector for the organism. Infection reaches the skin through traumatization of the skin by the cat scratch or by cat biting.

General manifestations

Fever, malaise and anorexia are not uncommon following the cat scratch. Central nervous system involvement. Purpura, thrombocytopenia and eye involvement are rare complications of the disease.

Skin manifestations

Scratch marks or bite are apparent at the site of injured skin .A red papule appears after 1-2 weeks. The papule enlarges into a nodule where the draining lymph node become enlarged, tender, suppurate and are accompanied by lymphangitis. The lesions usually heal within two weeks leaving no scarring.

 

DIFFERENTIAL DIAGNOSIS

Cat scratch disease must be differentiated from infectious mononucleosis, brucellosis, tularemia, histoplasmosis and sporotrichosis.

 

TREATMENT

Usually the condition heals spontaneously.

Antibiotics such as Cephalosporin, Erythrocin may give good results.

Treatment of suppurating lymph nodes is by aspiration with a needle and syringe and not by incision.

 

DOG BITES

Dogs are perhaps the most common assailants. They are capable of infecting soft tissue with a number of organisms that are part of normal oral flora of healthy dogs ,cats and a number of other animals.

The injury varies from local wound infection to fulminate septicemia.

Clinical Manifestations

Skin lesions include a localized eschar at the site of the bite and cellulitis.

Non-specific macular or maculopapular lesions, petechiae, purpura fulminans and symmetrical peripheral gangrene are the mainfestations.

Septicemia and disseminated intravascular coagulation may occur in severe cases.

Treatment

Treatment of the lacerated wound.

Antibiotics: Penicillin, Cephalosporin, Erythromycin, Tetracycline and Clindamycin are effective medications .

Examination of the dog for the possibility of infection with rabies where that needs thorough and special treatment .

 

CHANCRIFORM PYODERMA

This is uncommon infection that affects mainly children.

The etiology is uncertain but a necrotizing reaction due to a strain of Staph. Aureus, inoculated by minor trauma, has been suspected.

The lesion is usually solitary and is often situated around the eyelids, near the mouth, or occasionally on the genitalia.

 

CLINICAL FEATURES

Skin lesion presents with a sharply marginated ulcer, sometimes exceeding 1 cm in diameter, with an indurated base and a bright red areola that enlarges slowly after a few days.

The regional lymph nodes are enlarged and tender.

The ulcer may persist for several weeks before healing. It leaves a superficial scar.

 

DIFFERENTIAL DIAGNOSIS

The disease has to be differentiated from:

Epithelioma, syphilis, primary tuberculosis, accidental vaccination, swimming-pool granuloma, leishmaniasis and drug reaction. These are common dermatoses that may cause confusion in the diagnosis of chancroid pyoderma.

 

TREATMENT

Antibiotics may improve the condition.

 

PYODERMA VEGETANS

Pyoderma vegetans is characterized by the development of epithelial hyperplasia and chronic granulomatous changes accompanied by crusting, sinus tract formation and ulceration.

Etiology

Dermatitis vegetans may develop in any site but the flexures are often involved. Commonly, either Staph. Aureus or Group A streptococci are isolated from lesions but as the rash does not usually respond to antibiotics alone the role of these bacteria in the pathogenesis of the condition is unclear. Pyoderma vegetans may accompany ulcerative colitis and lymphomas.


Fig. 48. Pyoderma vegetans


Fig. 49. Pyoderma vegetans

 

CLINICAL FEATURES

Hyperplastic and crusted plaques appear on the skin surface. These may break down and weep and there is often central clearing. When there is a prominent edge with crust formation, the lesions may mimic blastomycosis. Alternatively, there may be ulceration; the condition in this case simulates pyoderma gangrenosum.

In pyodermite vegetante, crusted red plaques containing pustules have been described in multiple sites of the oral cavity, the flexures and the scalp.

 

DIAGNOSIS

This is difficult and largely depends on the exclusion of other conditions such as specific infections, iododerma, pyoderma gangrenosum and pemphigus vegetans.

It is important to exclude the underlying diseases such as ulcerative colitis, lymphoma or leukemia. In doubt, repeated biopsies from the skin lesion may be necessary.

 

TREATMENT

Antibiotics may be of no value in controlling the condition.

Application of antiseptics.

Topical corticosteroids appear to produce some response.

Co2 laser skin resurfacing of the lesion may be considered as one of the new methods of treatment.

 

MASTITIS AND BREAST ABSCESSES

Infection of the breast is common in the second or third week of life, more often in girls than boys. It is almost always unilateral.

 

CLINICAL FEATURES

The affected breast is swollen, red, hot and tender. Systemic toxicity is usually absent. Fluctuation denotes abscess formation, which will require surgical drainage.

The development of long-term breast abscess may be associated with loss of some breast tissues.

  

TREATMENT

Hot compresses on the affected breasts

Proper antibiotics

Incision and drainage

 

REIER‘S SYNDROME

Reiter‘s disease is a rare disease of unknown exact cause. Chlamydia and Mycoplasma were suspected as causative organisms. It affects mainly adult males, although it may sometimes occur in young children. The disease is characterized by triad manifestations: Non-gonococcal urethritis, Conjunctivitis and Arthritis.

 

CLINICAL FEATURES

The disease is usually accompanied by skin and systemic manifestations.

Skin manifestations

Skin lesions appear as small, yellowish vesicles and ulcers. Thick, dry, horny crust may develop especially on the toes. Detachment of the crust and horny masses leaves a residual pigmentation. The sites involved are mainly, the hands, feet, genitalia, and the mucous membranes of the mouth, palate, pharynx, urethra and conjunctiva. The soles characteristically show heavy crustations and hyperkeratosis known as keratoderma blenorrhagica.

Systemic manifestations

Urethritis - is non-bacterial, which manifests with pyuria, and bloody discharge. Symptoms may be dysuria, stranguary, precipitancy and lower abdominal pain. Complications such as cystitis , urethral stricture , seminal vesiculitis and prostatitis may manifest with different signs and symptoms accordingly .

Conjunctivitis, corneal ulcer and iritis are other manifestations.

Arthritis - the onset is a sudden with pain in the heels. It may involve any joint but the knee joints are the ones commonly involved . The affected joint is swollen, tender and hot.

Cardiac manifestations: Endocarditis, myocarditis, pericarditis and aortic insufficiency are rare manifestations of the syndrome.

Leucocytosis and raised erythrocytic sedimentation rate are common findings.

 

DIFFERENTIAL DIAGNOSIS

  • Gonococcal urethritis

  • Rheumatoid arthritis

  • Psoriatic arthritis, serum sickness and rheumatic fever.

Histopathology

Epidermis - there is spongiform vesicopustules, acanthosis, parakeratosis, hyperkeratosis and elongated intrapapillary processes.

Dermis - shows dilated vessels and perivascular infiltrate.

  

TREATMENT

Rest

Special care to the eye.

Corticosteroids - systemic steroids and topical eye drops.

Antibiotics in the form of tetracycline may have good effect.

Antirheumatics and care to the affected joints.

 

LEPTOSPIROSIS
(Weil‘s disease)

Leptospirosis is a systemic disease that is caused by the strains of the genus Leptospira.

Modes of Infection

  • Infected animals such as cats, dogs and rodents.
  • Drinking or swimming on infected water.

  • Direct infection from humans that may have acquired the disease, accidentally from the urine or tissues of infected animals.

  • Indirect infection from contaminated soil with the organism.

 

CLINICAL MANIFESTATIONS

Systemic manifestations:

Sudden chills and high fever.

Severe jaundice.

Hemorrhagic tendency, hematuria and proteinuria.

Skin manifestations

Petechiae and purpura appear on the skin and mucous membranes.

Severe conjunctivitis.

 

DIAGNOSIS

Blood picture

Severe leucopenia

Azotaemia

Blood culture: Detection of the organism.

Rising of the antibodies begin in the second week.

Urinalysis shows hematuria and proteinuria.

 

TREATMENT

Symptomatic

Antibiotics such as Tetracycline and Chloramphenicol may be of value in the adult age.

Children may be given erythromycin or zithromax

 

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