Bacterial Infections

Bacterial Infections

THE skin is normally colonised by an innumerable flora of organisms most of which are hamless saprophytes such as anaerobic gram-positive cocci, diphtheroid bacilli, staphylococcus albus, Candida and the acne bacillus. These reside in crypts, hair follicles, sebaceous glands and their ducts and their number and distribution varies with climate, age, hygiene, clothing and from one site to another. This resident flora is only temporarily reduced by scrubbing or the application of antiseptics.

In addition, there is a transient flora largely confined to more exposed areas and including potential pathogens such as haemolytic streptococci, staphylococci etc. The healthy human skin disinfects itself, destroying haemolytic streptococci with unsaturated fatty acids contained in sebum and staphylococci by desiccation so that this transient flora is only able to establish itself for a few hours and may be got rid of by washing with soap and water or more effectively by chlorhexidine. In a heavily contaminated environment such as a hospital ward, transient pathogens may acquire temporary resident status. If the skin remains healthy such a state may be short lived, but if a breach of continuity of the skin occurs, or if the defence mechanism is impaired by a skin disease, active infection of the skin may take place.

Staphylococcal infection

Nasal carriage of pathogenic staphylococci is the most important source of infection. Over half the population are nasal carriers and contamination of their skin and especially their hands disseminates the organisms. Spread of infection is aided in winter by the sudden increase in upper respiratory infections and these have been found to coincide with increased skin sepsis.


The type of infection produced by staphylococci depends on the soil and the seed. In children impetigo is common, though it occasionally occurs in adults. About 80 per cent of cases are found to be due to staphylococci of phage type 71. A build-up of carriage of such a potentially infective strain in the nostrils of nursing staff or the umbilici of babies in a neonatal nursery may lead to an outbreak of impetigo among the babies, whose resistance to staphylococcal infection is negligible even though the skin of the new born is colonised by non- pathogenic staphylococci within a few days of birth. Widespread blistered areas result which become denuded and crusted with serum (‘pemphigus neonatorum’).

Bacterial InfectionsIn older children it seems possible that the initial lesion occurs in skin damaged by injury, or some other lesion such as herpes simplex. Once established the organism gains virulence by ‘passage’ and is then capable of infecting the skin of susceptible contacts.

Uncomplicated impetigo usually appears on the exposed areas of face, hands and knees as delicate vesicles which rupture so rapidly that they are rarely seen intact. Serous exudation coagulates in a honey coloured crust and the edge of the lesion may spread, still giving the appearance of a broken blister at the edge, with crusting proximal to this and healing at the centre of the lesion, which may thus produce circinate or gyrate pattern ; during the active stage of the disease fresh lesions appear and spread daily. The skin beyond the lesions is normal unless secondary infection with haemolytic streptococci occurs, in which case crusting becomes more severe and an inflammatory halo appears round the lesions and there is regional lymphadenitis.

In the adult in the tropics, heat and maceration of the skin cause such an increased activity of the disease that widespread bullous lesions appear.

Presence of skin damage from some other cause commonly provides an entry for the infection; atopic eczema becomes ‘impetiginised’ producing a crusted mess in which the role of infection may be overlooked. The presence of pediculosis capitis may be missed even more easily and should be looked for in every case of impetigo of the scalp.

Secondary invasion of the lesions by streptococci of certain strains may give rise to acute glomerulonephritis but this is rare in this country although common in the tropics. Swabs should therefore be taken for bacteriological examination and when haemolytic streptococci are present the patient should be treated with systemic penicillin. The staphylococcus is penicillin-resistant in a high proportion of cases, therefore local treatment with an antibiotic such as neomycin-bacitracin ointment should be applied 3 times daily after soaking off the crusts with liquid paraffin. If the crusts are thick equal parts of lead diachylon plaster and soft paraffin should be applied as a poultice spread thickly on strips of lint, moulded and bandaged on the affected area and left in place for 24 hours. The crusts are easily wiped off when it is removed. The lesions should heal in about 5 days but the child should be kept away from school until healed as this disease is contagious among children. In tropical climates even the infected adult may require systemic antibiotics to combat the staphylococcus.

Toxic epidermal necrolysis in children (Lyell-Ritter’s disease)

Certain strains of phage type 71 staphylococci produce a delta toxin which in children can produce widespread erythroderma in areas unaffected by the impetiginous crusts. This leads to fragility and shedding of sheets of epidermis. The child should be treated with flucloxacillin as well as neomycin-bacitracin ointment to the crusts.


Boils are uncommon in small children and do not begin to be troublesome until the pilosebaceous apparatus becomes active at puberty. Once the skin has become colonised by pathogenic staphylococci, friction seems to be one of the precipitating causes and is most obvious in the ‘salt water boils’ of deep sea fishermen; these occur in groups round the wrists where stiff wet oilskins rub the water-macerated skin. Even in those not exposed to such discomfort the wrist is a common site for boils, but the majority occur on the face, head and neck. Nasal carriage of staphylococci occurs in the majority of those developing boils and is an important reservoir for auto-inoculation with organisms and for spread of organisms in a home or community.

Once a boil is established, the traditional methods of treatment would appear designed to spread infection, the application of kaolin poultices macerating and warming the surrounding skin, or occlusion under adhesive plaster producing a poultice of pus. It is therefore hardly surprising that one boil is often followed by many others.

Skin damaged by eczema or dermatitis is much more susceptible to invasion by staphylococci and furunculosis is a common complication of such cases. The skin disease may not be obvious and hidden patches of eczema and lesions caused by pruritis ani or pruritis vulvae may be the nidus of infection. Rarely furunculosis may be a complication of diabetes mellitus or leukaemia therefore a blood count and urine test should not be omitted.

Treatment should be aimed at preventing surface spread of infection and eradicating nasal carriage. It is desirable to have the antibiotic sensitivities of the staphylococcus estimated, especially if the patient has been in hospital recently, as the organism may be resistant to many of the broad spectrum antibiotics. If sensitive, the organism can be cleared from the anterior nares by the daily application of chlorhexidine- neomycin cream (Naseptin). Chlortetracycline or sod. fusidate ointment should be applied to and about an inch around any boils or pimples until they have completely healed. Sticking plaster should be avoided as a dressing and if some cover is necessary gauze and bandage should be used. The use of soap containing irgasan (Cidal soap) helps to reduce the carriage of bacteria on the skin. Such a regime usually brings recurrences of boils to an end in about 4 weeks in the majority of patients where there is no complicating factor.

Systemic antibiotic therapy has little effect in shortening the life of a boil and none at all in preventing recurrences, the oilly indications for systemic therapy being severe regional lymphadenopathy or progression of a boil to a carbuncle with surrounding cellulitis.

In patients with widespread eczema and boils any local steroid therapy should be combined-with an antibiotic such as neomycin to prevent spread of sepsis. In these patients local antibiotic may not be sufficient to prevent spread of infection or the nature of the skin lesions may make such applications undesirable, in which case systemic antibiotics usually suppress infection and healing of the eczema prevents recurrence.

Infection of the apocrine glands in the axillae may occur in association with, or without, boils elsewhere. Tender red nodules are formed which may become large abscesses and cause great discomfort. Application of sodium fucidate ointment (Fucidin), painting with silver nitrate paint and systemic administration of tetracycline will usually heal these lesions, but if fluctuant the abscesses may require incision. When the anogenital areas as well as axillae are involved the lesions are more likely to be apocrine acne (q.v.).

Finally, there remain those patients in whom foci of staphylococci have been dealt with and complications disproved, but who still continue to develop boils. These people seem to have an abnormally low resistance to staphylococcal infection which may be due to an immunological abnormality. Generalised ultraviolet-light therapy sometimes helps either by increasing their resistance or by sterilising the skin. The use of autogenous vaccines has been proved valueless in controlled trials.

Folliculitis of the beard (Sycosis barbae)

This condition is now considerably less of a problem than it was before the advent of antibiotics. It is a chronic staphylococcal infection of the beard area, initiated by shaving. Chronic nasal infection and staphylococcal carriage may be the precipitating cause, most obviously in those whose moustache area is mainly affected. In many cases the disease is associated with seborrhoeic dermatitis and there may be foci of sepsis on the skin such as boils, blepharitis and otitis externa.

The lesions consists of small follicular pustules on a background of erythema, the localisation to the beard area is marked and in long standing cases some areas may become scarred and permanently epilated. Scaling and crusting may also be present and hypertrophic cellulitis and scarring may produce the fig-like appearance from which the name is derived.

Eradication of sepsis elsewhere and the application of chlortetracycline ointment (Aureomycin) or sod. fusidate (Fucidin) usually heal the lesions rapidly. In long standing cases a residual erythema may persist which is controlled by the addition of a local steroid to the antibiotic. The patient should be encouraged to shave during treatment and an electric razor is preferable.

Streptococcal infections

Streptococcal infection of the skin fluctuates from year to year in accordance with the marked fluctuations in the incidence of other streptococcal infections such as tonsillitis and scarlet fever. It is most commonly seen as a secondary invader, causing inflammation round the lesions of impetigo, or again in association with the staphylococcus, causing crusted ulcers scattered over the limbs known as ecthyma.

Erysipelas can occur in any area of the body where a break in the skin allows streptococci to gain entry but usually this break is a Assure at the eye, ear, nostril or angle of the mouth. The patient becomes acutely ill with high fever and rigors, sometimes before there is much evidence of skin infection. From the fissure of entry an indurated area of erythema, hot to the touch, spreads over the face, its spreading border being easily palpable and the oedema of the dermis causing an orange- skin appearance. Occasionally blisters may appear and in about 48 hours at least half the face may be involved, with oedema of the eyelids closing the eyes.

A course of systemic penicillin controls this dramatically.
Recurrent attacks, sub-acute in onset and with little constitutional disturbance may occur on the face giving rise to a less demarkated erythema. Treatment of the fissure of entry with chloretracycline ointment (Aureomycin) until it is completely healed prevents recurrence, though some cases may require prolonged systemic therapy with sul- phonamides. The systemic use of chlortetracycline is less reliable as about 40 per cent of haemolytic streptococci are now resistant to this antibiotic.

Long standing recurrences may damage lymphatic drainage of the face and produce chronic lymphatic oedema of the ears, eyelids or lips.

Recurrent cellulitis

Recurrent cellulitis, like recurrent erysipelas, is a streptococcal infection depending on some portal of entry in the skin. Most commonly it affects a leg, entering through Assuring between the toes usually due to tinea pedis. Like recurrent erysipelas, the infection may damage lymphatic drainage, each attack leaving increasing residual oedema which increases the likelihood of spread of infection in the next attack.

Many of these patients can be shown to have a congenitally deficient lymphatic drainage.

The attacks are acute in onset with rigors and high fever which often precede the obvious signs of the disease; the inguinal lymph nodes become enlarged and painful, the foot and lower leg oedematous, red and slightly tender, the redness having a poorly defined border.

In the acute stage systemic penicillin therapy controls the infection, in penicillin-sensitive patients Septrin is effective. Tinea pedis if present should be treated (q.v.) and the fissures healed. If chronic lymphatic oedema is established, massage and wearing of an elastic web bandage help to reduce this. In some cases prolonged systemic antibiotic therapy may be indicated.


Is an infection with a Gram positive rod Erysipelothrix rhusiopathiae, which enters through a cut or abrasion, usually on the hand. The infection is acquired from handling uncooked fish, shell fish, meat or poultry and is therefore encountered in fishermen, fishmongers, butchers and cooks. Starting at the site of abrasion a purplish red erythema with a well defined raised edge travels slowly over first one finger, then spreads to creep up other fingers and over the hand. The areas first affected tend to heal. There is usually no systemic disturbance which, with the slowness of spread, distinguishes this from erysipelas. The localised form lasts 2-4 weeks. Treatment with full doses of systemic penicillin overcomes the infection.


Tuberculosis of the skin was a major dermatological problem before the Second World War and is now a rarity.

Primary tuberculosis of the skin produces a small persistent sore at the site of inoculation, the indolent undermined edges of which are now more familiar in unhealed B.C.G. vaccination sites; the regional lymph nodes enlarge and suppurate. Most primary lesions are found on the lower limbs.

Lupus vulgaris most commonly develops in children between the ages of 2 and 15 years and it is probable that many cases are a secondary extension of a primary lesion though some result from blood borne spread of infection. The face and neck are the common sites but the lesion may appear anywhere. The affected area is red, telangiectatic and slightly scaly; when blood is expressed with a glass slide the small brownish (apple-jelly colour) nodules of individual tubercles can be seen. Scarring follows resolution in some areas and is an important feature. The skin forms an unfavourable environment for the tubercle bacillus, possibly because of exposure to light or low temperature and strains of tubercle bacilli isolated from skin lesions show an attenuated virulence. Progress of lupus vulgaris is therefore very slow and when it has arisen in childhood it is often accepted by the patient as a ‘birthmark’.

Bacterial InfectionsInoculation into the skin of adults who have already been sensitised or immunised by commoner primary pulmonary or alimentary infection produces warty plaques, whose bluish inflammatory halo is a clue to their possibly tuberculous origin. Once fairly commonly seen on the wrists of farmers and caused by contact with tuberculous cattle, lupus verrucosa cutis is now rare.

Treatment. All forms of tuberculosis of the skin respond to the administration of antituberculous drugs and, although the administration of isoniazid mg 100 three times daily is effective, it is wiser to use a combination with ethionamide. This should invariably be done if the lesion is ulcerated or there is evidence of active tuberculosis elsewhere.


Syphilis in its early stages has become uncommon in Britain except in the larger ports, where infection is brought in from abroad and in the cities with shifting populations; nevertheless the possibility of sporadic outbreaks should be remembered.

The primary sore or chancre is nearly always acquired by sexual intercourse or kissing and appears after about 3 to 5 weeks at the site of infection. The sites usually affected are the penis or the vulva but 44 per cent of chancres in women are cervical and not easy to detect. Extragenital lesions occur on lips, fingers and anus, the latter being an increasingly common site as syphilis has become rife among homosexual males. The chancre is an erosion, ulcer or papule, rarely over 1 cm in diameter, with an indurated base which can be lifted up like a button in the skin. About one week after its appearance one or more of the regional lymph nodes develop a rubbery painless enlargement.

Five to 6 weeks after the chancre, by which time this primary sore is healing, secondary manifestations appear as the result of dissemination of the organism throughout the blood stream. The rash may consist of macules, papules or scaly lesions but a mixture of these in a polymorphic eruption, lack of itching and a universal distribution are the characteristic points to be borne in mind.

The macular eruption appears at an early stage as pink or copper coloured, round or oval macules with an ill-defined edge, distributed on trunk, limbs, palms and soles. The lesions may be so delicate that they are difficult to see unless examined in daylight. Associated with the macules are papules or lenticular papules, these being a similar coppery or pink colour slightly scaly and characteristically infiltrated. In the later stages of secondary syphilis, numerous patterns of more florid papules and psoriasiform lesions may occur; the tendency to grouping and annular patterning of these lesions should arouse suspicions of the diagnosis. With the rash the patient often complains of vague malaise, headaches and pains in the limbs. There is generalised painless enlargement of lymph nodes, the epitrochlear glands being one of the characteristic groups enlarged. The buccal mucosa develops superficial erosions sometimes presenting as red patches and sometimes covered with mucous secretion which is likened to a snail track. Care should be taken to fold back the lips and examine their mucosal aspects.

Condylomata lata are found in the perianal and vulval areas, but may occur at the angles of the mouth or in any of the flexures. They consist of flat moist plaques and nodules, often purplish in colour. In the later stages of secondary syphilis there may be a diffuse but patchy fall of hair, giving a moth-eaten appearance to the male scalp.

Late cutaneous manifestations of syphilis appear 2 to 10 years after the infection, the most common forming serpiginous or arcuate nodular lesions, which may be slightly scaly or ulcerated. In the central area over which they have passed they leave scarring and the lesion may be mistaken for lupus vulgaris especially if it occurs on the face or neck, but it traverses in months an area which would take lupus years. Gum- mata may be found in association with the nodular lesions or alone. Starting as a small nodule in the subcutis a gumma enlarges, becomes red and eventually ulcerates forming a discrete punched-out circinate ulcer with a slough at the base. A unilateral hyperkeratosis of palm or sole is a rare manifestation of tertiary syphilis. Leukoplakia predominantly affecting the tongue may also be a manifestation of the tertiary stage, though in these days other forms of chronic irritation such as trauma from dentures and smoking are a more common cause. The tongue is atrophic, sometimes scarred and sheets of white thickened epithelium involve the tongue and buccal mucosa. Whatever its cause this change in the mouth is potentially neoplastic. The most serious of all types of late syphilis is involvement of the cardiovascular and nervous system and although the skin can be the only organ involved, a careful examination of other systems must always be made.

Congenital syphilis is now seen very rarely owing to routine antenatal serological examination. The earliest cutaneous manifestation is a coppery coloured bullous eruption on the palms and soles appearing a few days after birth. The liver is usually enlarged and the child may have a serous nasal discharge, ‘snuffles’, which obstructs breathing. A few weeks after birth the eruptions and other signs of secondary syphilis appear and changes in the long bones can be demonstrated on x-ray to consist of osteochondritis and periostitis.

The most rapid confirmation of the diagnosis of primary syphilis can be made by scarifying or abrading the sore and examininng the serous discharge microscopically by dark ground illumination for spirochaetes.

In secondary syphilis the Wassermann and Kahn reactions are positive in virtually every case, spirochaetes can also be detected by expressing serum from condylomata. In tertiary syphilis the W.R. is positive in 90 per cent of cases and in cases of doubt the Treponema pallidum immobilisation test should be performed.

Because of the importance of tracing contacts the help of a specialist should be sought in treatment which is nowadays mainly dependent on penicillin in massive dosage.


With improved ease of travel and recent immigration from the Commonwealth, leprosy is increasingly encountered in Britain and though rare, its recognition is of obvious importance. It should be thought of in unusual skin eruptions in those from tropical or sub-tropical countries. Spread of the disease depends on the opportunity for contact with open cases of this infection and the greater the intimacy of contact the greater the chance of infection; spread of infection may also occur because of a high genetic susceptibility. Such conditions make the natives of these countries more prone to infection than transient visitors.

Fortunately the form of the disease most frequently seen in Great Britain is tuberculoid, occurring in patients with an adequate degree of resistance to the disease and a negligible chance of transmitting the infection. Sharply defined asymetrical areas of hypopigmentation of the skin with a dry, slightly scaly surface; or infiltrated lesions with a sharply demarkated erythematous edge or forming a hypopigmented plaque are the common skin eruptions in this form of the disease. It is important to notice that while the macules resemble vitiligo, pigment has not completely disappeared. When such lesions are tested for sensation there is usually impairment of the senses of light touch, temperature and sometimes to pain induced by pin prick. In the presence of such skin lesions the ulnar, peroneal or great auricular nerves may be enlarged and easily palpable; if damage to these nerves is sufficient, foot drop or ulnar palsy may also be found.

At the other end of the scale is the patient with lepromatous leprosy in whom the tissue defences are overwhelmed by infection. Here the early skin lesions are symmetrical, small, vague edged, erythematous macules with a smooth and slightly shiny surface. Even at this stage there is a slight degree of infiltration which becomes more marked as the disease progresses to form plaques and nodules associated with diffuse infiltration of the facial tissues and pinnae. Polyneuritis is a late manifestation of this type of disease. Between these two extreme pictures is a spectrum of intermediate forms.

Diagnosis is established by biopsy of the skin, tuberculoid leprosy showing circumscribed dermal foci of epithelioid cells surrounded by histiocytes and lymphocytes in which bacilli are difficult to detect. Lepromatous leprosy shows a dense dermal infiltrate ofyacuolated cells which distort and destroy epidermal appendages and are teeming with acid fast bacilli. In this stage nasal ulceration may occur and scrapings from the nose show profuse bacilli.

Because of the social implications of the disease, final diagnosis and treatment should be on the advice of an expert. Sulphone therapy is successful in the majority of cases and in recent years other drugs such as thiambutosine and rifampicin have proved effective.