Pediatric Annals

Bacterial Infections and Venereal Diseases

James E Rasmussen, MD

Abstract

BACTERIAL INFECTION OF THE SKIN

Cutaneous infections commonly occur in infants and children. Many, such as impetigo and furuncles, are easily recognized; others, such as Hemophilus influenzae cellulitis, are medical curiosities. This presentation will not dwell on familiar ground but will focus on unusual diseases and controversial aspects of the common ones.

Impetigo is the most common bacterial infection of the skin. In spite of its banality, the treatment of impetigo and its sequelae remains the subject of a continuing controversy.

There are two clinical varieties - bullous and nonbullous - each having its own etiology and treatment.

Nonbullous impetigo (Figures 1 and 2). Nonbullous impetigo, the most common of the two varieties, has distinctive clinical features. Most patients are children or young adults, and most lesions occur on the head or extremities. Pathogenic streptococci can colonize the normal skin but cannot produce disease unless the integrity of the skin is damaged. Insect bites, herpes simplex, scratches, and scabies may provide a portal of entry for streptococci; this may explain the initial localization of impetigo on exposed areas.

Ackerman, A. B. Hemorrhagic bullae in gonococcemia. N. Engl. J. Med. 282 (1970). 793.

Bennett, J. V" et al. Staphylococcal interference studies. Am. J. Epidemiol. 88 (1968). 410-421.

Burnett, J. W. The route of antibiotic administration in superficial impetigo. N. Engl. J. Med. 268 (1963), 72-75.

Dajani, A. S., et al. Experimental infection of the skin in the hamster simulating human impetigo. II: Assessment of various therapeutic regimens. Pediatrics 48 (1971), 83-90.

Derrick, C. W., et al. Further studies on the treatment of streptococcal skin infection. J. Pediatr. 76 (1970), 696-700.

Dillenberg, H., and Waldron, M. P. D. A preventive approach to impetigo of treaty Indians using staphylococcus polyvalent somatic antigen vaccine. Can. Med. Assoc. J. 89 (1963). 947-949.

Dillon, H. C. Impetigo contagiosa: Suppurative and non-suppurative complications. I: Clinical, bactériologie, and epidemiologic characteristics of impetigo. Am. J. Dis. Child. 115 (1968), 530-541.

Dillon, H. C. The treatment of streptococcal skin infections. J. Pediatr. 76 (1970). 676-684.

Dillon, H. O, and Derrick, C. W. Clinical experience with clindamycin hydrochloride. I: Treatment of streptococcal and mixed streptococcal-staphylococcal skin infections. Pediatrics 55 (1975). 205-212.

Editorial. Emergency Medicine 7 (Oct., 1975), 139.

Esterly, N. B.. and Markowitz, M. The treatment of pyoderma in children. J.A.M.A. 212 (1970), 16671670.

Ferrieri, P., et al. Natural history of impetigo. I: Site sequence of acquisition and familial patterns of spread of cutaneous streptococci. J. Clin. Invest. 51 (1972). 2851-2871.

Hall, W. D., et al. Studies in children with impetigo: Bacteriology, serology, and incidence of glomerulonephritis. Am. J. Dis. Child. 125 (1973), 800-806.

Hays, G. O, and Mullard, J. E. Blistering distal dactylitis. Pediatrics 56 (1975). 129.

Holmes, K. K., et al. The gonococcal arthritisdermatitis syndrome. Am. Intern. Med. 75 (1971), 470.

Hughes, W. T.. and Wan, R. T. Impetigo contagiosa: Etiology, complications, and comparison of therapeutic effectiveness of erythromycin and antibiotic ointment. Am. J. Dis. Child. 113 (1967), 449-453.

The Medical Letter 25: 389 (1973), 101.

Melish, M. E., and Glasgow, L A. the staphylococcal scalded-skin syndrome: Development of an experimental model. N. Engl. J. Med. 282 (1970). 1114.

Rasmussen, J. E. Haemophilus influenzae cellulitis: Case presentation and review of the literature. Br. J. Dermatol. 88 (1973), 547.

Rasmussen, J. E. Toxic epidermal necrolysis. AVcft. Dermatol. 11 1 (1975), 1135.

Ruby, R. J., and Nelson, J. D. The influence of hexachtorophene scrubs on the response to placebo or penicillin therapy in impetigo. Pediatrics 52 (1973), 854-859.

Wannamaker, L W. Differences between streptococcal infections of the throat and of the skin. N. Engl. J. Med. 282 (1970). 23-31.

Wannamaker, L.…

BACTERIAL INFECTION OF THE SKIN

Cutaneous infections commonly occur in infants and children. Many, such as impetigo and furuncles, are easily recognized; others, such as Hemophilus influenzae cellulitis, are medical curiosities. This presentation will not dwell on familiar ground but will focus on unusual diseases and controversial aspects of the common ones.

Impetigo is the most common bacterial infection of the skin. In spite of its banality, the treatment of impetigo and its sequelae remains the subject of a continuing controversy.

There are two clinical varieties - bullous and nonbullous - each having its own etiology and treatment.

Nonbullous impetigo (Figures 1 and 2). Nonbullous impetigo, the most common of the two varieties, has distinctive clinical features. Most patients are children or young adults, and most lesions occur on the head or extremities. Pathogenic streptococci can colonize the normal skin but cannot produce disease unless the integrity of the skin is damaged. Insect bites, herpes simplex, scratches, and scabies may provide a portal of entry for streptococci; this may explain the initial localization of impetigo on exposed areas.

Figures 1 and 2. Impetigo of the face and hands. The crust appears moist and shiny.

Figures 1 and 2. Impetigo of the face and hands. The crust appears moist and shiny.

The initial lesion is a small vesicle or pustule that becomes encrusted as it expands. Multiple lesions are common, each covered by a sticky yellow-brown crust. Although regional adenopathy is expected, significant fever and leukocytosis are not. Impetigo does not occur ordinarily in the scalp unless there is extensive involvement of glabrous skin. Impetigolike lesions in the scalp of a prepubertal child are frequently due to ringworm.

Uncomplicated nonbullous impetigo does not usually need to be cultured. Nearly all recent lesions contain streptococci, and about 60 per cent also contain coagulaseStaphylococcus aureus. The presence or absence of penicillin-resistant staphylococci does not influence treatment or recovery, since they are probably secondary invaders.

The treatment of choice for an established pyoderma is a systemic antibiotic drug. Penicillin V, benzathine penicillin, or erythromycin produces 91 to 99 per cent clinical and bactériologie cures in seven to 14 days. Clindamycin is equally effective but offers no advantages, and its use for minor skin infections is controversial. Topical antibiotic preparations do not approach this rate of success and cannot eradicate nasopharyngeal and anogenital streptococci unless applied to these areas. Furthermore, their regular use produces resistant organisms (usually staphylococci) and may cause allergic eczematous contact dermatitis. Patients who develop a topical allergy to neomycin may also have spontaneous crosssensitivity to other aminoglycoside antibiotic drugs (streptomycin, kanamycin, and gentamicin), which might need to be used systemically in the future.

The most important complication of streptococcal impetigo is acute glomerulonephritis. In areas where nephritogenic streptococci are endemic, impetigo is frequently followed by glomerulonephritis. This complication probably results from streptococcal antigen-antibody complexes deposited in the glomerular basement membrane. Early, vigorous antibiotic treatment does not seem to decrease the incidence of poststreptococcal nephritis, which, once established, usually resolves without permanent sequelae.

Nephritogenic streptococci can usually be grouped by M (2, 49, 55, 56, 57) or T (25/IMP, 12, 19, 3/B3264, 14/49) typing. If the incidence of nephritogenic streptococci is high, the lesions of nonbullous impetigo should be cultured for prognostic and public-health measures.

Bullous impetigo (Figure 3). A coagulase- phage group II S. aureus is the causative agent. This organism probably produces a toxin (similar to or identical with the epidermolysin of the staphylococcal scalded-skin syndrome) that causes the epidermal blisters.

Bullous impetigo also occurs during the summer; however, the initial lesions, unlike those of nonbullous impetigo, enlarge rapidly, developing a thin central crust. Affected areas appear to be freshly varnished, and only a thin rim of bullous tissue remains; this may expand to 5-10 cm. Bullous impetigo is not associated with significant adenopathy or nephritis and is not usually responsive to penicillin. Use of erythromycin or penicillinase-resistant penicillin (dicloxacillin) is the treatment of choice, and cultures are mandatory. This disease can be very aggressive - especially in the very young, in whom the rapid onset of large blisters has inappropriately been called pemphigus neonatorum (Figure 3).

GENERAL CARE OF IMPETIGO

Before the availability of specific therapy, impetigo was treated exclusively with topical antiseptics. Untreated nonbullous lesions resolve spontaneously in four to eight weeks, which may explain some of the "responses" to these antiseptics. Although antiseptics - such as silver nitrate or potassium permanganate, wet dressings, peroxides, hexachlorophene, iodines, iodophors, and Castellani's paint - can be used as an adjunct to systemic therapy, several studies indicate that the use of soap scrubs actually prolongs healing or spreads the disease.

Figure 3. Bullous impetigo in a neonate. All blisters have ruptured, leaving a thin rim of scales.

Figure 3. Bullous impetigo in a neonate. All blisters have ruptured, leaving a thin rim of scales.

Figure 4. Acute bacterial toxic epidermal necrolysis. Tissue paper-thin blisters have quickly ruptured in this three-yearold boy.

Figure 4. Acute bacterial toxic epidermal necrolysis. Tissue paper-thin blisters have quickly ruptured in this three-yearold boy.

Figure 5. Typical facies of a child with bacterial toxic epidermal necrolysis.

Figure 5. Typical facies of a child with bacterial toxic epidermal necrolysis.

STAPHYLOCOCCAL TOXIC EPIDERMAL NECROLYSIS

Also known as staphylococcal scalded-skin syndrome (SSSS) (Figures 4-7), this unusual but distinctive disease is caused by an epidermolytic toxin liberated by a phage group II coagulase-S. aureus. Most patients are less than six years old, and males and females are affected equally. The pathogenic staphylococci usually colonize the mucous membranes of the eyes, nasopharynx, and gastrointestinal tract. From this vantage point they produce prodromal signs of purulent rhinitis and conjunctivitis; they also liberate the epidermolytic toxin, which is absorbed systemicalIy. This toxin produces erythema and a split in the outer portions of the epidermis. At this point the disease is characteristic - erythema of the trunk and especially of the skin-fold areas (neck, axillae, anticubital fossae, groin), bullae in areas of erythema, purulent conjunctivitis, and pharyngitis. The staphylococci can be cultured from most mucous membranes but are not usually found in the blood. In a minor variation, erythema may be limited to flexures and blisters are absent. This clinical presentation appears similar to scarlet fever and has been called the scarlatiniform variety of SSSS. Pharyngitis is unusual with SSSS, however, while rhinitis and conjunctivitis are uncommon in scarlet fever.

Almost all patients with SSSS recover rapidly, with or without treatment. Systemic antibiotics should be used in all patients, however, since a few may be septic and all harbor a large number of potentially infectious S. aureus. A systemic penicillinase-resistant penicillin (dicloxacillin) is the treatment of choice, since most of the organisms are resistant to penicillin and some to erythromycin.

The epidermolytic toxin is usually produced by a phage group II staphylococcus (usually type 71), but epidemics and solitary cases have developed after infections with a group I organism (type 29). In 1969, Melish and Glasgow developed a newborn mouse model of SSSS that has been useful in studying both the bacteria and host responses to treatment.

Circulating toxin has not been found in patients with acute SSSS, perhaps because it is rapidly bound to epidermis. Convalescent sera contain high titers of an antiepidermolytic toxin antibody, but what role this plays in the resolution of the disease in unknown.

Desquamation begins within a few days of the onset of the erythema and bullae, starting on the face. Dry, leafy scales soon cover side areas of the body. At this stage, topical lubricants (Eucerin,® Nivea®) will reduce itching.

Most patients are treated best in the hospital, but those with the scarlatiniform variety can be treated as outpatients.

BLISTERING DISTAL DACTYLITIS

Hays and Mullard described this distinct entity in 1975. Their patients were all children who developed a solitary pustule on the palmar surface of the fingertip. Cultures grew beta-hemolytic streptococci, usually in pure culture but with S. aureus also present in one-third. The pustules enlarged to cover most of the surface of the pad of the finger but resolved promptly with treatment. Penicillin and erythromycin are both effective, and the disease apparently leaves no local sequelae.

Figure 6. Neonate with staphylococcal toxic epidermal necrolysis.

Figure 6. Neonate with staphylococcal toxic epidermal necrolysis.

Figure 7. Dry, leafy exfoliation as the end stage of staphylococcal toxic epidermal necrolysis

Figure 7. Dry, leafy exfoliation as the end stage of staphylococcal toxic epidermal necrolysis

Figure 8. Hemophilus influenzae cellulitis of the cheek of a six-month-old child. The color is blue-red.

Figure 8. Hemophilus influenzae cellulitis of the cheek of a six-month-old child. The color is blue-red.

Figure 9. A hemorrhagic pustule on the hand of a patient with gonococcemia.

Figure 9. A hemorrhagic pustule on the hand of a patient with gonococcemia.

HEMOPHILUS INFLUENZAE CELLULITIS

Of all the cutaneous bacterial infections, H. influenzae cellulitis (Figure 8) is the most obvious and dramatic. Within 24 hours, the patient develops a gross cellulitis and appears quite toxic. Within two to four days, all of the symptoms and most of the signs will resolve.

A typical patient is less than five years old with a one-to-two-day history of a mild prodrome of rhinitis, conjunctivitis, or pharyngitis. Within the next eight to 24 hours, a rapidly spreading red-blue cellulitis develops - usually on the cheek, although the extremities have also been involved. Fever (39-41° C. rectally) and leukocytosis add to the clinical impression of severe toxicity. After nose, throat, blood, and conjunctiva (if involved) have been cultured, the patient should be admitted for treatment with ampicillin. If ampicillinresistant strains are prevalent, chloramphenicol therapy should be considered. Within 24 to 48 hours, the area of cellulitis will begin to resolve, changing from red-blue to yellow-blue, as in the resolution of a superficial hematoma.

FOLLICULITIS, FURUNCLES, AND CARBUNCLES

These diseases are caused by bacterial (usually staphylococcal) infections of the hair follicles. If the infection is confined to the superficial portion of the pore, a small pustule results. Although this is usually recognized without difficulty, the pustule can be so small and ephemeral and the surrounding lesions so erythematous that it can easily be confused with urticaria or insect bites. Common symptoms of itching in urticaria, insect bites, and folliculitis also confuse the diagnosis. The distribution of lesions and a careful search for fresh pustules will help to establish the correct diagnosis.

Deeper follicular infection produces a hard, hot, red nodule - the furuncle - which is frequently located on the neck, in the axillae, or in the perineal area. With multiple furuncles, a patient may appear toxic and subsequently become septic. The carbuncle represents several confluent furuncles.

Mild folliculitis tends to be chronic, and systemic antibiotic therapy alone may produce only a partial response. The patient should be bathed daily with an antibacterial soap. If the patient has repeated episodes, the nose, throat, and anogenital areas should be cultured. If these are positive, topical antibiotics should be used in these areas.

Furuncles and carbuncles should be treated immediately with erythromycin or dicloxacillin. Lesions should not be incised and drained until fully fluctuant, and then only a small incision is required. Chronic furunculosis requires persistent, long-term antibiotic therapy. Staphylococcal vaccines, although popular, are unsound. The induction of bacterial interference with nonvirulent strains of staphylococci has been employed, but their use has been associated with epidemics of infection with the non virulent strains. If the furuncles resist despite therapy, chronic granulomatous disease or an immunoglobulin defect should be considered. Patients with atopic eczema and high levels of IgE may also have chronic abscesses (usually not very inflammatory); this has been referred to as Job's syndrome or the hyper-IgE syndrome.

ERYTHRASMA

"Athlete's foot" is the usual diagnosis when a patient complains of a pruritic white macerated dermatitis in the toe webs. This term usually implies a fungal infection, but tinea pedis of any type is very uncommon in prepubertal children. Erythrasma, on the other hand, can be found in 1 to 5 per cent of selected pediatric populations. The causative organism, Corynebacterium minutissimum, can produce two clinical problems. The more common is an intertrigo of the toe web spaces, usually the third and fourth. The second variation is a dry brown fine scaling patch that can involve the upper thigh (simulating tinea cruris), axillae, or inframammary regions. This second variety does not occur in prepubertal children, but web-space disease is quite common in this age group. Both types of erythrasma are easily and dramatically diagnosed by their pink fluorescence under Wood's light. The color is due to a porphyrin metabolite of C. minutissimum.

STAPHYLOCOCCAL PUSTULOSIS

Staphylococcal pustulosis (Figure 13) is a common infection of infants and young children who still wear diapers. It characteristically occurs during the first four weeks of life with multiple erythematous papules, vesicles, and pustules on portions of the thigh and lower abdomen covered by the diaper. Although this may resemble candidiasis, it has no predilection for the skin folds and does not become confluent. Perhaps most characteristic of staphylococcal pustulosis is the soft, leafy scaling that surrounds many of the mature lesions. The skin appears to be exfoliating around each lesion yet retains a soft compliant texture. Sticky crusts are never present as they are with impetigo, and individual lesions have a large zone of surrounding erythema. Erythromycin or dicloxaciUin, given orally, is usually satisfactory.

Although topical antibiotics have been used for many years in the treatment of pustular dermatitis, recent studies have shown that they not only lack effectiveness but may even at times be responsible for allergic eczematous contact dermatitis. The Medical Letter has condemned the use of topical neomycin, and an article criticizing their use will appear in a forthcoming publication of the Antimicrobial II Panel of the Food and Drug Administration. Topical antibiotics have no place in the treatment of any superficial cutaneous infection.

VENEREAL DISEASES

Gonorrhea

Most gonococcal infections do not involve the skin, but some patients may develop a disseminated gonococcal infection, with characteristic cutaneous signs (Figure 9). The organism may also seed the large joint spaces, producing severe arthralgia or arthritis. Most of these patients are teenage girls with previously unrecognized gonorrhea, but it is usually the joint complaints that bring them to a physician. In addition to a genital discharge, hemorrhagic pustules may also occur on the extremities. These characteristic but not absolutely diagnostic papules are composed of two parts - a hemorrhagic macule topped by a small pustule. Although they are caused by gonococci, organisms are difficult to culture from these pustules, but they may be seen with Gram's stain or a special antigonococcal immunofluorescence test done on exudate or tissue. Treatment should be prompt, vigorous, and usually in the hospital (although there have been reports of successful treatment with penicillin V or ampicillin G on an outpatient basis). Aqueous penicillin G is the drug of choice, 8 to 12 million units a day given intravenously and continued orally or intramuscularly for two weeks. With Pen Vee® K, the dosage would be 2 gm. a day for two weeks.

Figure 10. Solitary chancre in a two-year-old girl. This patient had been sexually molested.

Figure 10. Solitary chancre in a two-year-old girl. This patient had been sexually molested.

Figure 11. Papulosquamous eruption of palms characteristic of secondary syphilis. Chancre is still present on the foreskin.

Figure 11. Papulosquamous eruption of palms characteristic of secondary syphilis. Chancre is still present on the foreskin.

Figure 12. Condylomata lata in the perianal area of a sixyear-old girl.

Figure 12. Condylomata lata in the perianal area of a sixyear-old girl.

Syphilis

Syphilis is not dead! Although its current importance has been socially and medically overemphasized, syphilis continues to occur. Its cutaneous and systemic lesions are easily diagnosed early in its course, but passing years produce only vague complaints of shortness of breath, poor memory, or general physical decline. The early cutaneous lesions are not common but are characteristic and will be briefly reviewed.

Chancre. This is a clear, firm, painless ulcer that may occur in sexually active patients or in those who have been molested (Figure 10). Significant adenopathy, often unilateral, is common in lymphatics draining the ulcer site. This usually resolves spontaneously in about six weeks.

Secondary syphilis. Several months after a chancre develops, secondary syphilis appears. In its most common form, broadly based red-brown scaly papules about 1 cm. in diameter occur. The palms and soles (Figure 11) are commonly involved, and this distribution usually differentiates syphilis from pityriasis rosea. When these papules occur on mucous membranes or in moist intertriginous areas, they appear flat, pink and white, and with no visible scaling (Figure 12).

Figure 13. Red papular pustules and leafy scale in the diaper area of a six-month-old boy.

Figure 13. Red papular pustules and leafy scale in the diaper area of a six-month-old boy.

Tertiary and congenital forms of syphilis are not common and will not be discussed here.

Treatment. All forms of syphilis are treated with penicillin - usually 2.4 to 4.8 million units of benzathine penicillin administered intramuscularly, depending on the stage. Children should receive 50,000 units/kg. A benzathine-procaine combination is not recommended.

GENERAL REFERENCES

Ackerman, A. B. Hemorrhagic bullae in gonococcemia. N. Engl. J. Med. 282 (1970). 793.

Bennett, J. V" et al. Staphylococcal interference studies. Am. J. Epidemiol. 88 (1968). 410-421.

Burnett, J. W. The route of antibiotic administration in superficial impetigo. N. Engl. J. Med. 268 (1963), 72-75.

Dajani, A. S., et al. Experimental infection of the skin in the hamster simulating human impetigo. II: Assessment of various therapeutic regimens. Pediatrics 48 (1971), 83-90.

Derrick, C. W., et al. Further studies on the treatment of streptococcal skin infection. J. Pediatr. 76 (1970), 696-700.

Dillenberg, H., and Waldron, M. P. D. A preventive approach to impetigo of treaty Indians using staphylococcus polyvalent somatic antigen vaccine. Can. Med. Assoc. J. 89 (1963). 947-949.

Dillon, H. C. Impetigo contagiosa: Suppurative and non-suppurative complications. I: Clinical, bactériologie, and epidemiologic characteristics of impetigo. Am. J. Dis. Child. 115 (1968), 530-541.

Dillon, H. C. The treatment of streptococcal skin infections. J. Pediatr. 76 (1970). 676-684.

Dillon, H. O, and Derrick, C. W. Clinical experience with clindamycin hydrochloride. I: Treatment of streptococcal and mixed streptococcal-staphylococcal skin infections. Pediatrics 55 (1975). 205-212.

Editorial. Emergency Medicine 7 (Oct., 1975), 139.

Esterly, N. B.. and Markowitz, M. The treatment of pyoderma in children. J.A.M.A. 212 (1970), 16671670.

Ferrieri, P., et al. Natural history of impetigo. I: Site sequence of acquisition and familial patterns of spread of cutaneous streptococci. J. Clin. Invest. 51 (1972). 2851-2871.

Hall, W. D., et al. Studies in children with impetigo: Bacteriology, serology, and incidence of glomerulonephritis. Am. J. Dis. Child. 125 (1973), 800-806.

Hays, G. O, and Mullard, J. E. Blistering distal dactylitis. Pediatrics 56 (1975). 129.

Holmes, K. K., et al. The gonococcal arthritisdermatitis syndrome. Am. Intern. Med. 75 (1971), 470.

Hughes, W. T.. and Wan, R. T. Impetigo contagiosa: Etiology, complications, and comparison of therapeutic effectiveness of erythromycin and antibiotic ointment. Am. J. Dis. Child. 113 (1967), 449-453.

The Medical Letter 25: 389 (1973), 101.

Melish, M. E., and Glasgow, L A. the staphylococcal scalded-skin syndrome: Development of an experimental model. N. Engl. J. Med. 282 (1970). 1114.

Rasmussen, J. E. Haemophilus influenzae cellulitis: Case presentation and review of the literature. Br. J. Dermatol. 88 (1973), 547.

Rasmussen, J. E. Toxic epidermal necrolysis. AVcft. Dermatol. 11 1 (1975), 1135.

Ruby, R. J., and Nelson, J. D. The influence of hexachtorophene scrubs on the response to placebo or penicillin therapy in impetigo. Pediatrics 52 (1973), 854-859.

Wannamaker, L W. Differences between streptococcal infections of the throat and of the skin. N. Engl. J. Med. 282 (1970). 23-31.

Wannamaker, L. W. Differences between streptococcal infections of the throat and of the skin (second of two parts). N. Engl. J. Med. 282 (1970), 78-85.

Zaynoun, S. T., et al. Topical antibiotics in pyodermas. Br. J. Dermatol. 90 (1974). 331-334.

10.3928/0090-4481-19761201-09

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