Staphylococcus aureus infections

Skin infections caused by S. aureus are relatively common in newborns and infants. Epidemic outbreaks are occasionally seen in newborn and intensive care nurseries. In recent years, methicillin-resistant S. aureus (MRSA) infections have been increasingly reported in hospital nursery and maternity units, paralleling a trend toward such infections in other settings. Interestingly, most have had the molecular fingerprint of community-acquired (CA-MRSA), rather than nosocomial MRSA. Two forms of S. aureus infection involving the skin can occur: direct skin infection and staphylococcal scalded skin syndrome, caused by staphylococcal toxins.

Staphylococcus aureus pyoderma

Superficial skin infections with S. aureus (staphylococcal pyoderma) can result in crusted impetigo, bullous impetigo, and pustular folliculitis ( Figs 10.1 , 10.2 ). Deeper skin infections can result in furunculosis, cellulitis, and abscesses. Infection is virtually never present at birth, but develops in the first days to weeks of life. It typically presents with discrete vesicles and pustules. Toxin-producing S. aureus can present with tense, fragile vesicles and bullae. As these rupture, they may often leave either moist superficial erosions or crusted areas with a collarette of scale ( Fig. 10.3 ). Superficial staphylococcal infection can also present with crusted impetigo without clinically obvious vesicles, pustules, or bullae.

Papules, pustules, and crusted erosions in a 9-month-old infant with S. aureus infection.

Note evolution of primary lesions (papules and pustules) to secondary crusted erosions.

Numerous pustules due to S. aureus infection with follicular accentuation.

Staphylococcal impetigo in this 9-month-old infant with features of exotoxin-producing S. aureus , including collarettes of scale, larger areas involvement and shellac-like superficial scale.

Common sites of involvement include the neck folds, diaper area, and axillae. More extensive cases of generalized bullous impetigo are occasionally seen. The patients are usually otherwise well, without signs of more generalized infection. In two reports of CA-MRSA outbreaks in a well-baby nursery, neonates presented in the first 2.5 weeks of life with discrete pustules often in the diaper area but also on the trunk or posterior auricular surface; two babies had cellulitis. The skin lesions cleared rapidly with topical and/or oral antimicrobials.

In older infants, superficial infection can progress to invasive disease, especially in the malnourished or otherwise compromised host. In one study in India, 26% of pediatric patients with invasive staphylococcal disease had a preceding history of pustules. Staphylococcal infection can also cause a persistent perianal rash that involves the buttocks, in contrast to more localized perianal streptococcal disease. Blistering distal dactylitis (bullae on the volar tip of the digits usually due to Group A streptococcal infection) can rarely be caused by Staph in infants. Methicillin-sensitive and -resistant Staphylococcus , as well as herpes simplex infections can cause similar bullae; co-infection with Staph and HSV has been documented in a child. Infants with atopic dermatitis and staphylococcal superinfection usually present with crusting rather than intact pustules because of the tendency to scratch the primary lesion. Diagnosis and management are discussed in Chapter 12 .

Staphylococcal scalded skin syndrome

Staphylococcal scalded skin syndrome (SSSS) is an acute, potentially life-threatening disease caused by exotoxin-producing S. aureus , usually phage types 1, 2, or 3. Although epidemics as well as sporadic outbreaks of SSSS have been reported, including in newborn nurseries, it is still an uncommon to rare condition. A population-based study in Germany found an incidence of approximately 0.1 cases per million inhabitants per year (including all ages) with a bimodal distribution of ages: young children and older adults. In a group of neonates and infants with erythroderma, SSSS was the etiology of their skin findings in only 7%. Only a few cases of congenital SSSS have been reported; the vast majority of infants present between 3 and 7 days of age or older, with an abrupt onset of cutaneous erythema, tenderness, and widespread areas of skin fragility, superficial blistering, and/or erosions. Erythema often begins on the face, especially around the mouth. In newborns, flaccid blisters usually appear within 24–48 h and quickly erode, producing areas of superficially denuded skin. These erosions are particularly prominent in areas of mechanical stress, such as the shoulders, buttocks, body folds, feet, and hands. When firmly rubbed, the skin is easily separated from the underlying epidermis (Nikolsky’s sign). A milder, but more common form of SSSS, characterized by erythema, tiny erosions or pustules, with or without a scarlatiniform rash is often seen in older infants and children. Periorificial accentuation with scale or crusting is a common feature of both forms ( Fig. 10.4 ).

Staphylococcal scalded skin syndrome in a young infant.

Note periorificial accentuation and fragile vesicles overlying erythema on neck.

Systemic signs such as temperature instability, irritability, and/or lethargy are common in neonates whereas infants are nearly always febrile. Perioral or periocular edema and mucopurulent conjunctivitis are sometimes present. Although the primary site of S. aureus infection is usually not the skin, occasionally a primary skin infection, such as an abscess, purulent umbilicus, or localized area of impetigo, may be the source of disease.

Diagnosis is made by skin biopsy, which demonstrates a cleavage plane in the upper epidermis with acantholytic cells and minimal dermal inflammation. To speed diagnosis, a snip biopsy of exfoliating portions of the skin can be sent for frozen section. The differential diagnosis includes toxic epidermal necrolysis, epidermolysis bullosa, boric acid poisoning, and certain metabolic disorders such as methylmalonic acidemia. The management of SSSS is discussed in Chapter 12 .

Streptococcal infection

Several epidemics of group A streptococcus (GAS) have been reported in the newborn period. Although most infants present with omphalitis or a moist umbilical cord stump, in rare cases isolated pustules may be the presenting sign of GAS infection. GAS can also cause a form of intertrigo in infancy. Generalized sepsis, cellulitis, meningitis, and pneumonia are occasionally seen. Because neonatal group A streptococcal infection can result in an invasive infection, parenteral antibiotics should be considered, and infants observed closely for signs of systemic illness. Although bacterial cultures are the ‘gold standard’ for diagnosis, rapid antigen testing for GAS can be used while awaiting culture.

In older infants, clinical presentations of localized cutaneous GAS infection include impetigo, streptococcal intertrigo, perianal streptococcal dermatitis, blistering dactylitis and atopic dermatitis with secondary streptococcal infection. GAS impetigo can be difficult to distinguish from that caused by S. aureus : both have crusting and erosions and occasional pustules. In addition, infants with GAS skin infections may be more irritable and may be febrile, a finding less common in S. aureus impetigo. Infants with streptococcal intertrigo, have moist eroded areas in the folds of the neck, axilla, groin, or perianal area that can be mistaken for candidal infection. In young children with blistering distal dactylitis, a large vesicle or bulla develops on the volar aspect of tips of fingers or toes. In infants with atopic dermatitis, GAS causes crusting and pustules that may be deep-seated and may involve the palms and soles – a feature less likely to be due to S. aureus alone; coinfection with staphylococcus can occur ( Fig. 10.5 ).

Group A streptococcal impetigo.

In contrast to S. aureus infection, palms and soles are more common sites of infection. Overlapping features of both bacteria make it virtually impossible to distinguish these without confirmatory bacterial culture.

Infection with group B β-hemolytic streptococci (GBS) is one of the most common causes of neonatal sepsis, but skin lesions resulting from GBS infection are very rare. In a few cases cellulitis, vesicles, bullae, erosions, and honey-crusted lesions resembling GAS impetigo have been described either at the time of birth or later in the neonatal period. Many areas of the body, including the scalp, face, submandibular area, torso, and extremities, can be affected, with lesion size varying from a few millimeters to several centimeters. Other manifestations of group B streptococcal disease (including bacteremia, pneumonia, and meningitis) should be sought. GBS is also an occasional cause of blistering dactylitis or impetigo.

Listeria infection

Listeria monocytogenes is an uncommon cause of a rare form of sepsis in the newborn period, typically acquired via vertical transmission from an affected mother. Epidemics and sporadic cases due to inadequately pasteurized and more rarely pasteurized dairy products have been reported. Skin disease, when it occurs, is associated with an early-onset form of infection which is present at birth or develops in the first few days of life (so-called granulomatosis infantiseptica). The rash, which is usually present at birth, consists of discrete but widespread pustules and petechiae over the trunk and extremities. In less severely affected infants, erythematous macules may progress to pustules with an erythematous halo. Salmon-colored papules concentrated on the trunk have also been described. Typically, maternal fever, fetal tachycardia, and meconium staining of amniotic fluid are present before delivery, and premature delivery is common. Affected infants are usually gravely ill, with respiratory distress, meningitis, and other signs of sepsis.

The differential diagnosis includes several other infections, including congenital candidiasis, intrauterine herpes infection, and Haemophilus influenzae infection. Further details of diagnosis and management are discussed in Chapter 12 .

Haemophilus influenzae infection

Haemophilus influenzae is a very rare cause of neonatal skin disease. Findings have included vesicles, pustules, crusted areas, and abscesses. Halal and colleagues provided the best descriptions of skin lesions in an infant with discrete vesicles on an erythematous base, as well as several 2–3 mm crusted areas, present at birth. Gram stains and culture from skin lesions confirmed the presence of H. influenzae type B, but cultures from other sites were negative. Onset of symptoms is at birth or in the first few days of life.

If H. influenzae is suspected, diagnostic evaluation should include Gram stain and culture of skin lesions, and cultures of the infant’s blood, urine, cerebrospinal fluid (CSF), and nasopharynx. Cultures of the placenta (if available) and of the maternal cervix and lochia should also be performed. The differential diagnosis includes other infections. A Gram stain demonstrating pleomorphic Gram-negative bacilli is strong evidence for H. influenzae infection. Treatment is discussed in Chapter 12 .

Pseudomonas infection

Pseudomonas aeruginosa in newborns nearly always occurs after 5 days of life, most commonly in infants weighing less than 1500 g at birth. Risk factors include feeding intolerance, parenteral nutrition, prolonged intravenous antibiotics, and necrotizing enterocolitis. Skin lesions are usually a result of septicemia and hematogenous spread of infection to the skin. However, in older infants, ulcerative skin lesions of Pseudomonas have been reported in the diaper area and in previously healthy young infants in the absence of documented blood-borne infection or immunodeficiency. Some of these patients are ultimately diagnosed with neutropenia or immunodeficiency. Thus, apparently healthy older infants with ecthyma gangrenosum should be thoroughly evaluated for predisposing conditions. Older infants immunocompromised from cancer treatment or transplant are also at risk for pseudomonas infection.

The skin lesions of Pseudomonas infection are known as ‘ecthyma gangrenosum’. They typically evolve from areas of erythema to hemorrhagic bullae or pustules. The pus may be green, caused by a dye produced by the bacteria. Lesions rapidly erode, becoming punched-out necrotic ulcerations with an indurated base.

In septicemic forms, the affected neonates or immunocompromised infants are usually gravely ill; prompt diagnosis and rapid institution of treatments are necessary to prevent death from overwhelming sepsis. Gram staining of fluid from a pustule or bulla will reveal Gram-negative rods. If lesions are eroded, biopsy and tissue Gram staining should be performed to expedite diagnosis. Cultures of both the skin and blood will confirm the diagnosis. Treatment of suspected infection must take into account the local patterns of antibiotic resistance and is discussed in Chapter 12 .

Congenital syphilis

Congenital syphilis is a very rare neonatal infection in the USA and most often occurs in the setting of inadequate prenatal care. Rarer still is presentation with blistering or ulcerations. These findings occur almost exclusively in early-onset disease and are present in approximately 3% of cases, usually at the time of birth. Bullae are most often located on the palms, soles, knees, or abdomen, superimposed on dusky, hemorrhagic, or erythematous skin. Moist areas of eroded skin may also occur around the mouth, nose, and anogenital area. Typical skin rashes in congenital syphilis are seen more often in preterm than term infants. Generalized erythema multiforme-like lesions with vesicular centers have also been reported in an infant with congenital syphilis.

Blistering congenital syphilis must be differentiated from other disorders causing blistering on the palms and soles, including congenital candidiasis, acropustulosis of infancy, scabies, and epidermolysis bullosa. The clinical findings, as well as serologies, potassium hydroxide (KOH) preparation, and skin biopsy when necessary, help in this differentiation. The details of the evaluation and therapy of congenital syphilis are discussed in Chapter 12 .

Candida

Candida albicans infection is very common in infants but presentation with a primarily vesiculopustular eruption is much more common in neonates and is the focus of this discussion. Several candidal species can cause infections in neonates. Depending on the case series, C. albicans, C. parapsilosis , and to a lesser degree C. tropicalis are the most frequent isolates.

Congenital candidiasis and invasive candidal ‘dermatitis’

The cutaneous signs associated with candidal infections have been most clearly delineated for Candida albicans infection. Congenital candidiasis , a rare condition, is due to exposure to C. albicans in utero. It typically presents at birth or within the first week of life as a widespread eruption. Risk factors include a foreign body in the uterus or cervix (such as a retained intrauterine device or cervical suture), premature delivery, and a maternal history of vaginal candidiasis. Several types of skin lesions may be present, including diffuse erythema, erythematous papules, vesicopustules, and fine scaling. Typically, a fine erythematous papular eruption involving the face and upper body develops first, evolving over time into a more widespread pustular and scaly eruption. In milder cases, sparse papules and incipient pustules are scattered over the upper chest, back, and extremities. Virtually any part of the skin may be involved; unlike many pustular eruptions (such as erythema toxicum and miliaria), the palms and soles are often involved ( Fig. 10.6 ). Nail dystrophy and oral thrush are occasionally present.

Congenital candidiasis in a 5-day-old infant.

Scaling, erythema and tiny pustules are the most common features. Palm and sole involvement is common.

(Courtesy of Vinod Bansal, MD.)

The terms ‘ invasive fungal dermatitis ’ or ‘ candida-like dermatitis ’ are used to describe a more severe type of candidal skin infection seen in very low-birthweight infants. This form of infection may not be present at birth but can typically be noticed within the first 2 weeks of life, occasionally later. Diffuse erythema and scaling with superficial erosions resembling a first-degree burn have been reported and may evolve into full-thickness skin infection and necrosis. This finding in very low-birthweight infants is associated with high rates of positive blood cultures, as well as pulmonary and other sites of infection. Skin abscesses have also been reported as an early finding of systemic candidiasis. Diagnosis can often be confirmed with potassium hydroxide (KOH) preparation and/or culture from involved skin. Organisms are often present in large numbers even in cases where pustules are relatively sparse, but if necessary, skin biopsy can also help confirm the diagnosis. Candida may also be present in the gastric aspirate.

Differential diagnosis includes Listeria and intrauterine herpes simplex infections, erythema toxicum neonatorum, pustular miliaria rubra, and neonatal pustular melanosis.

Treatment depends on the gestational age and weight: premature infants weighing <1500 g have a much greater risk of disseminated candidiasis and need further investigations, such as blood, spinal fluid, and urine cultures, and immediate institution of systemic therapy (see Chapter 14 ). Infants with a higher birthweight and gestational age, without evidence of disseminated disease must be observed closely because on rare occasions, systemic infection, with respiratory distress or other organ involvement, may develop; however, topical therapy with an imidazole cream may be curative.

Neonatal candidiasis is the term used for infants that present with Candida infection after 1 week of life and are infected due to peripartum or postnatal exposure, and can occur in both term and preterm infants. Colonization with C. albicans is very common, occurring in approximately one-quarter of infants >1500 g birthweight, and nearly one-third of those colonized develop mucocutaneous disease. The most common sites of involvement are the diaper area and the oral mucous membranes, but other intertriginous areas or areas which have had tape or occlusion may be affected, e.g., facial eruption if the infant has been intubated. The most typical presentation is beefy red scaly patches with satellite papules at the periphery. Pustules at the periphery of lesions can be seen, but are less common and can be very subtle. Topical therapy with an imidazole cream or nystatin ointment is usually sufficient because dissemination does not develop in immunocompetent infants, but closer monitoring is mandated for very low-birthweight infants with evidence of postnatally acquired candidiasis.

Candidal infection in older infants

In immunocompetent older infants outside the neonatal period, cutaneous candidal infection is usually limited to the diaper area, where vesicles and pustules may be located on the margin of a red confluent plaque ( Fig. 10.7 ). Candida colonizes the diaper area more heavily in infants with diaper dermatitis even without overt infection. Differential diagnosis of the pustules includes bacterial infections with staphylococcus or streptococcus (see Chapter 14 for further discussion). In the immunocompromised host, clinicians should maintain a high index of suspicion for invasive disease (see also Chapter 18 ).

Acquired Candida albicans diaper rash in a 3-week-old infant.

Peripheral tiny pustules are evident.

Aspergillus infection

Primary cutaneous aspergillosis has been reported in neonates, most of whom were very premature, but it can also occur at any age including infancy, most often in the setting of severe immunocompromise. Aspergillus fumigatus , A. niger , and A. flavus can all cause skin disease. The usual age at diagnosis in neonates typically ranges from 1 week to 1 month. Predisposing factors in addition to prematurity include prior treatment with systemic antibiotics or, less commonly, use of systemic corticosteroids.

In both primary and secondary skin disease, a variety of skin lesions have been reported, including pustules and ulcerations, often superimposed on indurated plaques, but the most common of these is skin ulceration, which may feature a central necrotic-appearing eschar, with punched-out ulcers at the periphery.

Skin lesions are usually the result of primary cutaneous disease, where the skin is the initial or only site of infection, often preceded by skin maceration or injury, e.g., abrasions from adhesive tape. Hospital renovations and construction are risk factors in some cases. Secondary cutaneous disease occurs after hematogenous spread to the skin from the primary site of infection, most commonly the lungs. In secondary disease, lesions may be more extensive; they are most commonly located on the perineum and buttock. A third form of aspergillosis reported in the immunocompromised is infection of a cavity such as a sinus, with contiguous mucocutaneous spread, similar to that seen in other fungal infections like mucormycosis.

Skin biopsies, which demonstrate dermal inflammation and broad anastomosing septate hyphae on special stains, are usually necessary for diagnosis, with culture for confirmation. (Management is discussed in Chapter 14 .) The prognosis is guarded, both because of possible systemic aspergillosis and because of other diseases associated with prematurity.

Trichosporosis and zygomycosis

More than a dozen cases of Trichosporon infection (see Chapter 14 ) have been reported in neonates, most of whom were very low-birthweight due to prematurity. Infection can be associated with generalized skin breakdown, peeling, and oozing without vesicles or pustules, as well as necrotic eschar formation. Mucormycosis has been reported more frequently, again nearly all in very low-birthweight or otherwise immunosuppressed infants. The age at diagnosis varied from 4 to 33 days. Damage to the skin from adhesive tape and/or invasive catheters is felt to be an important risk factor. This, combined with prematurity, broad-spectrum antibiotics, and in some, the systemic use of corticosteroids, is a factor conducive to these opportunistic pathogens. Mucormycosis in this setting typically presents as vesicles, pustules, or cellulitis, or an area of skin discoloration, which evolves into a black necrotic ulcer with surrounding erythema. Skin biopsy is usually needed for diagnosis. In older immunosuppressed infants, there is a similar clinical picture. Both types of infection have a poor prognosis but treatment with amphotericin B (with or without surgical debridement) has been successful in some cases.

Herpes simplex infection

Herpes simplex (HSV) infection is one of the most feared causes of blisters and pustules in the newborn. Subtle or inconspicuous skin lesions may herald the onset of infection, and the failure to promptly recognize and treat neonatal HSV infection can worsen the prognosis of this potentially devastating disease. Skin lesions are present in both intrauterine and neonatal herpes simplex infection, and although there is considerable overlap, the time of onset and many of the clinical features of the skin disease differ.

In intrauterine HSV infection , skin lesions are usually present at the time of birth, or develop within 24–48 h in 90% of affected infants. In addition to the characteristic vesicular eruption, widespread bullae and erosions resembling epidermolysis bullosa, absence of skin on the scalp (resembling aplasia cutis congenita), polycyclic plaques with erosions, scars on the scalp, face, trunk, or extremities, and absence of nail plates have been reported. Affected infants are often premature, weighing less than 2500 g, and most have other manifestations of TORCH infections e.g. microcephaly and chorioretinitis. Some have limb and bone abnormalities.

In contrast, neonatal HSV infection is acquired perinatally and presents with three characteristic patterns: mucocutaneous disease (limited to the skin, eyes, or mouth, or SEM); disseminated disease (with evidence of visceral organ involvement, including liver, lungs, or disseminated intravascular coagulation); and central nervous system disease (where CSF or brain abnormalities are present in the absence of other visceral disease). Skin lesions may occur in all three types.

Skin disease is the most characteristic finding in neonatal HSV infection, but it often lags behind other symptoms in onset and is noted in less than half of infants with disseminated and CNS disease at presentation. Feeding problems and lethargy are the most common presenting complaints. Other signs of infection in neonates include lethargy, temperature instability, jaundice, coagulopathy, hepatitis, respiratory distress and neurologic deterioration. The average age at onset of symptoms is 6–8 days but the average age at diagnosis is 11–13 days, in part due to the lack of specific symptoms or characteristic skin lesions early in the disease course. Of infants with neonatal HSV infection, 17–39% never develop vesicles. Conversely, most infants will develop vesicles at some point in the course of disease. These evolve over time into pustules, crusts, or erosions. Another important form of presentation is a poorly healing fetal scalp monitor site. Although grouped vesicles on an erythematous base are a hallmark of herpetic infection ( Fig. 10.8 ), neonatal herpes lesions frequently lack such grouping, and in some cases a widespread vesicular exanthem or zoster-like blistering localized to one or two dermatomes may occur. Oral ulcerations are present in nearly one-third of cases. Neonatal HSV can recur, more commonly with HSV-2 infection than HSV-1. Vesicles usually develop at the same site as the initial eruption.

Neonatal herpes simplex infection in a 13-day-old infant presenting as grouped pustules on an erythematous base.

(Courtesy of Jeff Lindenberg, MD.)

A maternal history of primary herpes simplex infection, genital ulcerations during pregnancy (even if not diagnosed as HSV), and history of discordant infection with paternal but not maternal history of genital HSV are all risk factors for infection. However, the majority of cases occur in women who are either asymptomatic or whose symptoms go unrecognized. Both intrauterine and neonatal herpes simplex infection can occur even when primary HSV infection is diagnosed during pregnancy and the mother is treated with prophylactic acyclovir, although vertical transmission may be reduced by prophylaxis.

If skin lesions suggest herpes infection, prompt diagnosis and institution of treatment is imperative. Skin scrapings of the blister base for Tzanck preparation are helpful in experienced hands, but direct immunofluorescent stains are more specific for rapid detection. Polymerase chain reaction (PCR) is another way to obtain fast preliminary diagnosis of HSV infection in skin, mucosa and CSF samples, and to assess treatment response. False-positive immunofluorescent studies have occasionally been reported. Viral cultures remain the gold standard of diagnosis, and cultures of the skin, conjunctiva, throat, cerebrospinal fluid, and urine should be obtained.

The differential diagnosis of herpetic skin lesions depends on the specific clinical presentation and is summarized in Table 10.5 . The rarity of neonatal HSV infection in the USA was demonstrated in a study by Caviness and colleagues, at the Texas Children’s Hospital, the largest children’s hospital in the USA: in a 14-year period, only 40 cases were identified, fewer than three per year. When neonates with HSV infection were compared with HSV-negative controls, infected neonates had the following associated factors: maternal primary HSV infection, maternal fever, vaginal delivery, prematurity, postnatal HSV contact, vesicular rash, hypothermia, lethargy, seizures, severe respiratory distress, hepatosplenomegaly, thrombocytopenia, elevated hepatic enzymes, and cerebrospinal fluid (CSF) pleocytosis and proteinosis.

This study serves to further emphasize that many other diseases share features with neonatal HSV. Vesicles and pustules per se are not specific or sensitive for diagnosing neonatal HSV. Moreover, there are some clinical presentations that are unlikely to represent herpes simplex infection . In particular, a vigorous, term infant with a widespread pustular eruption at the time of delivery or within a few hours thereafter is unlikely to have herpes simplex infection. This time course – if due to HSV – would be due to intrauterine infection, which is typically associated with findings of TORCH infection. A premature infant with a widespread vesiculopustular eruption involving the palms and soles could have herpes infection, but is more likely to have congenital candidiasis. Although a high index of suspicion for herpes infection is appropriate, fear of neonatal HSV should not preclude a rational and systematic approach to differential diagnosis. The management of the infant presumed to have herpes simplex infection includes strict isolation and prompt institution of intravenous antiviral therapy while awaiting cultures, and is discussed in more detail in Chapter 13 .

Varicella

Cutaneous stigmata of varicella infection may occur in the newborn period as a result of early intrauterine infection, also referred to as the ‘fetal varicella syndrome,’ ‘congenital varicella,’ and ‘varicella embryopathy.’ Varicella can also occur as a result of intrauterine exposure just prior to delivery. This condition, which should more properly called ‘neonatal varicella,’ is often referred to in the literature as ‘congenital varicella.’

The fetal varicella syndrome may occur as a result of primary varicella infection in the mother, almost always during the first trimester of pregnancy. Cutaneous features include dermatomal scarring and occasional skin ulcerations, but blisters and pustules are not usually present in the neonatal period.

Primary varicella in the neonatal period occurs in one-quarter of infants exposed to maternal varicella during the last 3 weeks of pregnancy, and can be especially severe if exposure occurs between 7 days before and 2 days after delivery. Onset is usually at 5–10 days of age. When maternal infection occurs between 1 and 3 weeks before delivery, partial transplacental immunity results in earlier onset of infection and milder disease.

The skin lesions in neonatal varicella begin as vesicles superimposed on an erythematous base, gradually becoming cloudy and then crusted. The clinical pattern often resembles that seen in immunocompromised hosts. Lesions may be extremely numerous, widespread, and monomorphic, with all lesions occurring at the same stage of development instead of varying. They may also be hemorrhagic and enlarge into bullae.

The most life-threatening complication of neonatal varicella is pneumonia. The diagnosis is usually obvious because of the maternal history. A positive Tzanck preparation and viral cultures are confirmatory. Management is discussed in Chapter 13 .

Young infants can develop primary varicella postnatally from community exposure. The characteristic rash begins as itchy red macules on the scalp, face or trunk that evolve into vesicles on an erythematous base that then crust.

Herpes zoster in healthy children is uncommon. In the newborn period, it almost invariably results from exposure to varicella in utero, including later in pregnancy. HZ can occur later in infancy following primary varicella in utero or infection early in infancy. Wild-type virus can rarely cause HZ even in children who have been vaccinated and have not had a clinically evident infection. Like older children and adults, infants with HZ develop vesicles in a dermatome of a sensory nerve that spread and coalesce. Multiple dermatomes can be involved. Associated symptoms like fever, adenopathy and irritability can accompany the rash. HZ can recur, usually in the same dermatome as the initial episode. Other causes of localized vesicles in infants include HSV infection, bullous impetigo, vesicular insect bite reactions and contact dermatitis.

Cytomegalovirus (CMV) is a relatively common cause of intrauterine and perinatal infection, but presentations with vesicles, bullae or ulcerations are quite rare. In one case report, a premature and growth-retarded infant with hepatitis had two vesicles on the forehead, and blister fluid, as well as saliva and urine, produced a cytopathic effect characteristic of CMV in cell culture. Another term infant who was immuno­competent presented at 3 weeks of age with CMV hepatitis and vesicles and bullae on the face, chest and buttocks that cleared with antiviral therapy. Perineal ulcers developed at 1 month of age in a patient who was biopsied after lack of response to numerous topical therapies. The biopsy demonstrated intranuclear inclusions and positive immunoperoxide staining for CMV.

Enteroviruses are well-recognized causes of vesicular exanthems and enanthems in infants and children. Enterovirus infections may occur congenitally or during neonatal life, particularly in the summer months. One infant with fatal neonatal echovirus 19 infection developed a hemorrhagic bulla associated with gangrene and necrosis of a portion of her hand and fingers. After the newborn period, enteroviruses become a relatively frequent cause of vesicles and erosions. In typical hand, foot and mouth disease, the primary lesion is a small, oval, gray vesicle characteristically located on the hands, feet, mouth and diaper area. However, infants and children with atypical enteroviral exanthems, particularly those due to Coxsackie A6 infection have been reported with impressive, widespread vesicles and bullae ( Fig. 10.9 ). These patients also develop erosions within skin affected by atopic dermatitis, a phenomenon referred to as ‘eczema coxsackium’.

Enterovirus exanthem in a 2-year-old infant.

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