Arch Dis Child 1998 Ladhani 85 8

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CURRENT TOPIC

Staphylococcal scalded skin syndrome

Shamez Ladhani, Robert W Evans

The diseaseStaphylococcal scalded skin syndrome (SSSS)is the clinical term used for a spectrum of blis-

tering skin diseases induced by the exfoliative(epidermolytic) toxins (ET) of Staphylococcus

aureus.1 Current synonyms include Ritters dis-

ease, bullous impetigo, pemphigus neonato-rum, and staphylococcal scarlatiniform rash. Itis a disease primarily aVecting infants and

young children,2 but cases have been reportedin adults.3 It seems that the location of lesions

depends on age. In neonates, the lesions aremostly found on the perineum or periumbili-

cally, or both, while the extremities are morecommonly aVected in older children.2 The dis-ease begins with erythema and fever, followed

by formation of large fluid filled bullae whichquickly rupture on slightest pressure (Nikolskysign) to leave extensive areas of denuded skin.

The form and severity of SSSS will vary withthe route of delivery of the toxin to the skin,ranging from the localised bullous impetigo to

generalised SSSS involving the entire skinsurface.24 In the latter, patients are susceptibleto poor temperature control, extensive fluid

losses, and secondary infections. They may also

develop sepsis and present with hypotension,neutropenia, and respiratory distress.5 Anti-biotic treatment with -lactamase resistantsemisynthetic penicillins such as flucloxacillinis usually eVective.3 6 Outbreaks of SSSSinvolving a large number of babies in neonatal

wards are not uncommon and may persist for along time if carriers of toxin producing S aureusare not rapidly identified and treated.69

Considering the severity of the disease andthe amount of published work, it is surprisinghow little progress has been made in under-standing the mode of action of the toxin andthe epidemiology of the disease. Much workover the years on SSSS has been uneventful

and repetitivea large outbreak or a fatal out-come usually results in a surge of interest in thedisease, which soon declines until the nextevent. There have been no major break-throughs in management or prevention overthe past 25 years. It is true that because of theease of treatment of SSSS with eVective antibi-otics and the lack of long term sequelae such asscarring, there is very little pressure forresearch into the disease and the toxins thatcause it. However, the mortality is still 3% inchildren,10 11 and over 50% in adults, reachingalmost 100% in those with underlying disease(see below), despite antibiotic treatment.3

Potential problems with antibiotic resistance

have also recently arisen with the isolation of a

methicillin resistant toxin producing strain of S

aureus in a case of SSSS in Japan. 12

The toxins

The role of the exfoliative toxins in SSSS was

demonstrated as far back as 1970,1 but their

mechanism of action remains elusive 25 years

later, even though their physicochemical prop-

erties and, more recently, aspects of their mode

of action have been extensively studied. The

two known toxins (ETA and ETB) act specifi-

cally in the zona granulosa of the epidermis,13

and even intraperitoneal inoculation will result

in exfoliation. Immunocytochemical studies

have shown that the toxin binds to the filaggrin

group of proteins in keratohyalin granules,14

and because filaggrins act as intracellular

anchors of desmosomes, many investigators

have speculated that epidermal splitting is a

result of rupture of these desmosomes, prob-

ably from proteolytic activity of the toxins.1517

The toxins in their native form, however, do

not have any significant proteolytic activity,18 19

and the hypothesis that they may be serine

proteases comes from indirect evidence: (1)

both toxins show significant sequence homol-

ogy with the staphylococcal V8 protease,

particularly in the region of the serineaspartic

acidhistidine catalytic triad that forms the

active site of trypsin-like serine proteases15 ; (2)

replacing any of the three amino acids that

form the catalytic triad of the toxins results in

complete loss of biological activity when

injected into newborn mice16 17 19; (3) incuba-

tion of ETA with neonatal mouse epidermis 18

or neonatal mouse epidermal extract19 results

in the induction of caseinolytic activity in the

supernatant; and (4) recent computer model-ling20 and crystallographic studies21 22 on the

three dimensional structure of the toxins have

revealed a high degree of structural similarity

with known glutamate specific trypsin-like ser-

ine proteases. Deletion studies have shown that

the highly charged amino terminal of the exfo-

liative toxins is essential for their activity,22 and

recent structural studies have led to specula-

tion that this region may be responsible for

binding an epidermal receptor, which in turn

may result in a conformational change that

exposes the toxins active catalytic site.21

Arch Dis Child1998;78:8588 85

Division of

Biochemistry and

Molecular B iology,

UMDS, Guys

Campus, London

Bridge, London

S LadhaniR W Evans

Correspondence to:

Dr Shamez Ladhani, 65

Littlemede, Cold Harbour

Estate, Mottingham, London

SE9 3ED, UK

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Epidemiology

Staphylococcus aureus is a Gram positive coccus

which colonises the nose, perineum, axillae,

eyes, wound sites, and toe webs.23 Two toxin

serotypes are knownETA and ETBbut

others may exist.24 In the West, 8085% of

toxin producing S aureus belong to phage

group II,3 and around 90% of toxin producing

strains produce ETA.25 In contrast, in Japan

there is a predominance of ETB producing

strains, which are less likely to be of phagegroup II.26 27 A recent Nigerian study showed

that healthy animals can carry exfoliatin

producing S aureus,28 and a previous study

identified toxin producing strains in inanimate

objects such as ventilation shafts in a hospital. 29

Both may act as reservoirs of infection, but

their impact on human SSSS has not been

determined.

Large epidemiological studies have found

toxin producing strains of S aureus in 5.1% of

944 isolates from 577 dermatological patients

screened,10 6.2% of 2362 isolates from hospital

inpatients,30 3% of isolates from 500 antenatal

women,31 and 4.0% of isolates from various

clinical sources in Nigeria.28 Hargiss andLarson found that up to 60% of newborn

babies discharged from the hospitals may be

nasal carriers ofS aureus.32 If approximately 5%

of the strains produce the exfoliative toxins,

then as many as 3% of all neonates may carry

toxin producing strains of S aureus.

However, the incidence of SSSS does not

seem to be as common as might be expected.

This might be the result of any combination of

poor data collection and reporting of the

disease, a lower than reported prevalence of

toxin producing S aureus carriage, or a lowincidence of disease in carriers, possibly

because of high levels of protective antitoxin

antibodies in the population. Studies in 1981showed ETA antibody in 88% of cord blood

samples, reflecting maternal antibody status.11

This level dropped to 30% at 3 months to 2years, then rose steadily to 91% at 40 years. In

cases of generalised SSSS, ETA antibody wasabsent in acute sera (five days) and present inconvalescent sera (14 days). This contrasts

with localised infection, when antibody waspresent in over 60% of acute samples (four to10 days) but was no predictor of spread of dis-

ease. Perhaps maternal antibodies play animportant role in preventing SSSS, as has beenshown in mice,33 and if so breast feeding may be

protective.Factors other than antibodies may also gov-

ern the development and severity of SSSS.

Organism factors may include subtle diVer-ences in S aureus strains or the toxinsthemselves, requirement of a triggering factorfor toxin production, requirement of a cofactor

for the toxins, or the quantity of toxin in theblood. Host factors may include an inappropri-ate immune response to bacteria or their

toxins, the presence of concurrent infectionswhich would lower the host immune response,or a genetically variable site of action of the

exfoliative toxins, which would make someindividuals more susceptible than others.

Healthy adults rarely develop SSSS, and theonly two reported cases have been due toETB,3 although it is not known whether this isa coincidence or whether ETB is morecommonly able to aVect healthy adults. Re-ported risk factors for adult SSSS includeimmunosuppression (including immunosup-pressive drugs and AIDS), renal failure, malig-nant disease, chronic alcohol abuse, andintravenous drug addiction.3 However, it is still

not clear whether the disease is the result of ahigher carriage rate of toxin producing Saureus, increased susceptibility to the toxins,lack of protective antitoxin antibodies, or just amanifestation of a generalised increase in therisk of infections.

DiagnosisIn the United Kingdom, SSSS diagnosis iscurrently based mainly on clinical grounds,supported by the presence of S aureus in nasal,conjunctival, pharyngeal, umbilical, or otherswabs, although these criteria are not alwaysreliable.34 If confirmation of the diagnosis isrequired, or when outbreaks occur, isolates can

be sent to the Public Health Laboratory(PHL), London, where the S aureus will bephage typed (this service is not routinely avail-able in hospital laboratories). The presence ofisolates in phage group II will strongly supportthe diagnosis of SSSS, even though other phagetypes have been shown to produce an identicalclinical picture.35 If further confirmation of thediagnosis is required, the PHL may test fortoxins using the immunological Ouchterlonymethod, which lacks sensitivity and specificity.

Other detection systems have been devel-oped for the exfoliative toxins, includingserological methods of gel immunoprecipita-tion, radioimmunological assays, enzymelinked immunosorbent assays, and detection of

gene sequences by DNA hybridisation andpolymerase chain reaction.36 False positiveresults may occur in serological studies due toprotein A, a 42 kDa protein produced by over90% of S aureus, which binds non-specificallyto the constant (Fc) domain of immunoglobulins.37 These detection systemswere developed for use in research laboratoriesrather than clinical settings and tend to beeither very expensive or too time consuming forroutine use.

ResearchWhile a great deal of information is stilllacking, two particular areas of research merit

more attention: the development of a standardassay for the exfoliative toxins, and elucidationof their mechanism of action.

DEVELOPING A STANDARDISED ASSAY

The availability of a sensitive, specific, reliableclinical diagnostic kit which is simple to usewould considerably alter the management ofSSSS. Such a kit would allow a confirmeddiagnosis of SSSS, with simple tests to detecttoxin levels in the blood or bullae, to beavailable within a few hours. DiVerential diag-nosis of generalised exfoliation includes druginduced and virus mediated toxic epidermal

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necrolysis, burns, epidermolysis bullosa, bul-lous erythema multiforme, listeria and syphilisinfections, diVuse cutaneous mastocytosis, andgraft versus host rejection.38 Rapid diagnosis ofindividual cases, particularly in adults wheremortality rates are high, is important forinitiating appropriate treatment and reducingmortality. Similarly, the rapid identificationand treatment of asymptomatic carrierswhomay be numerousshould reduce the risk of

large outbreaks of infection.The diagnostic kit would improve our

understanding of the organism responsible, itstoxins, and the diseases they cause. For exam-ple, simple epidemiological data on SSSS, suchas age distribution, sex ratio, ethnic suscepti-bilities, and community as well as nurseryattendant carrier rates, are still lacking. The kitwould also speed up research into the possiblerole of staphylococcal toxins in other condi-tions such as eczema39 and sudden infant deathsyndrome.40

ELUCIDATING THE MECHANISM OF ACTION

All the evidence for the exfoliative toxins being

glutamate specific trypsin-like serine proteasesis indirect and speculative and needs to be sub-stantiated with more research. The problemlies in the lack of a suitable model to study themechanism of action of the toxins. The goldstandard model still remains newborn1 orhairless41 mice, developed over two decadesago. Since then, various attempts have beenmade to develop a simpler and more humanemodel to work on; human epidermis from sur-gery, keratinocyte cultures, and mouse epider-mis have been used to demonstrate epidermalsplitting at the zona granulosa.13 14 42 43 All theseassays are diYcult to perform and replicate,thus hampering research.

However, research using the neonatal mouse

epidermis assay18 19 could be extended to inves-tigate whether the exfoliative toxins are indeedserine proteases and whether they bind to anyreceptors,44 and to elucidate events followingbinding. The model could also be used todetermine any changes occurring in ETA,including a conformational change after recep-tor binding to expose the active catalytic site, ashas recently been speculated from structuralmodels.21 22 The main diYculty is the use ofmouse epidermis, but keratinocytes cell cul-tures, for example, may provide an alternativesubstitute.

Understanding the mechanism of action ofthe toxins has several important implications.

For example, their ability to target a specificlayer within the epidermis could be used toinvestigate the normal physiology of the skin byidentifying, marking, and isolating specificgroups of cells and cell structures. Similarly, ifthe toxins targeting domain can be identified,it may be possible to attach and deliver potentdrugs, such as chemotherapeutic agents, tospecific sites within the skin, thereby reducingthe dose required and systemic side eVects.Other toxins, such as diphtheria and pseudo-monas exotoxin A,45 have already served asimilar purpose and provided novel treatmentsfor various carcinogenic, immunological, and

haematological disorders. Furthermore, if anti-toxin antibodies are shown to protect againstSSSS, then inactive toxoids may be developedto provide active immunisation in susceptiblepopulations.

The localised blistering seen in most healthyindividuals with SSSS could be exploitedto produce a localised and controlledexfoliationfor example, to remove a superfi-cial oVending skin lesion.

Finally, discovering the mechanism of actionof these toxins may lead to the development ofeVective antitoxins. Given concurrently withantibiotics, antitoxins may abort exfoliation ifSSSS is diagnosed early, or may decrease theextent of exfoliation in severe cases, as mayoccur in late presentation or delayed diagnosisof the disease, in antibiotic resistant S aureusstrains that do not respond to conventionalantibiotics and in patients with underlying dis-ease, where mortality rates are high.

ConclusionsAlthough SSSS is relatively uncommon, usu-

ally easily diagnosed on clinical grounds, andreadily treated with conventional antibiotics, itis important to emphasise that at presentmortality rates are still unacceptably high, out-breaks are diYcult to control, and the second-ary complications, which are particularly com-mon in neonates, can often be lethal.Furthermore, clinicians should be aware ofthree recently emerging trends. Firstly, al-though phage group II staphylococci onlyrarely develop antibiotic resistance,3 onesuch case has already been described recently,12

and it is well known that hospital outbreaks ofmultiresistant organisms are diYcult andexpensive to control and carry a high mortalityrate.

Secondly, in the 1980s several studiesshowed that the use of antiseptic neonatalumbilical cord care delayed the time of cordseparation,4648 and this may produce parentalconcern and increase midwives workload.Since then, there has been a gradual decline inthe use of antiseptic umbilical cord care in theUnited Kingdom. However, several studieshave shown that this practice has led to asignificant increase in staphylococcal umbilicalcolonisation, which in turn may lead to anincrease in neonatal infections, including SSSSand methicillin resistant S aureus outbreaks.4951

Finally, the recent pressure to dischargepatients early from hospitals, particularly

mothers and their newborn babies, may serveto dissipate outbreaks (including SSSS)caused by hospital staV in close contact withneonatesinto the community.6 While indi-vidual cases can easily be treated by theprimary health care team, delays in recognisingan outbreak mean that carriers still working inthe hospital will continue to infect morepatients until identified, isolated, and treated.StaV should therefore ensure rigorous aseptictechnique with hospital patients, particularlywith neonates, and clinicians should beware ofa possible outbreak, even if patients presentwith infection after hospital discharge.

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In conclusion, the chapter on SSSS is by nomeans closed. Much work has to be done byboth researchers and clinicians, and there isnow added pressure to do so more quickly.SSSS researchers should be encouraged topublish more of their work, including negativefindings, while clinicians should be collectingand combining more data and performing sim-ple epidemiological studies on the disease andthe organism responsible. It is only through

such collaborative work that wasteful repetitiveresearch will be reduced and a more integratedapproach taken to tackle the disease once andfor all.

This work is the result of ideas and suggestions derived fromgroup discussions and debates held within the Division of Bio-chemistry and Molecular Biology and the Division of Microbi-ology at UMDS,London. We would specifically like to thank DrS Poston, Dr C L Joannou, and Miss J Cameron. The work onSSSS has been supported by the Trustees of Guys Hospital,The Clothworkers Foundation, and The Agakhan Foundation.

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doi: 10.1136/adc.78.1.851998 78: 85-88Arch Dis Child

Shamez Ladhani and Robert W EvansStaphylococcal scalded skin syndrome

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Arch Dis Child 1998 Ladhani 85 8