Understanding host's response to staphylococcal scalded skin syndrome.
desmoglein‐1
exfoliative toxins
staphylococcal scalded skin syndrome
Journal
Acta paediatrica (Oslo, Norway : 1992)
ISSN: 1651-2227
Titre abrégé: Acta Paediatr
Pays: Norway
ID NLM: 9205968
Informations de publication
Date de publication:
16 Oct 2024
16 Oct 2024
Historique:
revised:
24
08
2024
received:
07
05
2024
accepted:
08
10
2024
medline:
16
10
2024
pubmed:
16
10
2024
entrez:
16
10
2024
Statut:
aheadofprint
Résumé
The aim of this review was to summarise the current knowledge on host-related factors that contribute to the development and severity of staphylococcal scalded skin syndrome (SSSS) in children. A comprehensive assessment and analysis of the existing literature on SSSS clinical features, pathogenesis and susceptibility factors. SSSS is a blistering skin disease caused by circulating exfoliative toxins (ETs) of Staphylococcus aureus (S. aureus), almost exclusively affecting infants, young children and immunocompromised individuals. ETs possess serine protease activity and target desmoglein-1 (Dsg-1) in the superficial epidermis. While the role of S. aureus ETs and site of action are well-described, other host factors such as impaired immune responses to ETs, poor renal clearance and genetic factors are crucial for the onset of and/or the severity of SSSS in children. The fate of desmosomal fractions after cleavage by ETs, as well as the role of dermal inflammatory cell infiltrates remain to be elucidated.
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© 2024 The Author(s). Acta Paediatrica published by John Wiley & Sons Ltd on behalf of Foundation Acta Paediatrica.
Références
Ross A, Shoff HW. Staphylococcal Scalded Skin Syndrome. StatPearls. StatPearls Publishing; 2023.
Staiman A, Hsu DY, Silverberg JI. Epidemiology of staphylococcal scalded skin syndrome in U.S. children. Br J Dermatol. 2018;178(3):704‐708.
Dollani LC, Marathe KS. Impetigo/staphylococcal scalded skin disease. Pediatr Rev. 2020;41(4):210‐212.
Hultén KG, Kok M, King KE, Lamberth LB, Kaplan SL. Increasing numbers of staphylococcal scalded skin syndrome cases caused by ST121 in Houston, Texas. Pediatr Infect Dis J. 2020;39(1):30‐34.
Ladhani S. Understanding the mechanism of action of the exfoliative toxins of Staphylococcus aureus. FEMS Immunol Med Microbiol. 2003;39(2):181‐189.
Mariutti RB, Tartaglia NR, Seyffert N, et al. Exfoliative toxins of Staphylococcus aureus. Rise Virulence Antibiot Resist Staphylococcus Aureus. 2017;2:1148‐1165.
Braunstein I, Wanat KA, Abuabara K, McGowan KL, Yan AC, Treat JR. Antibiotic sensitivity and resistance patterns in pediatric staphylococcal scalded skin syndrome. Pediatr Dermatol. 2014;31(3):305‐308.
Gray L, Olson J, Brintz BJ, Cipriano SD. Staphylococcal scalded skin syndrome: clinical features, ancillary testing, and patient management. Pediatr Dermatol. 2022;39(6):908‐913.
Patel GK. Treatment of staphylococcal scalded skin syndrome. Expert Rev Anti‐Infect Ther. 2004;2(4):575‐587.
Abaev I, Skryabin Y, Kislichkina A, et al. Draft genome sequences of Exfoliative toxin A‐producing Staphylococcus aureus strains B‐7772 and B‐7777 (CC8/ST2993) and B‐7774 (CC15/ST2126), isolated in a maternity hospital in the Central Federal District of Russia. Genome Announc. 2016;4(2):e00064‐16.
Aydin D, Alsbjørn B. Severe case of staphylococcal scalded skin syndrome in a 5‐year‐old child ‐ case report. Clin Case Reports. 2016;4(4):416‐419.
Oliveira D, Borges A, Simões M. Staphylococcus aureus toxins and their molecular activity in infectious diseases. Toxins (Basel). 2018;10(6):252.
Brazel M et al. Staphylococcal Scalded Skin Syndrome and Bullous Impetigo. Medicina (Kaunas, Lithuania) Vol 57; 2021:1157.
Leung AKC, Barankin B, Leong KF. Staphylococcal‐scalded skin syndrome: evaluation, diagnosis, and management. World J Pediatr. 2018;14:116‐120.
Sakr A, Brégeon F, Mège JL, Rolain JM, Blin O. Staphylococcus aureus nasal colonization: an update on mechanisms, epidemiology, risk factors, and subsequent infections. Front Microbiol. 2018;9:2419.
Panierakis C, Goulielmos G, Mamoulakis D, Maraki S, Papavasiliou E, Galanakis E. Staphylococcus aureus nasal carriage might be associated with vitamin D receptor polymorphisms in type 1 diabetes. Int J Infect Dis. 2009;13(6):e437‐e443.
Reiss‐Mandel A, Rubin C, Maayan‐Mezger A, et al. Patterns and predictors of Staphylococcus aureus carriage during the first year of life: a longitudinal study. J Clin Microbiol. 2019;57(9):e00282‐19.
Chatzakis E, Scoulica E, Papageorgiou N, Maraki S, Samonis G, Galanakis E. Infant colonization by Staphylococcus aureus: role of maternal carriage. Eur J Clin Microbiol Infect Dis. 2011;30(9):1111‐1117.
Geoghegan JA, Irvine AD, Foster TJ. Staphylococcus aureus and atopic dermatitis: a complex and evolving relationship. Trends Microbiol. 2018;26(6):484‐497.
Imanishi I, Nicolas A, Caetano AB, et al. Exfoliative toxin E, a new Staphylococcus aureus virulence factor with host‐specific activity. Sci Rep. 2019;9(1):16336.
Yamaguchi T, Hayashi T, Takami H, et al. Complete nucleotide sequence of a Staphylococcus aureus exfoliative toxin B plasmid and identification of a novel ADP‐ribosyltransferase, EDIN‐C. Infect Immun. 2001;69:7760‐7771.
Jenul C, Horswill AR. Regulation of Staphylococcus aureus virulence. Microbiol Spectr. 2019;7(2). doi:10.1128/microbiolspec.GPP3-0031-2018
Iwatsuki K, Yamasaki O, Morizane S, Oono T. Staphylococcal cutaneous infections: invasion, evasion and aggression. J Dermatol Sci. 2006;42(3):203‐214.
Mahoney MG, Wang Z, Rothenberger K, Koch PJ, Amagai M, Stanley JR. Explanations for the clinical and microscopic localization of lesions in pemphigus foliaceus and vulgaris. J Clin Invest. 1999;103(4):461‐468.
Chidgey M, Brakebusch C, Gustafsson E, et al. Mice lacking desmocollin 1 show epidermal fragility accompanied by barrier defects and abnormal differentiation. J Cell Biol. 2001;155(5):821‐832.
Nishifuji K, Shimizu A, Ishiko A, Iwasaki T, Amagai M. Removal of amino‐terminal extracellular domains of desmoglein 1 by staphylococcal exfoliative toxin is sufficient to initiate epidermal blister formation. J Dermatol Sci. 2010;59(3):184‐191.
Mohseni M, Rafiei F, Ghaemi EA. High frequency of exfoliative toxin genes among Staphylococcus aureus isolated from clinical specimens in the north of Iran: alarm for the health of individuals under risk. Iran J Microbiol. 2018;10(3):158‐165.
Andrade‐Figueiredo M, Luz ACO, Mota Silveira Filho VD, Leal‐Balbino TC. Comparison of genotyping methods and toxin gene profiles of Staphylococcus aureus isolates from clinical specimens. Genet Mol Biol. 2023;46:e20220321.
Fritsch P, Elias P, Varga J. The fate of staphylococcal exfoliatin in newborn and adult mice. Br J Dermatol. 1976;95(3):275‐284.
Plano LR, Adkins B, Woischnik M, Ewing R, Collins CM. Toxin levels in serum correlate with the development of staphylococcal scalded skin syndrome in a murine model. Infect Immun. 2001;69(8):5193‐5197.
Ouchi T, Kubo A, Yokouchi M, et al. Langerhans cell antigen capture through tight junctions confers preemptive immunity in experimental staphylococcal scalded skin syndrome. J Exp Med. 2011;208(13):2607‐2613.
Anzai H, Stanley JR, Amagai M. Production of low titers of anti‐desmoglein 1 IgG autoantibodies in some patients with staphylococcal scalded skin syndrome. J Invest Dermatol. 2006;126(9):2139‐2141.
Paquet P, Piérard GE. Differential pathomechanisms of epidermal necrolytic blistering diseases. Int J Mol Med. 2002;10(6):695‐699.
Rolle CE, Chen J, Pastar I, et al. Keratinocytes produce IL‐6 in response to desmoglein 1 cleavage by Staphylococcus aureus exfoliative toxin A. Immunol Res. 2013;57(1–3):258‐267.
Jin Jung W, Kim SW, Hwang YH. The characteristics of staphylococcal scalded skin syndrome in atopic dermatitis. Kosin Med J. 2019;34(2):138‐145.
Ogonowska P, Gilaberte Y, Barańska‐Rybak W, Nakonieczna J. Colonization with Staphylococcus aureus in atopic dermatitis patients: attempts to reveal the unknown. Front Microbiol. 2021;11:567090.
Conte AL, Brunetti F, Marazzato M, et al. Atopic dermatitis‐derived Staphylococcus aureus strains: what makes them special in the interplay with the host. Front Cell Infect Microbiol. 2023;13:1194254.
Capoluongo E, Giglio AA, Lavieri MM, et al. Genotypic and phenotypic characterization of Staphylococcus aureus strains isolated in subjects with atopic dermatitis. Higher prevalence of exfoliative B toxin production in lesional strains and correlation between the markers of disease intensity and colonization density. J Dermatol Sci. 2001;26:145‐155.
Yagi S, Wakaki N, Ikeda N, et al. Presence of staphylococcal exfoliative toxin a in sera of patients with atopic dermatitis. Clin Exp Allergy. 2004;34(6):984‐993.
Ayed MB, Martel P, Zitouni M, et al. Tunisian endemic pemphigus foliaceus is associated with desmoglein 1 gene polymorphism. Genes Immun. 2002;3(6):378‐379.
Basurto C, Baah‐Owusu N, Berreth K. Recurrent staphylococcal scalded skin syndrome in a 20‐month old‐a case report. Clin Case Reports. 2023;11(8):e7805.
Ajmi H, Jemmali N, Mabrouk S, et al. Staphylococcal scalded skin syndrome: an uncommon symptomatology revealing an immune deficiency. Arch Pediatr. 2018;25:126‐128.
Chao SC, Richard G, Lee JY. Netherton syndrome: report of two Taiwanese siblings with staphylococcal scalded skin syndrome and mutation of SPINK5. Br J Dermatol. 2005;152:159‐165.
Kurz H, Lehmberg K, Farmand S. Inborn errors of immunity with susceptibility to S. aureus infections. Front Pediatr. 2024;12:1389650.
Simpson CL, Kojima S, Cooper‐Whitehair V, Getsios S, Green KJ. Plakoglobin rescues adhesive defects induced by ectodomain truncation of the desmosomal cadherin desmoglein 1: implications for exfoliative toxin‐mediated skin blistering. Am J Pathol. 2010;177(6):2921‐2937.
Yang L‐Y et al. Protective effects of a nanoemulsion adjuvant vaccine (2C‐staph/NE) administered intranasally against invasive Staphylococcus aureus pneumonia. RSC Adv. 2018;8(18):9996‐10008.
Mancini F, Monaci E, Lofano G, et al. One dose of Staphylococcus aureus 4C‐staph vaccine formulated with a novel TLR7‐dependent adjuvant rapidly protects mice through antibodies, effector CD4+ T cells, and IL‐17A. PLoS One. 2016;11(1):e0147767.