Early diagnosis of staphylococcal toxic shock syndrome by detection of the TSST-1 Vbeta signature in peripheral blood of a 12-year-old boy

We report the case of a 12-year-old boy who developed staphylococcal toxic shock syndrome associated with S. aureus pharyngeal colonization or infection. The diagnosis was rapidly confirmed by detecting the Vbeta signature of the toxic shock syndrome toxin-1 in peripheral blood, based on transient T cell depletion rapidly followed by massive expansion of Vbeta 2-positive T cells.     

Bullous impetigo: a rare presentation in fulminant streptococcal toxic shock syndrome

Since the mid-1980s, an increase in incidence of invasive disease caused by group A streptococci has been noted among adults and children. The characteristic clinical and laboratory features of the streptococcal toxic shock syndrome include deep-seated infection associated with shock, skin manifestation, and multiorgan failure. However, bullous impetigo is invariably considered to be a staphylococcal disease. Staphylococcus aureus produces an epidermolytic toxin, assumed to be the cause of bullous formation in the skin. Here, we present a case of bullous impetigo in an infant with streptococcal toxic shock syndrome. This is a rare presentation of bullous impetigo caused by group A streptococcus.     

Toxic shock syndrome caused by a strain of Staphylococcus aureus that produces enterotoxin C but not toxic shock syndrome toxin-1

An 8-month-old infant presented with pneumonia and pleural effusion associated with clinical manifestation of toxic shock syndrome. A Staphylococcus aureus strain isolated from the pleural fluid produced enterotoxin C, but not toxic shock syndrome toxin-1 or other enterotoxins. Acute and convalescent sera showed an antibody rise to enterotoxin C but not to toxic shock syndrome toxin-1. These findings support the possibility that enterotoxin C was the primary toxin associated with this infant's illness.     

Toxic shock syndrome in a neonate

We report an unusual case of toxic shock syndrome in a 4-day-old baby, with mucosal isolates of Staphylococcus aureus (SEC, G, and I) and group G streptococcus. Treatment involved intravenous immunoglobulin and antibiotics. This case highlights the difficulties associated with the diagnosis and treatment of this condition in neonates.     

Necrotizing haemorrhagic pneumonia proves fatal in an immunocompetent child due to Panton-Valentine Leucocidin, toxic shock syndrome toxins 1 and 2 and enterotoxin C-producing Staphylococcus aureus

Panton-Valentine leucocidin (PVL) toxin-producing strains of Staphylococcus aureus (S. aureus) are associated with skin abscesses and furunculosis, with necrotizing pneumonia being a relatively rare problem. Here, we describe a fatal case of necrotizing pneumonia in a 14-year-old child who presented initially with sore throat and pyrexia. He deteriorated rapidly, developing hypotension, multiple organ failure and purpura fulminans. S. aureus was isolated from the tracheal aspirate, which was found to be positive for PVL, toxic shock syndrome toxins (TSST) 1 and 2 and staphylococcal enterotoxin C (SEC). It was postulated that purpura fulminans and toxic shock syndrome were a result of the abovementioned exotoxins. CONCLUSION: This case highlights the emergence of PVL-positive community-acquired S. aureus infection and association of purpura fulminans with superantigens. Practitioners should be aware of this illness in order to initiate appropriate treatment.     

Necrotizing haemorrhagic pneumonia proves fatal in an immunocompetent child due to Panton–Valentine Leucocidin, toxic shock syndrome toxins 1 and 2 and enterotoxin C-producing Staphylococcus aureus

Panton–Valentine leucocidin (PVL) toxin-producing strains of Staphylococcus aureus ( S. aureus ) are associated with skin abscesses and furunculosis, with necrotizing pneumonia being a relatively rare problem. Here, we describe a fatal case of necrotizing pneumonia in a 14-year-old child who presented initially with sore throat and pyrexia. He deteriorated rapidly, developing hypotension, multiple organ failure and purpura fulminans. S. aureus was isolated from the tracheal aspirate, which was found to be positive for PVL, toxic shock syndrome toxins (TSST) 1 and 2 and staphylococcal enterotoxin C (SEC). It was postulated that purpura fulminans and toxic shock syndrome were a result of the abovementioned exotoxins.
Conclusion: This case highlights the emergence of PVL-positive community-acquired S. aureus infection and association of purpura fulminans with superantigens. Practitioners should be aware of this illness in order to initiate appropriate treatment.     

Toxic Shock Syndrome in a neonate?

Toxic Shock Syndrome is an acute multisystemic disease, characterized by high fever, hypotension and involvment of the skin and mucous membrane, associated with multisystem dysfunction. It is a rare condition in the paediatric population. We describe a newborn child with asphyxia and meconium aspiration, who developed a temperature of ≥38.9°C, severe hypotension and rash with desquamation, associated with evidence of coagulopathy and renal and muscular dysfunction. Strict CDC criteria of toxic shock syndrome were fulfilled in our patient, with all major criteria verified. These criteria have never been validated in neonates, but in this case some symptoms favour a diagnosis of toxic shock syndrome since they are not associated with birth asphyxia, viral intrauterine infection or other disease. We believe a probable intrapartum transmission occurred through ingestion or aspiration of contaminated amniotic fluid. The patient described in this report is, to our knowledge, one of the youngest described to fulfil all of the strict CDC criteria for Toxic Shock Syndrome.     

Production of antibodies to staphylococcal superantigens in atopic dermatitis.

Staphylococcal superantigens (SAG) are implicated in the inflammation of atopic dermatitis. As SAG mediated diseases may be modified by specific antibodies, the antibody response to SAG in atopic dermatitis was investigated. Immunoglobulin (Ig) G to staphylococcal enterotoxin A (SEA), staphylococcal enterotoxin B (SEB), and toxic shock syndrome toxin 1 (TSST-1) were measured by sandwich enzyme linked immunosorbent assay (ELISA) in 74 children with atopic dermatitis and 111 controls. Controls had detectable IgG to SEA, SEB, and TSST-1, which increased with age. Atopic dermatitis subjects had an increased response to SEB at 6 months to 2 years (76% v 42%) and 2 to 7 years (79% v 57%), and equivalent responses to SEA and TSST-1, compared to controls. It is suggested that increased responses to SEB relate to increased colonisation and hence exposure to superantigen producing staphylococcus in atopic dermatitis, and that inflammation of atopic dermatitis is not caused by an inability to make antibody to SAG.     

Production of antibodies to staphylococcal superantigens in atopic dermatitis

Staphylococcal superantigens (SAG) are implicated in the inflammation of atopic dermatitis. As SAG mediated diseases may be modified by specific antibodies, the antibody response to SAG in atopic dermatitis was investigated. Immunoglobulin (Ig) G to staphylococcal enterotoxin A (SEA), staphylococcal enterotoxin B (SEB), and toxic shock syndrome toxin 1 (TSST-1) were measured by sandwich enzyme linked immunosorbent assay (ELISA) in 74 children with atopic dermatitis and 111 controls. Controls had detectable IgG to SEA, SEB, and TSST-1, which increased with age. Atopic dermatitis subjects had an increased response to SEB at 6 months to 2 years (76% v 42%) and 2 to 7 years (79% v 57%), and equivalent responses to SEA and TSST-1, compared to controls. It is suggested that increased responses to SEB relate to increased colonisation and hence exposure to superantigen producing staphylococcus in atopic dermatitis, and that inflammation of atopic dermatitis is not caused by an inability to make antibody to SAG.     

Infection with Staphylococcus aureus producing toxic shock syndrome (TSS) toxin-1 without TSS

Relevant findings are reported in an 8-year-old boy with skin infection due to Staphylococcus aureus producing toxic shock syndrome toxin-1 without shock but with an increase in antibody titre against the toxin.Abbreviations anti-TSST-1 antibody against toxic shock syndrome toxin 1 - TSS toxic shock syndrome - TSST-1 toxic shock syndrome toxin-1     

Exfoliative dermatitis in an infant. Association with enterotoxin F-producing staphylococci

A 2-month-old premature infant had an extensive exfoliative dermatitis with flaccid bullae, mucous membrane involvement, thrombocytopenia, and an elevated creatinine kinase level. A subepidermal cleavage plane with numerous necrotic epidermal cells and a polymorphonuclear cell infiltrate were present on a skin biopsy specimen. The isolates of Staphylococcus aureus obtained at the onset of her disease had a 29/52 bacteriophage lysis pattern and produced enterotoxins C and F and epidermal toxin, but no exfolliatins. In toxic shock syndrome (TSS), subepidermal blister formation has been described and a new toxin, epidermal toxin, which causes subepidermal cleavage in the newborn mouse model, has been identified. In some infants, exfoliative dermatitis may be a variant of the well-described TSS in older children and adults.     

Streptococcal toxic shock syndrome in children without skin and soft tissue infection: report of four cases

Streptococcal toxic shock syndrome is a fulminant, highly fatal disease characterized by evidence of group A beta-haemolytic streptococcus infection and early shock with consecutive organ failure. In adults, affected individuals usually have preceding skin or soft tissue infection. However, in paediatric patients, except for varicella, the background focus is usually respiratory tract infection, and early diagnosis of streptococcal toxic shock syndrome in such patients is difficult. We report four previously healthy children with streptococcal toxic shock syndrome. Pharyngitis was identified in three cases. All of them had constitutional symptoms such as fever, vomiting, diarrhoea, abdominal pain and physical findings of tachycardia and diffuse abdominal tenderness, but no concomitant skin infection. CONCLUSION: Streptococcal toxic shock syndrome should be considered in paediatric patients with fever, vomiting, diarrhoea, abdominal pain and early shock. Early diagnosis, prompt initiation of antibiotics and aggressive fluid therapy are lifesaving for such patients.     

Failure of viridans group streptococci causing bacteremia in pediatric oncology patients to express superantigens

Group A Streptococcus pyogenes causes a distinctive clinical disorder, streptococcal toxic shock syndrome, mediated by superantigenic bacterial exotoxins. Oncology patients with viridans group streptococcal sepsis frequently present with a streptococcal toxic shocklike syndrome of unclear pathogenesis. Viridans group streptococci isolated from pediatric oncology patients with streptococcal toxic shocklike illnesses do not possess homologs of known superantigen genes. Supernatants from cultures of these bacteria also fail to stimulate T-cell proliferation, suggesting these bacteria do not commonly elaborate superantigens. Adjunctive treatment with intravenous immunoglobulin, which is advantageous in streptococcal toxic shock syndrome, may not benefit these patients.     

Toxic shock syndrome and streptococcal myositis: three case reports

Group A streptococcal (GAS) infection is the most common cause of bacterial pharyngitis and has an important role in the pathogenesis of post-infective phenomena including rheumatic fever and glomerulonephritis. Mortality from GAS is uncommon, particularly in the paediatric population. Toxic shock syndrome reflects the most severe form of GAS-related disease and is often associated with fasciitis or myositis. CONCLUSION: We present three cases of toxic shock syndrome secondary to (GAS) myositis demonstrating the importance of early recognition and provision of intensive care management.     

Bacterial croup and toxic shock syndrome

An 8-year-old boy with bacterial tracheitis, treated by endotracheal intubation, humidification, airway toilet and antibiotics, experienced a toxic shock syndrome on the day after his admission. The course was favourable. Staphylococcus aureus was isolated from tracheal secretions. Bacterial tracheitis is an infrequent cause of non-menstrual toxic shock syndrome. The diagnosis of bacterial tracheitis should be suspected in a child with toxicity and croup who is not responding to the usual therapy. Endoscopy should be performed allowing for removal of the secretions. The maintenance of a clear airway is the main purpose of the treatment.Abbreviations TSS toxic shock syndrome - CNS central nervous system - CRP C-reactive protein - ICU intensive care unit     

Update on the COVID‐19‐associated inflammatory syndrome in children and adolescents; paediatric inflammatory multisystem syndrome‐temporally associated with SARS‐CoV‐2

We provide an update on the state of play with regards a newly described inflammatory condition which has arisen during the current SARS‐CoV‐2 pandemic. The condition has been named paediatric inflammatory multisystem syndrome temporally associated with SARS‐CoV‐2 or multisystem inflammatory syndrome in children. This condition has shown significant similarities to Kawasaki disease and toxic shock syndrome.     

Streptococcus pyogenes pyomyositis

Group A beta-hemolytic Streptococcus pyomyositis continues to be an uncommon disease. We present a case of a 7-year-old boy with an M protein type 1, streptococcal pyrogenic exotoxin A and B, Streptococcus pyogenes pyomyositis and streptococcal toxic shock syndrome.     

Syndrome de choc toxinique streptococcique ou syndrome de Kawasaki ? À propos de 2 cas cliniques d’enfants présentant une pleuropneumopathie à streptocoque bêta hémolytique du groupe A

We report 2 cases of children with group A streptococcus pyogenes pleuropneumonia, in one child associated with Kawasaki disease and in the other with streptococcal toxic shock syndrome. These 2 features, with theoretically well-defined clinical and biological criteria, are difficult to differentiate in clinical practice, however, likely due to their pathophysiological links. In case of clinical doubt, an echocardiography needs to be performed to search for coronary involvement and treatment including intravenous immunoglobulins, and an antibiotic with an anti-toxin effect such as clindamycin has to be started early.     

Streptococcus associated toxic shock.

In the past few years, there appears to have been a change in the spectrum of disease caused by group A beta-haemolytic streptococcus (GABHS), and a toxic shock-like syndrome caused by this organism has recently been described in adults. We report four children with an acute illness characterised by rapid progression of shock, erythematous rash, multisystem organ involvement, electrolyte derangements, and desquamation who fulfil the previously established diagnostic criteria for toxic shock syndrome. Three of the children had extensive cutaneous and soft tissue infection and the fourth had peritonitis. All four developed bacteraemia. Treatment included aggressive cardiovascular resuscitation and antibiotic therapy. Although no patient died, they suffered multiple and severe complications requiring prolonged treatment and hospitalisation. Streptococcal toxic shock syndrome is a separate and clearly defined entity occurring in previously healthy children.     

Coronary Artery Dilatation in Toxic Shock-Like Syndrome: The Kawasaki Disease Shock Syndrome

Kawasaki disease is a common systemic vasculitis of childhood that may result in life-threatening coronary artery abnormalities. Despite an overlap of clinical features with toxic shock syndrome, children with Kawasaki disease generally do not develop shock. We report two cases of older children who presented with a toxic shock-like illness, and were diagnosed with Kawasaki disease when coronary artery abnormalities were found on echocardiography, in keeping with the recently described ‘Kawasaki disease shock syndrome’. Clinicians should consider Kawasaki disease in all children presenting with toxic shock and assess for coronary artery damage.