Neonatal toxic shock syndrome-like exanthematous disease (NTED)

The author and colleagues recently discovered an emerging neonatal infectious disease: neonatal toxic shock syndrome-like exanthematous disease (NTED), which is induced by the superantigen toxic shock syndrome toxin-1 (TSST-1), produced by methicillin-resistant Staphylococcus aureus (MRSA). The massively expanded Vbeta2+ T cells were rapidly deleted in the peripheral blood of patients with NTED. A marked depletion of Vbeta2+ T cells was also observed in the peripheral blood before the expansion of these T cells. Anergy is specifically induced in the TSST-1 reactive T cells of patients with NTED. Rapid recovery from NTED without complications is expected to be related to the induction of immunologic tolerance in neonatal patients. Anti-TSST-1 IgG antibody of maternal origin was found to play a protective role in preventing the development of NTED. The number of hospitals that have experience caring for patients with NTED has increased threefold in the past 5 years. Most MRSA isolates from neonatal intensive care units in Japan were found to be a single clone of coagulase type II and to possess TSST-1 and staphylococcal enterotoxin C genes. The timing and increased incidence of NTED suggest the emergence of a new MRSA clone. By recognizing that TSST-1 can induce NTED, healthcare providers may give increased attention to this disease in neonatal wards.     

Fulminant liver failure in a child with invasive group A streptococcal infection

Liver involvement is mentioned in streptococcal toxic shock syndrome, but never as fulminant liver failure (FLF). We report the case of a 2-year-old child who developed isolated FLF secondary to invasive group A streptococcal infection without shock due to a M1T1-type strain expressing speA, speB and speC toxin genes. On antibiotics, he recovered rapidly without liver transplantation. CONCLUSION: A streptococcal pyrogenic exotoxin likely constituted the initial insult leading to FLF. This etiology can be included in the differential diagnosis of FLF and would support early introduction of antibiotics.     

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     

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.     

Toxic shock syndrome associated with poison oak dermatitis

Toxic shock syndrome commonly occurs in menstruating women, but it is known to be associated with a variety of staphylococcal infections. We report a case of nonmenstrual toxic shock syndrome in an 11-year-old male who presented with altered consciousness and infected poison oak dermatitis of the feet. This is the first reported case of toxic shock syndrome associated with poison oak dermatitis. The signs and symptoms, laboratory findings, and treatment of toxic shock syndrome are reviewed.     

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.     

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.     

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.     

A severe case of neonatal toxic shock syndrome-like exanthematous disease with superantigen-induced high T cell response

Most newborn patients with a neonatal type of toxic shock syndrome (TSS), called neonatal TSS-like exanthematous disease (NTED), exhibit mild clinical symptoms. We present the case of a patient with NTED who exhibited exceptionally severe clinical symptoms and an adult-type T cell response to the causative toxin TSS toxin-1.     

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     

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.     

Acute epidermal necrolysis of Lyell syndrome

Acute epidermal necrolysis may be caused by staphylococcal toxins (staphylococcal scalded skin syndrome and toxic shock syndrome) or may be related to usually drug-induced hyper-sensitivity mechanisms (toxic epidermal necrolysis). Diagnostic certainty can only be obtained by histologic localisation of a cleavage plane which is intraepidermal in staphylococcal scalded skin syndrome but situated at the dermo-epidermal junction in toxic epidermal necrolysis. Steroid therapy is indicated in toxic epidermal syndrome. This report of two cases of acute epidermal necrolysis emphasizes the importance of an early skin biopsy for accurate diagnosis and appropriate treatment.     

Pediatric streptococcal toxic shock syndrome.

Two children who presented with fever, rash, and hypotension were found to have group A beta hemolytic streptococcal toxic shock syndrome. These cases are reported to remind physicians who care for acutely ill children that exotoxin-producing streptococci can produce clinical features and multisystem failure similar to staphylococcal toxic shock syndrome.     

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 in a 6-year-old male

Toxic shock syndrome, caused by an exotoxin of staphylococcus aureus is very rare in children. On admission, beside the shock, abdominal problems as vomiting, diarrhoea and a developing adynamic ileus were outstanding in our patient. Not before additional symptoms as staphylococcal pneumonia with bacteriemia occurred and later desquamation of palms and feet, diagnosis of toxic shock syndrome could be confirmed.     

Toxic shock syndrome in 2 girls with pharyngeal infection and wound infection

In 1981, a 13 year old girl died of her shock lung. She had been admitted with the classical toxic shock syndrome then still unknown to us. Staphylococcus aureus had been cultured from a pharyngeal swab. But even in 1987, it took us 48 hours to correctly diagnose the toxic shock syndrome in a 17 year old girl. The diagnosis became evident when she was found to have a staphylococcus aureus wound infection after a surgical procedure. For pediatricians, it is crucial to know this syndrome well. Not only menstruating girls using tampons, but also quite young children can acquire this disease. Quick diagnosis and prompt institution of the correct therapy can be life saving.     

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.     

Systemic complications associated with bacterial tracheitis.

The toxic shock syndrome, septic shock, pulmonary oedema, and the acute respiratory distress syndrome (ARDS) were recognised in four children with bacterial tracheitis. ARDS has not previously been reported in association with bacterial tracheitis. Prompt recognition of the severe systemic complications of bacterial tracheitis could lead to a decrease in the morbidity and mortality of this condition.     

A family of selective immunodeficiency with normal immunoglobulins: possible autosomal dominant inheritance

We report here our findings in two Japanese siblings who experienced recurrent bacterial and viral infections since early infancy. Recent symptoms included diarrhoea, conjunctivitis, rashes, headache, sore throat, joint pain, vomiting and vertigo, all similar to those seen in toxic shock syndrome, except for shock. These symptoms improved following gammaglobulin treatment.Staphylococcus aureus with coagulase type IV was continuously isolated from nasal smears producing toxic shock syndrome toxin-1 (TSST-1). Serum antibodies did not or only poorly responded to TSST-1, diphtheria toxoid, varicella virus and rubella virus, whereas total and subclass levels of serum immunoglobulin and in vitro DNA synthesis of lymphocytes stimulated by TSST-1,Staph. aureus, varicella vaccine and mitogens were normal. In the family, ten other members in three generations (five males: five females) including the mother had similar clinical symptoms. Thus, the disease may be inherited in an autosomal dominant fashion.