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• W2093618066 abstract "Toxic shock syndrome (TSS) is a rare and potentially life-threatening condition that arises from exposure to 1 or more superantigens from Staphylococcus aureus, such as TSS toxin-1 (TSST-1). By binding simultaneously to invariant region of Major Histocompatibility Complex II and β chains of T cell receptors, the toxins cause polyclonal T cell activation, resulting in a cytokine storm and sepsis syndrome.1 Many individuals make antibodies to toxin moieties, which are thought to be protective.2 A small proportion of TSS cases develop during menstruation for reasons that are not well-defined. TSS may be recurrent; it is hypothesized that repeated episodes signify defects in the ability to generate appropriate antibodies.1 CASE PRESENTATION Patient AB was a healthy 15-year-old adolescent when she first developed TSS. Medical/Gynecologic/Family History AB had menarche at 13 years and her cycle length ranged from 28 to 44 days, with 5–7 days of bleeding. She had always used tampons. She had mild hay fever from the age of 13 years. She had tympanostomies formed as a toddler and had a cyst removed from her scalp. At 14 years of age, AB developed impetigo on both arms in the antecubital fossae, which resolved with the application of a topical antibiotic. Some 2–3 months before presentation, she had been seen by her general practitioner for fatigue and swollen glands. Testing for Epstein-Barr virus was negative and her routine blood count at the time was unremarkable. There was no family history relating to any predisposition to staphylococcal infections. Presenting Features, Investigations and Outcome AB presented to a hospital in Spain with a 24-hour history of vomiting and diarrhea, fever and drowsiness. On examination, she was hypotensive with a temperature of 38.5°C. A widespread rash developed—this was thought to be sunburn. Intravenous fluids, an intravenous cephalosporin and paracetamol were given. The initial diagnosis was traveler’s diarrhea with sunstroke. During the second hospital day, AB’s oxygen requirement increased and inotropic support was required. Renal and liver impairment developed. AB was transferred to the intensive care unit for 5 days but did not require ventilation. The provisional diagnosis was changed to sepsis syndrome, although her blood and urine cultures were negative. Desquamation, especially of the peripheral extremities, began a week after the onset of symptoms. This illness began a day after she started to use tampons for her period. Four weeks later, after commencing her period and while using tampons, AB developed a sore throat, headache and muscle aches. She felt nauseous, but had no vomiting or diarrhea. Her tongue was red and she had a temperature of 40°C. She was seen by her general practitioner who diagnosed tonsillitis and started flucloxacillin. Her mother gave her a double dose for the first 2 days, as well as probiotic drinks. AB missed school for 2 weeks and her symptoms slowly resolved. At the commencement of the next menstruation, when using tampons, AB again developed muscle aches, fever, nausea, vomiting and headache. She had an erythematous tongue, conjunctival injection and fever. A blood pressure measured at home recorded 80/40 mmHg and in hospital she was diagnosed with recurrent TSS. She required treatment with inotropes for 24 hours in intensive care. Investigations demonstrated raised creatinine and transaminases, as well as a high creatine phosphokinase. The white cell count was low, with a neutropenia. Clindamycin, flucloxacillin and gentamicin were started and she was given intravenous fluids. Blood cultures were negative. Desquamation of the feet and hands was noted around 10 days after admission. With her subsequent period, now no longer using tampons, AB developed stomach pain, muscle ache, myalgia and fever. On admission to hospital, she was found to be hypotensive. She was treated with flucloxacillin, clindamycin and intravenous Immunoglobulins. Ultrasound and computed tomography scans of the abdomen and pelvis were normal. She recovered rapidly with no evidence of infection on her blood cultures. However, Staphylococcus cultured from a perineal swab was found to be capable of producing TSST-1 toxin. Desquamation was again noted around 10 days after admission. Careful and extensive investigations of AB’s immune system were carried. From samples collected before intravenous immunoglobulin was given, she had antibody responses with haemophilus and meningococcal vaccines. However, no IgG antibody to TSST-1 could be identified from several samples collected (an enzyme-linked immunosorbent assay run by Professor Laurent in Lyon was employed for this purpose). Following this admission, AB and her family were treated with nasal decolonization using mupirocin cream (2% as a single, 1-off dose). Two years later, she remains well with no recurrence of symptoms. She has not yet developed IgG antibodies to TSST-1. DISCUSSION This teenager had recurrent menstrual TSS, 2 episodes associated with tampon use, 1 without. The case suggests that tampons per se are not critical for the development of recurrent TSS, but other predispositions to developing this condition, including perhaps a deficiency of appropriate IgG antibodies, are crucial. Antibody repertoires to S. aureus in healthy and acutely infected patients show extensive heterogeneity3 that change with successive infections. It is thought IgG1 and IgG4 antibodies specifically protect against superantigens or toxin-induced illness. Antibodies to superantigens have been identified in patients recovering from staphylococcal sepsis and in infants after colonization.4 Similar observations have been reported by those employing vaccines against staphylococci.5,6 Some individuals (females more often than males) do not make effective protective responses to staphylococcal superantigens until adulthood. Loch et al and Parsonnet et al7–9 reported rising titers in different populations of women until adolescence, when levels of neutralizing antibodies can be identified in >80% of subjects. This leaves a minority of individuals who may be more prone to developing illness from staphylococci by virtue of lower or absent antibody. Initial studies suggested staphylococcal infection in childhood is protective.10 Extensive animal and in vitro study on human cells shows that staphylococcal toxins may induce regulatory T cells in patients, providing a mechanism for impairment of immunity.11 They may cause clonal deletion of B cells in some. Perhaps the episode of impetigo or the first episode of TSS in our case induced a defect in her spectrum of protective responses to the superantigens. Epidemiological studies and case series do not indicate immunocompromise as a complication of TSS.12–14 Recurrent TSS has been observed in nonmenstrual situations15 and in a small number of other conditions possibly related to the effects of bacterial endotoxins, including recurrent perineal erythema16 and Kawasaki disease.17 Patients with recurrent illness, such as AB, offer a valuable resource to investigate the development and evolution of immunologic defects linked with staphylococcal superantigens. The application of nasal decolonization strategies in cases of vaginal TSS is debatable. Although it appeared effective in this case, this may have been coincidental. Awareness of the potential risk of recurrent TSS as a rare condition in adolescents is a useful clinical lesson for all pediatricians. ACKNOWLEDGMENTS The authors would like to thank AB for consenting to the recording of this case history. They wish to acknowledge the invaluable contributions made by Professor F. Laurent, University of Lyon and Dr Yousuf Karim, royal Surrey Hospital, with respect to the review of AB’s immunologic investigations." @default.
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• W2093618066 date "2014-07-01" @default.
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• W2093618066 title "Recurrent Menstrual Toxic Shock Syndrome With and Without Tampons in an Adolescent" @default.
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