Diagnosis Of Toxic Shock Syndrome Research Articles

Kawasaki disease with shock as the primary manifestation: How to distinguish from toxic shock syndrome?: A case report and literature review.

Kawasaki disease (KD) is a vasculitis syndrome of small to medium-sized arteries that has typical clinical characteristics such as fever, rash, cervical lymphadenopathy, conjunctivitis, and mucosal changes. Cardiac manifestations, including coronary artery aneurysms, myocarditis, myocardial infarction, and sudden cardiac death, are the most serious complications observed in KD. On rare occasions, it may accompanied with reduced organ perfusion due to systolic hypotension, a condition known as Kawasaki disease shock syndrome (KDSS). KDSS is a serious complication that can be presented to the emergency department as an initial feature when typical clinical symptoms of KD have not be detected. We report the case of a 12-year-old boy admitted with prolonged fever, bilateral non-purulent conjunctivitis, and signs of shock such as hypotension and tachycardia. Laboratory findings showed elevated inflammatory markers, hypoalbuminemia, and sterile pyuria. He was initially treated with intravenous cefotaxime and vancomycin considering the possible diagnosis of toxic shock syndrome, while the treatment was not effective. Subsequent chest computerized tomography and ultrasound identified pulmonary consolidation and polyserous effusion. Echocardiography revealed mild biatrial dilatation and mild valvular regurgitation with preserved left ventricular function. After a multidisciplinary consultation, a diagnosis of KDSS was made. To prevent coronary artery lesions and other severe complications, the patient immediately received immunoglobulin, corticoid, and acetylsalicylic acid. Soon afterwards, he showed significant improvement, with the temperature dropped to normal and hypotension corrected about 24 hours post-intravenous immunoglobulin therapy. Polyserous effusions also disappeared before discharge. Follow-up echocardiography revealed normal results. Clinicians should maintain a high index of suspicion for KD and consider pulmonary involvement and polyserous effusions as potential complications. For children with KD, any symptoms pointing to infection should be carefully considered. When there is no etiologic evidence, antibiotics should be used with caution. Our case also highlights the importance of considering KDSS as a differential diagnosis in children presenting with prolonged fever and shock. Early recognition, timely treatment, and close monitoring are key to preventing severe complications and ensuring favorable outcomes in patients with KDSS.

Acute kidney injury in pediatric toxic shock syndrome is associated with worse clinical course in the intensive care unit.

To explore the prevalence, severity, nature, and significance of acute kidney injury (AKI) among children admitted to the pediatric intensive care unit (PICU) with toxic shock syndrome (TSS). Bi-center, retrospective observational study. Children admitted for TSS to two intensive care units from 2009-2022 were included. We identified 41 children (median age 5years, 46% females) who met the Centers for Disease Control and Prevention (CDC) definitions of TSS. Staphylococcal TSS accounted for 63% of the patients and Streptococcal TSS accounted for the remaining 37%. AKI was diagnosed in 24 (59%) (stage 1: n = 6 [15% of total], stage 2: n = 10 [24%], and stage 3: n = 8 [20%]). The worst creatinine level was measured during the first day of admission in 34 (83%) patients. The median duration of AKI was 2days. Creatinine normalized by hospital discharge in all cases. Patients with AKI had a longer intensive care unit stay than those without AKI (6 vs. 3days, respectively, p = 0.01), needed more respiratory support (87% vs. 47%, p = 0.002), had fewer 28 ventilation-free days (25 vs. 28, p = 0.01), fewer vasopressor-free days (25 vs. 28, p = 0.001), and received more blood products (p = 0.03). Conclusion: Children admitted to the PICU with TSS, show a high prevalence of AKI at presentation. Creatinine levels and clearance normalize by hospital discharge in most cases. AKI in the setting of TSS could be used as an early marker for illness severity and a predictor of a more complex course. What is Known: • TSS is characterized according to the CDC by specific sets of clinical signs and symptoms in conjunction with specific laboratory findings one of which is AKI. • AKI is associated with worse outcomes in critically ill patients in general and in septic patients in particular. What is New: • AKI is found in about 60% of all patients admitted to the PICU with a diagnosis of TSS and hence is an important defining criteria. • AKI in the setting of TSS is associated with a more complex illness course and can serve as an early marker predicting such a course.

Nowadays a New MIS-C Mimicker: Group A Streptococcal Infections.

To the Editors: We show severe streptococcal infections in this report that mimicked the multisystem inflammatory syndrome in children (MIS-C) clinical presentation. At the start of December 2022, the cases were concurrently admitted to our hospital. We would want to share our study considering the Streptococcus pyogenes-related death cases that have recently been reported in many parts of Europe. An 8-year-old female patient complained of chest pain, headaches and fever for 3 days. The patient exhibited a maculopapular rash on the trunk, strawberry tongue, bilateral conjunctivitis, tonsillar hyperemia and cervical lymphadenopathy. Acute phase reactants were noticeably greater and acute renal failure was found in addition to the patient’s lymphopenia (C-reactive protein: 503 mg/L, procalcitonin: 49 μg/L, leucocyte count: 14.700 × 103/μL, lymphocyte count: 100 × 103/μL). The patient was receiving inotropic treatment because of hypotension. A prediagnosis of septic shock and MIS-C was made, and she was monitored in the critical care unit. Treatments with cefotaxime and clindamycin began. Intravenous immunoglobulin (IVIG) (1 g/kg/d for 2 days) and steroid (2 mg/kg/d) treatments were used when the SARS-CoV-2 antibodies were positive. The echocardiogram was normal. Streptococcus pyogenes was produced in the case’s blood culture during the follow-up, confirming the diagnosis of toxic shock syndrome. A 10-year-old female patient presented with complaints of fever, headache, vomiting and weakness for 2 days. The patient with weakness appearance had hyperemic tonsils and bilateral conjunctivitis. In the laboratory results at admission, lymphopenia and increased B-type natriuretic peptide were evident. In the acute phase reactants, the procalcitonin level was 3.7 μg/L and the CRP level was 41 mg/L. The patient had multiorgan involvement, which included the Centers for Disease Control and Prevention case description, thus treatment for MIS-C was initiated in addition to antibiotherapy even though there had been no appreciable increase in inflammatory markers. The patient showed clinical improvement within hours after fluid resuscitation and antibiotic therapy. Influenza was detected in the respiratory viral panel. Upon isolation of Streptococcus pyogenes in the throat culture during the follow-up, the diagnosis was finalized and MIS-C treatment was discontinued and targeted antibiotherapy was continued. This report was presented to highlight severe streptococcal infections mimicking MIS-C. Today, MIS-C, which is characterized by fever, elevated inflammatory markers and multisystem organ involvement, is seen in children following SARS-CoV-2 infection.1 MIS-C is an excluding diagnosis, careful consideration should go into the differential diagnosis. Given that it is overlapped with other prevalent diseases, it is a challenging process for the doctor to treat. In instances with fever, organ involvement and elevated inflammatory markers, empirical antibiotic therapy for potential bacterial agents should be started. In fact, if clinical suspicion is high, antibiotic therapy may be extended. By carefully observing the outcomes of the culture, antibiotherapy can be terminated early in instances where it is not necessary. Viral infections, such as influenza, facilitate the development of group a streptococcal infection, and this increase may have occurred due to the influenza epidemic in the northern hemisphere. The presence of SARS-CoV-2 antibodies in our case with streptococcal toxic shock syndrome increased the suspicion of MIS-C. However, it remains unclear how the antibody test should be interpreted. Because of the increasing prevalence of infection in the community, the usefulness of SARS-CoV-2 antibody testing seems to be limited.2 Therefore, cases with suspected MIS-C should be evaluated from a broad perspective in terms of bacterial infections. Delayed administration of antibiotics may result in mortality.

A Rare Case of Staphylococcal Toxic Shock Syndrome in a Neonate

Staphylococcus toxic shock syndrome (TSS) is not well described in neonates. The present criteria for diagnosis of TSS have not yet been validated in neonates. Here, we present a case of a 13-day-old female baby who presented with acute kidney injury (AKI). She had a pus-draining lesion on the head, and the pus grew Staphylococcus aureus. Based on the clinical criteria of fever, desquamation, hypotension, and AKI and laboratory criteria of absence of growth of any organisms in blood and cerebrospinal fluid, we diagnosed the case as TSS. She was treated with antibiotics, oxygen, and fluids, along with inotropic support and mechanical ventilation, and she recovered fully and was discharged on day 17 of admission. As there is no single test to diagnose TSS and it is uncommon in neonates, physicians should be familiar with the clinical presentation of the disease to make early diagnosis.

Post-surgical staphylococcal toxic shock syndrome in pediatrics: A case report

IntroductionToxic shock syndrome (TSS) is a rare but serious, life-threatening medical condition and potentially lethal if not detected and treated early. It is mainly caused by a toxin called toxin-1 produced by Staphylococcus aureus, and characterized by fever, hypotension, rash, skin desquamation and multisystem involvement.Case presentationHerein, we describe a nine-month-old male patient who presented to the hospital complaining of fever, vomiting and hypoactivity on day one post-orchidopexy. During hospitalization, his condition began to deteriorate with signs and symptoms of multisystemic failure. Laboratory tests and radiological images were done, leading to the decision to reopen and drain the surgical wound. Wound and nasal swabs were cultured and showed S. aureus infection, and the diagnosis of toxic shock syndrome was confirmed.DiscussionTSS is a systemic illness resulting from overwhelming host response to bacterial exotoxins, that cause T cells activation and the release of pro-inflammatory cytokines (IL-1 and TNF-α causing fever, hypotension, and tissue injury). Also, it can present with CNS signs that may be misdiagnosed with meningitis in pediatrics.It requires early identification and treatment despite its rarity with mortality rate of 81% even with treatment.The patient's presentation, examination and laboratories tests with the blood and wound cultures were highly suggestive for this condition.ConclusionPhysicians must maintain a high index of suspicion for TSS, as early diagnosis and treatment make a difference. This condition shouldn't be excluded even in young age patients or after simple procedure as in our case in which TSS occurred after orchidopexy.

Prevalence, comorbidities and mortality of toxic shock syndrome in children and adults in the USA.

Toxic Shock Syndrome (TSS), a superantigen-mediated illness, is characterized by rash, hypotension and multi-organ dysfunction. Predictors of TSS and related morbidity and mortality are poorly defined. In this study, data on 61,959,084 hospitalizations from the 2003-2012 Nationwide Inpatient Sample, a 20% stratified sample of US hospitalizations, were analyzed and ICD-9-CM coding used to identify 4491 hospitalizations with a diagnosis of TSS. Incidence, in-hospital mortality rate, comorbidities, length of stay and costs of care attributable to TSS were determined. In multivariate survey logistic regression models, TSS was associated with female sex (adjusted odds ratio [95% confidence interval], 1.54 [1.48-1.60]), younger age (0-17 years, 2.17 [2.06-2.29]; 40-59: 0.53 [0.50-0.56]; 60-79: 0.28 [0.26-0.30]; 80+: 0.13 [0.11-0.14] compared with 18-39) and race/ethnicity (black, 0.63 [0.59-0.67]; Hispanic: 0.60 [0.56-0.64]; Asian, 1.11 [1.00-1.11]; and other, 0.83 [0.75-0.92] compared with white). Patients with TSS had a three-fold greater cost of care (mean: $36,656 ± 942) and length of stay (LOS) (mean: 10.65 ± 0.23 days) than patients without TSS. Shared predictors of increased LOS and costs in patients with TSS were male sex; age 40-79 years; Black, Hispanic, Asian and other race/ethnicity; and more than one chronic condition. Predictors of in-hospital mortality included respiratory failure (13.66 [11.37-16.43]), liver disease/failure (3.36 [2.59-4.34]), chickenpox (91.26 [27.74-300.25]), coagulopathy (2.14 [1.85-2.48]), and higher age. In conclusion, there are significant racial/ethnic, socioeconomic, and comorbid disparities in the incidence and mortality of TSS in adults and children in the USA.

Is Procalcitonin Helpful in the Diagnosis of Toxic Shock Syndrome?

Is Procalcitonin Helpful in the Diagnosis of Toxic Shock Syndrome?

Toxic Shock Syndrome Following Influenza-like Illness: The First Case Report in a Young Child

: Toxic shock syndrome in children following infection with influenza is a very rare syndrome. If it is not diagnosed quickly, it may cause significant morbidity and mortality. For diagnosis of toxic shock syndrome, clinical and laboratory criteria are used. Our patient is a 3.5-year old boy who admitted to the hospital with high fever, weakness, toxicity, hypotension and skin rash due to influenza-like Illness (fever, pharyngitis, rhinitis and non-productive cough) associated with gastrointestinal symptoms, elevated liver enzymes levels, low platelet count and mucosal hyperemia. After the treatment, he recovered and was discharged from the hospital in good condition, but had mild scaling on the soles of the feet and between toes. To our knowledge, this is the first reported case in a young child. There is not any specific diagnostic test for toxic shock syndrome diagnosis, and the diagnosis is based on clinical and laboratory findings. Therefore, the early detection and treatment of the condition is very important because delay in treatment leads to increased mortality and morbidity.

An unusual case of Guillain–Barre syndrome following toxic shock syndrome in a burned child

A 13 month-old girl presented to our Burns Unit with a 4% circumferential, superficial partial thickness scald to her right arm. The cause of the injury was a hot tea scald, for which first aid was given. Born to consanguineous parents, she had no known co-morbidities and was up-to-date with immunisations. The burn was managed as per our standard protocol, with topical nitrofurazone cream and Mepitel (Molnlycke Health Care) dressing, and the patient discharged home the same day to local follow-up. No prophylactic antibiotics were given. Six days later, the child presented to the Emergency Department at our hospital with an erythematous rash involving her face, trunk and limbs. On admission, she was febrile (T 38.8C), tachycardic (HR 188) and had a prolonged peripheral capillary refill time of 3–4 s. Intravenous (IV) fluids and antibiotics (benzylpenicillin and flucloxacillin, later clindamycin) were commenced and the patient was admitted to the paediatric high-dependency unit (HDU), in accordance with our local protocol, with a clinical diagnosis of toxic shock syndrome (TSS). Burn wound cultures grew Staphylococcus aureus, sensitive to flucloxacillin and erythromycin. Neither IV immunoglobulin nor fresh frozen plasma (FFP) was given. Samples were not sent for toxic shock syndrome toxin (TSST-1) analysis. The patient responded well to treatment

In Vitro Studies of Toxic Shock Toxin-1–secreting Staphylococcus aureus and Implications for Burn Care in Children

The main etiologic agent of toxic shock syndrome is the toxic shock syndrome toxin-1 (TSST-1) protein secreted by Staphylococcus aureus. Diagnosis of toxic shock syndrome is difficult and is significantly underdiagnosed in young children with burns due to the nonspecific presentation coupled with a rapid deterioration in patient condition. The lytic and cytolytic activity of a number of clinical and laboratory TSST-1-positive strains of methicillin-susceptible S. aureus (101, 253, 279 and RN4282, respectively) and Pseudomonas aeruginosa PAO1 strain were tested in vitro using an assay designed to assess the relative exotoxin activity of bacteria using phospholipid vesicles and a T cell toxicity assay. In addition, the activity of lytic exotoxins such as δ -toxin and the secretion of nonlytic TSST-1 toxin from S. aureus was measured using the vesicle assay and Western blotting over the 20-hour growth of TSST-1-positive S. aureus culture. Both the vesicle and T cell assays suggest a lytic exotoxin-mediated mechanism of vesicle rupture and T cell death, with high levels of vesicle lysis and T cell toxicity. It is important to note that the clinical TSST-1-positive methicillin-susceptible S. aureus strains exhibited lytic exotoxin production as well as TSST-1 expression as confirmed by Western blot. We suggest that there is no correlation between the expression of TSST-1 and lack of exotoxin production. We also suggest that apurulence in an S. aureus-infected burn wound in a child should not be used to rule out toxic shock syndrome.

An Unusual Case of Toxic Shock Syndrome

Toxic shock syndrome is a multisystemic illness most often associated with toxins produced by Staphylococcus aureus and group A Streptococcus. An extensive review of available literature revealed many other microbial agents including viruses to be associated with toxic shock syndrome. Parvovirus B-19 is usually a self-limiting illness. There has been only 1 case report of acute Parvovirus B-19 infection in association with severe sepsis. We report the first case of acute Parvovirus B-19 infection that fulfilled the CDC criteria for the diagnosis of Toxic Shock Syndrome in an immunocompetent host.

Staphylococcal toxic shock syndrome presenting as acute respiratory distress and cor pulmonale

We describe a 7-year-old boy with staphylococcal toxic shock syndrome who presented with acute respiratory distress and cor pulmonale. We wish to highlight this unusual presentation as the diagnosis of toxic shock syndrome depends chiefly on a high degree of clinical suspicion. Early diagnosis and prompt institution of appropriate therapy will significantly reduce morbidity and mortality.

Delayed Development of Toxic Shock Syndrome Following Abdominal Tissue Expansion in a Pediatric Reconstruction Patient

Toxic shock syndrome (TSS) is a potentially fatal postoperative complication, and even more so if the diagnosis is delayed. We present the case of a 7-month-old male infant who developed TSS as a complication of tissue expansion using an external port device. There have been 5 documented cases of TSS after tissue expander or breast prosthesis placement occurring in the adult population, however, there has not been a reported case of TSS in an infant. The long interval to development of TSS like symptoms, 4 months in this case, should not exclude TSS from the differential diagnosis. In a pediatric patient, a diffuse macular rash without the severe systemic symptoms on initial presentation can present as a diagnostic challenge. New diagnosis techniques are discussed that can shorten the time to a diagnosis of TSS. In this case, because the local bacterial count was low, the expanded tissue was transferred without complication.

Toxic shock syndrome toxin-1 (TSST-1) antibody levels in Japanese children

Children with burns have a greater risk of developing toxic shock syndrome (TSS) than adults. This risk is thought to be associated with colonisation by toxic shock syndrome toxin-1 (TSST-1)-producing Staphylococcus aureus in children with insufficient antibody titers. The diagnosis of TSS is difficult because, in the early stages, its signs and symptoms resemble those of other common childhood illnesses such as scarlet fever. If the condition is not treated promptly, the mortality rate is high. This study was designed to determine the titers of TSST-1 serum antibody in Japanese children, in order to prevent TSS and facilitate its early diagnosis. Between May 2006 and May 2007, we studied 119 patients who were treated in the Department of Plastic and Reconstructive Surgery of Kanazawa Medical University Hospital. An enzyme-linked immunosorbent assay (ELISA) was used to test the level of the IgG antibody to TSST-1 in the patients’ serum samples. The percentage of cases testing for TSST-1 antibody in the patients under 6 months old was 78.6%, and it was lowest (21.3%) in the age group from 6 to 12 months old. The group of patients older than 41 years showed the highest rate of positivity (100.0%) for TSST-1 antibody. Higher titers of TSST-1 antibody were found within the first 6 months after birth, and lower titers were found between 6 months and 2 years old. The titers began to increase again after age three. The high morbidity of TSS in children around 2 years of age was proven to be related to changes in the titers of TSST-1 antibody. Infants under 6 months old are protected from TSS because of the high level of TSST-1 antibody they receive from their mother. Children are at risk of developing staphylococcal toxic shock syndrome when their immune system is immature and they have no protective circulating anti-TSS antibodies.

Choc toxique staphylococcique dans un contexte menstruel de port de tampons vaginaux d’évolution favorable après optimisation hémodynamique précoce et administration de protéine C activée

A 19-year-old woman was admitted in the intensive care unit for a septic shock recognized as a menstrual toxic shock syndrome with a Staphylococcus aureus. An early goal oriented therapy was started in order to correct in particular the venous central O(2) saturation (ScvO(2)) associated to an early empiric anti-infectious treatment. A multi-organ failure appeared in a second time, so that we began a protein C activated infusion. The outcome was also auspicious. Bacteriologic samples and specific samples for the research of Staphylococci toxins confirmed the diagnosis of toxic shock syndrome with Staphylococcus aureus. A genotypic study allowed us to identify many anomalies which could be involved in the incompletely understood physiopathology of this disease.

Diagnosis of toxic shock syndrome by two different systems; clinical criteria and monitoring of TSST‐1‐reactive T cells

Two methods of TSS diagnosis were evaluated: comparison of symptoms with clinical criteria and monitoring for evidence of selective activation of Vbeta2(+) T cells by the causative toxin, TSS toxin-1 (TSST-1). Ten patients with acute and systemic febrile infections caused by Staphylococcus aureus were monitored for increase in TSST-1-reactive Vbeta2(+) T cells during their clinical courses. Nine of the ten patients were diagnosed with TSS based on evidence of selective activation of Vbeta2(+) T cells by TSST-1; however, clinical symptoms met the clinical criteria for TSS in only six of these nine patients. In the remaining patient, clinical symptoms met the clinical criteria, but selective activation of Vbeta2(+) T cells was not observed. Time taken to reach the diagnosis of TSS could be significantly shortened by utilizing the findings from tracing Vbeta2(+) T cells. In vitro studies showed that TSST-1- reactive T cells from TSS patients were anergic in the early phase of their illness. Examining selective activation of Vbeta2(+) T cells could be a useful tool to supplement clinical criteria for early diagnosis of TSS.

Early diagnosis and treatment of toxic shock syndrome in paediatric burns

Young children with burns are at risk of developing toxic shock syndrome (TSS), which is an exotoxin mediated disease usually caused by Staphylococcus aureus ( S. aureus). The diagnosis of TSS is difficult because in the early stages the signs and symptoms resemble other common childhood illnesses such as scarlet fever. If the condition is not treated promptly it has a high mortality. The South West Regional Paediatric Burns Unit at Frenchay Hospital admits 150–200 burns per year. We have designed a protocol to facilitate the early diagnosis and treatment of TSS. We report our experience over a 3-year period in which almost one quarter of cases of TSS were admitted from home or another hospital. During this period all children with TSS survived and none needed ventilatory support. Typical cases presented within 2 days of thermal injury, in a child under 2 years old with a burn of less than 10% of body surface area (BSA).

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 ≥ 38.9oC, 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.

Exanthematous disease induced by toxic shock syndrome toxin 1 in the early neonatal period

We have seen a number of patients who developed systemic exanthema and thrombocytopenia in the first week of life. Although nearly 100% of the patients were carriers of meticillin-resistant Staphylococcus aureus (MRSA), no clear link between MRSA and this exanthematous disease has yet been made. 20 neonates with exanthema and thrombocytopenia were selected for study. To see whether superantigenic exotoxins from MRSA are involved in the pathogensis of the exanthematous disease, we studied the production of these exotoxins by MRSA isolates from the neonates. We studied the expression of T-cell-receptor Vbeta and CD45RO in T cells taken from four of the neonates. We also analysed the DNA sequences of 16 cloned Vbeta2-positive T-cell-receptor-chain genes taken from two of the neonates. Although most of the patients recovered within 5 days of onset of the exanthematous disease without any active treatment, two preterm infants died in the recovery phase. All patients showed colonisation by MRSA. The MRSA produced toxic shock syndrome toxin-1 (TSST-1). The number of T cells positive for T-cell-receptor Vbeta2, reactive to TSST-1, was increased in the four patients studied (p<0.0001), and these T cells expressed CD45RO (p=0.0185). None of the Vbeta2 clones had the same junctional sequences. The polyclonal expansion of Vbeta2-positive T cells in patients colonised by TSST-1-producing MRSA suggests that the pathogenic micro-organism of this neonatal exanthematous disease is S aureus, mainly MRSA, and that in its pathogenesis it activates T cells by TSST-1. Although the pathogenesis of both this exanthematous disease and toxic shock syndrome are fundamentally the same, a diagnosis of toxic shock syndrome cannot be made in this case, based on the clinical criteria for toxic shock syndrome. We propose neonatal toxic-shock-syndrome-like exanthematous disease (NTED) as the name for this disease.

Vaginal Mucositis in Measles

Background: Measles (rubeola), a common childhood exanthema, occurs infrequently in adults. Vaginal mucositis in association with measles is not commonly described. Case: During a recent measles epidemic, 2 female patients presented with high fever, myalgia, exanthema, and prostration. On examination, each patient had marked inflammation and tenderness of the vaginal mucosa, prompting the presumptive diagnosis of toxic shock syndrome. The evolution of the illness was consistent with measles. Cervicovaginal cultures were negative for pathogens. Acute and convalescent antibody titers for Rocky Mountain spotted fever, rubella, leptospirosis, and Proteus Ox-19 were not consistent with a recent infection. The sera also were negative for anti-toxic shock toxin-1 and anti-streptolysin. Measles antibody titers were consistent with a recent infection. Conclusion: Vaginal mucositis is an unusual manifestation of measles that may mimic toxic shock syndrome.