Severe Streptococcal Infections Research Articles

Multimodal Mass Spectrometry Identifies a Conserved Protective Epitope in S. pyogenes Streptolysin O.

An important element of antibody-guided vaccine design is the use of neutralizing or opsonic monoclonal antibodies to define protective epitopes in their native three-dimensional conformation. Here, we demonstrate a multimodal mass spectrometry-based strategy for in-depth characterization of antigen-antibody complexes to enable the identification of protective epitopes using the cytolytic exotoxin Streptolysin O (SLO) from Streptococcus pyogenes as a showcase. We first discovered a monoclonal antibody with an undisclosed sequence capable of neutralizing SLO-mediated cytolysis. The amino acid sequence of both the antibody light and the heavy chain was determined using mass-spectrometry-based de novo sequencing, followed by chemical cross-linking mass spectrometry to generate distance constraints between the antibody fragment antigen-binding region and SLO. Subsequent integrative computational modeling revealed a discontinuous epitope located in domain 3 of SLO that was experimentally validated by hydrogen-deuterium exchange mass spectrometry and reverse engineering of the targeted epitope. The results show that the antibody inhibits SLO-mediated cytolysis by binding to a discontinuous epitope in domain 3, likely preventing oligomerization and subsequent secondary structure transitions critical for pore-formation. The epitope is highly conserved across >98% of the characterized S. pyogenes isolates, making it an attractive target for antibody-based therapy and vaccine design against severe streptococcal infections.

Editorial introductions.

Editorial introductions.

SG-APSIC1155: Drug susceptibility patterns of fulminant group G Streptococcus (GGS) infection as a re-emerging infectious disease in Japan

Objectives: Severe streptococcal infections are invasive, re-emerging infections that rapidly worsen and lead to death. Not only group A Streptococcus (GAS) but also group g Streptococcus (GGS) are the causative agents of this infection. Moreover, GGS produces hemolytic toxins, proteolytic toxins, and other toxins like GAS. Furthermore, drug-resistant Streptococcus spp, like other pathogenic bacteria, are on the rise worldwide. However, drug resistance has not been studied extensively in invasive GGS. Therefore, we investigated the drug susceptibility of GGS clinical isolates that are closely related to fulminant streptococcal infections. Methods: We used GGS strains isolated from sterile sites of invasive infections at a hospital in Nagoya City, Japan, from 2017 to 2021. Bacterial identification and drug-susceptibility testing were performed using a VITEK-2 system. Results: Overall, 53 strains were included in the study. The GGS strains examined in this study were resistant to 3 different antibiotics (erythromycin, clindamycin, and minocycline). Also, 18 strains (34%) were resistant to erythromycin, 9 (17%) were resistant to clindamycin, and 18 (34%) were resistant to minocycline. Moreover, there were 5 strains (9.4%) of 2-drug–resistant bacteria and 8 strains (15.1%) of 3-drug–resistant bacteria. Conclusions: Acquired resistance not only to individual antibiotics but also to multiple antibiotics suggests that GGS tends to become multidrug resistant. Continued surveillance of the drug susceptibility of GGS as a potential cause of fulminant streptococcal infections will be necessary in the future.

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.

Editorial introductions.

Editorial introductions.

An Emerging Infection: Streptococcal Toxic Shock-Like Syndrome Caused By Group B Streptococcus (GBS), Streptococcus Agalactiae

Abstract Introduction/Objective Streptococcus agalactiae, Group B Streptococcus (GBS), is a major cause of neonatal sepsis and infections in pregnant women. However, incidence of invasive GBS infections has more than doubled in the last two decades with highest risk in adults 65 years or older. Other risk factors are diabetes, malignancy, and immunocompromised state. Bacteremia and skin soft tissue infections are the most common invasive infections in nonpregnant adults. Rarely GBS infection has a fulminating pyrogenic exotoxin-mediated course characterized by acute onset, multiorgan failure, shock, and sometimes death, referred to as toxic shock-like syndrome. Methods A 77-year-old hypertensive female with uncontrolled type 2 diabetes mellitus and a history of bilateral foot ulcers presented to the hospital in probable septic shock. Clinical diagnosis of necrotizing fasciitis was made and she underwent bilateral lower limb amputations. Results Grossly soft tissue appeared gray. Microscopically fascia was necrotic without neutrophils present and Gram stain revealed sheets of Gram positive cocci. These findings reflected histopathologic Stage III necrotizing fasciitis, which is associated with 47% mortality. Autopsy showed a similar histology of Stage III necrotizing fasciitis involving the surgical stump. Erythema and desquamation of the upper limbs bilaterally and multi-organ failure met the clinical picture of Streptococcal Toxic Shock Syndrome (STSS) and fulfilled the criteria for TSS due to Group A Streptococcus (GAS), defined by The Working Group on Severe Streptococcal Infections. Conclusion Group B Streptococcal Toxic Shock-Like Syndrome may have a similar outcome to STSS caused by GAS and other pathogens and, in limited studies, mortality has been 30% or greater.

Editorial introductions

Editorial introductions

Prothrombotic and Proinflammatory Activities of the β-Hemolytic Group B Streptococcal Pigment

A prominent feature of severe streptococcal infections is the profound inflammatory response that contributes to systemic toxicity. In sepsis the dysregulated host response involves both immunological and nonimmunological pathways. Here, we report a fatal case of an immunocompetent healthy female presenting with toxic shock and purpura fulminans caused by group B streptococcus (GBS; serotype III, CC19). The strain (LUMC16) was pigmented and hyperhemolytic. Stimulation of human primary cells with hyperhemolytic LUMC16 and STSS/NF-HH strains and pigment toxin resulted in a release of proinflammatory mediators, including tumor necrosis factor, interleukin (IL)-1β, and IL-6. In addition, LUMC16 induced blood clotting and showed factor XII activity on its surface, which was linked to the presence of the pigment. The expression of pigment was not linked to a mutation within the CovR/S region. In conclusion, our study shows that the hemolytic lipid toxin contributes to the ability of GBS to cause systemic hyperinflammation and interferes with the coagulation system.

The Oral Pheneticillin Absorption Test: An Accurate Method to Identify Patients with Inadequate Oral Pheneticillin Absorption.

Severe streptococcal infections are commonly treated with intravenous followed by oral penicillin (pheneticillin) therapy. However, switching from iv to oral therapy is complicated by the variability in oral pheneticillin absorption. We employed an Oral Absorption Test (OAT) for pheneticillin to identify patients in whom oral pheneticillin absorption is poor. Out of 84 patients 30 patients (36%) were identified as insufficient absorbers. Treatment failure due to pheneticillin malabsorption can be avoided by performing an OAT, and these patients should be treated by another antibiotic, which is known to be absorbed well.

Editorial introductions

Editorial introductions

Intracellular Streptococcal Uptake and Persistence: A Potential Cause of Erysipelas Recurrence

Erysipelas is a severe streptococcal infection of the skin primarily spreading through the lymphatic vessels. Penicillin is the treatment of choice. The most common complication consists in relapses which occur in up to 40% or more of patients despite appropriate antibiotic treatment. They cause lymphatic damage resulting in irreversible lymphedema and ultimately elephantiasis nostras and lead to major health restrictions and high socio-medical costs. Prevention of relapses is an unmet need, because even long-term prophylactic penicillin application does eventually not reduce the risk of recurrence. In this article we assess risk factors and causes of erysipelas recurrence. A systematic literature search for clinical studies addressing potential causes and measures for prevention of erysipelas recurrence was combined with a review of experimental and clinical data assessing the ability and clinical relevance of streptococci for intracellular uptake and persistence. The literature review found that venous insufficiency, lymphedema, and intertrigo from fungal infections are considered to be major risk factors for recurrence of erysipelas but cannot adequately explain the high recurrence rate. As hitherto unrecognized likely cause of erysipelas relapses we identify the ability of streptococci for intracellular uptake into and persistence within epithelial and endothelial cells and macrophages. This creates intracellular streptococcal reservoirs out of reach of penicillins which do not reach sufficient bactericidal intracellular concentrations. Incomplete streptococcal elimination due to intracellular streptococcal persistence has been observed in various deep tissue infections and is considered as cause of relapsing streptococcal pharyngitis despite proper antibiotic treatment. It may also serves as endogenous infectious source of erysipelas relapses. We conclude that the current antibiotic treatment strategies and elimination of conventional risk factors employed in erysipelas management are insufficient to prevent erysipelas recurrence. The reactivation of streptococcal infection from intracellular reservoirs represents a plausible explanation for the frequent occurrence erysipelas relapses. Prevention of erysipelas relapses therefore demands for novel antibiotic strategies capable of eradicating intracellular streptococcal persistence.

The Emergence of Hypervirulent M1T1 Clone of Group A Streptococcus via Genetic Recombination and Host Selection.

Streptococcus pyogenes (Group A Streptococcus, GAS) is a strictly human bacterial pathogen. Since the mid-1980s, GAS M1T1 clone has been the most prevalent and globally disseminated serotype and is the culprit causing invasive and severe streptococcal infections, urging a better understanding of the emergence of hypervirulent M1T1 clone from an evolutionary perspective. This review highlights the molecular and evolutionary events leading to pandemic M1T1 strains, and discusses the pressure driving the genetic acquisition of novel virulence genes and the selection of hypervirulent isolates in host. By understanding the evolutionary selection and pressures that select and shape the pandemic M1T1 clone, we could potentially develop new therapeutic strategies to tackle challenges when dealing with the globally disseminated M1T1 GAS clone.

Association of ficolin-2 (FCN2) functional polymorphisms and protein levels with rheumatic fever and rheumatic heart disease: relationship with cardiac function.

IntroductionA role for ficolin (FCN) 2 gene polymorphisms in the pathogenesis of recurrent severe streptococcal infections and rheumatic carditis has been suggested. The aim of the study was to evaluate a possible relationship between single nucleotide polymorphisms located at positions -602 and -4 of the FCN2 gene and FCN2 serum levels and risk of development of rheumatic fever (RF) and rheumatic heart disease (RHD).Material and methodsSeventy-seven Caucasian Egyptian patients with RF were recruited with a control group of 43 healthy subjects. DNA was extracted for analysis of the FCN2 gene at positions -602 and -4 and serum protein level was measured by ELISA.ResultsFCN2 AA genotype at the -4 position was more frequently observed in RF and RHD patients, as compared to healthy subjects (p = 0.005 and p = 0.013, respectively); furthermore, the A allele was identified as a possible risk factor for the development of RF (p = 0.023, OR = 1.852, 95% CI: 1.085–3.159). The haplotype –602/–4 G/A, which was associated with low median levels of L-ficolin, was observed more frequently in the RF group when compared to the healthy subjects (74/162, 48.1% vs. 29/420, 33.7%, OR = 1.834, 95% CI: 1.034–3.252, p = 0.038). Low serum ficolin-2 level was associated with ESV and EDV increases. FCN 2 level was significantly lower with AA genotypes than GG+AG genotypes of the -4 position (56.68 ±17.90 vs. 66.05 ±18.79, p = 0.008).ConclusionsPolymorphisms linked to low levels of L-ficolin may render an individual at risk of recurrent and/or severe streptococcal infection. The -4 AA genotype and -602/-4 G/A haplotype are possible risk factors for the development of carditis.

Management Dilemma: A Case of Acute Epiglottitis Secondary to Group A Streptococcus (GAS)

SESSION TITLE: Shock SESSION TYPE: Affiliate Case Report Poster PRESENTED ON: Tuesday, October 31, 2017 at 01:30 PM - 02:30 PM INTRODUCTION: In adults, epiglottitis has a male preponderance with the potential for rapid airway obstruction. Risk factors include hypertension, diabetes mellitus (T2DM), substance abuse and immune deficiency. CASE PRESENTATION: A 52-year-old male with history of T2DM, obesity and alcohol abuse presented with shortness of breath and choking sensation. Intubation was attempted in the ER for respiratory distress using a size 6 endotracheal tube. Chest X-ray revealed poor tube position despite multiple attempts to advance it. Epinephrine and pulse steroids were administered. Emergent bronchoscopy showed swelling of the supraglottis and an emergent tracheostomy was performed. Labs revealed leukocytosis with bandemia. Neck CT scan confirmed acute epiglottitis with critical airway stenosis. Bronchoalveolar lavage and blood cultures grew GAS. Bacteremia cleared two days after admission with Ceftriaxone and Vancomycin. Patient had spiking fevers and was noted to be extremely agitated. He received steroids for five days after a second CT neck revealed no interval change in edema.(Image 2) Two weeks after persistent fevers and hemodynamic instability requiring pressors, antibiotics were switched to Penicillin (PCN) G and Clindamycin without resuming steroids. After 24 hours, patient had significant clinical improvement and was subsequently weaned off the ventilator. He was seen in the clinic after discharge with complete resolution of symptoms. DISCUSSION: Multiple retrospective studies have noted that epiglottitis in adults can be managed conservatively with airway support required in only 6.6 - 16% of patients. We encountered a severe case of acute epiglottitis in an adult male who failed to respond clinically after two weeks of appropriate antibiotic coverage and a trial of steroids but responded to the addition of Clindamycin. The loss of penicillin binding proteins in ‘stationary growth phase’ bacteria occurs in more invasive streptococcal infections rendering PCNs less effective. Clindamycin suppresses bacterial toxin production, enhances opsonization, decreases cytokine activation and has a post-antibiotic effect.1 A recent in-vivo and in-vitro study endorsed the addition of Clindamycin to PCN in severe streptococcal infections.2 CONCLUSIONS: GAS epiglottitis can present in adults with risk factors: male sex, diabetics and substance abuse. With poor clinical response, complications such as toxic shock syndrome should be considered. The addition of Clindamycin to PCN in severe streptococcal infections may be beneficial with its action on slow growing bacteria and ability to inhibit bacterial toxin production. Reference #1: 1.Russell NE, Pachorek RE. Clindamycin in the treatment of streptococcal and staphylococcal toxic shock syndromes. Ann Pharmacother. 2000;34(7-8):936-939. Reference #2: 2.Andreoni F, Zürcher C, Tarnutzer A, et al. Clindamycin Affects Group A Streptococcus Virulence Factors and Improves Clinical Outcome. J Infect Dis. 2016;1:jiw229. DISCLOSURE: The following authors have nothing to disclose: Hisham Hakeem, Marnie Aguasvivas, Lokesh Dayal, Killol Patel No Product/Research Disclosure Information

Molecular epidemiology of macrolide resistant Group A streptococci from Puducherry, India.

In penicillin allergic patients, macrolides are the most commonly used antibiotics for treating streptococcal infections, irrespective of the higher resistance rates. The objective of this study was to evaluate the comparative prevalence, phenotypes, and genetic determinants of macrolide resistance and associated emm types among different clinical isolates of Streptococcus pyogenes. A total of 173 Streptococcus pyogenes isolates were examined for macrolide resistance phenotype by double-disc test, resistance determinants by multiplex PCR and emm genotyping. Erythromycin resistance was found in 51.4% of isolates, with MIC90 ≥ 256 µg/mL Inducible phenotype was commonly found (iMLS, 67.4%) followed by the M phenotype (32.5%). Among these isolates, 65.1% harboured ermB and 32.5% mefA as sole macrolide resistance gene, whereas presence of both, ermB plus mefA was observed in 2.2% cases. The most common types among resistant strains were emm63 (11.2%), emm44 (6.7%), emm42 (5.6%), and emm75.3, emm82, emm85, emm92, emm111.1 (4.4% each). Statistically significant association was observed between emm63, emm44 and erythromycin resistance (p ≤ 0.05). Association of these emm types and macrolide resistance have not been reported earlier. Higher macrolide resistance in this study can be attributed to overuse and misuse of this antibiotic. These findings indicate that macrolides should not be empirically used for treating severe streptococcal infections.

MBL2 and FCN2 gene polymorphisms in a cohort of Italian children with rheumatic fever: A case-control study.

Mannose-binding lectins and human ficolins are pattern-recognition proteins involved in innate immunity. A role for MBL2 and FCN2 gene polymorphisms in the pathogenesis of recurrent severe streptococcal infections and rheumatic carditis has been suggested. The aim of this study is to evaluate the presence of MBL2 and FCN2 gene polymorphisms (SNPs) in children with a history of rheumatic fever (RF) and to investigate their possible role in RF clinical presentation and disease course. A total of 50 Caucasian patients with RF were recruited with a control group of 52 healthy children. DNA was extracted for analysis of MBL2 gene (exon 1, codons: 52, 54, and 57) and FCN2 gene (promoter region at position -986, -602, and -4). The FCN2 AG genotype at the -986 position was more frequently observed in patients, as compared to healthy subjects (p = 0.006); furthermore, the A allele was identified as a possible risk factor for the development of RF (OR = 7.14, CI: 2.439-20.89). Conversely, the GG genotype at the same position was observed more frequently in the control group and can be considered a protective factor for the development of the disease (p = 0.001, OR = 8.37, 95% CI: 2.763-25.33). In addition, the FCN2 GG and AG genotypes in the -4 position were also found to be protective factors for the development of RF and for carditis respectively (OR = 3.32, CI: 1.066-10.364; OR = 0.15, 95% CI: 0.037-0.566). Finally, the AA genotype in the -602 position was associated with a late onset of RF (p = 0.006). The analysis of the MBL2 gene only resulted in a higher frequency of the AA genotype on position 57 in controls as compared to patients (p = 0.025). This is the first study evaluating the FCN2 gene polymorphisms in patients with RF and rheumatic carditis finding a protective effect of -986 GG and -4 GG genotypes in the development of RF and the -4 AG genotype for the development of carditis. Our data do not support a possible role for MBL2 polymorphisms in the pathogenesis and in the clinical manifestations of RF.

Cardiopulmonary morbidity of streptococcal infections in a PICU

The streptococci are important bacteria that cause serious childhood infections. We investigated cardiopulmonary morbidity associated with streptococcal infection and pediatric intensive care unit (PICU) admission. A retrospective study between 2002 and 2013 of all children with a laboratory isolation of streptococcus. There were 40 (2.3%) PICU patients with streptococcal isolations including Streptococcus pyogenes (Group A streptococcus, GAS, n = 7), Streptococcus agalactiae (Group B streptococcus, GBS, n = 5), Streptococcus pneumoniae (SP, n = 20), alpha-hemolytic (n = 4), beta-hemolytic (n = 2) and gama-hemolytic (n = 2) streptococci. Comparing among GAS, GBS and SP, respiratory isolates were more likely positive for GAS or SP (P = 0.033), whereas cerebrospinal fluid was more likely positive for GBS (P = 0.002). All GAS and GBS, and the majority of SP (90%) were sensitive to penicillin. All SP specimens were sensitive to cefotaxime and vancomycin. These infections were associated with high PICU mortality of 43%, 20% and 25%, respectively. Isolation of streptococci was associated with a 30% mortality and high rates of need for mechanical ventilatory and inotropic supports. Patients with GAS, SP or any streptococcal isolation had relative risks [95% confidence interval (CI), P value] of PICU deaths of 7.5 (CI 3.1-18.1, P < 0.0001), 4.5 (CI 2.0-9.8, P < 0.0002) and 5.7 (CI 3.4-9.5, P < 0.0001), respectively. In SP, older children had significantly higher prevalence of premorbid conditions such as malignancy, mental retardation/cerebral palsy ± seizure disorders, chromosomal or genetic disorders (P = 0.003) than children <5 years of age. Serotypes were available for some of these specimens that included 19A, 6B, 3 and 6C. There were four SP deaths with multiorgan system failure and hemolytic uremic syndrome (two 19A and two serotype 3). Severe streptococcal infections are associated with significant morbidity and mortality despite treatment with systemic antibiotics and intensive care unit support. GAS and SP affect the lungs of children, whereas GBS more likely causes meningitis in infants. The expanded coverage of newer polyvalent pneumococcal vaccines can probably prevent infections by serotypes 19A, 19F, 6B and 3.

Beyond the traditional immune response: bacterial interaction with phagocytic cells

The human immune response is well equipped to sense and react to infectious agents in order to achieve efficient immune defence in most instances. A major event in the early control of infection is phagocytic killing of the pathogen. However, important human pathogens have evolved sophisticated mechanisms to modulate the immune response and thereby promote their own survival. In this review, we focus on pathogen-mediated modulation and/or exploitation of phagocytic cells. In particular, the mechanisms employed by Streptococcus pyogenes are described, with special attention given to intracellular persistence and stimulation of phagocytic cells leading to disease severity. The crucial role of these mechanisms in the pathogenesis of severe invasive streptococcal infections, such as necrotising fasciitis and streptococcal toxic shock syndrome, is described.

A群&beta;溶血性レンサ球菌肺炎から劇症型溶血性レンサ球菌感染症，急性膿胸を合併した1症例

A群β溶血性レンサ球菌肺炎が劇症化し，さらに急性膿胸を合併して治療に難渋した症例を経験したので報告する。症例は27歳，女性。生来健康。2011年1月下旬より感冒症状あり，近医で内服治療を受けていた。2月に近医を受診し急性咽頭炎の診断を受けたが，夜間になって呼吸苦が出現し急性肺炎と診断され緊急入院となった。翌日，多臓器障害の進行を認めたため，当院救命救急センター転院となった。臨床所見，検査結果から劇症型溶血性レンサ球菌感染症と診断，治療を開始した。その後，全身状態は安定したが，急性膿胸の合併を認めた。胸腔ドレナージを施行したが改善せず，第19病日に胸腔鏡下膿胸腔掻爬術を施行した。胸膜肥厚による肺拡張障害を認めたが，徐々に改善し第35病日に退院となった。肺炎に起因する劇症型溶血性レンサ球菌感染症では，急性膿胸の併発を念頭に置く必要があるが，その早期治療に関しては今後さらなる検討を要する。

劇症型溶血性レンサ球菌感染症

劇症型溶血性レンサ球菌感染症