Group A streptococcal sepsis

Stevens, Dennis L.

doi:10.1007/s11908-003-0017-7

Cited by 42 publications

(40 citation statements)

References 51 publications

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“…The role of lincosamides in addition to penicillin would be an attractive proposition if toxin production was proven. Lincosamides, which act on bacterial RNA to inhibit protein synthesis, might abort the duration of myocarditis by limiting toxigenicity (Stevens, 2003). However there are no precedents to recommend them as routine at this juncture.…”

Section: Discussionmentioning

confidence: 99%

Non-rheumatic streptococcal myocarditis – warm hands, warm heart

Chaudhuri

Dooris

Woods

2013

Journal of Medical Microbiology

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Acute myopericarditis in the developed world is ascribed predominantly to viral infections. Enteroviruses and adenoviruses are commonly implicated but are not routinely tested for, as the condition is self-limiting and has a good prognosis. However, we recently encountered two cases of acute myopericarditis associated with concomitant Streptococcus pyogenes [group A Streptococcus (GAS)] pharyngotonsillitis. A microbiological aetiology was pursued because of the severity of the upper respiratory tract infection and associated systemic illness rather than to explain the myopericarditis per se. We report these two cases and review the literature of this potentially under-recognized condition. In the absence of features of rheumatic fever, we hypothesize a toxin-mediated process as opposed to an immune-mediated one. We suggest that perhaps all patients with myopericarditis be assessed for GAS pharyngitis. Case reports Case 1A 29-year-old male was brought to our emergency department with left-sided chest pain and high fevers. He had developed a sore throat 3 days prior to admission which progressed to odynophagia and mild trismus at the time of admission. Urgent ENT consultation confirmed a peritonsillar abscess, which was treated with incision and drainage under local anaesthesia. Simultaneous investigation of his chest symptoms revealed widespread 'saddleshaped' ST elevation and a raised serum cardiac troponin I (cTnI) (peak level 25 ng l 21 ). An echocardiogram revealed mild segmental systolic dysfunction and regional wall motion abnormalities (Table 1). The temporal pattern of cTnI levels was not monophasic and the ECG evolution was not typical of myocardial infarction. Coronary artery disease was a possibility, which prompted additional investigations of cardiac magnetic resonance imaging (MRI) and left heart catheterization. MRI showed moderate systolic dysfunction left ventricular ejection fraction 39 % which was segmental but no obstructive coronary artery disease was found on coronary angiogram. Abnormal MRI was consistent with diffuse myopericarditis, with oedema and late gadolinium enhancement in subepicardial and intramural regions (Fig. 1). Left heart catheterization revealed abnormal haemodynamics of relative hypotension with elevated left ventricular enddiastolic pressure. A diagnosis of myopericarditis was made and the patient was admitted with cardiac monitoring.Intravenous penicillin was commenced for peritonsillar abscess, which shortly grew group A Streptococcus (GAS). Streptococcal serology done soon after admission was negative. The patient remained febrile, appeared flushed with warm bounding peripheries but was haemodynamically robust (heart rate of 90-100 b.p.m.; blood pressure of 130/70 mmHg; mean arterial pressure of 90 mmHg). Minimal improvement of his pharyngeal symptoms prompted a repeat incision and drainage, plus the addition of intravenous lincomycin for presumed anaerobic bacterial infections potentially resistant to penicillin. He made a gradual recovery over 5 days and lincomycin w...

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Section: Discussionmentioning

confidence: 99%

Non-rheumatic streptococcal myocarditis – warm hands, warm heart

Chaudhuri

Dooris

Woods

2013

Journal of Medical Microbiology

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“…Another important cause of morbidity and mortality is invasive infection caused by the bacteria. Streptococcal toxic shock syndrome and necrotizing fasciitis have a higher mortality rate than invasive disease caused by other Gram-positive bacteria (9). S. pyogenes can be classified into different serotypes based on variations in the cell surface M protein, an important virulence factor for the bacteria (10).…”

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confidence: 99%

Platelet Activation by Streptococcus pyogenes Leads to Entrapment in Platelet Aggregates, from Which Bacteria Subsequently Escape

et al. 2014

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Platelet activation and aggregation have been reported to occur in response to a number of Gram-positive pathogens. Here, we show that platelet aggregates induced by Streptococcus pyogenes were unstable and that viable bacteria escaped from the aggregates over time. This was not due to differential activation in response to the bacteria compared with physiological activators. All the bacterial isolates induced significant platelet activation, including integrin activation and alpha and dense-granule release, at levels equivalent to those induced by potent physiological platelet activators that induced stable aggregates. The ability to escape the aggregates and to resist the antibacterial effects of platelets was dependent on active protein synthesis by the bacteria within the aggregate. We conclude that S. pyogenes bacteria can temporarily cover themselves with activated platelets, and we propose that this may facilitate survival of the bacteria in the presence of platelets.

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“…Noninvasive infections, including acute pharyngitis and superficial skin infection, result in substantial morbidity and economic loss globally (3,30). Severe invasive GAS infections, such as necrotizing fasciitis, bacteremia, and streptococcal toxic shock syndrome, are associated with high mortality rates (28,32,39). Necrotizing fasciitis is characterized as a rapidly progressive infection, causing necrosis of the fascia and subcutaneous tissue that leads to systemic infection (42).…”

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confidence: 99%

The Secreted Esterase of Group A Streptococcus Is Important for Invasive Skin Infection and Dissemination in Mice

et al. 2009

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Virulence factors regulated by the CovRS/CsrRS two-component gene regulatory system contribute to the invasive diseases caused by group A Streptococcus (GAS). To determine whether the streptococcal secreted esterase (Sse), an antigen that protects against subcutaneous GAS infection, is one of these virulence factors, we investigated the phenotype of a nonpolar sse deletion mutant strain (⌬sse). In addition, we examined the effects of covS mutation on sse expression. As assessed using a mouse model of subcutaneous infection, the virulence of the ⌬sse strain is attenuated and the overall pathology is reduced. Furthermore, GAS was detected in the blood and spleens from mice subcutaneously infected with the parental strain, whereas mice subcutaneously infected with the ⌬sse strain had no GAS present in their blood and spleens. The ability of the mutant to survive in the subcutis of mice appeared to be compromised. The growth of the ⌬sse strain in rich and chemically defined media and nonimmune human blood and sera was slower than that of the wild-type strain. Complementation restored the phenotype of the ⌬sse strain to that of the wild-type strain. The wild-type, ⌬sse, and complement strains had no detectable SpeB activity. Expression of Sse is negatively controlled by CovRS. These findings suggest that Sse is a CovRS-regulated virulence factor that is important for the virulence of GAS in subcutaneous infection and plays an important role in severe soft tissue infections and systemic dissemination of GAS from the skin.

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Group A streptococcal sepsis

Cited by 42 publications

References 51 publications

Non-rheumatic streptococcal myocarditis – warm hands, warm heart

Non-rheumatic streptococcal myocarditis – warm hands, warm heart

Platelet Activation by Streptococcus pyogenes Leads to Entrapment in Platelet Aggregates, from Which Bacteria Subsequently Escape

The Secreted Esterase of Group A Streptococcus Is Important for Invasive Skin Infection and Dissemination in Mice

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