Posts filed under ‘FIEBRE y RASH’

Cluster of Fatal Group A Streptococcal emm87 Infections in a Single Family: Molecular Basis for Invasion and Transmission.

J Infect Dis. June 1, 2017 V.215 N.11 P.1648-1652.      

La enfermedad hipervirulenta debida a Strep pyogenes puede ser el resultado de cepas con mutaciones que mejoran la expresión del gen de virulencia pero reducen la transmisión posterior.

Los autores utilizan la secuenciación del genoma completo para investigar la diseminación intra-familiar entre 4 hermanos, de una infección debido a una cepa de Strep pyoegenes hipervirulenta que resultó en la muerte de uno de ellos.

Todos los aislamientos de Strep pyoegenes invasivos y faríngeos tenían una mutación idéntica en un gen que codifica una proteína reguladora clave que producía un fenotipo hiperinvasivo.

Estos datos desafían la teoría prevaleciente de la transmisión reducida inducida por mutaciones que conducen a un Strep pyoegenes hipervirulento con alta diseminación grupal.




September 25, 2018 at 8:13 am

Description of the Pathogenic Features of Streptococcus pyogenes Isolates from Invasive and Non-Invasive Diseases in Aichi, Japan.

Jpn J Infect Dis. 2016 Jul 22;69(4):338-41.

Matsumoto M1, Yamada K, Suzuki M, Adachi H, Kobayashi S, Yamashita T, Minagawa H, Tatsuno I, Hasegawa T.


We identified hypervirulent Streptococcus pyogenes in 27 and 420 isolates from patients with invasive and non-invasive diseases, respectively, in Aichi Prefecture, Japan, between 2003 and 2012, in an attempt to understand why the prevalence of streptococcal toxic shock syndrome (STSS) suddenly increased in this location during 2011. Hypervirulent strains belong to the emm1 genotype, with a mutation in the covR/S genes that regulate many other genes, encoding virulence determinants and resulting in the absence of the proteinase streptococcal exotoxin B and the production of virulence factors such as the superantigen streptococcal exotoxin A, the nuclease streptococcal DNase, the cytotoxin NAD-glycohydrolase, and the hemolysin streptolysin O. We found 1 strain from invasive disease and 1 from non-invasive disease with traits similar to those of hypervirulent strains, except that the sda1 gene was absent. We also found 1 non-emm1 strain with phenotypic and genetic traits identical to those of the emm1 hypervirulent strains except that it did not belong to emm1 genotype, from non-invasive diseases cases in 2011. These findings suggested that hypervirulent and hypervirulent-like strains from invasive and non-invasive disease cases could have at least partially contributed to the sudden increase in the number of patients with STSS in Aichi during 2011


September 21, 2018 at 8:21 am

Invasive streptococcal disease: a review for clinicians.

Br Med Bull. 2015 Sep;115(1):77-89.

Parks T1, Barrett L2, Jones N3.



Streptococci are a genus of Gram-positive bacteria which cause diverse human diseases. Many of these species have the potential to cause invasive infection resulting from the presence of bacteria in a normally sterile site.


Original articles, reviews and guidelines.


Invasive infection by a streptococcus species usually causes life-threatening illness. When measured in terms of deaths, disability and cost, these infections remain an important threat to health in the UK. Overall they are becoming more frequent among the elderly and those with underlying chronic illness. New observational evidence has become available to support the use of clindamycin and intravenous immunoglobulin in invasive Group A streptococcal disease.


Few interventions for the treatment and prevention of these infections have undergone rigorous evaluation in clinical trials. For example, the role of preventative strategies such as screening of pregnant women to prevent neonatal invasive Group B streptococcal disease needs to be clarified.


Studies of invasive streptococcal disease are challenging to undertake, not least because individual hospitals treat relatively few confirmed cases. Instead clinicians and scientists must work together to build national and international networks with the aim of developing a more complete evidence base for the treatment and prevention of these devastating infections.



September 21, 2018 at 8:20 am

Changes in the clinical and epidemiological features of group A streptococcal bacteraemia in Australia’s Northern Territory.

Trop Med Int Health. 2015 Jan;20(1):40-7.

Gear RJ1, Carter JC, Carapetis JR, Baird R, Davis JS.



Invasive group A streptococcus (iGAS) disease is an important cause of mortality globally. The incidence of iGAS in Australia’s tropical Northern Territory (NT) has been previously reported as 32.2/100 000 in Indigenous people for the period 1991-1996. We aimed to measure the incidence and severity of iGAS disease in the NT since this time.


We collected demographic data for all GAS blood culture isolates over a 12-year period (1998-2009) from the three hospital laboratories serving the tropical NT. We then collected detailed clinical information from hospital records and databases for the subset of these patients who were admitted to Royal Darwin Hospital during 2005-2009.


There were 295 confirmed cases of GAS bacteraemia over the study period, with a mean (SD) age of 42.1 (22.0) years, and 163 (55.0%) were male. The annual age-adjusted incidence was 15.2 (95% CI 13.4-16.9)/100 000 overall and 59.4 (95% CI 51.2-67.6) in Indigenous Australians. For 2005-2009, there were 123 cases with the most common focus of infection being skin/soft tissue [44 (35.6%)]; 29 patients (23.6%) required intensive care unit admission and 20 (16.3%) had streptococcal toxic shock syndrome. Antecedent sore throat or use of non-steroidal anti-inflammatory drugs was rare, but current or recent scabies, pyoderma and trauma were common.


The incidence and severity of iGAS are high and increasing in tropical northern Australia, and urgent attention is needed to improve surveillance and the social determinants of health in this population. This study adds to emerging data suggesting increasing importance of iGAS in low- and middle-income settings globally.



September 21, 2018 at 8:19 am

The contribution of group A streptococcal virulence determinants to the pathogenesis of sepsis.

Virulence. 2014 Jan 1;5(1):127-36.

Reglinski M1, Sriskandan S1.


Streptococcus pyogenes (group A streptococcus, GAS) is responsible for a wide range of pathologies ranging from mild pharyngitis and impetigo to severe invasive soft tissue infections. Despite the continuing susceptibility of the bacterium to β-lactam antibiotics there has been an unexplained resurgence in the prevalence of invasive GAS infection over the past 30 years. Of particular importance was the emergence of a GAS-associated sepsis syndrome that is analogous to the systemic toxicosis associated with TSST-1 producing strains of Staphylococcus aureus. Despite being recognized for over 20 years, the etiology of GAS associated sepsis and the streptococcal toxic shock syndrome remains poorly understood. Here we review the virulence factors that contribute to the etiology of GAS associated sepsis with a particular focus on coagulation system interactions and the role of the superantigens in the development of streptococcal toxic shock syndrome.


September 21, 2018 at 8:18 am

Group A Streptococcus Toxic Shock Syndrome: An outbreak report and review of the literature.

J Infect Public Health. 2012 Dec;5(6):388-93.

Al-ajmi JA1, Hill P, O’ Boyle C, Garcia ML, Malkawi M, George A, Saleh F, Lukose B, Ali BA, Elsheikh M.


Group A Streptococcal (GAS) Toxic Shock Syndrome (TSS) is an acute, rapidly progressive, and often fatal illness. Outbreaks can occur in hospitals. However, early infection control measures may interrupt transmissions and prevent morbidity and mortality. Two cases of invasive GAS TSS were diagnosed within 48h after two uncomplicated laparoscopic surgeries that were performed in the same operating room of a women’s hospital. Investigations conducted by the infection prevention and control department of the hospital identified 46 obstetrical staff members who were involved in the surgeries and/or had contact with either of the patients. All of the staff members were interviewed regarding any recent history of upper respiratory tract infections, the presence of skin lesions and vaginal or rectal symptoms. Throat, rectal, and vaginal cultures were obtained two times from all of the involved staff members. Throat colonization with GAS was detected in the cultures from one obstetrical intern who attended the 1st surgery and from one nurse who had formerly worked in the postnatal ward. These two strains were epidemiologically different from each other and from the outbreak strain. Both carriers were suspended from direct patient care and were treated with a ten-day course of oral clindamycin. The success of their decolonization status was assessed at the end of therapy and at three, six, nine and twelve months thereafter before reassigning them to routine work. Unfortunately, in spite of the extensive investigation of all involved personnel and of the environment, the mode of transmission to the second patient could not be established. However, droplet or airborne transmission could not be ruled out. Early and meticulous implementation of infection control measures was crucial and instrumental in the successful management and control of this outbreak. Furthermore, there were no subsequent GAS cases detected during the 24 months following the outbreak.


September 21, 2018 at 8:17 am

Superantigenic activity of emm3 Streptococcus pyogenes is abrogated by a conserved, naturally occurring smeZ mutation.

PLoS One. 2012;7(10):e46376.

Turner CE1, Sommerlad M, McGregor K, Davies FJ, Pichon B, Chong DL, Farzaneh L, Holden MT, Spratt BG, Efstratiou A, Sriskandan S.


Streptococcus pyogenes M/emm3 strains have been epidemiologically linked with enhanced infection severity and risk of streptococcal toxic shock syndrome (STSS), a syndrome triggered by superantigenic stimulation of T cells. Comparison of S. pyogenes strains causing STSS demonstrated that emm3 strains were surprisingly less mitogenic than other emm-types (emm1, emm12, emm18, emm28, emm87, emm89) both in vitro and in vivo, indicating poor superantigenic activity. We identified a 13 bp deletion in the superantigen smeZ gene of all emm3 strains tested. The deletion led to a premature stop codon in smeZ, and was not present in other major emm-types tested. Expression of a functional non-M3-smeZ gene successfully enhanced mitogenic activity in emm3 S. pyogenes and also restored mitogenic activity to emm1 and emm89 S. pyogenes strains where the smeZ gene had been disrupted. In contrast, the M3-smeZ gene with the 13 bp deletion could not enhance or restore mitogenicity in any of these S. pyogenes strains, confirming that M3-smeZ is non-functional regardless of strain background. The mutation in M3-smeZ reduced the potential for M3 S. pyogenes to induce cytokines in human tonsil, but not during invasive infection of superantigen-sensitive mice. Notwithstanding epidemiological associations with STSS and disease severity, emm3 strains have inherently poor superantigenicity that is explained by a conserved mutation in smeZ.


September 21, 2018 at 8:16 am

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