Group A streptococcus: A continued threat

This issue includes two articles on the consequences of group A streptococcal (GAS) pelvic and peritoneal infection. The first appears to have no predisposing factors while the second follows gynaecological intervention (Saha et al. 2006; El Toukhy and Hanna 2006). Obstetricians are no strangers to this bacteria – it was the causative organism of puerperal sepsis – and will be aware that this organism still features in ‘Why Women Die’. A recent case report in this journal (Abouzeid et al. 2005) highlighted several important messages relating to puerperal sepsis. But do gynaecologists have the same respect and awareness of its virulence? Prior to 1730, management of pregnancy and delivery was almost entirely in the hands of midwives, but in the 1730s and 1740s came the lying-in hospitals and the manmidwives or accoucheurs and with it the increasing problem of puerperal sepsis. In 1760, the maternal mortality in the British Lying-in Hospital was 60 per 1000 with the majority of deaths due to sepsis (Loudon 1986). Puerperal sepsis occurred in epidemics and was the leading cause of maternal mortality in the UK from the 18th to the early 20th centuries. Alexander Gordon, with a description of an outbreak in Aberdeen between 1783 and 1792 first recognised its transmissibility (Willocks 1990). In the early 19th century, Semmelweis, in Vienna, introduced handwashing with disinfectants for doctors and medical students between autopsies and vaginal examinations (Adriaanse et al. 2000). This occurred because he realised that puerperal sepsis rates were higher in wards attended by doctors than wards attended by nurses. Pasteur identified streptococci in the blood of a patient with puerperal sepsis in 1879. During a lecture at the Academy of Medicine in Paris, Pasteur interrupted a lecturer who was theorising on the causes of epidemics in lying-in hospitals with the statement that ‘nursing and medical staff carry the microbe from an infectious woman to a healthy one’ (Adriaanse et al. 2000). He then drew an illustration of a chain of small circles depicting the streptococcus he had isolated from the blood and uterine pus cultures from a case of puerperal sepsis. However, despite the fact that this syndrome was well recognised, puerperal sepsis related mortality only started to decline after the introduction of antibiotics in the 1930s and 1940s. Prior to this time 37% of deaths directly attributable to pregnancy were related to puerperal sepsis. The first UK confidential enquiry into maternal death documented a reduction in deaths from puerperal sepsis to 3.8% (MoH 1957). This rate continued to decline and the 1982 – 84 triennial report had no maternal deaths from puerperal sepsis (DoH 1989). Rather upsettingly, this has not continued and 13 deaths from sepsis are documented in the most recent report (CEMACH 2004). This enquiry into maternal deaths identified that puerperal sepsis is occurring with an increase in maternal sepsis involving GAS in the last decade. Similar results were identified in other European countries (Lamagni et al. 2005). Indeed since the 1990s, there has been a global increase in the reporting of invasive GAS cases with a re-emergence of more virulent strains. In 2003 the incidence of invasive disease (blood or cerebrospinal fluid) reported in the UK (excluding Scotland) was 3.5 per 100,000 of the population. The organism was first called Streptococcus pyogenes by Rosenbach in 1884 (Edwards et al. 2002). When the current classification of beta haemolytic streptococci by Lancefield in 1933 was introduced it was found that most pathogenic strains were Group A. It is a gram-positive coccus that grows in chains. The most frequent clinical manifestations of GAS are pharyngitis and pyoderma (Edwards et al. 2002). However, 90% of invasive GAS cases reported in the UK in 2003 presented with bacteraemia (Anonymous 2004a). In those invasive cases where a specific diagnosis was available the following were recorded: septic arthritis 10%, pneumonia 9%, toxic shock syndrome 6%, necrotising fasciitis 5%, puerperal sepsis 3%, and meningitis 1%. In addition one in five cases was reported to have died within seven days of initial presentation. This is similar to published reviews where the mortality rate has varied between 20% and 40% (Edwards et al. 2002; Anonymous 2004a; Barnham 1989). There are a number of products and constituents of GAS that have been identified as virulence factors (Edwards et al. 2002). M-protein contributes to invasiveness through preventing phagocytosis of streptococci by neutrophils and strains lacking this protein appear to be less virulent. Other virulence factors, for example, streptococcal pyrogenic exotoxins potentiate endotoxin induced shock, fever, suppress antibody synthesis, are cytotoxic and act as superantigens. However, specific virulence factors for individual clinical presentations have not been identified, though typing of the isolates through M protein may assist