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NCID > For Healthcare Professionals > Joint MOH/ NCID Guidances > Group A Streptococcus (GAS) Infection

Group A Streptococcus (GAS) Infection

Group A Streptococcus (GAS) Infection

​            In a recent surveillance review, there were signs of potential increase in the number of laboratory confirmed GAS infections treated at KKH, NUH, SGH and TTSH from January 2010 to March 2018. While the first phase of genotype analysis showed no dominant circulating invasive GAS strains and does not suggest ongoing outbreaks of GAS infections in the community, these findings warrant a continued monitoring of the local situation. GAS infection is not a notifiable disease under the Infectious Disease Act (IDA). However medical practitioners who notice clusters of GAS infections should report via email (, or MD-131 form under ‘Others’ via the online Communicable Diseases Live and Enhanced Surveillance System (CD-LENS) or by fax (6221 5528, 6221 5538 and 6221 5567).


           Streptococcus pyogenes (Group A Streptococcus; GAS) is a ubiquitous human-adapted Grampositive bacterium which colonises the throat, skin and anogenital tract of humans. It is spread by close contact between individuals, through respiratory droplets and direct skin contact. It can also be transmitted via contact with contaminated objects, such as towels or bedding, and ingestion of food inoculated by a carrier.

           GAS causes a variety of superficial and invasive infections, with occasional immunological sequelae. Globally, the incidence of major syndromes caused by GAS has seen striking changes over the decades. Rates of acute rheumatic fever have fallen worldwide over the past century, while a surge in severe invasive cases was noticed in many countries including Singapore in the 1980’s to 1990’s. In the past decade, scarlet fever outbreaks – infrequently reported since the 19th century – have occurred in multiple countries including UK, China, USA, Hong Kong, and Canada.

Superficial GAS Infections

           The vast majority of GAS infections comprise of pharyngitis and impetigo. Streptococcal pharyngitis – typically presenting with acute onset fever accompanied by exudative inflammation of the pharynx and tonsils, with occasional cervical lymphadenopathy – is difficult to distinguish from viral pharyngitis. Impetigo most commonly affects children, presenting as contagious pustules that enlarge and rupture with yellowish crusts. As with most other skin manifestations of GAS, the clinical syndrome can also be caused by Staphylococcus aureus.

           Scarlet fever rarely develops from pharyngitis and is caused by strains of GAS that produce streptococcal erythrogenic toxins, manifesting as a deep red, generalised papular rash, with an erythematous face and “strawberry tongue” that accompany the exudative pharyngitis. It occurs primarily in childhood (majority of cases between 5 to 15 years of age), and the rash usually persists for up to a week.

Invasive GAS Infections

           Invasive GAS infections – in which the organism has breached skin and/or mucosal barriers – are far less common than superficial infections. The majority of these infections are bacteraemia in association with cutaneous infections (e.g. cellulitis) and accounts for up to 80% of GAS invasive diseases. It is important to note that cellulitis may also be caused by S. aureus – both are
indistinguishable without the benefit of positive bacterial cultures. Bacteremia occurs when GAS strains are introduced into the bloodstream, classically following childbirth (puerperal sepsis), but more commonly today as a consequence of injury, superficial infection, or transiently from colonisation.

           Less commonly, necrotizing fasciitis and myositis can occur, along with focal infection such as septic arthritis, osteomyelitis, and abscess formation. Pneumonia, endocarditis and meningitis are rarely seen today. Necrotizing fasciitis is a severe and rapidly progressive infection of skin, deep soft tissue, and muscle that is associated with mortality rates that exceed 25% even in high income countries.

           Any invasive disease may rarely be complicated by streptococcal toxic shock syndrome (STSS) – a rapidly progressing illness with hypotension, disseminated intravascular coagulopathy and organ failure triggered by GAS superantigens. The presence of STSS tends to increase the risk of mortality.

Immunologic Sequelae of GAS Infections

           The major post-infectious sequelae of GAS are acute rheumatic fever and acute poststreptococcal glomerulonephritis. Acute rheumatic fever most commonly occurs after untreated GAS pharyngitis. Rheumatic heart disease is a potential long-term sequela of carditis occurring during an episode or recurrent episodes of acute rheumatic fever. Acute post-streptococcal glomerulonephritis may result from impetigo or pharyngitis caused by “nephritogenic” strains of GAS. The antecedent infection may no longer be clinically apparent, but may be elicited from history. It is an acute nephritic syndrome with sudden oedema, proteinuria, gross hematuria, and hypertension resulting from immune complex-mediated injury of the glomerulus. The prognosis is excellent in children, resolving completely within weeks.

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Prepared by:

Communicable Diseases Division                    National Centre for Infectious Diseases
Ministry of Health, Singapore      

Date:  18 October 2018                    

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