GAS pharyngitis or ‘strep throat’
Acute pharyngitis due to GAS infection can be differentiated form a viral sore throat by the presence of high temperature [>38degC], swollen cervical lymph nodes, swollen tonsils with or without exudates [pus], and the absence of a cough or coryza [runny nose, etc.]. High-risk groups
And those with confirmed GAS infection are treated with a 10-day course of oral penicillin. There is evidence that as long as therapy starts within nine days of the onset of symptoms, the risk of progression to ARF is minimized.
GAS is vulnerable to the effects of penicillin, which is remarkable considering the extensive use of the antibiotic and the development of resistance to it by many other types of bacteria. Most resistance to penicillin is conferred by beta-lactamase activity in bacterial species. GAS does not possess the gene for beta-lactamase, possibly because it [the enzyme] may be toxic to GAS. An alternative mechanism of resistance is modification of the penicillin binding [PBP] in the bacterial cell wall. When GAS with modified PBPs were created in the laboratory, there were such severe changes in the bacteria structure and function that they could not survive.
Amoxicillin is a broader spectrum antibiotic. It is as effective penicillin but may have better compliance due to more palatable taste, once-daily dosing and because it does not need to be administered on an empty stomach.
Box 1. Why is there no vaccine for GAS?
Since the 1930s, when the Lancefield categories were established, there has been little research on the immune responses to Group A streptococci [GAS]. This, in combination with the lack of global epidemiological data on the different of GAS, has impeded the development of a vaccine against the bacteria. Also, there has been a theoretical risk that a vaccine may trigger the same autoimmune events leading to ARF and RHD as infection with GAS itself. While there is some research evidence to support this, the quality of that research has been questioned and recent early-stage vaccine trials have not demonstrated any increased risk.
Since 1923, only 19 vaccines against GAS have progressed as far as clinical trials. Currently there are several vaccines in development and early trial stages, but their ability to cover strains of GAS in developed vs third world nations is variable.
At issue is the variability in strains of GAS as determined by the M-protein on the bacterial cell surface. The M-protein is the main virulence factor involved in GAS infections. Emm-typing is the main method used to identify strains of GAS and these are known to vary considerably around the world. Unfortunately, data from developing nations is lacking compared with what from first world countries, so vaccine development is targeted for these known but less prevalent strains. In addition, there has been a lack of collaboration between research groups and with vaccine manufacturers regarding M-subtypes.
Multivalent vaccines [targeting up to 30 different emm-types] are entering clinical trials, but vaccines targeting other, less variable GAS bacterial proteins are still in early development. These other protein targets may not be able to induce immune response in humans to the same extent as the multivalent vaccines, because they are less virulent than M-proteins. They would, however, theoretically provide broader coverage against more strains of GAS than the multivalent vaccines.
GAS pharyngitis or ‘strep throat’
Acute pharyngitis due to GAS infection can be differentiated form a viral sore throat by the presence of high temperature [>38degC], swollen cervical lymph nodes, swollen tonsils with or without exudates [pus], and the absence of a cough or coryza [runny nose, etc.]. High-risk groups
And those with confirmed GAS infection are treated with a 10-day course of oral penicillin. There is evidence that as long as therapy starts within nine days of the onset of symptoms, the risk of progression to ARF is minimized.
GAS is vulnerable to the effects of penicillin, which is remarkable considering the extensive use of the antibiotic and the development of resistance to it by many other types of bacteria. Most resistance to penicillin is conferred by beta-lactamase activity in bacterial species. GAS does not possess the gene for beta-lactamase, possibly because it [the enzyme] may be toxic to GAS. An alternative mechanism of resistance is modification of the penicillin binding [PBP] in the bacterial cell wall. When GAS with modified PBPs were created in the laboratory, there were such severe changes in the bacteria structure and function that they could not survive.
Amoxicillin is a broader spectrum antibiotic. It is as effective penicillin but may have better compliance due to more palatable taste, once-daily dosing and because it does not need to be administered on an empty stomach.
Box 1. Why is there no vaccine for GAS?
Since the 1930s, when the Lancefield categories were established, there has been little research on the immune responses to Group A streptococci [GAS]. This, in combination with the lack of global epidemiological data on the different of GAS, has impeded the development of a vaccine against the bacteria. Also, there has been a theoretical risk that a vaccine may trigger the same autoimmune events leading to ARF and RHD as infection with GAS itself. While there is some research evidence to support this, the quality of that research has been questioned and recent early-stage vaccine trials have not demonstrated any increased risk.
Since 1923, only 19 vaccines against GAS have progressed as far as clinical trials. Currently there are several vaccines in development and early trial stages, but their ability to cover strains of GAS in developed vs third world nations is variable.
At issue is the variability in strains of GAS as determined by the M-protein on the bacterial cell surface. The M-protein is the main virulence factor involved in GAS infections. Emm-typing is the main method used to identify strains of GAS and these are known to vary considerably around the world. Unfortunately, data from developing nations is lacking compared with what from first world countries, so vaccine development is targeted for these known but less prevalent strains. In addition, there has been a lack of collaboration between research groups and with vaccine manufacturers regarding M-subtypes.
Multivalent vaccines [targeting up to 30 different emm-types] are entering clinical trials, but vaccines targeting other, less variable GAS bacterial proteins are still in early development. These other protein targets may not be able to induce immune response in humans to the same extent as the multivalent vaccines, because they are less virulent than M-proteins. They would, however, theoretically provide broader coverage against more strains of GAS than the multivalent vaccines.
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