Streptolysin A and deoxyribonuclease B are two further proteins that generate antibody formation on infection with GAS. In the absence of clinical manifestations, measurement of the antibodies for these two antigens (ASO and Anti-DNaseB) can indicate recent GAS infection. It is important the antibody titre be repeated 10 to 14 days after first measurement if the first results were low--rising titres indicate infection, while persistent low titres are associated with carrier status or chronic infection. (2)
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 strains of GAS, has impeded
the development of a vaccine against the bacteria. (19) 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. (10)
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. (19)
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 that 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. (10)
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.
(10) 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. (10,19)
Streptolysin A and deoxyribonuclease B are two further proteins that generate antibody formation on infection with GAS. In the absence of clinical manifestations, measurement of the antibodies for these two antigens (ASO and Anti-DNaseB) can indicate recent GAS infection. It is important the antibody titre be repeated 10 to 14 days after first measurement if the first results were low--rising titres indicate infection, while persistent low titres are associated with carrier status or chronic infection. (2)
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 strains of GAS, has impeded
the development of a vaccine against the bacteria. (19) 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. (10)
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. (19)
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 that 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. (10)
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.
(10) 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. (10,19)
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