Asymptomatic Strep

[matis_mom]

I am bringing up this from another post... I am trying to make sense of this as it sounds a lot like what is going on around here. Last strep bout none of my children had symptoms (except for my little canary, of course). Other families in our circle have had it too, with maybe only 1 child showing symptoms. I am reading this article over and over but I'm getting brain fog.

 

Is it saying that certain STRAINS are carried without symptoms, and that antibodies usually do not rise in that case?

 

Thanks to anyone out there who might be a little bit more scientifically inclined and less tired than me (or is it I)!

 

Isabel

 

 

The antibody response of 40 institutionalized children involved in an epidemic associated with asymptomatic pharyngeal acquisition of a group A, M-11, T-11 typeable Streptococcus was studied. Titers of antibody to streptolysin O and to deoxyribonuclease B determined in sera collected from patients within two weeks of positive throat cultures were significantly higher than those in sera of controls (P < 0.001). However, there was no rise in antibody titers in sera obtained from these patients after an interval of three weeks. Type-specific antibody to the group A Streptococcus (type M-11) was assayed in the sera of 24 patients. No detectable antibody activity was found either in the initial sera or in sera collected eight months after the epidemic. Thus, the asymptomatic nature of this epidemic could not be attributed to the presence of detectable type-specific antibody in this population at the time of the epidemic. These observations suggest that asymptomatic pharyngeal acquisition of group A Streptococcus may occur in epidemic fashion in certain populations and may not be associated with evidence of an antibody response to the streptococcal organism.

 

http://www.jstor.org/pss/30105590

[Buster]

Hi Isabel,

 

This paper is unusual for several reasons. This was an institutional study that happened to be sampling children for GABHS infection and detected an outbreak of an epidemic that did not cause symptoms of strep throat. This meant 47 of 50 children had culturable strep, but the children did not have a rise in ASO or Anti-DNAse B.

 

This result could be treated two ways. Either colonization is all that happened (i.e., no infection), or an infection occcured and the bacteria did not produce significant amounts of Streptolycin O or DNAse B.

 

The result was surprising because instead of only 20% of the children getting "asymptomatic carriage" 80% had asymptomatic carriage.

 

What was also surprising was that while the culture revealed that strain was one that is normally invasive (M-11), none of the children (barring one) had antibodies to that particular strain -- i.e., it doesn't look like the colonized M-11 actually invaded.

 

However further study showed that there were antibodies to another strain derived from a common parent of M-11 (how they figured this out is not disclosed). This other strain lacks the M-protein. Other researchers had found this type specific antibody to the "base" type seemed to only occur in those with carriage and not in those with symptomatic response. This seems to indicate that some transformation to the M strain occurred in each child .

 

Another interesting item was that when the M-11 strain was isolated it produced very little streptolysin O but produced significant amount of DNAseB. There was clearly something odd about the strain or something that was keeping the strain in check. Kaplan had found in other studies that other bacteria in the throat could hold strains of GABHS in check, he also found that in certain individuals, the M-protein is not replicated (i.e., the strain changes type within a person with carriage -- a form of mutation). It's unclear whether that was occuring in this case.

 

Perhaps the most interesting comment in the paper is the sentence around "benign pharyngeal acquisition". They write "Despite increasing evidence for the occurrence of "benign" pharyngeal acquisition of Streptococcus and the absence of an association of nonpurulent complications with this entity in contrast to the high risk of such complications with symptomatic disease [2, 3, 5, 14, 15, 27-29], it is premature, at this stage of our knowledge, to use these data as a basis for not treating patients with mild streptococcal pharyngitis."

 

What this says is that there is a lack of evidence that carriage is actually benign. Kaplan says this too in his paper about carriage being an enigma. Furthermore the authors of this paper highlight that in studies of recent increases in acute rheumatic fever, many who got the disease had no recollection of a preceeding sore throat.

 

I realize that the above is probably more than most want to know, but:

 

The bottom line is that if you get a positive throat culture, treat it.

 

Buster

 

I am bringing up this from another post... I am trying to make sense of this as it sounds a lot like what is going on around here. Last strep bout none of my children had symptoms (except for my little canary, of course). Other families in our circle have had it too, with maybe only 1 child showing symptoms. I am reading this article over and over but I'm getting brain fog.

 

Is it saying that certain STRAINS are carried without symptoms, and that antibodies usually do not rise in that case?

 

Thanks to anyone out there who might be a little bit more scientifically inclined and less tired than me (or is it I)!

 

Isabel

 

 

The antibody response of 40 institutionalized children involved in an epidemic associated with asymptomatic pharyngeal acquisition of a group A, M-11, T-11 typeable Streptococcus was studied. Titers of antibody to streptolysin O and to deoxyribonuclease B determined in sera collected from patients within two weeks of positive throat cultures were significantly higher than those in sera of controls (P < 0.001). However, there was no rise in antibody titers in sera obtained from these patients after an interval of three weeks. Type-specific antibody to the group A Streptococcus (type M-11) was assayed in the sera of 24 patients. No detectable antibody activity was found either in the initial sera or in sera collected eight months after the epidemic. Thus, the asymptomatic nature of this epidemic could not be attributed to the presence of detectable type-specific antibody in this population at the time of the epidemic. These observations suggest that asymptomatic pharyngeal acquisition of group A Streptococcus may occur in epidemic fashion in certain populations and may not be associated with evidence of an antibody response to the streptococcal organism.

 

http://www.jstor.org/pss/30105590

[sf_mom]

THANK YOU BUSTER......... once again!!!!!!!

 

In all your free time, I'd love your interpretation of the paper posted for IOWA DAWN. It talks about cloning of the T-cell? From throat to skin?

 

No worries if there is not the time.

 

FOREVER GRATEFUL FOR YOUR INSIGHT.

 

-Wendy

Edited May 6, 2010 by SF Mom

[EAMom]

What this says is that there is a lack of evidence that carriage is actually benign. Kaplan says this too in his paper about carriage being an enigma. Furthermore the authors of this paper highlight that in studies of recent increases in acute rheumatic fever, many who got the disease had no recollection of a preceeding sore throat.

 

I realize that the above is probably more than most want to know, but:

 

The bottom line is that if you get a positive throat culture, treat it.

 

Buster

 

The extremely frustrating thing is that most peds/docs don't think treating carriage is warranted.

[kim]

I have to wonder if these were the Willowbrook children again. I also wonder if there isn't a little something more here than meets the eye (could be wrong but something seems pretty strange)?

 

This would not have been the first time institutionalized children had been used. Why do you go looking for an asymptomatic epidemic? Am I missing something (can't get whole paper).

 

Mentally defective and inmates is how they are referred to in this paper. 7 mos to 10 year olds were used in this study for a measles vaccine

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1522575/?page=4

 

Of the 32 willowbrook children 94% had a fever over 101 40% of this group had a fever btwn 103 and 105

 

Some history on the use of children in experiments

 

http://www.hss.energy.gov/healthsafety/OHR...re/chap7_2.html

 

 

bolding mine

http://www.sciencedirect.com/science?_ob=A...31b885df044a8ac

 

M.D.Myron M. Levineb, , M.D.Eugene J. Gangarosaa, M.D.Max Wernerc and Ph.D.George K. Morrisa

 

aBureau of Epidemiology, Center for Disease Control, Atlanta, Ga. USA

 

bDivision of Infectious Diseases of the University of Maryland School of Medicine, Baltimore, Md. USA

 

Willowbrook State School, Staten Island, N. Y. USA

 

Shigellosis in custodial institutions: III. Prospective clinical and bacteriologic surveillance of children vaccinated with oral attenuated shigella vaccines

 

 

 

http://www.jpeds.com/article/S0022-3476(73)80312-9/abstract

 

Abstract

Serial monitoring of rubella hemagglutination-inhibiting antibodies in institutionalized children revealed that 4 of 16 nonvaccinated rubella-susceptible children had developed antibodies and 4 of 29 children immunized with Cendehill rubella vaccine had a fourfold or greater rise in antibody titer during the same 4 year interval. This apparent spread of wild virus occurred within three building with a population estimated to be 91 per cent “immune.” The vaccinees have shown a slight fall in hemagglutination-inhibiting antibody titers over the four years, and both the vaccines and naturally immune children who experienced the “booster” response had titers lower than the others. These observations cast doubt on the ability of “herd immunity” to prevent the spread of wild rubella virus.

Edited May 6, 2010 by kim