IgA and infections: a preliminary miscellany

x x IgA and infections: a preliminary miscellany
IgA and INFECTIONS a preliminary miscellany
by Teresa Binstock
My writings do not constitute medical advice. Instead, they represent a seeking to understand autism-spectrum disorders and their causes and associated traits.
                                          >>> Posting number 7880, 
                                          dated 10 Mar 1997 12:05:41

.....IgA DEFICIENCY, CANDIDA, STAPHYLOCOCCUS AUREUS
The fact that a child tests positive for IgA deficiency does not
necessarily mean that the child's IgA-deficiency is due to the presence
of ongoing Candidiasis. However, in some individuals, low IgA might be
derived from an infection with Candida albicans.
      An enzyme produced by Candida albicans "...can break down a number of
host substrates, including albumin..., collagen..., immunoglobulin A
(IgA)..., keratin..., and hemoglobin..."
      Also, Candida albicans induces weakening of immune responses against
Staphyloccocus aureus, a common pathogen in human intestines. "The
ability of human polymorphonuclear leukocytes to kill Staphyloccocus
aureus was greatly reduced when the bacteria were opsonized [a complement
process] with human serum treated with... [the aforementioned C. albicans
enzyme]."

1. Kaminishi H et al.  Degradation of humoral host defense by Candida albicans
proteinase. Infection and Immunity 63.3.984-8 1995.

                                *****

Personal anecdote:

A friend who has been treated for Candida albicans since she was a very
young child, recently received her test results from the Great Plains
(Shaw) and Great Smokies labs. Her metabolites were described as
indicating presence of high levels of Staphylococcus aureus.

Teresa

                  >>> Posting number 2318, dated 20 Jan 1997 22:08:08
                  IgA & CD5+: was Re: Heavy Metal Toxicity

Hillary,

IgA is the primary immunoglobulin focused upon by Kroese et al, which is
reference 3 in my CD5+ paper; evidently, IgA is very significant in
protecting our natural microflora or in some cases, protecting pathogenic
microbes that if present early enough in the intestines, would always be
able to colonize... (which just seems to be another phrase for "bacterial
overgrowth").

Teresa

On Mon, 20 Jan 1997, robert wrote:
> ...I'll ask him then the name of the lab he's using. All I did at
> the appointment was write down the names of the various
> Ig tests. I have a good URL for IgA deficiency which I've
> found very thorough but down-to-earth. Have you seen the
> following?
> http://www.mssm.edu/iga-defi.html
>
> My son's immunologist liked this reference so well that he's
> now copying it to hand out to his IgA-deficient patients !!


                                          >>> Posting number 11480, 
                                          dated 17 Apr 1997 03:48:26

.....NEW IgA/AUTOIMMUNE STUDY by Reed Warren et al.....
A possible IgA connection in some cases of autism may be that of secretory IgA in
the GI-tract. As outlined and cited in my CD5+ paper, gastrointestinal IgA is very
important in establishing long term immunity to various intestinal pathogens. At
least hypothetically, sub-par IgA (if not induced later in life) might allow various
GI-pathogens to be seen as normal, not to be reacted against (reference 1 and cites
therein).
      I find myself thinking of Bob's thalidomide example and of the SSPE
example. Most mothers who took thalidomide did not have kids with defects.
Most kids who get measles do not develop SSPE. In other words and as
possibly relevant to IgA deficiencies, a contributing factor need not have
100 percent applicability (across all kids within a syndrome) in order to be a
causal factor.

Here is a garish analogy. Recently in Denver, a fellow walked into a bank
and shot two employees (one of whom died). The fellow then robbed the
bank, ran from the scene and has not been caught. Mr. Lee (who died from
the gunshot) would not have died from that gunshot had he not gone to work
that day. His going to the bank was a contributing factor. His going to
work was not the cause of his death; the gun-shot was the cause. Yet had
he stayed home or taken the day off, he would still be alive (probably).
In other words, contributing factors can be important, even if they are
not the primary cause.
      The parallel to IgA deficiency is not that IgA deficiency causes autism, but
that *in some cases and depending upon other factors* IgA deficiency may allow the
more primary causal factor to occur. This is very parallel to Reed Warren et al's
findings of enhanced rates of complement 4 deficiencies in ADHD and autism. The
complement deficiency is not the
cause of autism or ADHD but is likely to be a contributing factor, ie, a
factor increasing the likelihood of severe effects from infectious
events that can induce the more primary causes -- eg, cerebral edema,
atypically elevated bilirubin, etc.

Teresa

1. Binstock T. Hypothesis: Intestinal microflora and CD5+ B cells: their possible
significance in some cases of autism. Bit.Listserv.Autism        January 14 1997.

POSTING HISTORY FOR THE ABOVE E-MAILS

>>> Posting number 7880, dated 10 Mar 1997 12:05:41
Date:         Mon, 10 Mar 1997 12:05:41 -0700
Sender:       SJU Autism and Developmental Disablities List
              
From:         Teresa Binstock
Subject:      Re: IgA Deficiency & Candida & Staphylococcus aureus

>>> Posting number 2318, dated 20 Jan 1997 22:08:08
Date:         Mon, 20 Jan 1997 22:08:08 -0700
Sender:       SJU Autism and Developmental Disablities List
              
From:         Teresa Binstock
Subject:      IgA & CD5+: was Re: Heavy Metal Toxicity

>>> Posting number 11480, dated 17 Apr 1997 03:48:26
Date:         Thu, 17 Apr 1997 03:48:26 -0600
Sender:       SJU Autism and Developmental Disablities List
              
From:         Teresa Binstock 
Subject:      Re: Warren's new autoimmune study: IgA
return to: Contents e-mail to: Teresa Binstock