Many who feel they are very sick from mold tell me their IgE comes back normal, so their doctors say it's not mold. (Allergists call this the RAST IGE testing for mold).  But  a false negative is very likely,,,, My IgE was normal, yet the tests below were all positive {see NOTES below}.. My treating physician stated the importance of correct tests. Your doctor should be able to order the IgA, IgG, IgM mold and mycotoxin panels.  Do NOT let them tell you all you need is IGE, as that is just not true, as you'll see below..

Testing is no longer offering these tests thru Immuno-Sciences, but we're confident they will be available again soon. The most prestigious awards and recognition given Dr. Aristo Vojdani for his expertise and years of devotion to environmental medicine is well-deserved. I hope this info below helps someone.  I’ll keep you posted on any testing available..

The exact mechanism by which molds and particularly mycotoxins induce neurotoxicity is yet unclear. As a result of the assault of mycotoxins on the nervous system and the degenerative process, proteins, which act as antigens to provoke humoral responses in the form of IgG, IgM and IgA, are liberated. It can therefore be said that promising candidates for monitoring neurotoxicity caused by mycotoxins are the presence of autoantibodies against neurotypic and gliotypic proteins.

While the mechanisms have yet to be elucidated, we believe that antibodies against neuron-specific antigens and their cross-reactive epitopes may play a role in the pathogenesis of neurotoxicity induced by mycotoxins.

Immunotoxicity Induced by Molds and Mycotoxins

The exposure of animals to molds has shown a significant effect on the immune system.
In animals, this was manifested as increased susceptibility to infectious diseases.It is important to note that almost all mycotoxins have an immunosuppressive effect, although the exact target within the immune system may differ. Many are also cytotoxic, so that they have route of entry effects that may be damaging to the gut, the skin, or the lungs. Such cytotoxicity may affect the physical defense mechanisms of the respiratory tract, decreasing the ability of the airways to clear particular contaminants (including bacteria or viruses). It may also damage alveolar macrophages, thus preventing the clearance of contaminants from the deeper lung cavity.

Studies on the adverse immunological effects of fungal bio-aerosol on individuals were conducted at our laboratory facility and both cellular and humoral immune abnormalities were detected. The cellular abnormalities included abnormal T-cell function, B-cell function, and NK cell activity, as well as abnormal helper-suppressor ratios and cytokine production. Humoral abnormalities were observed in levels of anti-nuclear antibodies, anti-tissue antibodies, anti-neuronal antibodies, anti-thyroid antibodies, anti-adrenal antibodies, rheumatoid factor,
immune complexes, C3 and C4 complements, and fungal and mycotoxin antibodies.

Symptomatology of Patients Exposed to Toxigenic Molds

Soon after exposure to molds and their byproducts, patients are most likely to exhibit one of the following neurological and behavioral symptoms: allergy, blurred vision, fatigue, general cognitive deficits, headache, hyperthyroidism, loss of balance, memory loss, migraine, multiple chemical sensitivity, nausea, nosebleeds, painful lymph nodes, rashes, rhinitis, sinusitis.
Symptomologies are rather similar to those experienced by patients with Chronic Fatigue Syndrome with a history of exposure to toxic environmental chemicals.
Therefore, patients with Chronic Fatigue, Fibromyalgia, and Chemical Sensitivity Syndromes should also be examined for possible exposure to toxigenic molds at the home, as well as work environments.


Symptomatology of Patients Exposed to Toxigenic Molds – See Below

*Allergies

*Blurred vision
• Fatigue
• General cognitive deficits
• Headache
• Hyperthyroidism
• Loss of balance
• Memory loss
• Migraine
• Multiple chemical sensitivity
• Nausea
• Nosebleeds
• Painful lymph nodes
• Rashes
• Rhinitis
• Sinusitis



IMMUNOSCIENCES LAB., INC.

1. Allergy evaluation by skin or an in-vitro test for the detection of IgE mediated allergies are not enough for patients exposed to toxigenic molds in water-damaged building environments.
2. Depending on the individual immune response to toxigenic mold antigens,some people may respond by producing IgG, while others may produce IgM and IgA antibodies against different fungal antigens.
3. The measurement of IgG, IgM and IgA antibodies against toxigenic mold
is necessary for the detection of exposure to mold spore antigens and mycotoxins.
4. Intranasal and enteric exposure to mold antigens and mycotoxins leads
to the production of specific IgA antibodies in saliva and other secretions.
5. In addition to IgG, IgM and IgA antibodies in the blood, the measurement
of total specific salivary IgA against mold antigens and mycotoxins is necessary in order to increase the sensitivity and specificity of mold exposure detection.
6. Different parameters pertaining to the cellular (T-cell, B-cell, helper/ suppressor cell numbers, NK cell activity, T- and B-cell function, apoptosis)
and the humoral immune system (immunoglobulins, C3 and C4 complement, immune complexes, ANA, thyroid and other tissue antibodies) should be measured for documentation of immune competency dysfunction in patients exposed to toxigenic molds.
7. Mold antigens and/or mycotoxins can compromise the blood-brain barrier
and induce a neurodegenerative process of protein and antigen libera-
tion, provoking IgG, IgM or IgA against different neuronal antigens.
8. Detection of autoantibodies against myelin basic protein (MBP), myelin
associated glycoprotein (MAG), gangliosides, sulfatide, chondroitin sulfate, glutamate receptor, cerebellar, Purkinje cells, neuron-axon filament protein, glial fibrillary acidic protein, tubulin, and other neurological antigens, indicating a neurotoxicity process initiated by toxigenic molds, may result in: chronic sensory neuropathy, demyelinating sensorimotor neuropathies or Multiple Sclerosis-
Like Syndrome.
9. Prolonged and intense exposure to toxigenic molds and mycotoxins is
associated with disorders of the respiratory and central nervous systems,
the mucous membrane, mucosal immunity, as well as cellular and humoral immune dysfunction.


After Exposure to Toxigenic Molds Laboratory Tests



IMMUNOSCIENCES LAB., INC. •
In conclusion, we believe that mold-specific antibodies, when accompanied by
mycotoxin antibodies, can indeed be effectively used as biomarkers to assess
exposure to molds and mycotoxins. However, appropriate medical history,
physical exam, environmental laboratory examination, and documentation of
high viable microbial activity by means of testing for mold and mycotoxins specific IgG, IgM, IgA and IgE antibodies in blood or saliva, as well as other diagnostic procedures, such as monitoring abnormal immune parameters can assist in the diagnosis of fungal hypersensitivity and non- hypersensitivity reaction. Extraction of the patients from the mold environment and improvements in laboratory testing and in the patient's clinical conditions will be the best strategy for the demonstration of the cause and effect relationship.

Conclusion




IMMUNOSCIENCES LAB., INC. •

IgG, IgA, IgM and IgE Antibodies in Blood and IgA Antibodies in Saliva Against Molds and Mycotoxins

NOTE: [My bloodwork (IgA & IgG) showed very high abnormal levels to 9 the 14 molds listed below]


MOLD ANTIBODIES PANEL

IgG, IgM, IgA and IgE Antibodies in Blood and IgA
Antibodies in Saliva against the following:
• Alternaria tenuis
• Aspergillus fumigatus
• Aspergillus niger
• Aspergillus versicolor
• Chaetomium globosum
• Cladosporium herbarum
• Epicoccum nigrum
• Geotrichum candidum
• Penicillium notatum
• Phoma herbarum
• Pullularia pullulans
• Rhizopus nigricans
• Rhodotorula glutinis
• Stachybotrys chartarum
• Others by request
* Specimen Requirements: 2ml serum and/or saliva

NOTE: [My bloodwork showed excessively high abnormal antibodies the 6 of the 10  mycotoxins listed below per IgG, IgA]

MYCOTOXIN ANTIBODIES PANEL

IgG, IgM, IgA and IgE Antibodies in Blood and IgA
Antibodies in Saliva against the following:
• Aflatoxin
• Satratoxin-H
• Tricothecene-B
• Cladosporium HSP70
• Aspergillus Hemolysis
• T-2 Toxin
• Mycophenolic Acid
• Alternariol
• Chaetoglobosins2
• Vomitoxin
* Specimen Requirements: 2ml serum and/or saliva

NOTE: Of the 4 molds listed below we were tested by PCR/DNA analyses to find an active systemic infection, both Tlee and I were positive in our sputum and white blood cells. The only one not found was legionella pneumophila. Dr. Vojdani and Wilson documented the findings as extreme. We are very fortunate to be alive, and we thank God.  Our white blood cell count / activity was also very low….

Plus our Natural Killer Cell Cytotoxic Activity - very low

MOLECULAR DETECTION OF MOLDS AND BACTERIA [PCR Testing]
• Aspergillus fumigatus
• Aspergillus niger
• Stachybotrys chartarum
• Legionella pneumophila
* Specimen Requirements: 1ml lung secretions

NOTE: [My bloodwork revealed an abnormal natural killer cell activity which often happens after a toxic exposure such as ours]
• Lymphocyte Subset Analysis
• Natural Killer Cell Cytotoxic Activity
• T- and B-cell Function
• Autoimmune Panel
• Thyroid Antibodies Panel
• Immune Complexes
• C3 and C4 Complement
• Myelin Basic Protein, Neurofilament, Ganglioside and
Sulfatide Antibodies
• Total Secretory IgA in Saliva
• IgG, IgM, IgA and IgE Antibodies against the most
common Molds
• IgG, IgM, IgA and IgE Antibodies against Mycotoxins
• Salivary IgA Antibodies against Molds & Mycotoxins


IMMUNOTOXICOLOGY PANEL

Evaluation of Patients Exposed to Toxigenic Molds and Mycotoxins


Andersson et al., (1997). Bacteria, molds and toxins in water-
damaged building materials. Applied and Environ Microbio
63, 387-393.
Apter et al., (1989). Fluctuation of serum IgA and its subclasses
in allergic bronchopulmonary aspergillosis. J Allergy Clin
Immunol 84, 367-372.
Baxter et al., (1981). A prospective analysis of the potential
reaction associated with the inhalation of aflatoxin-contami-
nated grain dusts. Food and Cosmetic 19, 763-69.
Bozza et al., (2002). Dendridic cells transport conidia and
hyphae of Aspergillus fumigatus from the airways to the drain-
ing lymph nodes and initiate disparate TH responses to the fun-
gus. J of Immunology 168, 1362-1371.
Cresia et al., (1987). Acute inhalation toxicity of T-mycotoxin in
mice. Fund. Applied Toxicol. 8 (2), 230-235.
Flannigan et al., (1991). Allergenic and toxigenic microorgan-
isms in houses. J. Appl Bact Sym (Suppl) 70, 61-73.
Flükigers et al., (2002). Comparison of the crystal structure of
human manganese superoxide dismutase and the homologous
Aspergillus fumigatus allergen at 2-Ao resolution. J of
Immunology 168, 1267-1272.
Gareis, M. (1995). Cytotoxicity testing of samples originat-
ing from problem buildings.
Proceedings of the
International Conference: Fungi and Bacteria in Indoor
Environments: Health Effects, Detection and Remediation
(Eckart Johanning and Chin S. Yang, Eds.) pp. 139-144.
....Saratoga Springs.., ..NY.....
Hodgson et al., (1998). Building-associated pulmonary disease
from exposure to Stachybotrys chartarum and Aspergillus versi-
color. J Occ Env Med 40(3), 241-249.
Hyvarinen et al., (1999). Fungal exposure and IgG-levels of
occupants in houses with and without mold problems in
Bioaersols,
Fungi and Mycotoxins: Health Effects,
Assessment, Prevention and Control. Ed. Johanning E.
Eastern New York Occ. & Env. ..Health.. ..Center.., ....Albany.., ..NY.....
99, 166-168.
Jakab et al., (1994). Respiratory aflatoxicosis:suppression of
pulmonary and systemic host defenses in rats and mice. Toxicol.
Applied Pharm. 125, 198-205.
Jarvis et al., (1996). Toxigenic molds in water damaged build-
ings: dechlorogriseofulvins from Memnoniella echinata. J. Nat.
Prod. 59, 553-554.
Johanning et al., (1996). Health and immunology study follow-
ing exposure to toxigenic fungi (Stachybotrys chartarum) in a
water-damaged office environment. Int Arch Occup Environ
Health 68, 207-218.
Knutsen et al., (1994). Serum anti-Aspergillus fumigatus anti-
body immunoblot and ELISA in cystic fibrosis with allergic bron-
chopulmonary aspergillosis. J Clin Immunol 93, 926-931.
Liu Biing-Hui et al., (2002) The effects of mycotoxins, Gumonisin
B1 and Aflatoxin B1 on primary swing alveolar macrophages.
Toxicology and Applied Pharmacology 180,197-204.
Mahfoud et al., (2002) The mycotoxin patulin alters the barrier
function of the intestinal epithelium: mechanism of action of
the toxin and protective effects of glutathione. Toxicology and
Applied Pharmacology 181, 209-218.
Nikulin et al., (1996). Experimental lung mycotoxicosis in mice
induced by Stachybotrys atra. Int. J. Exp. Path. 77, 213-218.
Nikulin et al., (1997). Effects of intranasal exposure to spores of
Stachybotyrs atra in mice. Fundamental and Applied Toxicology
35, 182-188.
Ojanen et al., (1990). Class-specific antibodies during follow-up
of patients with farmer's lung. Eur Respir J 3, 257-260.
Paolo et al., (1993).Acute renal failure from inhalation of myco-
toxins. Nephron 64:621-625.
Paris et al., (1990) Comparison of different extraction methods
of Alternaria allergens. J. Allergy Clin. Immunol 85, 941-948.
Peebles et al., (2001).Antigen-specific IgE and IgA antibodies in
bronchoalveolar lavage fluid are associated with stronger anti-
gen-induced late phase reactions. Clin Exp Allergy 31, 239-248.
Pestka et al., (1989). Dysregulation of IgA production and IgA
nephropathy induced by trichothecene vomitoxin. Food Chem
Toxicol 27, 361-368.
Raunio et al., (2001). Preliminary description of antigenic com-
ponents of Stachybotrys chartarum. Environmental Research
Section 85, 246-255.
References
IMMUNOSCIENCES LAB., INC