Types:
Click below:
Aspergillus
Chaetomium
Fusarium
Penicillium
Stachybotrys
Mycotoxins
Location
RealTime Laboratories, LLC
13016 Bee Street
Suite 203
Dallas, Texas 75234
Ph: 972.243.7754
Fax: 972.243.7759
Email:
mscmd@cox.net
"In the
summer of 2005 I was 49 and
in top
physical condition. I was a
dedicated
white water kayaker,
a passionate skier, dancer, and
I delighted
in running up mountains.
I had
pneumonia in 2004 and again
in 2005.
After that I got progressively
worse
with my breathing. I was
referred to
Beth Israel Hospital
in Boston.
After many
examinations, I had an
open lung
biopsy in 2005. The diagnosis
was
“idiopathic pulmonary fibrosis”.
They
told me there are no effective
treatments.
Life expectancy is 2-5
years from
diagnosis. One of the
treatments is a lung
transplant.
I was able to kayak
only if
I had oxygen on.
In 2006,
while on a trip, (wearing oxygen)
I met a
doctor in the Grand Canyon,
from Benson,
Arizona, who treated
mold patients and
knew of
patients he had seen
with my
diagnosis.
He suggested
that I have
my biopsy from Beth Israel
Hospital sent
to RealTime Laboratories
in
Dallas, Texas, for examination for
mycotoxins
and DNA to molds.
I did that.
RTL
found molds and mycotoxins in my
biopsy.
After many conversations with
the doctors
in Boston, I began treatment
with standard
antifungal medication,
itraconazole
and ketoconozole.
One year
later, I am happy to report I
have had no
acute exacerbations. I have
not had
to have a lung transplant and it
doesn’t look
like that is in my future!! I
am
delighted to be alive and healthy.
Had I not met
the physician from Arizona,
I would have
never heard of RTLs. I
believe I
would be dead or very close to it.
I will speak
with anyone on this topic
anytime.
Please feel free to email me
at took@worldpath.net"
- Seth K.
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Mold
Information - Type
Aspergillus
Aspergillus
is a group of molds, which are found
everywhere world-wide. The are also called filamentous fungi. Of the more
than 200 species, only a few of these molds cause illness in humans and
animals. Most people are naturally immune and do not develop disease caused by
Aspergillus. Diseases caused by aspergillus can take many different
forms. Patients can have allergy-type illness due to Aspergillus or they can
have life-threatening generalized infections. The severity of aspergillosis
is determined by various factors but one of the most important is the state of
the immune system of the person. The poisons or mycotoxins produced by
Aspergillus sp. are
aflatoxins or ochratoxins.
The conditions or diseases are allergic
broncopulmonary aspergillosis (ABPA), Aspergilloma and chronic pulmonary
aspergillosis, aspergillus sinusitis, and invasive aspergillosis.
A lot of encouraging research is being done at the moment to
speed up diagnosis of this invasive aspergillosis and to improve its
treatment. RTL has tests that can find the Aspergillus in sinus specimens,
urine, and tissue. DNA and aflatoxin
(mycotoxins)
can be found in these specimens.
Cultures
and
DNA can be used to identify the molds. The
most common Aspergillus species are: A. fumigatus: fungus ball
and invasive disease, A. flavus: nasal sinus lesions,
invasive disease, and A. niger: "Swimmer's ear," and invasive
disease. All the conditions listed below can affect children and should be
diagnosed and treated in the same way.
Conditions:
Aspergillus
is a genus of molds, which are found everywhere world-wide. The are also
called filamentous fungi. Of the approximately 200 species found in patients
with serious health conditions, only a few of these molds cause illness in
humans and animals by producing toxins. Most people are naturally immune to
molds and do not develop disease caused by Aspergillus. Diseases
caused by Aspergillus can take many different forms. Patients can have
allergy-type illness due to Aspergillus or they can have life-threatening
generalized infections. The severity of aspergillosis is determined by
various factors but one of the most important is the state of the immune
system of the person. The poisons or mycotoxins produced by Aspergillus
species (sp.) are
aflatoxins and/or ochratoxins. The conditions or
diseases are: allergic broncopulmonary aspergillosis (ABPA), Aspergilloma and
chronic pulmonary aspergillosis, aspergillus sinusitis, and invasive
aspergillosis.
Allergic bronchopulmonary aspergillosis (ABPA) -
Exposure to Aspergillus may produce an allergy which is very common in
asthmatics. Many health professionals and government agencies believe that
5-10 % of adults with asthma may get ABPA. This is also common in cystic
fibrosis patients. Patients can have coughing, wheezing, and episodes of
feeling “bad”. The diagnosis can be made by X-ray, sputum cultures, skin
biopsies or cultures, and NOW
mycotoxin tests.
Treatment varies using prednisone taken by either
pills or sprays in the nose. Sometimes antifungal drugs are used.
Aspergilloma and chronic pulmonary aspergillosis –
Aspergillus can grow in a cavity of the
lung which may have been caused by an early disease like tuberculosis or
sarcoidosis. While in the lung, the fungus secretes toxic and allergic
products which can make the person have many of the symptoms described above.
Aspergillus sinusitis -
Aspergillus
disease can happen in the sinuses leading to Aspergillus sinusitis.
Three diseases - allergic sinusitis, a fungal ball or invasive aspergillosis
have been described. You may have a runny, blocked up nose which could lead
to nasal polyps. You may need surgical drainage, including removal of
polyps. You may need careful attention to treatment of bacterial infection.
Antibiotics, antifungal agents and local steroids are approaches to therapy.
In patients with normal immune systems,
stuffiness of the nose, chronic headache or discomfort in the face is common.
Drainage of the sinus, by surgery, usually cures the problem, unless the
Aspergillus has entered the sinuses deep inside the skull. Then antifungal
drugs and surgery is usually successful. When patients have damaged immune
systems due to cancer, leukemia or a bone marrow transplant, an Aspergillus
sinusitis is more serious. In these cases the sinusitis is a form of invasive
aspergillosis. The symptoms include fever, facial pain, nasal discharge and
headaches. The diagnosis is made by finding the fungus in fluid or tissue from
the sinuses and with scans. Surgery is done in most cases as it is important
to find out what is exactly wrong and is often helpful in eradicating the
fungus.
Treatment with powerful antifungal medicines is
essential. Choices of treatment can include amphotericin B, caspofungin,
voriconazole or itraconazole. We are familiar with doctors that treat
aspergillus sinusitis with amphotericin B nasal spray or voriconazole or
itraconazole; the role of caspofungin is uncertain, as there is little
experience.
Invasive aspergillosis
- Many people with damaged or impaired immune systems die from invasive
aspergillosis. Their chances of living are improved the earlier the diagnosis
is made but unfortunately there is no good single diagnostic test. Often
treatment has to be started when the condition is only suspected. People with
invasive aspergillosis usually have a fever and lungs (cough, chest pain or
discomfort or breathlessness) which do not respond to standard antibiotics.
X-rays and scans are usually abnormal and help to localize the disease.
Bronchoscopy (inspection of the inside of the lung with a small tube inserted
via the nose) is often used to help confirm the diagnosis. Cultures and
blood tests usually necessary to confirm the disease. In people with
particularly poor immune systems, the fungus can transfer from the lung
through the blood stream to the brain or to other organs, including the eye,
the heart, the kidneys and the skin. Usually this is a bad sign as the
condition is more severe and the person is sicker with a higher risk of death.
However, sometimes infection of the skin enables the diagnosis to be made
earlier and treatment to be started sooner.
Treatment is with antifungal drugs such as
voriconazole, caspofungin, itraconazole or
amphotericin B. Some other drugs used
for the treatment of tuberculosis or epilepsy reduce the blood levels of
voriconazole. Voriconazole can be given orally or intravenously. It is better
than amphotericin B, but may require dose modification to maximize success,
especially in children, those with liver disease or cirrhosis, and possibly
the elderly.
Caspofungin can only be given intravenously, and
is also partially effective. It has been used as rescue therapy and in
combination with other anti-fungals with reasonable success.
Amphotericin B has to be given by vein in large
doses. In some patients, the treatment can damage the kidney and other organs.
Newer forms of amphotericin B (Amphotec or Amphocil, Abelcet or AmBisome) are
useful, especially when the patient experiences side-effects, as they usually
cause fewer side effects, especially less renal dysfunction.
Itraconazole is generally given orally (also in
large doses, e.g. at least 400 mg daily), although an intravenous preparation
is available now.
The earlier treatment is started the better the chances of
survival. In patients with low numbers of white cells (infection fighters),
recovery of these cells can be important in stopping the growth of the fungus.
Sometimes surgery is also required. Overall, a third to a half of patients
survive invasive aspergillosis if treated, and none survive if they are not
treated.
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Chaetomium
Chaetomium
is a large
ascomycetous fungus producing rope like structures (perithecia). It is found
on a variety of materials containing cellulose including paper and plant
compost. It can be readily found on the damp or water damaged paper in
sheetrock. Most species are strong decomposers of cellulose and occur
wherever this material is abundant, such as in soil, dung, or rotting plants.
Chaetomium globosum, the most common species within this genus,
produces chaetoglobosins A and C when cultured on building material.
Relatively low levels of these compounds have been shown to be lethal to
various tissue culture cell lines. Studies recently reported that of 794
water-damaged buildings, Chaetomium species were isolated in 49% of
these structures.
Clinically, cases of
invasive Chaetomium perlucidum and review of the literature regarding
invasive Chaetomium infections show fatal disseminated disease involving the
brain, heart, lungs, and spleen and has been found in immune compromised
patients. The organisms have been demonstrated in patients with a history of
asthma and chronic bronchiectasis. Literature also shows the organism's
ability to disseminate beyond the central nervous system which is important
when considering that Chaetomium is and continues to be found in homes,
schools, and work sites.
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Fusarium
Fusarium
is a large genus of molds that are widely distributed in soil and in
association with plants. Most species are harmless and are relatively
abundant members of the soil. Some species produce
mycotoxins in cereal crops that can affect human and animal health if
they enter the food chain. The main toxins produced by these Fusarium
species are trichothecenes
and fumonosins. As
well as being common plant pathogens, Fusarium spp. are causative
agents of superficial and systemic infections in humans. Infections due to
Fusarium spp. are collectively referred to as fusariosis. The most
virulent Fusarium spp. is Fusarium solani. Patients can develop
Fusarium infections if there is physical trauma. Disseminated
opportunistic infections, on the other hand, develop in immunosuppressed
hosts.
Outbreaks of nosocomial (hospital acquired) fusariosis
have also been reported. Existence of Fusarium in hospital water
systems may result in disseminated fusariosis in immunosuppressed patients.
Fusarium may also exist in soil of potted plants in hospitals. These
plants constitute a hazardous fungal reservoir for nosocomial fusariosis.
Eye, ear, and skin infections can occur with
fusarium. Furthermore, pulmonary infections, endocarditis, peritonitis,
central venous catheter infections, septic arthritis, disseminated infections
and fungemia due to Fusarium spp. have been reported. Recently,
Fusarium has been isolated in contact lenses and solutions. These findings
prompted the manufacturers and FDA to recall some solutions for fear that such
organisms in the wash solutions may cause severe eye infections and even
blindness.
Fusarium
has been used in biological warfare. There were many casualities in the
Soviet Union in the 1940’s when it was found that wheat flour was contaminated
with Fusarium. The troops had alimentary toxic aleukia with a high
mortality rate. Symptoms were abdominal pain, diarrhea, and vomiting.
Patients developed skin lesions and bleeding from the lungs and intestinal
tract. The Soviets used the toxins from and dubbed it “yellow rain” in Laos
and Afghanistan between 1975 and 1981. The fungus has been implicated in the
birth of 31 anencephalic (without brains or skulls) children in the Rio Grande
region of Texas in 1991.
Fusarium
spp. produce mycotoxins. Although they are not the most toxic of all types of
Fusarium mycotoxins, fumonisins (Fm) and
Deoxynivalenol (DON)
are the most frequently detected and, therefore, most often associated with
illness in farm animals or humans. Ingestion of grains or inhalation of dust
contaminated with these toxins may give rise to allergic symptoms or be
carcinogenic (cancer producing) in long-term consumption or exposure.
Fumonisins are the mycotoxins produced by Fusarium moniliforme and
Fusarium proliferatum. Fumonisins cause a neurological disease, equine
leucoencephalomalacia in horses, pulmonary edema in swine, hepatotoxic and
nephrotoxic effects in other domestic animals, and carcinogenesis in
laboratory animals. The may cause cancer of the esophagus. Another group of
mycotoxins, zearalenones, may also be produced by some Fusarium spp.
growing in grains and hence there presence in the environment. Tricothecenes
are also produced by Fusarium spp. The trichothecenes that Fusarium
can produce are potent inhibitors of DNA, RNA, and protein synthesis, and have
been well studied in animal models because of concern about their potential
misuse as agents of biological warfare, due to their ability to destroy human
health, alter DNA, and affect the mind.
Fusarium
attacks cells in humans much the way it attacks cells in plants -through the
secretion of mycotoxins that it itself is immune to. These mycotoxins dissolve
the cell walls, and the fungus is then free to absorb the cell's contents, and
enter the cell cavity, reproduce, and continue the process attacking other
cells which will eventually kill the cells.
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Penicillium
Penicillium
is genus of molds, which are found everywhere
world-wide. They are widespread and are found in soil, decaying vegetation,
and the air. These fungi (or molds) are commonly considered as contaminants
but may cause infections, particularly in immunocompromised hosts. One
species, Penicillium marneffei is pathogenic particularly in patients
with AIDS and when it is found in a patient’s blood it is considered as an HIV
marker. In addition to their infectious potential, Penicillium species
(spp). are known to produce
mycotoxins.
Penicillium
spp. are occasional causes of infection in humans
and the resulting disease is known generically as penicilliosis.
Penicillium has been isolated from patients with eye infections, ear
infections, pneumonia, heart disease, as well as intestinal and urinary tract
infections. Asthmatics have also had Penicillium isolated from their
sinuses. Most Penicillium infections are also found in
immunosuppressed hosts. In addition to its infectious potential,
Penicillium species like verrucosum produces a mycotoxin,
ochratoxin A, which is damaging to the kidney
(nephrotoxic) and could be cancer causing (carcinogenic). The production of
the toxin usually occurs in cereal grains at cold climates but has been
isolated in buildings contaminated with Penicillium.
P.marneffei
is a pathogenic fungus and specifically infects patients with AIDS.
Penicillium marneffei infections have also been reported in non-AIDS
patients with hematological malignancies and those receiving immunosuppressive
therapy. Penicillium marneffei infection, so called penicilliosis is
acquired via inhalation and results in initial pulmonary infection, followed
by fungemia and dissemination of the infection. The lymphatic system, liver,
spleen and bones are usually involved. Acne-like skin papules on face, trunk,
and extremities are observed during the course of the disease. Penicilliosis
infection can be fatal.
Encouraging research is being done at the moment
to speed up diagnosis of penicillosis and to improve its treatment. RTL has
tests that can find the Penicillium in sinus specimens, urine, and tissue.
DNA and
ochratoxin A (mycotoxins)
can be found in these specimens.
Cultures and DNA can be used to identify the
molds. The most common Penicillium species are: Penicllium verrucosum,
P. chrysogenum, and P. exspansum.
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Stachybotrys
Stachybotrys
is a greenish-black fungus found worldwide
that lives in high-cellulose material, such as straw, hay, paper, dust,
lint, and cellulose-containing building material such as fiber board, and
gypsum board that becomes chronically moist or water damage due to
excessive humidity, water leaks, condensation or flooding . This mold
grows and produces spores in the temperature range of 36°-104°F. It is
also capable of producing several
mycotoxins, however, researchers still know little about the
temperature and moisture conditions under which these toxins are produced.
It is believed that moist high-cellulose and low-nitrogen materials at a
temperature range of 32-104°F can provide sufficient conditions for
production of
Tricothecenes.
Surfaces exposed to air with a relative
humidity above 55% and subjected to temperature fluctuations are ideal for
toxin production. Individuals with chronic exposure to the toxin produced
by this fungus have reported cold and flu symptoms, sore throats,
diarrhea, headaches, fatigue, and dermatitis (skin rashes). These fungi
can produce a component that paralyzes sperm.
The tricothecenes have been used as bio- warfare
agents in the Vietnam era and also used by the Russians during the
Russian-Afghanistan war. There has also been documentation that
tricothecenes can cause bleeding in the lungs of infants and in those
patients with weak immune systems.
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Mycotoxins
Mycotoxins
are toxins produced by molds or fungi. The mycotoxins discussed here are
the
Tricothecenes, (which include T-2, macrocyclic tricothecenes,
Zearalenone,
Fumonosins, Aflatoxins,
and Ochratoxins.
Where conditions are right, fungi proliferate into colonies and mycotoxin
levels become high. Toxins vary greatly in their severity. Some fungi
produce severe toxins only at specific levels of moisture, temperature or
oxygen in the air. Some toxins are lethal, some cause identifiable
diseases or health problems, some weaken the immune system without
producing symptoms specific to that toxin, some act as allergens or
irritants, and some have no known effect on humans. Some mycotoxins
generally have more negative impacts on farm animal populations than on
humans. Some mycotoxins are harmful to other micro-organisms such as other
fungi or even bacteria (penicillin is one example).
Mycotoxins can appear in the food chain as a result of fungal infection of
crops, either by being eaten directly by humans, or by being used as
livestock feed. Mycotoxins don’t decompose easily so they remain in the
food chain in meat and dairy products. Even temperature treatments, such
as cooking and freezing, do not destroy mycotoxins.
Buildings are another source of mycotoxins. Public concern over mycotoxins
increased following multi-million dollar toxic mold settlements in the
1990s. The negative health effects of mycotoxins are a function of the
concentration, the duration of exposure and the individual's
sensitivities. The concentrations experienced in a normal home, office or
school are often too low to trigger a health response in occupants.
However, concentrations experienced in a home or building which has
experienced water leaks are often high enough to trigger health responses
in the occupants. Such health responses are noted in the
symptoms section.
Trichothecenes:
Tricothecenes are mycotoxins produced by a number of different fungi such
as Stachybotrys and Fusarium. Their mechanism of
action is the inhibition of protein synthesis, therefore they are known to
kill cells and are extremely dangerous. It is known that when
Stachybotrys grows in a mold infested building, the organism produces
tricothecene mycotoxins. It is also known that these toxins can get into
the air where than can be inhaled. It is also known that they are inhaled
by human beings and animals as well (e.g. cats). However it is not known
if the concentration of tricothecenes inhaled by animals or humans inside
these buildins is sufficient to cause disease. However, because of the
extreme toxicity of these compounds, this is felt to be a potentially
dangerous situation. The tricothecene mycotoxins produced by Stachybotrys
are macrocyclic tricothecene mycotoxins. Other tricothecenes are called
simple tricothecene mycotoxins. These include most prominently T-2 toxin,
HT-2 toxin, neosolaniol and fusarenon-X. These are stongly toxic
compounds. Like the macrocyclic tricothecenes mentioned above, their
primary toxic methancism is the inhibition of protein synthesis at the
level of the ribosome. For the most part, their effects are known from
instances in which humans or animals ate contaminated grain, or from
laboratory animal or in vitro (in lab) studies. The major effects (of
symptoms) observed in humans exposed to these mycotoxins include
"vomiting; inflammation; diarrhea; cellular damage of the bone marrow,
thymus, spleen and mucous membranes of the intestines; and depression of
circulating white blood cells." Humans who have eaten contaminated grain
develop "alimentary toxic aleukia," which begins with burning sensations
of the mouth, throat, esophagus and stomach, continues with vomiting,
diarrhea and gastric cramps, and finally progresses to severe leucopenia
(drop in white blood cell count), which renders the patient susceptible to
infections. Death may then be a result. Skin contact with material
contaminated with these trichothecenes induces contact dermatitis, and in
stronger exposures, lesions may be necrotizing (that is, may contain dead
tissue, a significant risk factor for the development of bacterial
infections). Effects on immune system components apart from the
above-mentioned killing of thymus and spleen cells include inhibition of
lymphocyte (white cells in the blood) responses and disruption and
killing of alveolar (lung) macrophages (clean up cells). Clotting
factors in the blood are also significantly affected and the patient
could bleed excessively if cut. Trichothecenes in general seem to have
little effect on producing cancer, but when consumed or administered in
pregnancy some scientist believe that they may have some teratogenicity
(inducing deformed offspring) or abortifacient (abortion producing)
properties.
When a person is exposed to Tricothecenes, the first symptoms exhibited
are general discomfort, dry eyes, and drowsiness. A red skin rash appears
shortly, starting in blotches and swiftly covering the entire body.
Symptoms of a classic hemorrhagic fever set in, which include blood-red
eyes, vomiting/urinating of blood, nosebleed, and patches of skin ranging
in size from a quarter- to a silver dollar begin to bleed without
reason. Brain function is also impaired, with the victim progressing
from slurred speech to classic 'fever dreams' to various psychological
conditions from Multiple Personality Disorder to Paranoia. The victim
succumbs because of loss of blood, fever, or an infection brought on by
the weakened immune system, whichever comes first.
If
the patient survives, he will recover from most of the symptoms, although
patches of skin will still bleed spontaneously for short periods of time.
His immune system remains weakened, and his mental faculties will be
severely damaged.
Zearalenone:
A few isolates of Fusarium. sporotrichoides have been verified as
producing this toxin. This compound is an estrogen mimic, most commonly
causing vulvovaginitis (swelling and reddening of the vulva) in gilts
(young female pigs) and sows which have consumed contaminated feed. This
condition sometimes leads to vaginal or rectal prolapse which commonly
results in reduced litter size, loss of pregnancy, and poor milk
production in affected swine. Males may be feminized to some extent.
Similar syndromes occur in cattle and sheep fed zearalenone-contaminated
feed.
Fumonosins:
These toxins were first described in 1984 after a thorough search for the
cause of equine leukoencephalomalacia, a disease of horses in which brain
tissue is damaged and horses show ataxia (inability to coordinate
walking), facial and other paralysis, partial blindness, lethargy or
excitement, and in later stages lameness, inability to stand, seizures and
death. After the purification of fumonisins, the disease was induced in
horses with purified material, confirming the etiologic role of the
mycotoxin. Liquefactive necrosis of white matter areas of brain tissue is
the main pathological sign observed. Hepatotoxicity (liver damage) is
also seen. Experimental animals often experience hepatotoxicity,
nephrotoxicity (kidney damage) or both; rats have also been shown to
experience necrosis (destruction) of stomach lining and heart muscle
(myocardium). Liver cancers can be caused by Fumonisins . Fumonisins are
also among the chief suspects for the agent(s) of elevated levels of
esophageal cancer in certain parts of the world.
Aflatoxins
are naturally occurring mycotoxins that are produced by many species of
Aspergillus. The organisms that usually produce aflatoxins are
Aspergillus flavus and Aspergillus parasiticus. Aflatoxins are toxic and
can be cancer producing. . After entering the body, aflatoxins are
metabolized by the liver to a reactive intermediate, aflatoxin M1.
High-level aflatoxin exposure
produces an acute damage and cirrhosis of the liver as well as cancer of
the liver. It appears that no animal species is immune to the acute
toxic effects of aflatoxins including humans; however, humans appear to
have an extraordinarily high tolerance for aflatoxin exposure and rarely
die to acute aflatoxicosis.
Chronic, of long term exposure
does not lead to as dramatic of symptoms as seen in acute aflatoxicosis.
Children, however, are particularly affected by aflatoxin exposure which
leads to stunted growth and delayed development. Chronic exposure also
leads to a high risk of developing liver cancer due to the metabolite
aflatoxin M1.
Chronic, of long term exposure
does not lead to as dramatic of symptoms as seen in acute aflatoxicosis.
Children, however, are particularly affected by aflatoxin exposure which
leads to stunted growth and delayed development. Chronic exposure also
leads to a high risk of developing liver cancer due to the metabolite
aflatoxin M1.There are two techniques that have been used most
often to detect levels of aflatoxin in humans.
The first method is measuring the
AFM1-guanine adduct in the urine of subjects. Many believe
that the presence of this breakdown product indicates exposure to
aflatoxin in the past 24 hours. However, this technique has a significant
flaw in that it only produces a positive result in approximately one-third
of positive test subjects. Additionally, due to the half life of this
metabolite, the level of AFM1-guanine measured can vary
significantly from day to day, based on diet, and thus is not useful for
assessing long term exposure.
Another technique that has been
used is a measurement of the AFB1-albumin adduct level in the
blood serum. This approach is significantly more accurate, as positive
results are generated in 90% of positive test subjects. This test is also
useful for measuring long-term exposure, as it remains positive for two to
three months.
Many patients and physicians are
concerned about infestation of the sinuses with Aspergillus in patients
who have sinusitis. Thus, there is also a concern of whether or not the
organism present produces the toxin aflatoxin. RTL measures the presence
of toxins and orgnaisms in sinus fluids, nasal washes, urine, and tissues
(especially respiratory biopsies, ie. Bronchoscopy specimens).
RTL has isolated aflatoxins from tissues from lung biopsies
(See
Seth K. testimonial),
tissues from animals, and also from urines and sinus washes. RTL uses
immuno-affinity columns for isolation of the aflatoxins from body
fluids and tissues.
Ochratoxin A, a
mycotoxin produced by Aspergillus ochraceus and Penicillium
verrucosum and is one of the most abundant food-contaminating
mycotoxins in the world. Human exposure occurs mainly
through consumption of improperly stored food products,
particularly contaminated grain and pork products, as well as coffee,
wine grapes, and dried grapes. The toxin has been found in the tissues and
organs of animals, including human blood and breast milk.
Ochratoxin A is potentially carcinogenic (cancer
producing) to humans. There is sufficient evidence in experimental
animals for the carcinogenicity of ochratoxin A. Ochratoxin A was tested
for production of cancer by oral administration in mice and rats. It
increased the incidence of liver tumors in mice of each sex and produced
renal-cell (kidney) tumors and cancers in male mice and in rats of each
sex. Ochratoxin A can cause suppression of white cells and immunity (immunosuppression)
in animals.
Little is documented concerning the actual presence of
Ochratoxin A in the air or dust of samples taken from the environment.
This mycotoxin, however, has been found in food samples and in storage
areas where foods known to have these toxins are stored. The organisms
that produce these toxins have also been documented to be isolated in the
respiratory tract of patients. Thus, it would not be surprising to find
Ochratoxin A in the body fluids of some patients. RTL uses immunoaffinity
columns to as screening procedures to isolate this toxin from urine and
other body fluids and/or tissues.
Methods are available to examine urine for determination
of ocratoxin A. The level of detection used at RTL is 2.0 ppb. At
present, the test used at RTL is a qualitative test only. In other words,
RTL can determine whether the toxin is present or not present. New
methods for the determination of ocratoxin A in human urine samples have
been reported in 2007 in medical literature. Thus, it is not surprising
to find Ochratoxin A in some fluids from the human body.
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