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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.
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.
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 Fursarium 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.
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.
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.
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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