RE: RE: Molds, Medics, and the Pursuit of Factual Clarifications

[Guest guest]

ph/ALL (In response to your recent post re; vote)

Molds, Medics, and the Pursuit of Factual Clarifications By R.

HaneyCopyright© May 2008 Just because medical doctors are ignorant because

they profess to know or understand virtually little or nothing about the

live-celled " pathogenic " mold species doesn't mean the rest of the world has to

be as dumb! Let's look at what they are saying to those who are patients behind

closed doors on HIV/AIDS, cancer, and other serious neurological and disease

wards and bring the " allergen " myth to the test. First: What do most doctors

refer to live disease-causing bacteria cells as? Bacteria: Single-celled

microorganisms which can exist either as independent (free-living) organisms or

as parasites (dependent upon another organism for life). The term bacteria was

devised in the 19th century by the German botanist Ferdinand Cohn (1828-98) who

based it on the Greek bakterion meaning a small rod or staff. In 1853, Cohn

categorised bacteria as one of three types of microorganisms -- bacteria (short

rods), bacilli (longer rods), and spirilla (spiral forms). The term bacteria was

preceded in the 17th century by the microscopic animalcules described by Antony

van Leeuwenhoek

(1632-1723).http://www.medterms.com/script/main/art.asp?articlekey=13954

Bacteria are very small living organisms made of only one cell . They are

present just about everywhere : the air, the soil, and the skin, for example.

Many of them are microbes that cause diseases (rhinitis, listeriosis, and

others), but others are very helpful to humans. For example, bacteria in the

intestine help digestion and we often use bacteria to make food products

(yoghurt, sauerkraut, and

others).http://lexicon.cvfm.com/biology/definition_31.html Notice the word

" Microorganisms? " Notice the wording " very small living organisms? " Second: What

do most doctors refer to allergens as? An antigen, a substance capable of

inducing allergy or specific hypersensitivity.

www.cdc.gov/oralhealth/infectioncontrol/glossary.htm

A substance that provokes an allergic response.

www.olympianlabs.com/html/glossary.aspx

The substance that triggers an allergic reaction.

www.uchicagokidshospital.org/online-library/content=P01686

A substance capable of causing an allergic reaction because of an individual's

sensitivity to that substance.

www.madison.k12.wi.us/cso/news/chavez/iaq_glossary.htm

Any substance that causes an allergy; A substance capable of producing an

immediate hypersensitive (allergic) reaction.

www.respironics.com/Glossary.asp

A substance that causes the body to react hypersensitively to it.

www.i-sis.org.uk/Glossary.php

A harmless substance that triggers the immune system to mount an inappropriate

response known as an allergic reaction.

www.health.harvard.edu/dictionary/A.htm

A substance which reacts with the body's immune system to produce a type of

irritation known as an allergic reaction.

www.hs101.ca/glossary.htm

A substance that causes an allergic response. Examples include pollen, molds

and certain foods.

www.mdanderson.org/patients_public/about_cancer/display.cfm

A substance (such as a food or pollen) that your body perceives as dangerous

and can cause an allergic reaction.

www.webmd.com/asthma/guide/asthma-glossary

An antigen that provokes an immune response.

www.biobasics.gc.ca/english/View.asp

A substance, usually a protein such as pollen, animal dander, food, or

medication, which can trigger an allergic reaction.

www.allergyasthma.wordpress.com/2006/11/08/glossary-of-common-allergy-terms/

Any substance that induces an allergy (mold, grasses, antibiotics, etc.).

www.repro-med.net/glossary.php

Is anything that can produce an allergic reaction, such as weed pollens, mold

spores, cat dander and house dust mites.

www.allernet.com/newsletter/dict.html

A protein molecule (antigen) that can trigger the immune system to produce

antibodies and thereby cause an allergic reaction. Examples are proteins in

pollen, house dust mites and animal dander (dead skin cells). Can also be called

" hypersensitivity reaction " . www.asthmacure.com/Glossary/ASTHMAGLOSSARY.html

Any substance that can cause an allergic reaction; typical examples are pollen,

dust and pet dander.

www.chop.edu/consumer/jsp/division/generic.jsp

A substance, such as pollen or pet dander, that causes an allergy.

www.apluspetgoods.com/petsupplies/cat-glossary.php

A protein substance that may provoke an allergic response in a susceptible

person. Common allergens include house-dust mite faeces, grass pollen and cat

danderwww.synairgen.com/investors_glossary.asp A substance that causes

sensitivity and the release of antibodies and histamine typically causing

itching and

sneezing.www.saltairesinusrelief.com/learn-about-sinus-cleansing/glossary/ Any

substance that causes an allergy. It may, for example, be pollen that can

trigger hay fever or peanuts that can cause anaphylactic

shock.www.lucyburney.co.uk/glossary/index.html a substance which produces an

allergyhttps://www.thepetmedsite.com/definition.htm Any substance, such as food

or drug, that causes an allergic response. A common allergen among infants is

cow's milk protein.

www.infobreastfeed.com/Glossary.htm

A compound that produces an allergic reaction, such as a food or chemical, that

can produce itchy hives, rashes or other irritations on the skin. Some common

foods that produce itchy hives are strawberries, tomatoes and nuts.

www.lanacane.co.uk/itch_glossary.shtml

A nonparasitic antigen capable of stimulating a type I hypersensitivity reaction

in atopic individuals is called an allergens.

www.[1]sitewide.org/balo/allergens.html ********* Any substance that causes a

hypersensitivity reaction, such as dust, pollens, fungi, smoke, perfumes

[inhalents]; wheat, eggs, milk, chocolate, strawberries [foods]; aspirin,

antibiotics, serums [drugs], bacteria, viruses, animal parasites [infectious

agents]; and chemicals, animals, plants.

www.newtrience.com/Definitions.html

Any substance that can cause an allergy.

www.wordnet.princeton.edu/perl/webwn

An allergen is any substance (antigen), most often eaten or inhaled, that is

recognized by the immune system and causes an allergic reaction. Reference:

Health Canada Website

www.hc-sc.gc.ca

Notice how the live-celled mold species is mentioned as an " allergen " and not a

pathogen or microorganism as is the live-celled " bacteria? " And, notice that

only one definition, a non-medical definition at that, mentions bacteria as an

allergen and all others do not? Now, lets look at the definition of " mold, " and

a couple of important statements about the serious disease properties of mold.

Parasitic, microscopic fungi (like Penicillin) with spores that float in the air

like pollen. Mold is a common trigger for allergies and can be.

www.webmd.com/asthma/guide/asthma-glossary

A potentially damaging fungus that forms on a cigar when it is stored at too

high a temperature.

www.tobaccoparadise.com/cigar_glossary.htm

A cavity left in firm sediment by the decayed body of an organism.

www.china.org.cn/english/features/Archaeology/98851.htm

Mold is a type of fungus (and not a plant). Like other fungi, molds do not

contain any chlorophyll (and cannot make their own food); molds live off the

food produced by plants or animals, or decaying matter. Molds are often

parasites on plants, animals, or even other fungi.

www.enchantedlearning.com/subjects/plants/glossary/indexm.shtml

Are you aware that the following is fact? Fungal Infections Carol A. Kauffman,

MD Infect Med 20(9):424-436, 2003. © 2003 Cliggott Publishing, Division of SCP

Communications Posted 10/24/2003 Abstract and IntroductionAbstractOpportunistic

fungal infections in immunocompromised patients are associated with a high

mortality rate. Endemic mycoses are often asymptomatic, but in appropriate

hosts, fungi can cause severe and even fatal infection. Skin lesions and

multiple nodules or mass-like lung lesions seen on CT scans or radiographs may

be clues to specific types of fungal infections. Some fungi grow better in the

presence of iron and may cause infection in patients being treated with deferox

amine. Face pain in an immunocompromised patient may signify invasive fungal

sinusitis. Treatment with antifungal agents needs to be individualized according

to factors such as the fungus involved, presence of renal failure, or pregnancy.

Combining antifungal agents or addition of other approaches, such as surgical

debridement or steps to control intracranial pressure, may be needed for

adequate treatment of certain types of fungal

infections.IntroductionOpportunistic fungal infections constitute an increasing

proportion of infections seen in immunocompromised patients; these infections

are associated with a very high mortality rate. On the other hand, the endemic

mycoses affect tens of thousands of persons who encounter the fungi that cause

these infections in the course of every day activities in certain geographic

areas. These infections are often asymptomatic, but endemic fungi can cause

severe and even fatal infection in the appropriate host. New antifungal agents

have changed the treatment of many fungal infections in the past few years. One

can now choose from multiple effective drugs for many of the invasive mycoses.

The following " clinical pearls " emphasize some clinical syndromes that aid in

the diagnosis of fungal infections and highlight various nuances of treatment

with antifungal agents.Diagnostic Pearls1. Fever, a pulmonary infiltrate, and

erythema nodosum in a young adult who just returned from working in Central

America could be either coccidioidomycosis or histoplasmosis.Both of these

mycoses are endemic to North America but also occur in many countries in Central

America. More travelers are participating in ecotours or working vacations and

are exposed to Coccidioides or Histoplasma in the course of these activities.[1]

Outbreaks are typically related to activities that disturb the soil or create a

cloud of dust, such as constructing churches and orphanages, digging at an

archaeological site, and spelunking.[2-4]The usual manifestation of acute

infection with endemic fungi that are inhaled from the environment is pneumonia,

which is generally accompanied by fever, myalgias, and fatigue. Erythema nodosum

is seen mostly in young adults who have acute coccidioidomycosis or

histoplasmosis; the rash appears to reflect a good host response to the

infection.The history is helpful in establishing the involvement of an endemic

mycosis, especially if multiple persons sharing in the same activity become ill.

Growth of Coccidioides immitis or Histoplasma capsulatum in cultures of sputum

or bronchoalveolar fluid is diagnostic for acute infection; however, this test

is not very sensitive. Testing for antibodies to C immitis or H capsulatum is

most useful for making the diagnosis of acute pulmonary infection with these

fungi, but it may take weeks for seroconversion to occur. The urine assay is

positive for Histoplasma antigen in as many as 75% of patients with severe acute

pulmonary histoplasmosis that occurs after exposure to a massive fungal

inoculum; it is usually negative in those with mild pneumonia that occurs after

exposure to a few organisms.[5]2. A mass-like lesion on a chest radio graph in a

former smoker in rural Arkansas is not necessarily lung cancer—it might be

blastomycosis.Blastomyces dermatitidis is endemic in the north central, south

central, and southeastern United States. Middle-aged to older men are the usual

hosts. In patients with blastomycosis, there is a propensity for mass-like

lesions to form; these lesions are frequently mistaken for lung cancer on chest

radiographs (Figure 1).[6] Cytologic examination of bronchoalveolar lavage fluid

or lung tissue stained with periodic acid– Schiff or silver stain often shows

the classic thick-walled yeast with a single, broad-based bud that is

characteristic of B dermatitidis (Figure 2). Definitive diagnosis is made by

growth of B dermatitidis in cultures of sputum, bronchoalveolar lavage fluid, or

lung tissue. Serologic testing currently plays no role in the diagnosis of

blastomycosis.[7] Figure 1. Chest radiographs show a right lower lobe mass-like

lesion in a middle-aged man who was thought to have lung cancer. Biopsy of the

lesion revealed granulomatous inflammation, and special stains revealed

yeast-like organisms. Figure 2. Periodic acid–Schiff stain of tissue obtained

from the patient whose chest radiograph is shown in Figure 1. Large,

thick-walled, broad-based budding yeasts typical of Blastomyces dermatitidis can

be seen.3. An ulcerated skin lesion with extension to local lymph nodes in a

person who cared for a cat with a draining skin lesion may not be caused by

Bartonella.Although Bartonella infection might be the first diagnosis

entertained in this scenario, there is a high likelihood that this could be

sporotrichosis. Zoonotic transmission from squirrels, armadillos, and birds is

well described, but most cases of animal-associated sporotrichosis are in

persons caring for cats with the disease.[8] In cats, ulcerated lesions tend to

develop on the head and face; these lesions frequently are teeming with the

yeast-like tissue form of Sporothrix schenckii.Most cases of sporotrichosis, of

course, are not animal-associated. The usual environmental exposure is through a

cut or puncture wound from a thorn, a pine needle, timber, straw, or other sharp

objects that are contaminated with soil.[9] The diagnosis is made most often by

culture of material aspirated from a lesion or from a tissue biopsy. The

cigar-shaped yeasts can be sought using special stains for fungi in tissue, but

often very few organisms are present. Serologic testing is not well established

as a diagnostic tool for sporotrichosis.4. A positive result on a serum

Cryptococcus antigen test from a patient with neutropenia who has fever,

multiple nodular skin lesions, and pneumonia does not always signify infection

with Cryptococcus neoformans.Trichosporon asahii (formerly known as Trichosporon

beigelii) is a yeast-like fungus that is found in water and soil.[10] In normal

hosts, several species of Trichosporon cause superficial cutaneous lesions and

onychomycosis. Disseminated trichosporonosis most often occurs in a patient with

leukemia who has profound neutropenia.[11,12] In this type of patient,

pneumonia, multiple nodular cutaneous lesions, and widespread visceral abscesses

are found. Mortality rates approach 80% to 90%.The organism is able to grow in

blood cultures, and on initial Gram stain of the fluid from the blood culture

bottle it may look like a Candida species; further studies reveal Trichosporon

species. Antigens in the cell wall of T asahii cross-react with the capsular

polysaccharide of C neoformans and may lead to a positive result in the serum

latex agglutination test for Cryptococcus antigen.[12] Biopsy specimens of skin

lesions usually reveal a characteristic mixture of blastoconidia, arthroconidia,

and hyphae typical of Trichosporon species.5. Zygomycosis is the most likely

diagnosis in a patient with myelodysplastic syndrome who is being treated with

deferoxamine for iron overload and who exhibits a pulmonary mass-like

lesion.Certain fungi, among them Rhizopus species, grow best with additional

iron. Rhizopus species have evolved the capacity to use exogenous compounds as

siderophores to capture iron to enhance their growth. Deferoxamine, used to

chelate iron in patients with iron excess as a result of multiple transfusions,

is usurped by Rhizopus species, bringing iron to the fungus.[13] Thus, these

molds are able to grow luxuriantly in the presence of the iron chelator.

Rhinocerebral, pulmonary, and disseminated forms of zygomycosis have been

described in patients receiving deferoxamine, and the infection tends to be very

aggressive (Figure 3). Figure 3. Extensive bilateral pulmonary infiltrates are

demonstrated in this chest radio graph from a patient who on biopsy was found to

be infected with Rhizopus. Extension into the pericardium and myocardium was

seen at autopsy.The diagnosis of infection caused by a fungus of the Zygomycetes

class must be made quickly so that appropriate therapy can be initiated as soon

as possible.[14] Initial diagnosis is usually made by a tissue biopsy specimen

that shows broad nonseptate hyphae invading blood vessels. It is somewhat ironic

that it is often difficult to grow Zygomycetes in vitro from tissue samples, in

spite of their aggressive in vivo growth; this is likely related to damage to

the hyphae during the processing of tissue for culture in the laboratory.[15]

The clinician must treat the patient based on results from histopathologic

examination; positive culture results provide confirmatory evidence of the

specific fungus involved. There are no rapid antigen or antibody tests for the

Zygomycetes.6. Infective fungi with acutely branching septate hyphae: Not always

Aspergillus.Aspergillus is the most common nonpigmented acutely branching

septate filamentous fungus that causes infections in immunocompromised hosts.

However, other opportunistic fungi are increasingly seen in immunocompromised

hosts, often cannot be distinguished from Aspergillus on histopathologic

examination of tissues, are frequently resistant to amphotericin B, and are

often associated with dismal outcomes.[16]Scedosporium apiospermum, also known

as Pseudallescheria boydii when it assumes the sexual state in vitro, is a

nonpigmented filamentous fungal organism that mimics the appearance of

Aspergillus in tissues. S apiospermum is found in soil, sew age, manure, and

water. It is a cause of pneumonia and lung abscess in near-drowning victims, and

increasingly is reported as a cause of invasive pulmonary and disseminated

infection in patients with neutropenia, transplant recipients, and patients

receiving corticosteroids.[17] The organism is readily grown in the mycology

laboratory. Importantly, this mold is resistant to amphotericin B, emphasizing

the point that all biopsy specimens must be sent for both histopathologic

examination and culture. Voriconazole has been effective for treating infections

with S apiospermum.7. A patient with leukemia and neutropenia in whom fever, a

pulmonary infiltrate, and painful nodular skin lesions develop and whose blood

cultures are positive for a mold most likely is infected with Fusarium.The genus

Fusarium includes nonpigmented septate filamentous fungi that commonly cause

disease in plants. Fusarium species cause onychomycosis and locally invasive

infections, usually after traumatic inoculation, in nonimmunocompromised hosts.

Disseminated infection is the rule in patients with hematologic malignancies,

especially when they have neutropenia or have received a stem cell

transplant.[18] The source of the infection can be either aerosolization into

the lungs from an environmental source[19] or inoculation through the skin,

often beginning as a paronychia.Widespread hematogenous dissemination is

frequent, and multiple painful nodular cutaneous lesions are characteristic.[20]

The diagnosis can be made by biopsy and culture of a skin lesion. The histologic

picture is similar to that of Aspergillus, showing acutely branching,

nonpigmented hyphae that invade through blood vessel walls. Fusarium grows in

routine blood culture media, a phenomenon that is rarely encountered with other

molds. Fusarium species are often resistant to amphotericin B, and the mortality

rates are as high as 100% in infected patients who remain neutropenic.

Voriconazole has shown success in the treatment of Fusarium infection.8.

Infection with angioinvasive fungi leads to characteristic findings on

high-resolution CT scan of the lung.The most common angioinvasive fungal

infections are those caused by the genera Aspergillus, Fusarium, and

Scedosporium (Pseudallescheria) and the class Zygomycetes (mostly Rhizopus and

Mucor). Hyphae of these fungi have the propensity to invade through blood vessel

walls, leading to local tissue infarction and necrosis. With early infection,

the chest radiograph may appear normal or show only a small nodule or

infiltrate. High-resolution CT scans have become invaluable in the diagnosis of

infection with angioinvasive fungi.[21] They often reveal multiple nodules when

only 1 was seen on the chest radiograph.A " halo sign " is an extremely helpful

finding on the CT scan (Figure 4). This sign is seen in approximately 90% of

cases at the onset of symptoms[22] and consists of an area of ground-glass

infiltrate surrounding a nodule, reflecting parenchymal hemorrhage secondary to

blood vessel invasion by the fungus. A " crescent sign " demonstrates cavitation

and is also indicative of infection with an angioinvasive fungus (Figure 5).

This occurs in as many as 63% of cases, but it appears late (usually in the

second week) and thus is not helpful for early diagnosis.[22] This sign occurs

with tissue necrosis and often appears when the patient's neutropenia has begun

to resolve. Figure 4. High-resolution CT scan shows a right upper lobe lung

lesion in a patient whose bronchoalveolar lavage specimen yielded Aspergillus

fumigatus. Note the so-called halo sign, seen as a blush around the lesion. This

sign is indicative of hemorrhage and highly suggestive of infection with an

angioinvasive fungal organism. Figure 5. This CT scan from the same person as in

Figure 4 was taken 1 month later and shows development of cavitation, or a

" crescent sign. " 9. Fever, right upper quadrant discomfort, nausea, and an

elevated alkaline phosphatase level in a patient with leukemia who has just

recovered from neutropenia is likely caused by chronic disseminated

(hepatosplenic) candidiasis.Candida disseminates widely in patients with

neutropenia. In many of them, the extent of visceral dissemination is not clear

until the patient experiences a return of circulating neutrophils.[23,24] At

that time, fevers (often high and spiking), right upper quadrant or abdominal

pain and tenderness, and nausea and vomiting occur. Generally, patients do not

appear terribly ill except when their temperature is elevated. Values of serum

liver enzymes, predominantly alkaline phosphatase, are modestly elevated in most

patients; white blood cell counts are within normal limits; and blood cultures

show no growth.A CT scan of the abdomen reveals multiple lucencies, some of

which can become quite large, in liver, spleen, and less often in kidneys

(Figure 6). Ultrasonography is less sensitive than CT for defining the lesions.

A liver biopsy specimen shows multiple well-circumscribed micro abscesses

containing neutrophils and organisms that suggest Candida species. Culture often

yields no growth even though organisms are clearly seen on the biopsy specimen.

The clinical, laboratory, and radiologic findings are so characteristic that

liver biopsy does not need to be performed in all patients before starting

antifungal therapy. However, if a patient does not respond to therapy, a biopsy

should be done because other organisms, including Trichosporon and Aspergillus,

uncommonly can cause a similar syndrome. Figure 6. Typical punched-out lesions

are seen on this CT scan from a patient with hepatosplenic (chronic

disseminated) candidiasis.10. Acute onset of face pain in an immunocompromised

patient: Suspect invasive fungal sinusitis.Pain out of proportion to initial

physical findings is often the presenting manifestation of an invasive mold

infection.[25] Most often the pathogen is Aspergillus; Fusarium; Scedosporium;

one of the Zygomycetes; or less commonly, a pigmented dematiaceous fungus, such

as Alternaria or Bipolaris.[26] All of these organisms are commonly found in

air, water, and soil. The usual host is a patient who has a hematologic

malignancy and neutropenia and has been receiving broad-spectrum antimicrobial

agents.Findings from the initial examination may be within normal limits or

there may be only slight swelling of the face over the maxillary or frontal

sinuses. The infection worsens rap idly, and further examination will often

reveal nasal mucosal hypesthesia, pallor, and bleeding when the area is swabbed

and later, formation of a necrotic eschar and/or serosanguineous drain age from

the nares.Plain radiographs of the sinuses may show an air-fluid level, but

radiography is generally insensitive. CT scans of the sinuses are needed to

assess the extent of mucosal involvement and whether the infection has spread

into bone.[27] An otolaryngologist should be consulted immediately, and

endoscopic evaluation of all sinuses should be undertaken. Culture of purulent

material usually reveals the organism, and biopsy, if it can safely be

performed, will reveal the extent of invasion into the walls of the sinuses.

Drainage of the involved sinuses is carried out at the time of endoscopy, and

surgical debridement of adjacent infected structures is often necessary.

Follow-up endoscopy is essential to assess response to therapy and to ensure

that drainage is adequate.Therapeutic Pearls11. Coccidioidal meningitis requires

lifelong antifungal treatment.The treatment of choice for isolated coccidioidal

meningitis is oral fluconazole, 800 mg/d.[28] Most patients will respond to this

therapy within several weeks. If the patient does not respond to fluconazole,

itraconazole can be tried, but most physicians would go directly to intrathecal

administration of amphotericin B. This can be accomplished through lumbar

injection initially, but almost always will require a lumbar, cisternal, or

ventricular reservoir for long-term therapy.[29] If the patient has severe

disseminated coccidioidomycosis as well as meningitis, intravenous amphotericin

B should be used along with fluconazole initially. Experience clearly shows that

this infection is rarely, if ever, cured and thus therapy should be given for

life.[30]12. Cryptococcal meningitis: Combination antifungal therapy and

aggressive control of intra-cranial pressure is required.Several randomized

controlled trials in patients with AIDS have shown excellent results when

induction therapy is given with amphotericin B combined with flucytosine,

followed by consolidation therapy with fluconazole.[31,32] It should be noted

that the dosage of flucytosine should never exceed 100 mg/kg/d, which is less

than the dosage listed in the package insert (150 mg/kg/d). Flu cytosine

exhibits dose-related marrow toxicity, which can be decreased by using the lower

dosage noted above. Fluconazole is not as effective as amphotericin B when used

for initial therapy.[33] Therapy is the same for patients who do not have HIV

infection, even though no controlled trials have been performed to compare

azoles with amphotericin B in this population.[34] Fluconazole alone can be used

for isolated pulmonary and other forms of cryptococcal infection unless the

patient is severely ill.An important finding that emerged from treatment trials

in patients with AIDS was that increased intracranial pressure was common in

cryptococcal meningitis and was associated with increased mortality.[31,33,35]

It is postulated that there is increased brain edema because of the osmotic

effect from the large polysaccharide capsule surrounding each organism and the

huge burden of cryptococci found in patients with AIDS; an alternative postulate

is that the arachnoid villi are plugged by the large amount of capsular

polysaccharide.An opening pressure should always be obtained when a lumbar

puncture is performed. A pressure greater than 200 mm H2O, and especially a

pressure above 300 mm H2O, requires lowering; this is most easily done by

removing spinal fluid. A patient in whom the intracranial pressure is elevated

should have repeated lumbar punctures over the succeeding few days to be certain

that the pressure remains low. If repeated taps are required to keep the

pressure low, a temporary shunting device, either lumbar or ventricular, should

be placed to lower the pressure. Most patients will respond to antifungal

therapy and will not require a permanent shunting device.[32,35]13. Infection

with Zygomycetes: Use amphotericin B combined with aggressive surgical

debridement.Despite recent advances in antifungal therapy, infections with the

Zygomycetes remain quite difficult to treat.[14] These organisms are relatively

resistant to amphotericin B, and current azoles have no activity against these

fungi. Invasion through blood vessels with tissue infarction and necrosis is

characteristic. Aggressive early and repeated surgical debridement to remove all

necrotic tissue is essential for cure of the infection, and it should be

combined with treatment with high doses of amphotericin B.It is appropriate to

use a lipid-based formulation of amphotericin B so that a higher daily dose can

be administered. The initial dosage of lipid formulation amphotericin B should

be no lower than 5 mg/kg/d, and increasing the dosage to 10 mg/ kg/d or higher

has proved helpful in individual cases. Therapy must be continued until all foci

of infection are eradicated. Decreasing immunosuppression, reversing diabetic

ketoacidosis, and stopping any iron chelators that the patient may have been

taking are also essential.14. Candidemia: Treat all patients with an antifungal

agent.Candidemia has become the most common serious fungal infection in

hospitalized patients. Candida species now rank as the fourth most common cause

of nosocomial bloodstream infections and are associated with the highest crude

mortality rate.[36] Currently, patients at greatest risk for candidemia are not

those with neutropenia, but those who are in an ICU. These patients usually have

multiple medical problems, including renal failure that requires dialysis; have

been treated with broad-spectrum antibiotics; and have urinary, endotracheal,

and central venous catheters in place.[37]The source of candidemia is most often

the GI tract or a central venous catheter.[38] Some patients will clear the

organism from the blood following removal of the intravenous catheter if that is

the source, but many will not. Unfortunately, it is impossible for a clinician

to know which patients will and which will not clear the infection without

antifungal therapy.[39]The risks of persistent candidemia include seeding of the

infection to the eye, osteoarticular structures (especially the vertebrae), the

endocardium, and multiple other organs. The recommendations from a selected

consensus panel and from the Infectious Diseases Society of America guidelines

are that all patients with candidemia should be treated with an antifungal

agent[39,40]; therapy most often is continued for 2 weeks after blood cultures

have been shown to no longer yield Candida.15. Options for the treatment of

invasive aspergillosis.Amphotericin B has been the treatment of choice for

invasive aspergillosis for the past 4 decades. Lipid formulations of

amphotericin B are all approved only for refractory invasive aspergillosis, but

many clinicians caring for patients who already have renal disease or are at

risk for nephrotoxicity use a lipid formulation as primary therapy for

aspergillosis. Although few comparison studies are available, the lipid

formulations appear to have the same efficacy as standard amphotericin B.[41]

The dosage used is usually 5 mg/kg/d, but higher dosages have been used for

severe disease.Voriconazole is approved for the primary treatment of invasive

aspergillosis, based on the results of a randomized, controlled multicenter

trial that included 277 patients with proven or probable invasive disease.[42]

Outcomes with voriconazole were superior to those noted with amphotericin B;

voriconazole will likely assume a more prominent role in the primary treatment

of aspergillosis.Caspofungin is approved for the treatment of patients who have

refractory aspergillosis or those who cannot tolerate other agents. There are no

data for primary treatment of invasive aspergillosis with caspofungin, and thus

this drug should be saved for use as salvage therapy or in combination with

another agent active against Aspergillus species.[43] Absorption of itraconazole

is problematic, and the activity of this drug against Aspergillus species is

less than that noted with voriconazole; itraconazole should, therefore, not be

considered first-line therapy for invasive aspergillosis.16. In pregnant women,

amphotericin B is the antifungal agent of choice.Although associated with more

serious side effects than any other antifungal agent, amphotericin B is the only

agent that has been given to pregnant women with no serious con sequences for

the fetus. The azoles are teratogenic in animals and have caused birth defects

in humans receiving long-term therapy with fluconazole.[44] All azoles should be

considered contraindicated in pregnancy. It is important to note that

single-dose 150-mg fluconazole therapy for Candida vaginitis in women later

found to be pregnant has not been reported to be associated with birth defects.

Flucytosine has been associated with birth defects in animals and in humans. The

echinocandins are teratogenic in animals and are contraindicated in

pregnancy.17. Be aware of the individual absorption characteristics of oral

azole formulations.Fluconazole has the best absorption characteristics of all

the azoles.[45] The drug is essentially 100% bioavailable, and absorption is not

influenced by the presence of food in the stomach or by gastric acidity.The

original capsule formulation of itraconazole requires both gastric acid and the

presence of food in the stomach for adequate absorption. Ad ministering H2

blockers, antacids, or proton pump inhibitors will markedly reduce serum levels

of itraconazole. The oral suspension of itraconazole was developed to obviate

this issue. The suspension should be given on an empty stomach, rather than with

food, and gastric acidity is not essential for adequate absorption.[46] Thus, if

the patient requires a gastric acid modifying agent, the itraconazole suspension

should be used.Voriconazole is approximately 95% bioavailable when given without

food in the stomach (1 to 2 hours before or after eating); however, the presence

of food reduces bioavailability to 80% to 85%.[47] Gastric acid is not required

for absorption.18. Although relatively nontoxic, each of the azoles has certain

side effects that should be monitored.All azoles have the potential to cause

hepatitis; measurement of liver enzymes should be done at baseline and after

several weeks of therapy. During long-term treatment with an azole, liver enzyme

tests should be done every month. The hepatotoxicity seen with voriconazole may

be related to serum levels of the drug, which is different from other azoles, in

which the occurrence of hepatotoxicity appears to be

idiosyncratic.[47]Itraconazole can cause a syndrome of hypertension,

hypokalemia, and edema; this occurs mostly in older patients and often requires

stopping the drug. Itraconazole is also uniquely associated with ventricular

dysfunction; again, this occurs mostly in older adults and requires that the

drug be stopped.[48] Itraconazole should be used with great caution in patients

who have underlying heart failure.Fluconazole causes alopecia in many patients

who receive the drug for several months.[49] This may involve only thinning of

scalp hair, but it can involve loss of all body hair. The effect is reversible

when the drug is stopped. Dry, chapped lips are also noted frequently with

fluconazole use.Although rashes are an uncommon side effect of all azoles,

voriconazole has been noted to cause a rash in up to 8% of patients. The rash

has been related to photosensitivity in some patients; these patients experience

severe blistering of sun-exposed skin.[47] A side effect noted only with

voriconazole is photopsia, in which the patient perceives bright lights, wavy

lines, or enhanced colors within 30 to 60 minutes after administration of either

the oral or the intravenous formulation of the drug.[42,47,50] This side effect

occurs in as many as 30% of patients receiving the drug, lasts about 30 to 60

minutes, and eventually fades after several weeks despite continuation of

therapy. It is not associated with any long-term visual consequences.19. The

echinocandins will assume an increasing role in the treatment of Candida

infections.Caspofungin is the only echinocandin currently available; 2 other

agents will likely be available soon. The echinocandins are fungicidal for all

Candida species. Results from a multicenter, randomized, blinded trial comparing

caspofungin with amphotericin B for serious Candida infections showed equivalent

efficacy of the 2 agents.[51] Approximately 80% of the patients had candidemia,

and the others had peritonitis or deep-seated abscesses. There were fewer side

effects noted with caspofungin than with amphotericin B. The relative lack of

toxicity of the echinocandins makes them attractive for use in ICU patients who

have multiple underlying diseases.[43] These agents are available only as

intravenous formulations that are given once daily.20. For patients in renal

failure, antifungal therapy must be individualized.Amphotericin B should be

avoided if at all possible, and lipid formulations should be substituted if

amphotericin B must be used. Obviously, if the patient is already on dialysis,

there is no need to use a lipid formulation to avoid nephrotoxicity.Flucytosine

is renally excreted; in renal failure, this agent accumulates to toxic levels,

causing severe bone marrow suppression and hepatotoxicity. If serum flucytosine

levels cannot be obtained, it is safer to not use this agent in patients with

renal failure.Fluconazole is also renally excreted, and the dosage should be

reduced when renal failure is present. However, fluconazole is relatively

nontoxic; following suggested dos age reduction recommendations in the package

insert allows safe use of intravenous or oral fluconazole in patients with renal

failure.The intravenous formulations of both voriconazole and itraconazole are

solubilized in cyclodextrins. Because of concerns over the nephrotoxic potential

of these cyclodextrin components, which are cleared through glomerular

filtration, it is recommended that neither drug be used in patients who have

creatinine clearances below 30 to 50 mL/ min.[45,47] The oral formulations of

these 2 azoles can be used safely in patients with renal failure. Because

caspofungin is not nephrotoxic or excreted through the kidneys, it is a good

choice for treating patients with renal failure.[43]References Cano MV, Hajjeh

RA. The epidemiology of histoplasmosis: a review. Semin Respir Infect.

2001;16:109-118. Cairns L, Blythe D, Kao A, et al. Outbreak of

coccidioidomycosis in Washington state residents returning from Mexico. Clin

Infect Dis. 2000;30:61-64. Mardo D, Christensen RA, Nielson N, et al.

Coccidioidomycosis in workers at an archeological site—Dinosaur National

Monument, Utah, June-July 2001. MMWR. 2001;50:1005-1008. JE, Kabler JD,

Gourley MF, et al. Cave-associated histoplasmosis—Costa Rica. MMWR.

1988;37:312-313. Wheat LJ. Laboratory diagnosis of histoplasmosis: update 2000.

Semin Respir Infect. 2001; 16:131-140. Sheflin JR, JA, GP.

Pulmonary blastomycosis: findings on chest radio graphs in 63 patients. AJR.

1990;154:1177-1180. Areno JP, GD Jr, RB. Diagnosis of

blastomycosis. Semin Respir Infect. 1997; 12:252-262. KD, FM, Geiger

G, Stemper ME. Zoonotic transmission of sporotrichosis: case report and review.

Clin Infect Dis. 1993;16:384-387. Kauffman CA. Sporotrichosis: state-of-the-art

review. Clin Infect Dis. 1999;29:231-237. Mahal M, Saiman L, Bitman L, et al.

Review of trichosporonosis with a report of a case of disseminated Trichosporon

asahii infection. Infect Dis Clin Pract. 1998;7:175-179. Erer B, Galimberti M,

Lucarelli G, et al. Trichosporon beigelii: a life-threatening pathogen in

immunocompromised hosts. Bone Marrow Transplant. 2000;25:745-749. Fleming RV,

Walsh TJ, Anaissie EJ. Emerging and less common fungal pathogens. Infect Dis

Clin North Am. 2002;16:915-933. Daly AL, Velazquez LA, Bradley SF, Kauffman CA.

Mucormycosis: association with deferoxamine therapy. Am J Med. 1989;87:468-471.

Kontoyiannis DP, Wessel VC, Bodey GP, Rolston KV. Zygomycosis in the 1990s in a

tertiary-care cancer center. Clin Infect Dis. 2000;30:851-856. Ribes JA,

Vanover-Sams CL, Baker DJ. Zygomycetes in human disease. Clin Microbiol Rev.

2000;13:236-301. Marr KA, RA, Crippa F, at al. Epidemiology and outcome

of mould infections in hematopoietic stem cell transplant recipients. Clin

Infect Dis. 2002;34:909-917. Castiglioni B, Sutton DA, Rinaldi MG, et al.

Pseudallescheria boydii (anamorph Scedosporium apiospermum) infection in solid

organ transplant recipients in a tertiary medical center and review of the

literature. Medicine (Baltimore). 2002;81:333-348. Boutati EI, Anaissie EJ.

Fusarium, a significant emerging pathogen in patients with hematologic

malignancy: ten years' experience at a cancer center and implications for

management. Blood. 1997;90:999-1008. Anaissie EJ, Kuchar RT, Rex JH, et al.

Fusariosis associated with pathogenic Fusarium species colonization of a

hospital water system: a new paradigm for the epidemiology of opportunistic mold

infections. Clin Infect Dis. 2001;33:1871-1878. Nucci M, Anaissie E. Cutaneous

infection by Fusarium species in healthy and immunocompromised hosts:

implications for diagnosis and management. Clin Infect Dis. 2002;35:909-920.

Caillot D, Casasnovas O, Bernard A, et al. Improved management of invasive

pulmonary aspergillosis in neutropenic patients using early thoracic computed

tomographic scan and surgery. J Clin Oncol. 1997;15:139-147. Caillot D,

Couaillier JF, Benard A, et al. Increasing volume and changing characteristics

of invasive pulmonary aspergillosis on sequential thoracic computed tomography

scans in patients with neutropenia. J Clin Oncol. 2001;19: 253-259. Thaler M,

Pastakia B, Shawker TH, et al. Hepatic candidiasis in cancer patients: the

evolving picture of the syndrome. Ann Intern Med. 1988;108:88-100. Anttila VJ,

Elonen E, Nordling S, et al. Hepatosplenic candidiasis in patients with acute

leukemia: incidence and prognostic implications. Clin Infect Dis.

1997;24:375-180. Malani PN, Kauffman CA. Invasive and allergic fungal sinusitis.

Curr Infect Dis Rep. 2002;4: 225-232. Iwen PC, Rupp ME, Hinrichs SH. Invasive

mold sinusitis: 17 cases in immunocompromised patients and review of the

literature. Clin Infect Dis. 1997;24:1178-1184. Gillespie MB, O'Malley BW Jr,

Francis HW. An approach to fulminant invasive fungal rhinosinusitis in the

immunocompromised host. Arch Otolaryngol Head Neck Surg. 1998;124:520-526.

Galgiani JN, Ampel NM, Catanzaro A, et al. Practice guidelines for the treatment

of coccidioidomycosis. Clin Infect Dis. 2000;30:658-661. s DA, Shatsky SA.

Intrathecal amphotericin B in the management of coccidioidal meningitis. Semin

Respir Infect. 2001;16:263-269. Dewsnup DH, Galgiani JN, Graybill JR, et al. Is

it ever safe to stop azole therapy for Coccidioides immitis meningitis? Ann

Intern Med. 1996;124: 305-310. van der Horst CM, Saag MS, Cloud GA, et al.

Treatment of cryptococcal meningitis associated with the acquired

immunodeficiency syndrome. N Engl J Med. 1997;337:15-21. Saag MS, Graybill RJ,

Larsen RA, et al. Practice guidelines for the management of cryptococcal

disease. Clin Infect Dis. 2000;30:710-718. Saag MS, Powderly WG, Cloud GA, et

al. Comparison of amphotericin B with fluconazole in the treatment of acute

AIDS-associated cryptococcal meningitis. N Engl J Med. 1992;326:83-89. Pappas

PG, Perfect JR, Cloud GA, et al. Cryptococcosis in human immunodeficiency

virus-negative patients in the era of effective azole therapy. Clin Infect Dis.

2001;33:690-699. Graybill JR, Sobel J, Saag M, et al. Diagnosis and management

of increased intracranial pressure in patients with AIDS and cryptococcal

meningitis. Clin Infect Dis. 2000;30:47-54. Edmond MB, Wallace SE, McClish DK,

et al. Nosocomial bloodstream infections in United States hospitals: a

three-year analysis. Clin Infect Dis. 1999;29:239-244. Blumberg HM, Jarvis WR,

Soucie JM, et al. Risk factors for candidal bloodstream infections in surgical

intensive care unit patients: the NEMIS prospective multicenter study. Clin

Infect Dis. 2001;33:177-186. Nucci M, Anaissie E. Should vascular catheters be

removed from all patients with candidemia? An evidence-based review. Clin Infect

Dis. 2002; 34:591-599. JE Jr, Bodey GP, Bowden RA, et al. International

conference for the development of a consensus on the management and prevention

of severe candidal infections. Clin Infect Dis. 1997;25:43-59. Rex JH, Walsh TJ,

Sobel JD, et al. Practice guidelines for the treatment of candidiasis. Clin

Infect Dis. 2000;20:662-678. Bowden R, Chandrasekar P, White MH, et al. A

double-blind, randomized, controlled trial of amphotericin B colloidal

dispersion versus amphotericin B for treatment of invasive aspergillosis in

immunocompromised patients. Clin Infect Dis. 2002;35:359-366. Herbrecht R,

Denning DW, TF, et al. Voriconazole versus amphotericin B for primary

therapy of invasive aspergillosis. N Engl J Med. 2002;347:408-415. Deresinski

SC, s DA. Caspofungin. Clin Infect Dis. 2003;36:1445-1457. Pursley TJ,

Blomquist IK, Abraham J, et al. Fluconazole-induced congenital anomalies in

three infants. Clin Infect Dis. 1996;22:336-340. Kauffman CA, Carver PL. Use of

azoles for systemic antifungal therapy. Adv Pharmacol. 1997; 39:143-189. Barone

JA, Moskovitz BL, Guarnieri J, et al. Enhanced bioavailability of itraconazole

in hydroxypropyl-b-cyclodextrin solution versus capsules in healthy volunteers.

Antimicrob Agents Chemother. 1998;42:1862-1865. LB, Kauffman CA.

Voriconazole: a new triazole antifungal agent. Clin Infect Dis. 2003;36:630-637.

Ahmad SR, Singer SJ, Leissa BG. Congestive heart failure associated with

itraconazole. Lancet. 2001;357:1766-1767. Pappas PG, Kauffman CA, Perfect J, et

al. Alopecia associated with fluconazole therapy. Ann Intern Med.

1995;123:354-357. Walsh TJ, Pappas P, Winston DJ, et al. Voriconazole compared

with liposomal amphotericin B for empirical antifungal therapy in patients with

neutropenia and persistent fever. N Engl J Med. 2002;346:225-234. Mora-Duarte J,

Betts R, Rotstein C, et al. Comparison of caspofungin and amphotericin B for

invasive candidiasis. N Engl J Med. 2002;347: 2020-2029. Carol A. Kauffman, MD,

Ann Arbor (Michigan) Veterans Affairs Healthcare System, University of Michigan

Medical School, Ann Arbor. Dr Kauffman is chief, infectious diseases, Ann Arbor

Veterans Affairs Healthcare System, and professor of internal medicine,

University of Michigan Medical School, Ann Arbor. Are you also aware of the

fact that? It is interesting to note what laboratory protocol medical students

and students destined for future laboratory work are being instructed on prior

to working with micro fungi in university laboratory settings. In her text,

Introduction to Diagnostic Microbiology (1997), Associate Professor and Director

of Medial Laboratory Programs, Dannessa Delost, M.S., M.T. (ASCP) of the

Department of Allied Health, College of Health and Human Services Youngstown

State University writes, concerning the health and safety of her students:

“Conidia and spores may remain dormant in the air or environment or may be

transported through the air to other locations. The spores of pathogenic molds

can be inhaled and enter the respiratory tract. This is a common rout of

infection, and because of this, it is imperative to practice good laboratory

safety when working in mycology. All work, including the preparation of slides,

plating and transferring cultures, and nay biochemical work, must be performed

in a biological safety cabinet. Because airborne conidia and spores are readily

released from a fungal culture, one should never smell a fungal culture.

Screw-cap test tubes should be used in place of test tubes with a cotton, metal,

or plastic lid. In addition, Petri plates must be sealed tightly with either an

oxygen-impermeable tape or Parafilm. As always, gloves should be worn and any

breaks or cuts in the skin covered to prevent the transmission of fungal

infection.” Also that? A good example of this activity is observed when a person

drinks alcohol. Alcohol is a naturally produced product that within minutes

after consumption changes neural activity, and generates an adverse accumulative

chemical effect on virtually every cell in the human body as the person’s

drinking progresses. If enough alcohol is consumed over a short period of time

“alcohol poisoning” could result causing a comatose condition in the drinker, or

even lead to death. Smoking or chewing of tobacco is also a great example.

According to a research study on tobacco released by E. L. Maghraby and M. A.

Abdel-Slater of the Botany Department, Faculty of Science at Sohag University in

Egypt, titled, Mycoflora and natural occurrence of Mycotoxins in Tobacco from

Cigarettes in Egypt, the following facts relating to tobacco state: “Forty-two

species and 4 varieties belonging to 21 genera [of fungal species] were

collected from 40 tobacco samples…” The research continues to report that

among the many mold species were: Aspergillus, Penicillium, Fusarium,

Chaetomium, and Stachybotrys (the so called “Black Mold”) which has been the

mainstay of mold reports by assorted national and local news media. What is

very important as a result of this study is the fact that: “Four samples (out of

40) had toxicity and four compounds of mycotoxins were detected namely;

aflatoxin B1, aflatoxin B2, zearalenone, and T-2 toxin,” all of which are known

to be associated with lung cancer, liver cancer, birth defects, and other

serious diseases. According to research data published by the American Lung

Association: “Tobacco use causes 90% of lung cancer deaths of deaths from

chronic lung disease, 33% of all cancer deaths, 10% of newborn deaths and

increases the risk of miscarriage by 80%. A third of smokers will eventually die

from smoking, and smoking is responsible for one in five deaths in the U.S.”

What this epidemiological research and many others similar to it relate is that

pathogenic micro fungi live eukaryotic cells (structurally and chemically

similar to animal and human cells), unlike prokaryotic pathogenic bacteria and

virus exposures grows and poisons cells, especially lung and liver cells very

slowly. All of these microbes are “live cells,” and as people tend to think of

“molds” as simply “allergens” or “plant-life” irritants that come and go

seasonally, they are not. Pathogenic micro fungi as Professor Wong

explains it to his students at the University of Hawaii, Department of Botany,

in a class lecture titled, Fungi as Human Pathogens: “The successful treatment

of fungal diseases is more difficult than those caused by bacteria. Because

bacteria are prokaryotes, the makeup of their cells are very different than our

own eukaryotic cells and pharmaceutical products, such as antibiotics, can

successfully destroy bacteria without harming our cells, tissues and organs.

However, because fungi are eukaryotes, finding a treatment that will kill the

fungus and not harm our own cells is more difficult.” (Source:

http://www.botany.hawaii.edu/faculty/wong/BOT135/LECT09.htm) Noted environmental

researcher Harriet Ammann, Ph.D., D.A.B.T., a Sr. Toxicologist with the State of

Washington, explains in her article about cytotoxic micro fungi and their

secondary mycotoxins, “Is Indoor Mold Contamination a Threat to Health?” the

health dangers of prolonged indoor exposures: “Mycotoxins… are not essential to

maintaining the life of the microfungi cell in a primary way (at least in a

friendly world), such as obtaining energy or synthesizing structural components,

informational molecules or enzymes. They are products whose function seems to be

to give microfungi a competitive advantage over other microfungi species and

bacteria. Mycotoxins are nearly all cytotoxic, disrupting various cellular

structures such as membranes, and interfering with vital cellular processes such

as protein, RNA and DNA synthesis. Of course they are also toxic to the cells

of higher plants and animals, including humans. Mycotoxins vary in specificity

and potency for their target cells, cell structures or cell processes by species

and strain of the microfungi that produces them. Higher organisms are not

specifically targeted by mycotoxins, but seem to be caught in the crossfire of

the biochemical warfare among microfungi species and microfungi and bacteria

vying for the same ecological niche.”SO, IN OTHER WORDS, EVEN A HIGHLY PAID

MEDICAL SPECIALIST WITH LITTLE OR NO MEDICAL RESEARCH OR FORMAL MEDICAL SCHOOL

EXPERIENCE IN MICROORGANISM SURVIVAL AND BEHAVIOR, GENETICS, OR CELLULAR

EVOLUTION, MIGHT TAKE A HINT! Even in people with immune competent systems live

mold cells are more than simply " allergens " . Far removed from bacteria, that are

observed as much older species without a formed nucleus, molds and yeasts (which

some molds can form into based on body temp), live-celled, multinucleated mold

species such as many forms of Aspergillus, Fusarium, Trichoderma, Culvularia,

Stachybotrys, Penicillum, etc., are very close to human cells in structure,

chemistry, and genetics. In fact, in the scientific Phylogenetic Tree of Life

under the family " Eucaryota " places these live celled potential serious

disease-causing pathogens second to Humans.

http://en.wikipedia.org/wiki/Biology I believe that it is time for medical

science/the medical field to reevaluate their belief that live-celled

" opportunistic " (internal in the body) and " pathogen " (external entering the

body) are simply " allergens. " These dangerous cells technically and by all known

standards are not factually classifiable as allergens, the enzymes, mycotoxins,

and volatile organic compounds may fit that definition, but live, functioning

cells are not. And, most importantly, molds are not classifiable as plant life

either. They are live microorganisms that can recreate themselves and destroy

weakened living cells in a " fermenting " process of decay based on the chemical

ability to genetic mutate dying or dead organisms. So, I vote that molds are

not true allergens, and medical science already knows this or at least they

should since the molds we are discussing herein have been thoroughly studied in

the disease processes for well over two centuries. It is about time those who

continue to play " ignorant " in the medical field start to catch on. Much

respect, R. HaneyBio-Health Environmental PsychologyEmail:

_Haney52@...

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_052008

[Guest guest]

Oh my god. Thank you for this post. This makes absolute sence. I will be

makeing a phone call to the pathologist to find out just what test were done on

the biopsy from my lungs. As well as looking into further testing done on the

skin biopsys done on skin sores that were a direct result of exposure.

Thank you, thank you thank you...

Chris...