Re:Vote For Mold Today, Tuesday

[Guest guest]

You can vote all week, on this poll. When I voted today, the tally was 44%

voting for mold, the largest percentage of the 4 choices. Please vote " early and

often " , to get the attention of the medical community. Remember to " delete your

cookies " before each vote, to enable re-voting. We are always talking, on this

board, about how to get doctors to believe us, and treat us. Please remember the

old joke about the farmer telling his friend that nothing seems to work, when

trying to get the mule to move forward, The friend stands in front of the mule

and punches the mule right in the face. The farmer says: " what did you do that

for?' The friend replies: " first, you've got to get his attention " .

The results of this poll might get the attention of the " mules " who won't move

forward for us.

Click both of the below links, (one of them should connect)

http://tinyurl.com/3hjmd6

www.myallergynetwork.com

[Guest guest]

Great idea, Joe!! I voted and had my husband do the same!

[Guest guest]

The vote for most troublesome allergen, on a web site that doctors look

at, as of 8PM, Friday, is Mold 48%, which is TWICE as much as the next

closest allergen. Please keep voting. I don't know when this weekly

poll closes. If we can shatter the misconception of most allergists,

that mold is " no big deal " compared with other allergens, the whole

medical community might re-evaluate their " mold can't hurt you "

attitude.

Click here to vote:

http://tinyurl.com/3hjmd6

or type it into your address bar and hit your " enter " key

.........................................

--- In , Joe Salowitz <josephsalowitz@...>

wrote:

Please remember the old joke about the farmer telling his friend that

nothing seems to work, when trying to get the mule to move forward, The

friend stands in front of the mule and punches the mule right in the

face. The farmer says: " what did you do that for?' The friend

replies: " first, you've got to get his attention " .

>

> The results of this poll might get the attention of the " mules " who

won't move forward for us.

> Click both of the below links, (one of them should connect)

>

> http://tinyurl.com/3hjmd6

> www.myallergynetwork.com

[Guest guest]

ph/All:

Molds, Medics, and the Pursuit of Factual Clarifications

By R. Haney

Copyright© May 2008

Just because medical doctors are ignorant as hell because the virtually know

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) reactionwww.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

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

Any substance that induces an allergy (mold, grasses, antibiotics,

etc.).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.

[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 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 http://www.hc-sc.gc.ca en.wikipedia.org/wiki/Allergen

http://www.google.com/search?hl=en & defl=en & q=define:Allergen & sa=X & oi=glossary_de\

finition & ct=title

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 Introduction

Abstract

Opportunistic 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.

Introduction

Opportunistic 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 Pearls

1. 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 Pearls

11. 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]

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Blumberg HM, Jarvis WR, Soucie JM, et al. Risk factors for candidal bloodstream

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candidemia? An evidence-based review. Clin Infect Dis. 2002; 34:591-599.

JE Jr, Bodey GP, Bowden RA, et al. International conference for the

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Bowden R, Chandrasekar P, White MH, et al. A double-blind, randomized,

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for treatment of invasive aspergillosis in immunocompromised patients. Clin

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Herbrecht R, Denning DW, TF, et al. Voriconazole versus amphotericin B

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

Pursley TJ, Blomquist IK, Abraham J, et al. Fluconazole-induced congenital

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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

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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. Haney

Bio-Health Environmental Psychology

Email: _Haney52@...

@...: josephsalowitz@...: Sat, 10 May

2008 00:42:01 +0000Subject: [] Re:Vote For Mold Today, Tuesday

The vote for most troublesome allergen, on a web site that doctors look at, as

of 8PM, Friday, is Mold 48%, which is TWICE as much as the next closest

allergen. Please keep voting. I don't know when this weekly poll closes. If we

can shatter the misconception of most allergists, that mold is " no big deal "

compared with other allergens, the whole medical community might re-evaluate

their " mold can't hurt you " attitude.Click here to

vote:http://tinyurl.com/3hjmd6 or type it into your address bar and hit your

" enter " key........................................Please

remember the old joke about the farmer telling his friend that nothing seems to

work, when trying to get the mule to move forward, The friend stands in front of

the mule and punches the mule right in the face. The farmer says: " what did you

do that for?' The friend replies: " first, you've got to get his attention " . > >

The results of this poll might get the attention of the " mules " who won't move

forward for us.> Click both of the below links, (one of them should connect)> >

http://tinyurl.com/3hjmd6 > www.myallergynetwork.com

_________________________________________________________________

With Windows Live for mobile, your contacts travel with you.

http://www.windowslive.com/mobile/overview.html?ocid=TXT_TAGLM_WL_Refresh_mobile\

_052008

[Guest guest]

Thank you Doug, for that graduate school education in biology that

you posted, in response to my request that we all vote for " Mold " as

our most troublesome " allergen " . The problem is, that by the time I

re-read your posting for the fourth time, to understand the massive

content, I had already exceeded the total amount of time that most

medical school students spend on studying the place of fungi in

cellular biology. So, when you say that it is " about time " , that

these medical students, who are NOW doctors, " catch on " , it is just

wishful thinking on your part, because they are NOT " playing

ignorant " of the subject matter. They " ARE ignorant " of the subject

matter. And they are far too busy raking in the bucks to take any

continuing medical education course that will not result in MORE

bucks to rake in.

My intention, in promoting our voting in the poll, was to send a

message to allergists and pulmonologists that " MOLD is a great way to

make a buck " , since so many people suffer from the effects of it. MY

hope, is that once they start treating us as if we have an illness,

ANY ILLNESS, instead of treating us as if we were mental cases, they

might stumble upon the TRUTH that WE have all known, since the day

that each of us became sick.

So, I'm NOT asking you to validate their misconception that, at

worst, all we have is an allergy. I'm just trying to give the medical

profession a REASON to treat our health problems. That reason is,

that we constitute a vast market for their talents, and they can

choose the medical coding of their choice, as long as they listen to

us long enough to learn something. Someone's got to educate these

bozos. The medical schools are not doing that job. So, as unfair as

it is, the task falls to us to accomplish.

By the way, when I clicked on your link to the Wikipedia biology

page, I was astounded, myself, to see that our CLOSEST biological

relatives are " SLIME MOLD " . I also liked your analogy to humans being

caught in the " cross fire " between mold and other mold and bacteria,

for survival. Kind of reminds me of the present situation in Iraq.

....................................................

R. Haney, in Sickbuildings, wrote, in reply to my request for

our board members to vote for " Mold " as being the most

troublesome " allergen " in ther life:

" 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. Haney

> Bio-Health Environmental Psychology

> Email: _Haney52@...

>

>

[Guest guest]

ph: Thank you for your very kind comments and support. When I read your

" vote " post, I was both aware of its intent and conception. And, I am deeply

appreciative that you would take the time to do this as it motivated me to write

something that I have been slow to publish for a couple of years now.

It is my contention however, that if the medical field is specifically trained

to work with dangerous medicines in attempting to cure serious diseases and make

huge salaries in the process, I figure that they should also be held directly

accountable for misinformation and lack of education in medicine. I do not give

a rats ass to any degree whether or not they have an excuse for not knowing or

being ignorant of the facts. Tell that to the poor deceased soul who might have

listened to his or her untrained doctor while dying a cruel death. We are

Americans! Aside from that we are suppose to be a nation that promised that we

would live " Under God, Indivisible, with Liberty and Justice for all! " When we

went to war, we were taught nearly everything there was to know about survival

and how to kill. Our very lives depended upon what we learned and how we used

what we learned. Many of us returned home for that reason. We were entrusted to

keep liberty and freedom safe and out of harms way. We did just that! That is

what I feel we should also expect from the medical field as well. What is the

difference in dying from an enemy during war, and having to fight human diseases

in which our enemy happens to be a medical doctor who did not care enough about

his Hippocratic oath to be " The Best He or She Could Be " or work as an " Army of

One! "

If the information that I have related is absolutely out there for medical

doctors to read and heed, as well as use in their medical practices, then it

should be compelled and imperative that doctors " STOP " playing the " Ignorance

card. " At some point all of the technicalities and semantics the medical field

uses to minimize the facts of disease were micro fungi are implicated; resorting

to the labeling of a person as malingerer or depressed, or; worse yet, an

" idiopathic " illness is absolute nonsense. Medical doctors should be fined,

imprisoned, or just plain hanged for allowing a patient to die simply because he

or she did not want to keep up with what medical science is teaching

(figuratively speaking, of course). However, lacking the education to fully

understand what allergies are in comparison to live-celled bacteria, molds, and

yeasts is blatantly inexcusable! It certainly does not take a PhD or M.D. to

understand it. It is time for the medical field to enter the world of 21st

century medical science in order to earn their money or cut the BS, and greatly

reduce their salaries. We as patients on the other hand, should form and

petition Medical Schools to teach and research in depth the molecular and

biochemistry of human molecular activity and micro fungi genetic and chemical

integration... it is all there for the taking, now!

Finally, we as patients should also demand more of our government and American

industry in regulating the massive products that have virtually no controls in

inhibiting micro fungi, mycotoxins, volatile organic compounds, and particulate

matter in materials and products that America sells. If you believe that wars

kill people, and I will certainly attest that they do, all of the wars ever

fought and all of the enemies ever confronted do not begin to number the

casualties that pathogenic molds and yeasts knowing used in American products

have tallied. Our voice in confronting the indignity of the medical field,

government, and various other entities directly or indirectly connected to moldy

product sales (i.e., perfumes and colognes, cereals, fuels, alcoholic beverages,

tobacco, medicines, citric beverages, bleaching products, and literally

thousands of other solid and liquid products).

This perpetuated ignorance is much more of a war than I was ever involved in

during Vietnam, by a long shot! And we who are so acutely aware, are the

frontline of defense for our fellow countrymen/women.

Again, thank you; God Bless and take care.

Doug Haney

@...: josephsalowitz@...: Sun, 11 May

2008 22:47:28 +0000Subject: [] Re:Vote For Mold Today, Tuesday

Thank you Doug, for that graduate school education in biology that you posted,

in response to my request that we all vote for " Mold " as our most troublesome

" allergen " . The problem is, that by the time I re-read your posting for the

fourth time, to understand the massive content, I had already exceeded the total

amount of time that most medical school students spend on studying the place of

fungi in cellular biology. So, when you say that it is " about time " , that these

medical students, who are NOW doctors, " catch on " , it is just wishful thinking

on your part, because they are NOT " playing ignorant " of the subject matter.

They " ARE ignorant " of the subject matter. And they are far too busy raking in

the bucks to take any continuing medical education course that will not result

in MORE bucks to rake in. My intention, in promoting our voting in the poll, was

to send a message to allergists and pulmonologists that " MOLD is a great way to

make a buck " , since so many people suffer from the effects of it. MY hope, is

that once they start treating us as if we have an illness, ANY ILLNESS, instead

of treating us as if we were mental cases, they might stumble upon the TRUTH

that WE have all known, since the day that each of us became sick. So, I'm NOT

asking you to validate their misconception that, at worst, all we have is an

allergy. I'm just trying to give the medical profession a REASON to treat our

health problems. That reason is, that we constitute a vast market for their

talents, and they can choose the medical coding of their choice, as long as they

listen to us long enough to learn something. Someone's got to educate these

bozos. The medical schools are not doing that job. So, as unfair as it is, the

task falls to us to accomplish. By the way, when I clicked on your link to the

Wikipedia biology page, I was astounded, myself, to see that our CLOSEST

biological relatives are " SLIME MOLD " . I also liked your analogy to humans being

caught in the " cross fire " between mold and other mold and bacteria, for

survival. Kind of reminds me of the present situation in Iraq.

.................................................... R. Haney, in

Sickbuildings, wrote, in reply to my request for our board members to vote for

" Mold " as being the most troublesome " allergen " in ther life: " 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. Haney> Bio-Health Environmental Psychology> Email:

_Haney52@...> >

_________________________________________________________________

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rive_052008

[Guest guest]

Doug, this is very well written and I agree with its content 110%. While I

understand what ph is trying to say he is not taking into consideration what

I would refer to as the whole picture. He is probably right in saying that your

last post took longer to read than most students spend learning and that is

inexcusable these days which is precisely what you both are saying. My ex has

just about finished up nursing school and still knows nothing whatsoever about

my illness or mold, toxins etc. I find this more disturbing than I can even

explain.

To both posters I want you to know I am enjoying the discussion and can

honestly say I continue to be interested and learn from discussions just like

this. Also as a vet myself with a family member who has fought in every war

since the civil war I would like to reiterate what Doug has said from his

Vietnam experience. The medical and pharmaceutical companies in this country had

better wake up and do it soon. The agent orange and idiocies of the like will

pale in comparison to what we are now facing. Just my two cents.

Chris...