Textos coletatos com perspectiva didática por Luiz Meira 

As mais Recentes Controvérsias: Alimento para o Pensamento ou a Zona da Penumbra.

Síndrome da Guerra de golfo

Uma das correntes mais controversas dos assuntos médicos são se os múltiplos sintomas agudos e crônicos achados em veteranos da Guerra do Golfo Persa foram causados por exposição química, agentes infecciosos, ou problemas psicológicos, ou se uma Síndrome da Guerra de Golfo não existe no todo. A enfermidade clínica inclui uma coleção de sintomas incluindo fadiga crônica, dores em geral, enxaquecas e erupções cutâneas da pele. Um estudo sugere que micoplasmas patogênicos sejam os responsáveis por um grande número de casos entre os veteranos, na base de hibridação do DNA e a responsabilidade dos veteranos pelo tratamento antibiótico prolongado. De vez que a evidência experimental é escassa, incompleta e mal disseminada (bem-controlada), é necessário um detalhado estudo através de laboratórios independentes. Se a Síndrome da Guerra do Golfo tem causas infecciosas, os micoplasmas, com suas credenciais biológicas requeridas, são os candidatos mais potenciais.

A Doença de Crohn

Vários estudos epidemiológicos correlatam infecções respiratórias com exacerbação da doença de Crohn e outras doenças inflamatórias crônicas do intestino. Sintomas iniciais gastro-intestinais agudos em pacientes com estas doenças são acompanhados através de soro-conversão a vírus específicos ou antígenos de M. pneumoniae. Como indicado anteriormente, micoplasmas podem induzir imuno-respostas pleiotrópicas e podem ser de difícil eliminação em pacientes, apesar de tratamento antibiótico apropriado. Terapia de esteróides para controlar sintomas gastro-intestinais nestes pacientes, junto com as multi-facetedas propriedades biológicas associadas com micoplasmas patogênicos, pode precipitar o aparecimento de exacerbações agudas de doença inflamatória crônica do intestino.

Artrite Reumatóide e Outras Artritides Humanas

A ocorrência de vários Micoplasmas e espécies Ureaplasmas em tecidos das juntas de pacientes com artrite reumatóide, artrite reativa sexualmente transmitida, e outras artritides humanas, já não podem ser ignoradas [8]. Uma tentativa clínica de terapia antibiótica (doxyciclina) de longo termo (6 a 12 meses) antes da destruição da cartilagem poderia provar benefícios no gerenciamento de tais freqüentes e debilitantes infecções.

Extensiva evidência clínica e microbiológica indica que micoplasmas sozinhos podem extrair um espectro da enfermidade para a qual nenhum outro agente é incriminado. A erradicação deste micoplasmas patogênicos de vários locais do tecido requer um sistema imune intacto e funcional, embora as pessoas com sistemas imunes completamente competentes podem ter dificuldades de eliminar micoplasmas, até mesmo com longa terapia com drogas recomendadas. Todavia, ainda são vistos micoplasmas como subordinados para outros agentes infecciosos e são relegados a uma categoria de comensais que desgraçadamente causam doença em pacientes cujos sistemas imunes oferecem pouca resistência a tensão e sobrecarga microbiana.

A importância fundamental dos micoplasmas em doenças específicas de humanos, animais, insetos e plantas são irrefutáveis, e suas propriedades biológicas sem igual são consistentes com sua associação íntima com células hospedeiras designadas. Estas bactérias notáveis têm que continuar recebendo a atenção científica de micoplasmologistas, culturistas de célula, clínicos, imunologistas e pesquisadores de DNA, que recentemente estão compilando bancos de dados extensos que podem dissecar qualquer elemento micoplasmal acessível, que eventualmente defina o ser biológico e genético deles. Todavia, micoplasmas permanecem misteriosos e enigmáticos e os dados disponíveis e as hipóteses propostas que correlatam micoplasmas com patogenesis de doenças variam de definitivo, provocativo e excitante para inconclusivo, confuso e herético. Controvérsias parecem ser companheiras reincidentes de micoplasmas, contudo boa ciência e mentes abertas deveriam superar o legado acarretado durante décadas.

Sobre os Autores

Dr. Baseman é o professor e catedrático do Departamento de Microbiologia do Centro Científico de Saúde da Universidade do Texas, San Antonio. Sua pesquisa enfoca em interações patogênicas da célula hospedeira com interesse especial na definição da biologia e determinantes da virulência patogênica de micoplasmas em humanos.

Dr. Tully encabeça a Seção de Micoplasma, Laboratório de Microbiologia Molecular, Instituto Nacional de Alergia e Doenças Infecciosas, Frederick, Maryland,. Seu interesse cobre a distribuição dos hospedeiros, patogenicidade e taxonomia de mollicutes.

Endereços para correspondência: Joel B. Baseman, Departamento de Microbiologia, do Centro Científico de Saúde da Universidade do Texas, em San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78284-7758; fax: 210-567-6491; e-mail: baseman@uthscsa.edu.

Reconhecimentos:

Este estudo foi em parte apoiado pelo NIH (National Institutes of Health), concessões AI 27873, AI 32829 e AI 41010.
 

Jorge Timenetsky & Elena Metiffogo.
Depto. de Microbiologia/ICB II. Universidade de São Paulo.
Av. Prof. Lineu Prestes, 1374. São Paulo - SP.
CEP 05508-900.
 

1. Características gerais
2. Estrutura genômica
3. Patogenicidade nos diferentes hospedeiros
4. Processos patogênicos
5.Aspectos imunológicos
 

"As propriedades biológicas dos micoplasmas e as suas características de parasitismo, evidenciam a complexicidade destes organismos como patógenos e oportunistas por execelência, desafiando de forma singular, a homeostasia do hospedeiro."
 

1. CARACTERÍSTICAS GERAIS.
Micoplasma usualmente é o termo para se referir a qualquer gênero desta classe de bactérias. Foi derivada das palavras gregas, mykes para fungos e plasma para designar a forma ou o molde das células. O primeiro isolamento de micoplasma foi realizado por NOCARD & ROUX na França, em 1898, a partir de um surto de pleuropneumonia contagiosa bovina. As espécies descobertas posteriormente foram denominadas genericamente de PPLO (Pleuropneumonia-Like Organisms ou organismos semelhantes aos da pleuropneumonia ).
Esses procariontes pertencem à Divisão Tenericutes e à Classe dos Mollicutes (do latin, molli, suave; cutes, cútis ou derme), nome de cuja origem se deve à característica peculiar da total ausência de parede e da molécula de peptidioglicano, sendo o citoplasma, envolvido por uma membrana trilaminar. Algumas espécies possuem cápsula e/ou projeção polar, em forma de clava. Não possuem esporos, fímbrias, corpúsculos de inclusão ou flagelos. No entanto apresentam deslizamento em superfícies ou contração celular como nos Spiroplasmas. Filogeneticamente os micoplasmas descendem de bactérias Gram positivas. Adquirem coloração Gram negativa pela ausência da parede celular.
Os micoplasmas são considerados os menores microrganismos de vida livre. Apesar da ausência de parede celular, sua forma estável, é usualmente ovóide. Entretanto, poucas espécies apresentam-se espiraladas atingindo cerca de 100µm. As suas dimensões, em geral, estão próximas aos maiores vírus (0,2 a 0,4 m m). A forma filamentosa é "multinucleada", pode ocorrer em determinados momentos metabólicos, pela falta de sincronia da septação na divisão celular e replicação do DNA. Assim além da fissão binária, a partir dos filamentos, formam-se cadeias ou conjuntos de pequenas células de micoplasma viáveis que se desprendem, e sob pressão em filtros, podem transpor a porosidade de 0,22µm .
Em meios sólidos, geralmente produzem colônias em forma de "ovo frito" observada em lupa. Em caldo, raramente turvam os meios mesmo com densidade de 108 células /mL.
Estas bactérias possuem alta sensibilidade aos agentes descontaminantes químicos e físicos. São também sensíveis à detergentes e alterações osmóticas, são naturalmente resistentes à penicilina pela ausência do alvo pertinente. A tetraciclina é citada classicamente, mas dependendo da espécie incluem-se alguns macrolídios. Atualmente a ciproflaxina e a azitromicina tem sido os antimicrobianos mais escolhidos.
Em função do reduzido genoma (580 a 2200 kpb) da maioria das espécies, os micoplasmas apresentam metabolismo e vias biossintéticas limitadas. Desta maneira o seu cultivo exige meios enriquecidos, contendo precursores para a biossíntese do ácido nucléico, proteínas e lipídios.
Os micoplasmas podem ser divididos em fermentadores e não fermentadores de carboidratos (glicose). Os fermentadores acidificam os caldos. Os não fermentadores, oxidam ácidos graxos e álcoois, não diminuindo significativamente o pH. Quando a arginina é utilizada por ambos os grupos, há produção de ATP, CO2 e NH3, alcalinizando o meio. Usualmente o pH ótimo para o crescimento in vitro é de 7,8 ± 0,2. Os ureaplasmas hidrolizam a uréia e exigem pH entre 5,8 e 6,5.
As superfícies das mucosas oral, ocular, trato respiratório, urogenital e digestivo dos animais e do homem, além da glândula mamária e das articulações são o habitat primário desses organismos, em que a maioria das espécies, permanecem aderidas à células. Além dos mamíferos, esses organismos são encontrados em peixes, aves e répteis, como patógenos, oportunistas ou comensais. Em insetos podem ser patógenos ou vetores de transmissão de doenças para certas plantas. De forma singular, foram constatadas espécies de micoplasmas no solo e na água. Contudo, os micoplasmas usualmente exibem estrita especificidade em relação ao hospedeiro e ao sítio de colonização, refletindo suas características de exigência nutricional e de parasitismo obrigatório.

2. ESTRUTURA GENÔMICA
O genoma circular de fita dupla dos micoplasmas pode ser cinco vezes menor do que em E. coli e possui baixo teor de G+C (24 a 43%). De acordo com o tamanho do genoma, os micoplasmas conhecidos, podem ser divididos em dois grupos: o primeiro, composto por espécies dos gêneros Mycoplasma e Ureaplasma, apresentando genoma de aproximadamente 500 MDa ou de 600 a 1350 kbp e o segundo, abrangendo as espécies pertencentes aos gêneros Anaeroplasma, Asteroleplasma, Acholeplasma, Spiroplasma, Mesoplasma e Entoplasma, aproximadamente com 1000 MDa ou de 790 a 2200 kbp. Recentemente, a seqüência genômica do M. genitalium e do M. pneumoniae foi determinada, e apresentaram DNA de fita dupla circular com 580,07 e 816,39 kbp, respectivamente.
Presume-se que os genomas com 500 MDa são limitados à algumas espécies dos gêneros Mycoplasma e Ureaplasma e que, até o momento, representam a menor carga genética de um microrganismo de vida livre. Assim, de acordo com os resultados convencionais da biologia molecular, os micoplasmas são considerados os representantes do menor sistema de vida, desde que a sua capacidade de codificação limita-se à aproximadamente 700 proteínas essenciais para o seu metabolismo codificadas por não mais do que 500 genes. Apesar do pequeno genoma, os micoplasmas facilitam a reorganização do DNA, pela repetição de seqüências gênicas, promovendo alteração genética e patogenica maximizando o potencial da diversidade de proteínas. Os micoplasmas possuem de uma a duas cópias de RNA 16S, podem conter fagos, plasmídios e alguns possuem o codon UAG para triptofano.
 

3. PATOGENICIDADE NOS DIFERENTES HOSPEDEIROS
Os micoplasmas são amplamente distribuídos entre os seres vivos e podem causar diversas doenças, cujos sinais clínicos podem se apresentar na forma aguda, porém, normalmente são de caracter crônico.

3.1. Nos animais
A maioria das espécies de micoplasmas são de origem animal e portanto existe grande diversidade na relação parasito-hospedeiro neste campo da micoplasmologia.
Entre os animais de interesse econômico, laboratório, ou os considerados "de companhia", os micoplasmas são potenciais causadores de patologias no sistema respiratório, urogenital, glândula mamária, articulações, sistema nervoso e conjuntiva ocular. A detecção de micoplasmas em animais silvestres diferentes é crescente.
Para a avicultura, o M. gallisepticum é a espécie de maior importância econômica, em função das perdas decorrentes da Doença Crônica Respiratória (DCR). Severa aerosaculite e sinusite são as principais afecções em galinhas poedeiras, frangos de corte, perus, codornas e outras aves, levando à baixa conversão alimentar, diminuição na produção de ovos e acentuada condenação de carcaça. Outras espécies patogênicas para as aves são o M. synoviae, M. iowae e M. meleagridis.
Nos suínos, o M. hyopneumoniae é o agente da Pneumonia Enzoótica que ocorre em todas as regiões do mundo onde a suinocultura é explorada comercialmente. A doença caracteriza-se pela alta morbidade e baixa mortalidade nos rebanhos, tosse crônica não produtiva, diminuição no crescimento e baixa conversão alimentar. O M. hyorhinis e o M. hyosynoviae são habitantes comumente encontrados no trato respiratório superior dos suínos e ocasionalmente provocam poliartrite e poliserosite.
Nos bovinos, a Pleuropneumonia Contagiosa Bovina (PPCB), causada pelo M. mycoides subsp. mycoides é considerada a principal doença infecto-contagiosa do trato respiratório, caracterizada por intensa pleurite sero-fibrinosa e edema nos lóbulos e nos tecidos alveolares. A doença é considerada de notificação obrigatória e, segundo o Órgão Internacional de Epizootias (OIE), até 1997, apesar da erradicação na Europa, América do Norte e Austrália, ainda encontra-se disseminada em países da África e da Ásia. Além da PPCB, os problemas respiratórios nos bovinos são também causados pelo M. bovis e o M. dispar. Considerado a segunda espécie de maior patogenicidade entre os micoplasmas que afetam os bovinos, o M. bovis é responsável também por distúrbios reprodutivos, artrite, meningite e a mais grave e freqüente forma de mastite por micoplasmas em vários países do mundo. Outras espécies de micoplasmas estão relacionadas com a mastite, tais como o M. bovigenitalium, M. canadense, M. bovirhinis, M. californicum, M. arginini, M. alkalescens e A. laidlawii e com distúrbios reprodutivos em vacas e touros ¾ M. bovigenitalium, M. canadense e o U. diversum.
Nos pequenos ruminantes, especificamente os caprinos, a cepa de micoplasma F-38, atualmente designada M. capricolum subsp. capripneumoniae subsp. nov., é considerada o agente responsável pela Pleuropneumonia Contagiosa Caprina (PPCC). Além desta espécie, o M. mycoides subsp. mycoides, M. mycoides subsp. capri, M. agalactiae e o M. capricolum causam pneumonia e septicemia, com conseqüentes manifestações em outros órgãos ¾ mastite, poliartrite ou queratoconjuntivite. O M. agalactiae é uma espécie de considerável importância na agalactia contagiosa e na pneumonia em ovinos; o M. ovipneumoniae, em sinergismo com a Pastereulla haemolytica e outros agentes, causa a pneumonia exsudativa proliferativa.
Em animais de laboratório (ratos e camundongos), o M. pulmonis é o mais frequente, é o agente etiológico da micoplasmose respiratória murina (MRM). A morbidade e a mortalidade podem ocorrer de forma significante. No entanto, o maior impacto da infecção pelo M. pulmonis é a interferência com as interpretações de resultados, quando estes animais são utilizados na pesquisa biomédica. M. arthritidis, M. muris, M. collis e M. neurolyticum são também espécies indesejáveis em animas de laboratório.

3.2. No homem foram isoladas 16 espécies. A minoria possui interesse médico e causam principalmente infecções no trato respiratório e urogenital. Infecções não usuais ocorrem geralmente em indivíduos imunodeprimidos como a artrite séptica entre outras. As associações com outras afecções tem sido controversa. Neste contexto inclui-se: artrite reumatóide, cofator na AIDS, oncogênese, Síndrome do Golfo e Doença de Chron. Mais recentemente, encontrou-se DNA de Spiroplasmas (micoplasmas de vegetais) em tecido nervoso apresentando encefalite spongiforme. O M. pneumoniae é um patógeno primário importante, causa pneumonia e outras patologias do trato respiratório, tais como traqueíte e faringite, bem como de manifestações extra pulmonares, síndromes hematopoiéticas, do sistema nervoso central, articulações, fígado, pâncreas e coração. No trato urogenital, duas espécies de micoplasmas são implicadas como principais causadoras de infecções e distúrbios da reprodução: o Ureaplasma urealyticum, que provoca infertilidade, aborto e nascimento de crianças fracas ou prematuras e o M. genitalium, agente de uretrite não gonocócica em homens e infecções no trato genital inferior em mulheres. A etiologia de uretrites por M. hominis e U. urealyticum continua controversa, pois estas espécies, pertencem à microbiota do trato genito-urinário. As espécies M. fermentans (incognitus), M. pirum, M. hominis e M. penetrans estão sendo consideradas como patógenos humanos e possíveis cofatores na infecção pelo vírus HIV, contribuindo e acentuando os sintomas desenvolvidos na AIDS.

3.3. Nas plantas, insetos e artrópodes
Os organismos da Ordem Entomoplasmatales, além de algumas espécies de Acholeplasma, são encontrados em plantas, artrópodes e insetos, sugerindo evidências da interação parasita, vetor e hospedeiro na transmissão de doenças nas plantas. Os Spiroplasmas são freqüentemente encontrados na superfície das plantas, sendo associados a várias doenças em citrus e à doença da "planta amarela". As flores são consideradas uma rica fonte de Spiroplasmas e Acholeplasmas e, possivelmente outros micoplasmas.

3.4. Culturas celulares.
Adicionalmente, os micoplasmas são responsáveis por inoportunas e persistentes infecções em células de cultivo primário ou de linhagem. Esses organismos causam diversos efeitos citogenéticos: alterações no metabolismo, diminuição na taxa de divisão celular pela interferência na síntese de DNA, RNA e proteínas, aberrações cromossômicas e morte com desprendimento da monocamada. Além disso, podem induzir à redistribuição e modificação dos antígenos de superfície na membrana da célula hospedeira, interferindo na propagação de vírus.
As espécies mais frequentes são; M. orale, M. fermentans, A. laidlawii, M. hyorhinis e M. arginini, sendo as duas primeiras de origem humana, e as duas últimas, de origem animal. O A. laidlawii é encontrado na microbiota humana e de bovinos; o M. fermentans, apresenta-se como uma espécie emergente, devido ao uso crescente de culturas primárias de linfócitos e macrófagos de origem humana empregadas nos estudos imunológicos e virológicos. Os micoplasmas são isolados principalmente dos cultivos celulares e do soro animal. Apesar da principal fonte original ser o soro animal, o intercambio de doações de linhagens entre os institutos de pesquisa, tem sido a principal causa.
A infecção por micoplasmas em culturas celulares traz prejuízos consideráveis aos laboratórios de pesquisa e rotina, bem como às indústrias farmacológicas e biotecnológicas que utilizam-se destes sistema para a elaboração de vários produtos biológicos.
Ironicamente, dada a diversidade de efeitos dos micoplasmas nas culturas celulares, este binômio, pode ser utilizado como modelo auxiliar no esclarecimento dos fatores de patogenicidade dos micoplasmas, células e outros agentes infeciosos através de coinfecções.

4. PROCESSOS PATOGÊNICOS
Nos animais e no homem, os micoplasmas podem ser vistos aderidos intimamente às células do trato respiratório, urogenital e articulações. Esta aderência pode ser íntima a ponto de promover trocas antigênicas ou mesmo a fusão celular, mas raramente invadem os tecidos e a corrente circulatória.
A clava polar possui proteínas interativas, denominadas adesinas. No entanto a adesão de micoplasmas às células pode ocorrer mesmo na ausência da clava. Em algumas espécies verificou-se que a adesão é realizada provavelmente por sialoglicoconjugados e glicolipídios sulfatados da célula hospedeira. A presença temporária ou prolongada de micoplasmas na superfície de uma célula pode interferir de várias maneiras a sua integridade. Os micoplasmas podem provocar autoimunidade, destruir uma organização celular (i.e. epitélio brônquico mucociliar) ou mesmo não destruir a célula, mas eliminar compostos do metabolismo primário como H2O2 ou NH3, sufciente para alterar a fisiologia celular. A presença de superantígenos, lipoproteínas e a diversidade antigênica nos micoplasmas induz modulação da resposta imune. Desta maneira, justifica-se em parte, a permanência e/ou a reincidência de micoplasmoses e a disseminação de outros agentes infeciosos nos hospedeiros.
As adesinas têm sido muito bem caracterizadas em algumas espécies de micoplasmas, a exemplo da proteína P1 (168 kDa) do M. pneumoniae e a de 140 kDa do M. genitalium. Outras espécies de micoplasmas igualmente exibem proteínas de superfície responsáveis pela adesão: M. hominis, M. bovis, M. gallisepticum e M. pulmonis, enquanto que espécies de micoplasmas que não possuem tais estruturas como M. hyorhinis, M. bovigenitalium e U. urealyticum, são também capazes de realizar a cito-aderência, provavelmente por outras proteínas ou mecanismos alternativos de parasitismo.
A falta da parede celular facilita a fusão da membrana do micoplasma com a do hospedeiro e, embora evidências desta hipótese sejam discutíveis, é considerada um indicativo da interação de estruturas entre a membrana do hospedeiro e do parasita. Essa associação íntima proporciona um microambiente, no qual ocorre a concentração de produtos tóxicos excretados pelo parasita, tais como H2O2 e NH3 que se acumulam e causam danos aos tecidos do hospedeiro. Esta função é evidenciada pelo M. pneumoniae: o peróxido de hidrogênio (H2O2) e radicais superóxidos (O2-) gerados pelos micoplasmas aderidos, penetram na célula hospedeira, gradualmente provocam o acúmulo destes componentes e induzem à inibição irreversível da catalase endógena. A inibição da catalase pode causar, por conseguinte, a diminuição do superóxido dismutase. O processo se perpetua e resulta no aumento das concentrações de H2O2 e O2-, os quais induzem progressivos danos oxidativos aos constituintes vitais da célula hospedeira.
A limitação na síntese dos componentes para o metabolismo e a dependência do meio externo, somada à capacidade de interação com a célula hospedeira, sugerem que os micoplasmas necessitam utilizar os componentes do hospedeiro e transformar este mecanismo em fator de patogenicidade. Os ureaplasmas possuem fosfolipases na membrana, e possivelmente a ação direta destas enzimas nos substratos do hospedeiro produzem ácido aracdônico, diacilglicerol e lisofosfolipídios. Estas substâncias alteram a biossíntese de prostaglandinas e das funções normais da célula hospedeira. A necessidade de obtenção externa de ácidos nucléicos e proteínas para o seu metabolismo, evocam a síntese de nucleases e proteases. As nucleases de M. penetrans reduzem a atividade da transcriptase reversa do vírus HIV, bem como possuem amplo espectro de atividade em outros substratos, incluindo DNA e RNA de células eucarióticas.
Determinadas espécies de micoplasmas apresentam uma estrutura externa à membrana constituída de polissacarídios, a cápsula. O M. dispar e o M. penetrans sintetizam esta estrutura, envolvida na supressão de várias funções dos macrófagos alveolares e, conseqüentemente na imunossupressão local.
As hemolisinas são produzidas por vários micoplasmas, no entanto são poucas as evidências sobre a função direta das hemolisinas na indução de doenças. As toxinas produzidas por cepas de M. mycoides subsp. capri, demonstraram citopatogenicidade em células embrionárias da traquéia de galinhas. Endotoxinas foram demonstradas em cinco espécies de Acholeplasma e caracterizadas como lipoglicanos, moléculas complexas constituídas de vários açúcares neutros, amino açúcares, glicerol e ácidos graxos. Estas moléculas não somente demonstraram uma estrutura diferente dos lipopolissacarídios-LPS das bactérias Gram negativas, como também foram consideradas mais potentes do que o LPS de Escherichia coli..
O M. gallisepticum sintetiza diferentes substâncias solúveis neurotóxicas, provocando uma síndrome neurológica letal com lesões histopatológicas primárias nas artérias cerebrais em perus. As lesões histopatológicas se caracterizam pelo edema nos capilares cerebrais, os quais provocam oclusão vascular, resultando em fibrose necrótica. No caso do M. bovis, uma fração polissacáride foi descrita como citotóxica. Finalmente, a neurotoxina produzida pelo M. neurolyticum seletivamente altera a permeabilidade das células endoteliais dos capilares do cérebro, produzindo a clássica e fatal rolling disease em camundongos, sintomatologia nervosa típica, fazendo o animal girar ao longo do áxis do corpo e desenvolver paralisia ascendente progressiva.

5. ASPECTOS IMUNOLÓGICOS
Os micoplasmas normalmente provocam infecções crônicas ou de longa duração. Isto sugere que estas bactérias, possuem um mecanismo de escape à resposta do sistema imune do hospedeiro, seja em decorrência da variação das proteínas de superfície, ou na capacidade de provocar alterações nos constituintes imunológicos. Embora os achados histopatológicos variam de acordo com a doença e a espécie de micoplasma, a reação inflamatória crônica sempre ocorre, devido à infiltração clássica de células mononucleares nos tecidos afetados.
No trato respiratório, os micoplasmas são capazes de alterar a motilidade dos cílios ou mesmo provocar efeitos que levam à degeneração destas estruturas e das células epiteliais, ambos considerados como a primeira barreira física dos mecanismos de defesa. Os macrófagos alveolares são as principais células de defesa imunológica pulmonar contra os agentes infecciosos. As alterações funcionais destas podem levar à conseqüências adversas. Determinadas espécies de micoplasmas, incluindo M. dispar, M. bovis, M. pulmonis, M. arthritidis, M. hominis e o M. penetrans, demonstraram capacidade de provocar efeitos supressores nos macrófagos alveolares, inibindo as atividades de fagocitose..
Demonstrou-se que o LPS da cápsula de algumas espécies de micoplasmas, seja o responsável pelos efeitos supressores da fagocitose e lise dos micoplasmas e outras bactérias. O LPS interfere no Fator de Necrose Tumoral (TNF-a ), na produção de interleucinas (IL-1, IL-6), estimula resposta imune primária timo independente e permite a ocorrência de infecções crônicas pela dificuldade de eliminar os micoplasmas e outros microrganismos.
Espécies como M. bovis, M. hominis e M. pulmonis, podem rapidamente alterar a expressão e a estrutura das suas proteínas de superfície, contribuindo na cronicidade das micoplasmoses. A variação antigênica justifica em parte a dificuldade de obtenção de vacinas eficazes contra algumas espécies de micoplasmas.
Outras espécies como M. arthritidis, M. fermentans, M. capricolum e o U. diversum, são mitogênicos para linfócitos de camundongos, induzindo blastogênese e produção de citocinas. A capacidade destas espécies em induzir um largo espectro de eventos imuno-moduladores como a produção de citocinas e interferência nos macrófagos, linfócitos B e T e células glias, evidencia os atributos de mediadores primários nos processos patogênicos.
Nos últimos anos, várias espécies de micoplasmas, tais como M. fermentans, M. penetrans e M. pirum e M. hominis foram isoladas de indivíduos infectados pelo HIV e implicadas como cofatores na progressão da AIDS nos pacientes. Os mecanismos envolvidos incluem a ativação do sistema imune, produção de super antígenos que estimulam a liberação de várias citocinas imuno-moduladoras ou a produção de radicais livres que contribuem para o estresse oxidativo observado nas infecções pelo HIV.
Recentemente, com a aplicação das técnicas da biologia molecular, algumas possíveis respostas foram sugeridas para o esclarecimento destes mecanismos. O fenômeno de mimetismo molecular é especialmente interessante, desde que as adesinas dos micoplasmas, ricas em prolinas, demonstraram homologia nas seqüências de aminoácidos com as proteínas da classe II do Complexo de Histocompatibilidade Principal dos linfócitos CD4 humanos, os quais podem gerar anticorpos autoreativos e desencadear morte celular e imunossupressão. O M. fermentans, detectado no sangue e na urina de pacientes aidéticos, por sua vez, apresentou capacidade de sinergismo com o HIV, acentuando os efeitos citopáticos dos linfócitos CD4 e estimulando outras atividades imunomoduladoras. Os micoplasmas podem atuar como mitógenos de linfócitos T e B e induzirem doenças auto-imunes pela ativação de linfócitos policlonais anti-T e anti-B.
As propriedades biológicas dos micoplasmas, a sua capacidade de provocar alterações nas células, bem como as características singulares de parasitismo e interação, evidenciam o caracter complexo e singular destes organismos como potenciais patógenos, desafiando de modo diferenciado, a homeostasia do hospedeiro.

Extracted from Nexus Magazine, Volume 8, Number 5 (August-September 2001)
PO Box 30, Mapleton Qld 4560 Australia. editor@nexusmagazine.com
Telephone: +61 (0)7 5442 9280; Fax: +61 (0)7 5442 9381
From our web page at: www.nexusmagazine.com

© by Donald W. Scott, MA, MSc © 2001
President
The Common Cause
Medical Research Foundation
190 Mountain Street, Suite 405
Sudbury, Ontario, Canada P3B 4G2
Tel/fax: +1 (705) 670 0180

PATHOGENIC MYCOPLASMA

A Common Disease Agent Weaponised

There are 200 species of Mycoplasma. Most are innocuous and do no harm; only four or five are pathogenic. Mycoplasma fermentans (incognitus strain) probably comes from the nucleus of the Brucella bacterium. This disease agent is not a bacterium and not a virus; it is a mutated form of the Brucella bacterium, combined with a visna virus, from which the mycoplasma is extracted.

The pathogenic Mycoplasma used to be very innocuous, but biological warfare research conducted between 1942 and the present time has resulted in the creation of more deadly and infectious forms of Mycoplasma. Researchers extracted this mycoplasma from the Brucella bacterium and actually reduced the disease to a crystalline form. They "weaponised" it and tested it on an unsuspecting public in North America.

Dr Maurice Hilleman, chief virologist for the pharmaceutical company Merck Sharp & Dohme, stated that this disease agent is now carried by everybody in North America and possibly most people throughout the world.

Despite reporting flaws, there has clearly been an increased incidence of all the neuro/systemic degenerative diseases since World War II and especially since the 1970s with the arrival of previously unheard-of diseases like chronic fatigue syndrome and AIDS.

According to Dr Shyh-Ching Lo, senior researcher at The Armed Forces Institute of Pathology and one of America's top mycoplasma researchers, this disease agent causes many illnesses including AIDS, cancer, chronic fatigue syndrome, Crohn's colitis, Type I diabetes, multiple sclerosis, Parkinson's disease, Wegener's disease and collagen-vascular diseases such as rheumatoid arthritis and Alzheimer's.

Dr Charles Engel, who is with the US National Institutes of Health, Bethesda, Maryland, stated the following at an NIH meeting on February 7, 2000: "I am now of the view that the probable cause of chronic fatigue syndrome and fibromyalgia is the mycoplasma..."

I have all the official documents to prove that mycoplasma is the disease agent in chronic fatigue syndrome/fibromyalgia as well as in AIDS, multiple sclerosis and many other illnesses. Of these, 80% are US or Canadian official government documents, and 20% are articles from peer-reviewed journals such as the Journal of the American Medical Association, New England Journal of Medicine and the Canadian Medical Association Journal. The journal articles and government documents complement each other.
 

How the Mycoplasma Works

The mycoplasma acts by entering into the individual cells of the body, depending upon your genetic predisposition.

You may develop neurological diseases if the pathogen destroys certain cells in your brain, or you may develop Crohn's colitis if the pathogen invades and destroys cells in the lower bowel.

Once the mycoplasma gets into the cell, it can lie there doing nothing sometimes for 10, 20 or 30 years, but if a trauma occurs like an accident or a vaccination that doesn't take, the mycoplasma can become triggered.

Because it is only the DNA particle of the bacterium, it doesn't have any organelles to process its own nutrients, so it grows by uptaking pre-formed sterols from its host cell and it literally kills the cell; the cell ruptures and what is left gets dumped into the bloodstream.

II &endash; CREATION OF THE MYCOPLASMA

A Laboratory-Made Disease Agent

Many doctors don't know about this mycoplasma disease agent because it was developed by the US military in biological warfare experimentation and it was not made public. This pathogen was patented by the United States military and Dr Shyh-Ching Lo. I have a copy of the documented patent from the US Patent Office.1

All the countries at war were experimenting with biological weapons. In 1942, the governments of the United States, Canada and Britain entered into a secret agreement to create two types of biological weapons (one that would kill, and one that was disabling) for use in the war against Germany and Japan, who were also developing biological weapons. While they researched a number of disease pathogens, they primarily focused on the Brucella bacterium and began to weaponise it.

From its inception, the biowarfare program was characterised by continuing in-depth review and participation by the most eminent scientists, medical consultants, industrial experts and government officials, and it was classified Top Secret.

The US Public Health Service also closely followed the progress of biological warfare research and development from the very start of the program, and the Centers for Disease Control (CDC) and the National Institutes of Health (NIH) in the United States were working with the military in weaponising these diseases. These are diseases that have existed for thousands of years, but they have been weaponised--which means they've been made more contagious and more effective. And they are spreading.

The Special Virus Cancer Program, created by the CIA and NIH to develop a deadly pathogen for which humanity had no natural immunity (AIDS), was disguised as a war on cancer but was actually part of MKNAOMI.2 Many members of the Senate and House of Representatives do not know what has been going on. For example, the US Senate Committee on Government Reform had searched the archives in Washington and other places for the document titled "The Special Virus Cancer Program: Progress Report No. 8", and couldn't find it. Somehow they heard I had it, called me and asked me to mail it to them. Imagine: a retired schoolteacher being called by the United States Senate and asked for one of their secret documents! The US Senate, through the Government Reform Committee, is trying to stop this type of government research.

Crystalline Brucella

The title page of a genuine US Senate Study, declassified on February 24, 1977, shows that George Merck, of the pharmaceutical company, Merck Sharp & Dohme (which now makes cures for diseases that at one time it created), reported in 1946 to the US Secretary of War that his researchers had managed "for the first time" to "isolate the disease agent in crystalline form".3

They had produced a crystalline bacterial toxin extracted from the Brucella bacterium. The bacterial toxin could be removed in crystalline form and stored, transported and deployed without deteriorating. It could be delivered by other vectors such as insects, aerosol or the food chain (in nature it is delivered within the bacterium). But the factor that is working in the Brucella is the mycoplasma.

Brucella is a disease agent that doesn't kill people; it disables them. But, according to Dr Donald MacArthur of the Pentagon, appearing before a congressional committee in 1969,4 researchers found that if they had mycoplasma at a certain strength--actually, 10 to the 10th power (1010)--it would develop into AIDS, and the person would die from it within a reasonable period of time because it could bypass the natural human defences. If the strength was 108, the person would manifest with chronic fatigue syndrome or fibromyalgia. If it was 107, they would present as wasting; they wouldn't die and they wouldn't be disabled, but they would not be very interested in life; they would waste away.

Most of us have never heard of the disease brucellosis because it largely disappeared when they began pasteurising milk, which was the carrier. One salt shaker of the pure disease agent in a crystalline form could sicken the entire population of Canada. It is absolutely deadly, not so much in terms of killing the body but disabling it.

Because the crystalline disease agent goes into solution in the blood, ordinary blood and tissue tests will not reveal its presence. The mycoplasma will only crystallise at 8.1 pH, and the blood has a pH of 7.4 pH. So the doctor thinks your complaint is "all in your head".

Crystalline Brucella and Multiple Sclerosis

In 1998 in Rochester, New York, I met a former military man, PFC Donald Bentley, who gave me a document and told me: "I was in the US Army, and I was trained in bacteriological warfare. We were handling a bomb filled with brucellosis, only it wasn't brucellosis; it was a Brucella toxin in crystalline form. We were spraying it on the Chinese and North Koreans."

He showed me his certificate listing his training in chemical, biological and radiological warfare. Then he showed me 16 pages of documents given to him by the US military when he was discharged from the service. They linked brucellosis with multiple sclerosis, and stated in one section: "Veterans with multiple sclerosis, a kind of creeping paralysis developing to a degree of 10% or more disability within two years after separation from active service, may be presumed to be service-connected for disability compensation. Compensation is payable to eligible veterans whose disabilities are due to service." In other words: "If you become ill with multiple sclerosis, it is because you were handling this Brucella, and we will give you a pension. Don't go raising any fuss about it." In these documents, the government of the United States revealed evidence of the cause of multiple sclerosis, but they didn't make it known to the public--or to your doctor.

In a 1949 report, Drs Kyger and Haden suggested "the possibility that multiple sclerosis might be a central nervous system manifestation of chronic brucellosis". Testing approximately 113 MS patients, they found that almost 95% also tested positive for Brucella.5 We have a document from a medical journal, which concludes that one out of 500 people who had brucellosis would develop what they call neurobrucellosis; in other words, brucellosis in the brain, where the Brucella settles in the lateral ventricles--where the disease multiple sclerosis is basically located.6

Contamination of Camp Detrick Lab Workers

A 1948 New England Journal of Medicine report titled "Acute Brucellosis Among Laboratory Workers" shows us how actively dangerous this agent is.7 The laboratory workers were from Camp Detrick, Frederick, Maryland, where they were developing biological weapons. Even though these workers had been vaccinated, wore rubberised suits and masks and worked through holes in the compartment, many of them came down with this awful disease because it is so absolutely and terrifyingly infectious.

The article was written by Lt Calderone Howell, Marine Corps, Captain Edward Miller, Marine Corps, Lt Emily Kelly, United States Naval Reserve, and Captain Henry Bookman. They were all military personnel engaged in making the disease agent Brucella into a more effective biological weapon.

III &endash; COVERT TESTING OF MYCOPLASMA

Testing the Dispersal Methods

Documented evidence proves that the biological weapons they were developing were tested on the public in various communities without their knowledge or consent.

The government knew that crystalline Brucella would cause disease in humans. Now they needed to determine how it would spread and the best way to disperse it. They tested dispersal methods for Brucella suis and Brucella melitensis at Dugway Proving Ground, Utah, in June and September 1952. Probably, 100% of us now are infected with Brucella suis and Brucella melitensis.8

Another government document recommended the genesis of open-air vulnerability tests and covert research and development programs to be conducted by the Army and supported by the Central Intelligence Agency.

At that time, the Government of Canada was asked by the US Government to cooperate in testing weaponised Brucella, and Canada cooperated fully with the United States. The US Government wanted to determine whether mosquitoes would carry the disease and also if the air would carry it. A government report stated that "open-air testing of infectious biological agents is considered essential to an ultimate understanding of biological warfare potentialities because of the many unknown factors affecting the degradation of micro-organisms in the atmosphere".9

Testing via Mosquito Vector in Punta Gorda, Florida

A report from The New England Journal of Medicine reveals that one of the first outbreaks of chronic fatigue syndrome was in Punta Gorda, Florida, back in 1957.10 It was a strange coincidence that a week before these people came down with chronic fatigue syndrome, there was a huge influx of mosquitoes.

The National Institutes of Health claimed that the mosquitoes came from a forest fire 30 miles away. The truth is that those mosquitoes were infected in Canada by Dr Guilford B. Reed at Queen's University. They were bred in Belleville, Ontario, and taken down to Punta Gorda and released there.

Within a week, the first five cases ever of chronic fatigue syndrome were reported to the local clinic in Punta Gorda. The cases kept coming until finally 450 people were ill with the disease.

Testing via Mosquito Vector in Ontario

The Government of Canada had established the Dominion Parasite Laboratory in Belleville, Ontario, where it raised 100 million mosquitoes a month. These were shipped to Queen's University and certain other facilities to be infected with this crystalline disease agent. The mosquitoes were then let loose in certain communities in the middle of the night, so that the researchers could determine how many people would become ill with chronic fatigue syndrome or fibromyalgia, which was the first disease to show.

One of the communities they tested it on was the St Lawrence Seaway valley, all the way from Kingston to Cornwall, in 1984. They let out hundreds of millions of infected mosquitoes. Over 700 people in the next four or five weeks developed myalgic encephalomyelitis, or chronic fatigue syndrome.

IV &endash; COVERT TESTING OF OTHER DISEASE AGENTS

Mad Cow Disease/Kuru/CJD in the Fore Tribe

Before and during World War II, at the infamous Camp 731 in Manchuria, the Japanese military contaminated prisoners of war with certain disease agents.

They also established a research camp in New Guinea in 1942. There they experimented upon the Fore Indian tribe and inoculated them with a minced-up version of the brains of diseased sheep containing the visna virus which causes "mad cow disease" or Creutzfeldt&endash;Jakob disease.

About five or six years later, after the Japanese had been driven out, the poor people of the Fore tribe developed what they called kuru, which was their word for "wasting", and they began to shake, lose their appetites and die. The autopsies revealed that their brains had literally turned to mush. They had contracted "mad cow disease" from the Japanese experiments.

When World War II ended, Dr Ishii Shiro--the medical doctor who was commissioned as a General in the Japanese Army so he could take command of Japan's biological warfare development, testing and deployment--was captured. He was given the choice of a job with the United States Army or execution as a war criminal. Not surprisingly, Dr Ishii Shiro chose to work with the US military to demonstrate how the Japanese had created mad cow disease in the Fore Indian tribe.

In 1957, when the disease was beginning to blossom in full among the Fore people, Dr Carleton Gajdusek of the US National Institutes of Health headed to New Guinea to determine how the minced-up brains of the visna-infected sheep affected them. He spent a couple of years there, studying the Fore people, and wrote an extensive report. He won the Nobel Prize for "discovering" kuru disease in the Fore tribe.

Testing Carcinogens over Winnipeg, Manitoba

In 1953, the US Government asked the Canadian Government if it could test a chemical over the city of Winnipeg. It was a big city with 500,000 people, miles from anywhere. The American military sprayed this carcinogenic chemical in a 1,000%-attenuated form, which they said would be so watered down that nobody would get very sick; however, if people came to clinics with a sniffle, a sore throat or ringing in their ears, the researchers would be able to determine what percentage would have developed cancer if the chemical had been used at full strength.

We located evidence that the Americans had indeed tested this carcinogenic chemical--zinc cadmium sulphide--over Winnipeg in 1953. We wrote to the Government of Canada, explaining that we had solid evidence of the spraying and asking that we be informed as to how high up in the government the request for permission to spray had gone. We did not receive a reply.

Shortly after, the Pentagon held a press conference on May 14, 1997, where they admitted what they had done. Robert Russo, writing for the Toronto Star11 from Washington, DC, reported the Pentagon's admission that in 1953 it had obtained permission from the Canadian Government to fly over the city of Winnipeg and spray out this chemical--which sifted down on kids going to school, housewives hanging out their laundry and people going to work. US Army planes and trucks released the chemical 36 times between July and August 1953. The Pentagon got its statistics, which indicated that if the chemical released had been full strength, approximately a third of the population of Winnipeg would have developed cancers over the next five years.

One professor, Dr Hugh Fudenberg, MD, twice nominated for the Nobel Prize, wrote a magazine article stating that the Pentagon came clean on this because two researchers in Sudbury, Ontario--Don Scott and his son, Bill Scott--had been revealing this to the public. However, the legwork was done by other researchers!

The US Army actually conducted a series of simulated germ warfare tests over Winnipeg. The Pentagon lied about the tests to the mayor, saying that they were testing a chemical fog over the city, which would protect Winnipeg in the event of a nuclear attack.

A report commissioned by US Congress, chaired by Dr Rogene Henderson, lists 32 American towns and cities used as test sites as well.

V &endash; BRUCELLA MYCOPLASMA AND DISEASE

AIDS

The AIDS pathogen was created out of a Brucella bacterium mutated with a visna virus; then the toxin was removed as a DNA particle called a mycoplasma. They used the same mycoplasma to develop disabling diseases like MS, Crohn's colitis, Lyme disease, etc.

In the previously mentioned US congressional document of a meeting held on June 9, 1969,12 the Pentagon delivered a report to Congress about biological weapons. The Pentagon stated: "We are continuing to develop disabling weapons." Dr MacArthur, who was in charge of the research, said: "We are developing a new lethal weapon, a synthetic biological agent that does not naturally exist, and for which no natural immunity could have been acquired."

Think about it. If you have a deficiency of acquired immunity, you have an acquired immunity deficiency. Plain as that. AIDS.

In laboratories throughout the United States and in a certain number in Canada including at the University of Alberta, the US Government provided the leadership for the development of AIDS for the purpose of population control. After the scientists had perfected it, the government sent medical teams from the Centers for Disease Control--under the direction of Dr Donald A. Henderson, their investigator into the 1957 chronic fatigue epidemic in Punta Gorda--during 1969 to 1971 to Africa and some countries such as India, Nepal and Pakistan where they thought the population was becoming too large.13 They gave them all a free vaccination against smallpox; but five years after receiving this vaccination, 60% of those inoculated were suffering from AIDS. They tried to blame it on a monkey, which is nonsense.

A professor at the University of Arkansas made the claim that while studying the tissues of a dead chimpanzee she found traces of HIV. The chimpanzee that she had tested was born in the United States 23 years earlier. It had lived its entire life in a US military laboratory where it was used as an experimental animal in the development of these diseases. When it died, its body was shipped to a storage place where it was deep-frozen and stored in case they wanted to analyse it later. Then they decided that they didn't have enough space for it, so they said, "Anybody want this dead chimpanzee?" and this researcher from Arkansas said: "Yes. Send it down to the University of Arkansas. We are happy to get anything that we can get." They shipped it down and she found HIV in it. That virus was acquired by that chimpanzee in the laboratories where it was tested.14

Chronic Fatigue Syndrome/ Myalgic Encephalomyelitis

Chronic fatigue syndrome is more accurately called myalgic encephalomyelitis. The chronic fatigue syndrome nomenclature was given by the US National Institutes of Health because it wanted to downgrade and belittle the disease.

An MRI scan of the brain of a teenage girl with chronic fatigue syndrome displayed a great many scars or punctate lesions in the left frontal lobe area where portions of the brain had literally dissolved and been replaced by scar tissue. This caused cognitive impairment, memory impairment, etc. And what was the cause of the scarring? The mycoplasma. So there is very concrete physical evidence of these tragic diseases, even though doctors continue to say they don't know where it comes from or what they can do about it.

Many people with chronic fatigue syndrome, myalgic encephalo-myelitis and fibromyalgia who apply to the Canada Pensions Plan Review Tribunal will be turned down because they cannot prove that they are ill. During 1999 I conducted several appeals to Canada Pensions and the Workers Compensation Board (WCB, now the Workplace Safety and Insurance Board) on behalf of people who have been turned down. I provided documented evidence of these illnesses, and these people were all granted their pensions on the basis of the evidence that I provided.

In March 1999, for example, I appealed to the WCB on behalf of a lady with fibromyalgia who had been denied her pension back in 1993. The vice-chairman of the board came to Sudbury to hear the appeal, and I showed him a number of documents which proved that this lady was physically ill with fibromyalgia. It was a disease that caused physical damage, and the disease agent was a mycoplasma. The guy listened for three hours, and then he said to me: "Mr Scott, how is it I have never heard of any of this before? I said: "We brought a top authority in this area into Sudbury to speak on this subject and not a single solitary doctor came to that presentation."

VI &endash; TESTING FOR MYCOPLASMA IN YOUR BODY

Polymerase Chain Reaction Test

Information is not generally available about this agent because, first of all, the mycoplasma is such a minutely small disease agent. A hundred years ago, certain medical theoreticians conceived that there must be a form of disease agent smaller than bacteria and viruses. This pathogenic organism, the mycoplasma, is so minute that normal blood and tissue tests will not reveal its presence as the source of the disease.

Your doctor may diagnose you with Alzheimer's disease, and he will say: "Golly, we don't know where Alzheimer's comes from. All we know is that your brain begins to deteriorate, cells rupture, the myelin sheath around the nerves dissolves, and so on." Or if you have chronic fatigue syndrome, the doctor will not be able to find any cause for your illness with ordinary blood and tissue tests.

This mycoplasma couldn't be detected until about 30 years ago when the polymerase chain reaction (PCR) test was developed, in which a sample of your blood is examined and damaged particles are removed and subjected to a polymerase chain reaction. This causes the DNA in the particles to break down. The particles are then placed in a nutrient, which causes the DNA to grow back into its original form. If enough of the substance is produced, the form can be recognised, so it can be determined whether Brucella or another kind of agent is behind that particular mycoplasma.

Blood Test

If you or anybody in your family has myalgic encephalomyelitis, fibromyalgia, multiple sclerosis or Alzheimer's, you can send a blood sample to Dr Les Simpson in New Zealand for testing.

If you are ill with these diseases, your red blood cells will not be normal doughnut-shaped blood cells capable of being compressed and squeezed through the capillaries, but will swell up like cherry-filled doughnuts which cannot be compressed. The blood cells become enlarged and distended because the only way the mycoplasma can exist is by uptaking pre-formed sterols from the host cell. One of the best sources of pre-formed sterols is cholesterol, and cholesterol is what gives your blood cells flexibility. If the cholesterol is taken out by the mycoplasma, the red blood cell swells up and doesn't go through, and the person begins to feel all the aches and pains and all the damage it causes to the brain, the heart, the stomach, the feet and the whole body because blood and oxygen are cut off.

And that is why people with fibromyalgia and chronic fatigue syndrome have such a terrible time. When the blood is cut off from the brain, punctate lesions appear because those parts of the brain die. The mycoplasma will get into portions of the heart muscle, especially the left ventricle, and those cells will die. Certain people have cells in the lateral ventricles of the brain that have a genetic predisposition to admit the mycoplasma, and this causes the lateral ventricles to deteriorate and die. This leads to multiple sclerosis, which will progress until these people are totally disabled; frequently, they die prematurely. The mycoplasma will get into the lower bowel, parts of which will die, thus causing colitis. All of these diseases are caused by the degenerating properties of the mycoplasma.

In early 2000, a gentleman in Sudbury phoned me and told me he had fibromyalgia. He applied for a pension and was turned down because his doctor said it was all in his head and there was no external evidence. I gave him the proper form and a vial, and he sent his blood to Dr Simpson to be tested. He did this with his family doctor's approval, and the results from Dr Simpson showed that only 4% of his red blood cells were functioning normally and carrying the appropriate amount of oxygen to his poor body, whereas 83% were distended, enlarged and hardened, and wouldn't go through the capillaries without an awful lot of pressure and trouble. This is the physical evidence of the damage that is done.

ECG Test

You can also ask your doctor to give you a 24-hour Holter ECG. You know, of course, that an electrocardiogram is a measure of your heartbeat and shows what is going on in the right ventricle, the left ventricle and so on. Tests show that 100% of patients with chronic fatigue syndrome and fibromyalgia have an irregular heartbeat. At various periods during the 24 hours, the heart, instead of working happily away going "bump-BUMP, bump-BUMP", every now and again goes "buhbuhbuhbuhbuhbuhbuhbuhbuh". The T-wave (the waves are called P, Q, R, S and T) is normally a peak, and then the wave levels off and starts with the P-wave again. In chronic fatigue and fibromyalgia patients, the T-wave flattens off, or actually inverts. That means the blood in the left ventricle is not being squeezed up through the aorta and around through the body.

My client from Sudbury had this test done and, lo and behold, the results stated: "The shape of T and S-T suggests left ventricle strain pattern, although voltage and so on is normal." The doctor had no clue as to why the T-wave was not working properly. I analysed the report of this patient who had been turned down by Canada Pensions and sent it back to them. They wrote back, saying: "It looks like we may have made a mistake. We are going to give you a hearing and you can explain this to us in more detail."

So it is not all in your imagination. There is actual physical damage to the heart. The left ventricle muscles do show scarring. That is why many people are diagnosed with a heart condition when they first develop fibromyalgia, but it's only one of several problems because the mycoplasma can do all kinds of damage.

Blood Volume Test

You can also ask your doctor for a blood volume test. Every human being requires a certain amount of blood per pound of body weight, and it has been observed that people with fibromyalgia, chronic fatigue syndrome, multiple sclerosis and other illnesses do not have the normal blood volume their body needs to function properly. Doctors aren't normally aware of this.

This test measures the amount of blood in the human body by taking out 5 cc, putting a tracer in it and then putting it back into the body. One hour later, take out 5 cc again and look for the tracer. The thicker the blood and the lower the blood volume, the more tracer you will find.

The analysis of one of my clients stated: "This patient was referred for red cell mass study. The red cell volume is 16.9 ml per kg of body weight. The normal range is 25 to 35 ml per kg. This guy has 36% less blood in his body than the body needs to function." And the doctor hadn't even known the test existed.

If you lost 36% of your blood in an accident, do you think your doctor would tell you that you are alright and should just take up line dancing and get over it? They would rush you to the nearest hospital and start transfusing you with blood. These tragic people with these awful diseases are functioning with anywhere from 7% to 50% less blood than their body needs to function.

VII &endash; UNDOING THE DAMAGE

The body undoes the damage itself. The scarring in the brain of people with chronic fatigue and fibromyalgia will be repaired. There is cellular repair going on all the time. But the mycoplasma has moved on to the next cell.

In the early stages of a disease, doxycycline may reverse that disease process. It is one of the tetracycline antibiotics, but it is not bactericidal; it is bacteriostatic--it stops the growth of the mycoplasma. And if the mycoplasma growth can be stopped for long enough, then the immune system takes over.

Doxycycline treatment is discussed in a paper by mycoplasma expert Professor Garth Nicholson, PhD, of the Institute for Molecular Medicine.15 Dr Nicholson is involved in a US$8-million mycoplasma research program funded by the US military and headed by Dr Charles Engel of the NIH. The program is studying Gulf War veterans, 450 of them, because there is evidence to suggest that Gulf War syndrome is another illness (or set of illnesses) caused by mycoplasma.

Endnotes:
1. "Pathogenic Mycoplasma", US Patent No. 5,242,820, issued September 7, 1993. Dr Lo is listed as the "Inventor" and the American Registry of Pathology, Washington, DC, is listed as the "Assignee".
2. "Special Virus Cancer Program: Progress Report No. 8", prepared by the National Cancer Institute, Viral Oncology, Etiology Area, July 1971, submitted to NIH Annual Report in May 1971 and updated July 1971.
3. US Senate, Ninety-fifth Congress, Hearings before the Subcommittee on Health and Scientific Research of the Committee on Human Resources, Biological Testing Involving Human Subjects by the Department of Defense, 1977; released as US Army Activities in the US Biological Warfare Programs, Volumes One and Two, 24 February 1977.
4. Dr Donald MacArthur, Pentagon, Department of Defense Appropriations for 1970, Hearings before Subcommittee of the Committee on Appropriations, House of Representatives, Ninety-First Congress, First Session, Monday June 9, 1969, pp 105&endash;144, esp. pp. 114, 129.
5. Kyger, E. R. and Russell L. Haden, "Brucellosis and Multiple Sclerosis", The American Journal of Medical Sciences 1949:689-693.
6. Colmonero et al., "Complications Associated with Brucella melitensis Infection: A Study of 530 Cases", Medicine 1996;75(4).
7. Howell, Miller, Kelly and Bookman, "Acute Brucellosis Among Laboratory Workers", New England Journal of Medicine 1948;236:741.
8. "Special Virus Cancer Program: Progress Report No. 8", ibid., table 4, p. 135.
9. US Senate, Hearings before the Subcommittee on Health and Scientific Research of the Committee on Human Resources, March 8 and May 23, 1977, ibid.
10. New England Journal of Medicine, August 22, 1957, p. 362.
11. Toronto Star, May 15, 1997.
12. Dr Donald MacArthur, Pentagon, Department of Defense Appropriations for 1970, Hearings, Monday June 9, 1969, ibid., p. 129.
13. Henderson, Donald A., "Smallpox: Epitaph for a Killer", National Geographic, December 1978, p. 804.
14. Blum, Deborah, The Monkey Wars, Oxford University Press, New York, 1994.
15. Nicholson, G. L., "Doxycycline treatment and Desert Storm", JAMA 1995;273:618-619.

Recommended Reading:
¥ Horowitz, Leonard, Emerging Viruses: Aids and Ebola, Tetrahedron Publishing, USA, 1996.
¥ Johnson, Hillary, Osler's Web, Crown Publishers, New York, 1996.
¥ Scott, Donald W. and William L. C. Scott, The Brucellosis Triangle, The Chelmsford Publishers (Box 133, Stat. B., Sudbury, Ontario P3E 4N5), Canada, 1998 (US$21.95 + $3 s&h in US).
¥ Scott, Donald W. and William L. C. Scott, The Extremely Unfortunate Skull Valley Incident, The Chelmsford Publishers, Canada, 1996 (revised, extended edition available from mid-September 2001; US$16.00 pre-pub. price + US$3 s&h in US).
¥ The Journal of Degenerative Diseases (Donald W. Scott, Editor), The Common Cause Medical Research Foundation (Box 133, Stat B., Sudbury, Ontario, P3E 4N5), Canada (quarterly journal; annual subscription: US$25.00 in USA, $30 foreign).

Additional Contacts:
¥ Ms Jennie Burke, Australian Biologics, Level 6, 383 Pitt Street, Sydney NSW 2000, Australia tel +61 (0)2 9283 0807, fax +61 (0)2 9283 0910. Australian Biologics does tests for mycoplasma.

¥ Consumer Health Organization of Canada, 1220 Sheppard Avenue East #412, Toronto, Ontario, Canada M2K 2S5, tel +1 (416) 490 0986, website www.consumerhealth.org/.

¥ Professor Garth Nicholson, PhD, Institute for Molecular Medicine, 15162 Triton Lane, Huntington Beach, CA, 92649-1401, USA, tel +1 (714) 903 2900.

¥ Dr Les Simpson, Red Blood Cell Research Ltd, 31 Bath Street, Dunedin, 9001, New Zealand, tel +64 (0)3 471 8540, email rbc.research.limited@xtra.co.nz. (Note: Dr Simpson directs his study to red cell shape analysis, not the mycoplasma hypothesis.)

¥ The Mycoplasma Registry for Gulf War Illness, S. & L. Dudley, 303 47th St, J-10 San Diego, CA 92102-5961, tel/fax +1 (619) 266 1116, fax (619) 266 1116, email mycoreg@juno.com.

About the Author:
Donald Scott, MA, MSc, is a retired high school teacher and university professor. He is also a veteran of WWII and was awarded the North Atlantic Star, the Burma Star with Clasp, the 1939&endash;1945 Volunteer Service Medal and the Victory Medal. He is currently President of The Common Cause Medical Research Foundation, a not-for-profit organisation devoted to research into neurosystemic degenerative diseases. He is also Adjunct Professor with the Institute for Molecular Medicine and he produces and edits the Journal of Degenerative Diseases. He has extensively researched neurosystemic degenerative diseases over the past five years and has authored many documents on the relationship between degenerative diseases and a pathogenic mycoplasma called Mycoplasma fermentans. His research is based upon solid government evidence.

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