Harold Clark Memorial Web Page


Internationally known Harold Clark, PhD (1922-2007) specialized in the study of mycoplasmas and their pathogenic/immune system interactions with their hosts. He was the author of the 1997 book Why Arthritis?, reviewed at the Arthritis Trust website. See Amazon's Book Listing. Graduated from College of Wooster (`46); married Bonnie Greer (`46); earned a PhD from University of Rochester School of Medicine (‘53); worked at George Washington University in Washington, D.C. (`52-`70) as associate research professor of medicine and research director of the Medical Rehabilitation Center.

In 1970 Dr. Clark joined the newly established Arthritis Institute of National Orthopedic Hospital, Arlington, VA, as research director and vice chair with Dr. Thomas McPherson Brown. He retired in 1987 and established the Mycoplasma Research Institute in Florida, publishing technical papers on mycoplasmas, antibiotic antimicrobial protocols, and the causes of rheumatic illnesses. His professional memberships included the International Organization for Mycoplasmologists, the American Society for Microbiology, and the American Association for the Advancement of Science.

Dr. Clark studied and worked for more than 45 years, investigating and documenting the role and biochemical mechanisms of mycoplasma bacteria as a cause of rheumatoid autoimmune diseases. He published more than 65 papers detailing evidence of the infectious pathogenicity, the cellular affinities, and the antibiotic suppression of these cell wall deficient (CWD) microbes. He presented his scientific findings in the U.S. and abroad in Australia, Canada, Brazil, Egypt, France, Germany, Japan, Mexico, Peru, the Philippines, and Scotland.

For many years (1952-1987) Dr. Clark worked with Dr. Thomas McPherson Brown as his lab manager.  In 1939, Dr. Brown, with Doctors Homer Swift and Albert Sabin at the Rockefeller Institute Medical Research Hospital, published their findings, proving that pleuropneumonia-like organism (PPLO) microbes cause arthritis in mice. See the March 1939 NY Times Science Article announcing that arthritis is caused by a PPLO (a.k.a. Eaton Agent, a.k.a. Mycoplasma pneumoniae) citing Science, Vol. 89, No. 2308. March 24, 1939. After joining Dr. Brown at George Washington University, Dr. Clark was to spend the rest of his life working to study how PPLO mycoplasmas cause and aggravate autoimmune/rheumatic diseases. He became a world-renowned expert in his chosen field.

When Dr. Thomas McPherson Brown, with Dr. Clark’s help, challenged the rheumatologists’ short-term cortisone cure, as a long-term failure, they became the enemy, much like Wyburn-Mason (founder of the Arthritis Trust) did after he published his infectious theory and his antibiotic therapy in 1978.  From that time forward, the National Institutes of Health (NIH) research establishment successfully obstructed the public’s efforts to get government study funds to support the nation’s most successful privately established center of excellence in arthritis treatment that Doctors Brown and Clark had established in Arlington, VA, across the river from the impressive NIH facilities being built and expanded in Bethesda, MD, using public research funding.

Activist patients among the tens of thousands of Dr. Brown’s grateful patients lobbied for federal funds to conduct a study, Minocycline in Rheumatoid Arthritis (MIRA), to test the already proven successful long-term antibiotic protocol for Rheumatoid Arthritis (RA). Funds were appropriated; the study was reluctantly conducted in a short term, using a partly defective design; results were published in 1995. It did prove the tetracycline-based protocol was successful in improving the symptoms, but only to a small degree above conventional anti-inflammation, symptomatic treatments for a too-short period of treatment.  Proving remarkable long term-improvements in active condition and even remissions were not part of these tests.

Short-term improvement itself is remarkable, considering that the most serious RA cases of infection often have a strong Herxheimer inflammation flare at the start of antibiotic treatment, and one must also use anti-inflammatory drugs to get past the initial microbe kill-off and the resulting flood of toxins. Following the Herx die-off, long-term, antibiotics gradually eliminate the microbes, leading to remission of many autoimmune RA symptoms.  Seriously infected patients always have a period of getting worse under intravenous (IV) antibiotics in order to achieve a long-term cure.

What the competing research teams ignored was that for many longer-term cases, the conventional anti-inflammatory-only treatments usually failed, leading to a painful death, while the Brown/Clark long-term, low dose antibiotic treatments led to remission and a long productive life. 

Requests were made to the NIH to study the MIRA antibiotic protocols over longer periods. Long-term treatment successes were already proven by many case histories to work quite well. Despite thousands of personal requests to the Congress, the appeals were denied and the statisticians won; the future patients lost. In retrospect, it appears that medical politics, obstructive gatekeepers, bureaucrats, and shortsighted, less-competent consensus had suppressed the successful maverick practitioners, yet again.

Culture of the Mycoplasmae and other CWD organisms is quite hard, due to the fastidious nature of the microbe. Mice given the PPLO show pneumonia and later show chronic arthritis. The original 1939 microbe came from a human case of rheumatic fever. It was unclear at that time whether the Streptococcus pneumoniae L-form (Pneumococcus) or the Mycoplasma pneumoniae bacteria (or both) were the reported troublemakers. 

Today the list of CWD bad actors includes both of these and the list is now much larger. But most of these bacteria are, in certain stages, susceptible to tetracyclines and other macrolides when used in long-term pulsed dosages, with probiotics to control dysbiosis, with antioxidants to suppress oxides and toxins, and also with various concurrent anti-inflammatory interventions.  Yeast overgrowth countermeasures may also be necessary, involving probiotics as supplements. The total treatment is highly individualized and can be quite complex and time-varying, requiring exceptional medical attention, special and frequent lab testing, and above average anti-microbe treatment skills.

We now have a polyvalent Pneumococcus vaccine, but attempts to produce a Mycoplasma pneumoniae vaccine have failed to produce a safe and effective one. There is also the problem of the huge number of mycoplasma sub-species and strains. See Dr. Clark’s Mycoplasma elephantis paper listed at the end of this article.

Private funds sources for the successful Arthritis Institute were drying up. Brown and Clark applied for further research funds to the NIH and were turned down by a committee of rival peer reviewers.  This enabled the NIH then to apply the Congressional appropriated study funds to support their own research bureaucracy, effectively diverting the money and subverting the will of Congress and the people.  NIH’s supported future results have proven to be much less effective than the clinical results obtained by Brown and Clark and documented by the Road Back Foundation.

After so many years of successful work and helping so many persons, Dr. Brown published his book, The Road Back, in 1988 with the help of the prolific popular science writer Henry Scammell. Sadly Dr. Brown died of cancer soon after completing the draft. At about the same time (1987), Dr. Clark retired, but he continued to educate on the topics of mycoplasmas and their long-term pathogenic characteristics in both humans and animals.  He turned his notes into the book Why Arthritis? Searching for the Cause and Cure of Rheumatoid Disease.

Dr. Joseph Mercola, D.O., participated actively in the medical conferences organized by Dr. Brown’s Arthritis Institute. Successful treatments at the time were made possible by Dr. Clark’s amazing microbe identification and specific immune reaction tests in the Institute’s own world-class laboratory, which he directed.

Dr. Clark wrote the foreword to the 2002 book Rheumatoid Arthritis: The Infection Connection by Katherine Poehlmann, PhD. This book was based on Dr. Brown’s antibiotic protocol consisting of long-term tetracycline antibiotics plus anti-inflammatory drugs, and nutritional improvements all taken together. Dr. Joseph Mercola describes the pulsed antibiotic protocol in Dr. Poehlmann’s book.

One of the great problems with propagating the knowledge into the future was that Dr. Clark’s skill and competence was so great that it was difficult for others in this country to duplicate his work.  His peers and collaborators in Mycoplasma bacteriology were worldwide. The U.S. NIH doctors had competing agendas and were rivals for public funds. 

No funds were available for educating the next generation of microbiologists and immunologists. Doctors Brown and Clark were so successful that they were able to obtain private donations to establish their Institute and to run it for many years.  However, the expectation of public support, given the demonstrated wide success, met with peer arthritis research opposition and never materialized.

Instead, age, retirements, illness, and deaths removed the key team members one by one, and the private funds dropped to the level of operational unsustainability for the Arthritis Institute.  The public health rivals grew to a huge bureaucracy of research gatekeepers that have consumed large amounts of funds, supporting favored projects and impressive building programs, but they have failed to duplicate the high levels of excellence achieved by Doctors Brown and Clark.

Today arthritis treatments remain symptomatic. Treating the microbial causes, though documented repeatedly in the literature, still remain officiallyunknown and/or “controversial.” It is as if the gatekeepers still do not even bother to read medical papers published, still do not want to understand or want to disprove the medical history of accomplishments of Drs Brown and Clark.


According to Dr. Clark:

“The problem is that rheumatoid diseases, among the most complex medical problems, are still thought to be controllable by some magic bullet. I wish it were that simple. There obviously is no quick fix. Starting with the premise that every patient is different, therapy should be customized to achieve complete and permanent remission and even prevention. It is not surprising that investigators have found so many different alternative therapies that could hit the diverse targets.”

“It took over 40 years for the tetracycline therapy to be proven safe and effective, but [it] is yet to be accepted by the FDA.”

“Most unfortunately Economics is driving Health Care and Research [and] …. Profits and not patients come first.” 

“When I retired in 1987 I formed the Mycoplasma Research Institute primarily as an information center. What started as a quarterly newsletter soon became the book [Why Arthritis?] at a sizable cost. My goal still is to educate the patients and doctors hoping it will help them to obtain and to provide the best appropriate treatment.”


Review of A sample article: Multiple Uses of Antibiotics by H. W. Clark, PhD, 2000/06

[A better title might be Multiple Actions of Tetracyclines]

Summary:  A tightly worded functional summary of tetracycline (macrolide antibiotics) actions—anti-inflammatory, chelating, in sera antimicrobial, intracellular antimicrobial, immunosuppressive, protein-synthesis suppression, collagenase neutralization, etc. This article is so rich in ideas that you may need to read this three times to understand all the concepts packed together in each paragraph.

The 1995 MIRA study was designed to test the short-term anti-inflammatory value of minocycline. The MIRA test’s pass/fail criteria were not set to measure or to record long term results. Thus the short-term failures of comparable treatments were not contrasted with the long-term successes of the MIRA antibiotics.


Antibiotic Treatment Case Histories:  Road Back Foundation Interrupted Journeys

The Road Back Foundation has documented treatment of more than fifty of the most remarkable of the tens of thousands of patients successfully treated by Dr. Thomas McPherson Brown using antibiotics in IV form, injected, and in pulsed dosages over a long time period at Dr. Brown’s Arthritis Institute. These case histories show conclusively that a long-term antibiotic (macrolide/tetracycline) protocol can effect a long-term improvement and often a remission. If re-infection occurs, a subsequent course of antibiotics can again quell the infection and stop the arthritis or autoimmune inflammation condition. The effectiveness of the treatments depended heavily on learning the patients’ microbe antibodies. This was accomplished using the immune system tests developed and applied in Dr. Clark’s laboratory.

Many other doctors worldwide have applied antibiotics in this way, successfully, to treat arthritic autoimmune conditions in humans and in many different wild and domestic animals.  The thoroughness, depth, and breadth of Dr. Clark’s practical understanding is found in the many of the papers that he and Dr. Brown published over the many years they worked together.



Online hot links to papers by Doctors Brown and Clark:

References:  Dr. Clark’s and other Authors’ Works Supporting Mycoplasma Pathogenicity

  1. Clark HW, et al, 1961, Antigenic Properties Of Pleuropneumonia-Like Organisms From Tissue Cell Cultures And The Human Genital Area, J Bacteriol. 82(4): 542–547
  2. Clark HW, et al, 1961, Preparation Of Pleuropneumonia-Like Organisms For Microscopic Study, J Bacteriol. 81(3): 500–502
  3. Clark HW, et al, 1963, Identification Of Mycoplasmataceae By The Fluorescent Antibody Method, J Bacteriol. 85(1): 111-8.
  4. Clark HW, et al, 1963, Growth Inhibitory Properties Of Mycoplasma Antibody,  J Bacteriol. 86(1): 147–150
  5. Clark HW, et al, 1965, Sedimentation Counting and Morphology of Mycoplasma, J. Bacteriol, 1373-1386.
  6. Clark HW, et al, 1969, Variations in mycoplasma antigen activity. In Mycoplasma diseases of Man, M. Sprossig, W. Witzleb eds., VEB Gustov Fischer Verlag, Jena. Germany.
  7. Clark HW, Bailey, JS, Brown, TMcP. 1985, Medium-dependent properties of mycoplasma, Diagn. Microbial. Infection Dis. 3:283-294.
  8. Robinson LB, Wichelhausen RH, Roisman B, 1956, Contamination of human cell cultures by pleuro-pneumonia-like organisms. Science~ 124:1147-1149.
  9. Himmelreich R, et al, 1997, Comparative analysis of the genomes of the bacteria Mycoplasma pneumoniae and Mycoplasma genitalium, Nucleic Acids Research, 25:701-'112..
  10. Sawaya MR, et.al. 1999, Crystal structure of the Helicase Domain from the Replicative Helicase-Prlmase of Bacteriophage T7. Cell, 99:167-177.
  11. Brown 'TMcP, Wichelhausen RH, Merchant, WR, Robinson, LB, 1951, A study of the antigen-antibody mechanism in rheumatic diseases, Ann. J Med. Science, 618-625.
  12. Clark HW, Bailey JS, Brown TMcP. 1982, Properties supporting the role of mycoplasma in rheumatoid arthritis. Reviews of Infectious Diseases,4:S238.
  13. Clark HW, Coker-Vann MR Bailey, JS, Brown, TMcP. 1988. Detection of mycoplasma ill immune complexes from rheumatoid arthritis synovial fluids. Ann Allergy 60: 394-398.
  14. Clark HW, 1991, The potential role of mycoplasma as autoantigens and immune complexes in chronic vascular pathogenesis. American J Primatology 24: 235-243.
  15. Cole BC HJ96 Mycoplasma Interactions with the Immune system: Implications for Disease Pathology ASM News 62: 471-475.
  16. Clark, HW, 1996, Mycoplasma and Diseases, ASM News, 62:617  Letters
  17. Falkow SF 1997, What Is a Pathogen?, ASM News, 63:359-365.
  18. Clark HW, 1997, What is a Pathogen? (Continued), ASM News, 64:1-2. Letters
  19. World Health Organization, 1977, The Role of Immune Complexes in Disease. Technical Report Series 606.
  20. Clark, HW, 1997, Why Arthritis? Searching for the Cause and the Cure of Rheumatoid Disease, from the Mycoplasma Research Institute.
  21. Razin S, et. al, 1998, Molecular Biology and Pathogenicity of Mycoplasmas, Microbiology and Molecular Biology Reviews, 62:1094-1166.

Townsend Letter For Doctors and Patients:

    Index of contributions by Harold W Clark, PhD

1.       Autoimmune Diseases Caused by Mycoplasmas (letter), #243, p.143+ Oct 2003

2.       The Case for Mycoplasma's Role as a Cause of Autoimmune Rheumatoid Diseases, #208, p.78-80

3.       Multiple Uses of Antibiotics, #226, p.47-48

4.       Mycoplasma Contaminated Vaccines (letter), #222, p.110

5.       The Role of Chelation Therapy (letter), #209, p.111


World-Class thoroughness in identifying pathogenic mycoplasmas characteristic of the work of the mycoplasma-specializing HW Clark colleague microbiologists in Europe.  (117 strains tested and ruled out)

Table 1 below is from Mycoplasma elephantis sp. nov., a New Species from Elephants (1996)  -- HELGA KIRCHHOFF, ROSEMARIE SCHMIDT, HEINER LEHMANN, HAROLD W. CLARK, AND AURIOL C. HILL. Institut fur Mikrobiologie und Tierseuchen, Tierarztliche Hochschule Hannover, 301 73 Hannover, ' and Botanisches Institut, and Medical Research Council Toxicology Unit, Carshalton, Surrey SM5 4EF, United Kingdom;  Tierarztliche Hochschule Hannover, 30559 Hannover, Germany; Mycoplasma Research Institute, Beverly Hills, Florida 32665


TABLE 1.  Mycoplasma, Entomoplasma, Mesoplasma, and Acholeplasma

Strains and antisera used in comparative serological tests with the new elephant mycoplasma. (1996)

Mycoplasmas Antisera Strains

Mycoplasmas Antisera Strains

Mycoplasmas Antisera Strains

Mycoplasmas Antisera Strains

Mycoplasma adleri G-145T               

M. dispar 462/2T            

M. maculosum PGIST

M. yeatsii GIHT

M. agalactiae PG2T      

M. edwardii PG24T       

M. rneleagidis 1 7529T

Entomoplasma ellychniae ELCN-lT

M. alkalescens DIZT     

M. equigenitalium T37T                         

M. moatsii MK405T

E. lucivorax PIPN-2T

M. alvi IlsleyT                   

M. falconis H/TIT           

M. mobile 163KT

E. luminosurn PIMN-lT

M. anatis 1340T              

M. fastidiosum 4822T  

M. molare H54ZT

E. melaleucae MIT

M. anseris 1219T            

M. faucium DC333T     

M. rnuris R1114T

E. somnilux PYAN-lT

M. arginini G230T         

M. felifaucium PUT       

M. mustelae MX9T

Mesoplasma entomophilum TACT

M. arthritidis PG6T       

M. feliminutum BenT    

M. mycoides subsp. mycoides PGIT

M. jlorum LIT

M. auris UIAT                  

M. felis COT                     

M. mycoides subsp. Capri PG3T

M. lactucae 831-C4T

M. bovigenitaliiim PGl lT                    

M. fermentans PG1gT

M. neurolyticum type AT

M. seifferti F7T

M. bovirhiizis PG43T   

M. gallinaceum DDT    

M. opalescens MH540gT

Acholeplasma axanthum S-743T

M. bovis DonettaT          

M. gallinarum PG16T  

M. orale CH19299T

A. cavigenitalium GP3T

M. bovoculi M 1 65/69T                      

M. gallisepticum PG3 lT

M. ovipneumoniae Y9gT

A. equgetale C112T

M. buccale CH20247T                         

M. gallopavonis WRIT                         

M. oxoniensis 12gT

A. granularum BTS39T

M. buteonis Bb/T2gT    

M. gateae CST                

M. penetrans GTU54T

A. hippikon CIT

M. calijomicum ST6T  

M. genitalium G37T      

M. phocacerebrale 1049T

A. laidlawii PGgT

M. canadense 275CT   

M. glycophilum 486T   

M. phocarhinis 852T

A. modicum PG49T

M. canis PG14T              

M. gypis Bl/TIT                

M. phocidae 105T

A. morum 72-43T

M. capricolum subsp. capricolum California KidT                 

M. hominis PG21T        

M. pirum HRC 70-159T

A. multilocale PN 525T

M. capricolum subsp. capripneumoniae F3gT                        

M. hyophalyngis H3-6BFT                         

M. pneumoniae FHT

A. oculi 19LT

M. caviae G122T           

M. hyorhinis BTS7T      

M. primatum HRC292T

A. parvum H23MT

M. cavipharyngis 1 1 7CT                  

M. hyosynoviae S16T   

M. pullorum CKKT

Bovine serogroup strain 7PG50

M. citelli RG-2CT          

M. imitans 4229T           

M. pulmonis PG34T


M. cloacale 383T           

M. indiense 3TT              

M. putrefaciens KS-IT


M. collis 58BT                  

M. iners PG30T               

M. salivarium PG20T


M. columbinasale 694T                        

M. iowae 695T                

M. simbae LXT


M. columbinum MMP-lT                    

M. equirhinis M432/72T

M. spermatophilum AH 159T


M. columborale MMP-4T                   

M. jlocculare M ~ 4 2 ~

M. spurnans PG13T


M. conjunctivae HRC581T                

M. hyopneumoniae JT

M. sualvi Mayfield BT


M. corogypsi BVT          

M. leocaptivus 3L2T

M. subdolum TBT


M. cottewii VIST            

M. leopharyngis LL2T

M. synoviae WVU 1853T


M. cricetuli CHT             

M. lipofaciens R171T

M. testudinis 01008T


M. cynos H831T             

M. lipophilum MaByT

M. verecundum 107T



If you know of other papers by Dr Thomas McPherson Brown or Dr Harold W Clark, please tell us about them and their web location.

We will undertake to update this memoriam page to include the references so that their contributions to medical science are more easily found.

Please email the information to kpoehlmann@RA-Infection-Connection.com with the title/subject:  “HW Clark Update Info”


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