Study Finds Bacteria in Milk Linked to Rheumatoid Arthritis

Study Finds Bacteria in Milk Linked to Rheumatoid Arthritis

A strain of bacteria commonly found in milk and beef may be a trigger for developing rheumatoid arthritis in people who are genetically at risk, according to a new study from the University of Central Florida.

A team of UCF College of Medicine researchers has discovered a link between rheumatoid arthritis and Mycobacterium avium subspecies paratuberculosis, known as MAP, a bacteria found in about half the cows in the United States. The bacteria can be spread to humans through the consumption of infected milk, beef and produce fertilized by cow manure.

The UCF researchers are the first to report this connection between MAP and rheumatoid arthritis in a study published in the Frontiers in Cellular and Infection Microbiology journal this week. The study, funded in part by a $500,000 grant from the Florida Legislative, was a collaboration between Saleh Naser, UCF infectious disease specialist, Dr. Shazia Bég, rheumatologist at UCF’s physician practice, and Robert Sharp, a biomedical sciences doctoral candidate at the medical school.

Naser had previously discovered a connection between MAP and Crohn’s disease and is involved in the first ever phase III-FDA approved clinical trial to treat Crohn’s patients with antibiotics. Crohn’s and rheumatoid arthritis share the same genetic predispositions and both are often treated using the same types of immunosuppressive drugs.  Those similarities led the team to investigate whether MAP could also be linked to rheumatoid arthritis.

“Here you have two inflammatory diseases, one affects the intestine and the other affects the joints, and both share the same genetic defect and treated with the same drugs. Do they have a common trigger? That was the question we raised and set out to investigate,” Naser said.

For the study, Bég recruited 100 of her patients who volunteered clinical samples for testing.  Seventy-eight percent of the patients with rheumatoid arthritis were found to have a mutation in the PTPN2/22 gene, the same genetic mutation found in Crohn’s patients, and 40 percent of that number tested positive for MAP.

“We believe that individuals born with this genetic mutation and who are later exposed to MAP through consuming contaminated milk or meat from infected cattle are at a higher risk of developing rheumatoid arthritis,” Naser said.

About 1.3 million adults in the U.S. have rheumatoid arthritis – an autoimmune and inflammatory disease that causes the immune system to attack a person’s joints, muscles, bones and organs. Patients suffer from pain and deformities mostly in the hands and feet. It can occur at any age but the most common onset is between 40 and 60 years old and is three times more prevalent in women.

Although case studies have reported that some RA patients suffer from Crohn’s disease and vice versa, the researchers say a national study needs to investigate the incidence of the two diseases in the same patients.

“We don’t know the cause of rheumatoid arthritis, so we’re excited that we have found this association,” Bég said. “But there is still a long way to go.  We need to find out why MAP is more predominant in these patientswhether it’s present because they have RA, or whether it caused RA in these patients. If we find that out, then we can target treatment toward the MAP bacteria.”

The team is conducting further studies to confirm findings and plan to study patients from different geographical and ethnic backgrounds.

“Understanding the role of MAP in rheumatoid arthritis means the disease could be treated more effectively,” Naser said.  “Ultimately, we may be able to administer a combined treatment to target both inflammation and bacterial infection.”

Naser holds a Ph.D in Medical Microbiology from New Mexico State University. He joined UCF in 1995. He has been investigating Crohn’s disease and other auto-immune diseases for more than 30 years. He has published more than 100 peer-reviewed articles and has presented his work at numerous conferences.  He has several patents including a licensed DNA technology for detecting MAP.

Bég, a board-certified rheumatologist, has been with UCF since 2011 after completing her fellowship in rheumatology at Baylor College of Medicine in Houston. In addition to practicing medicine at UCF Health, she is a full-time faculty member at the college. Her research and clinical interests include conditions such as rheumatoid arthritis, psoriatic arthritis, lupus and osteoporosis.



Lyme/MSIDS patients need to take note of this study as RA is often undiagnosed tick-borne infections – including Mycoplasma.  The genetic issue as well as consuming infected animal products should be a concern to us all; however, being infected with TBI’s is right up there on the list.

BTW:  Garth Nicholson has been sleuthing on the role of Mycoplasma and Lyme/MSIDS for years:

And previously to that, Dr. Brown way back in the 40’s and 50’s believed that RA was caused by mycoplasmas and used tetracycline rather than prednisone, the drug of choice. He eventually modified his treatment which included Minocycline and brought over 10,000 patients into remission.  (This demonstrates the importance of dealing with the infection)

I find it interesting that Minocycline was probably the drug that helped me the most:  This link also shows Nicholson’s discovery that 90% of evaluated ALS patients had Mycoplasma. 100% of ALS patients with Gulf War Syndrome had Mycoplasma and nearly all of those were specifically the weaponized M. fermentans incognitos.  One of the hallmark symptoms of Mycoplasma is fatigue.
And the bad news for us is that Nicholson’s experience has found Mycoplasma to be the number one Lyme coinfection, and similar to other coinfections in that it can be supposedly cleared for years only to reappear when conditions are right.

One other note is that immunosuppressive drugs for folks that have TBI’s are going to worsen their condition, so TBI’s must be ruled out before the administration of them, which is going to be tricky business as the tests for all of these pathogens is abysmal.  I highly recommend having patients fill out the Horowitz questionnaire along with testing and for doctors to make a clinical diagnosis not based on testing only:

This study also shows the dire need for medical professionals to be properly trained regarding TBI’s or they run the risk of putting patients on immunosuppressive drugs to their demise.  So far the education in med school on Tick borne infections is antiquated and brief, considering Lyme is the #1 vector borne disease in the U.S.  No one has accurate numbers on coinfections.  If you know of doctors who are willing to be trained in this area, please send them this: Betty Maloney, President, Partnership for Tick-borne Diseases Education created a website built specifically for the purpose of offering accredited, evidence-based continuing medical education (CME) modules on Lyme and other tick-borne diseases (TBD) for doctors and other healthcare professionals. Doctors will like the convenience of on-demand learning that’s available on PC and mobile devices. The modules I developed for LymeCME provide a concise review of the evidence, highlighting points that are especially relevant to patient care. And, they’re free!

More on Myco:  Dr. Rawls states:  “Borrelia, the microbe commonly associated with Lyme disease, could be a culprit. However, I would lay odds on mycoplasma and a closely related bacterium called ureaplasma. About 75% of chronic Lyme disease sufferers have been found to harbor at least one species of mycoplasma.

It fits. Mycoplasma and ureaplasma are the smallest of all bacteria. They are obligate intracellular microbes — which means they must live inside cells of a host to survive. They typically infect linings of the body — linings of lungs, intestines, joints, and the urinary tract.
Different species of mycoplasma and ureaplasma prefer certain areas of the body, but any species of these microbes can be found in different places the body. The most common species found in the urinary and reproductive tract are Ureaplasma urealyticum and Mycoplasma hominis. These microbes typically spread sexually, but they can be acquired by other routes. Mycoplasma pneumoniae, a frequent cause of respiratory infections, can also be found in the urinary tract.  Mycoplasma and ureaplasma are notoriously difficult to culture.”

But back to Mycobacterium…..Dr. Horowitz is finding that Mycobacterium drugs are working for his treatment resistant patients:    The case study has based on a woman with Borrelia burgdorferi, Borrelia hermsii, possible prior exposure to tularemia, exposure to Mycoplasma pneumonia, multiple viruses, fibromyalgia, and rheumatoid arthritis.
Under Dr. Horowitz’s care she improved from 30% to 50%, but with the addition of Dapsone had a sudden fourfold increase in tularemia titers as well as Bartonella titers turning positive.  While making continuous progress the patient had ongoing joint pain which interfered with sleep as well as ongoing severe blood-filled blisters, oral/genital ulcerations, and increased granulomas.
While a rheumatologist wanted to put her on an immunosuppressive, she and Dr. Horowitz chose to try 500mg (based on body weight) of PZA twice a day combined with rifampin and minocycline. Her liver was monitored every two weeks and was helped with alpha lipoid acid 600mg and milk thistle 250mg.  Two months later she reported up to 80% of normal functioning…

The fact that the addition of a mycobacterium drug that gave this woman 80% of normal functioning is something that needs to be noted.  It also leads to the conclusion that her prior diagnosis of RA is probably infectious in nature and improved with microbials.

Now if that isn’t a success story, I don’t know what is.  So something is going on here with Mycobacterium or a mycobacterium-like pathogen.  This needs to be hunted to ground.