Tuberculosis was historically called consumption.

Anyone that watched Gunsmoke series, or old western shows in the 60's knows this.

FYI: (Our old friend DMSO)

DMSO significantly enhances the treatment of many common bacterial infections (e.g., of the head, mouth, and skin) and many severe bacterial infections that require hospitalization (e.g., tuberculosis, sepsis, peritonitis, severe lung infections, osteomyelitis). In many cases, this has allowed an individual requiring an amputation of a chronically infected area to instead fully recover.

It can remove the antibiotic resistance of bacteria. This is particularly helpful in widespread problematic infections that have gradually developed a resistance to many existing antibiotics (e.g., tuberculosis) and challenging infections that are not responding to antibiotics (e.g., ones that would otherwise require an amputation).

DMSO and Bacterial Infections

DMSO has six properties that make it useful in treating bacterial infections.

First, data suggests DMSO increases bacterial cell membrane permeability and concurrently creates changes in the cell indicative of damage to its membrane. In addition to directly eliminating bacteria, it also reduces their ability to prevent antibiotics from entering them. In turn, existing data shows DMSO has a much greater ability to increase the potency of antibiotics that target structures inside bacteria rather than ones that target their cell wall (e.g., penicillin). Note: this property is particularly important for tuberculosis as it has a robust external barrier that impairs antibiotic entry.

In 1964, Stanley Jacob reported that 20% DMSO had a bacteriostatic effect (growth inhibiting activity that does not kill bacteria) against E. coli, Staph aureus, and Pseudomonas cultures, and that 1% DMSO made resistant tuberculosis more sensitive to antibiotics.

Tuberculosis

Despite over a century of work, Tuberculosis remains the worlds most deadly microbe (e.g., in 2023, it was estimated to have killed 1.25 million people). This is largely due this tiny bacteria’s unique characteristics making chronic tuberculosis infections quite challenging to eliminate and its high aptitude for developing resistance to the antibiotics that eliminate it.

Because of this, once the early DMSO researchers realized that DMSO could remove antibiotic resistance, their focus immediately went to tuberculosis (a decision which has also been influenced by the recognition DMSO is more effective at eliminating smaller bacteria). In turn, a variety of studies have demonstrated DMSO’s utility for this challenging infection. Non-Human Studies:

•According to Stanley Jacob, at a 1966 DMSO symposium, it was reported that pretreating tuberculosis bacteria in 5% DMSO made them 200 times more sensitive to streptomycin.

•A 1974 study of guinea pigs infected with isoniazid resistant tuberculosis found that while all guinea pigs treated only with isoniazid died within 80 days (with tuberculosis throughout their tissues), if a single oral dose of DMSO was given 2 weeks prior to isonizaid, they all survived (and a year later were still alive). This suggested DMSO could remove tuberculosis’s resistance to isonizaid. In a followup 1976 study, they then took cultures from tuberculosis patients and found that 5% DMSO made 19 of the 61 isonizaid resistant strains become susceptible to isoniazaid and 19 of the 19 rifampin resistant strains susceptible to rifampin.

•A 1980 study found that DMSO and 5-fluorouracil enhanced the antibacterial effects of isoniazid and streptomycin on tuberculosis bacterial cultures.

Note: DMSO has also been shown to prevent rifampin from degrading for at least 8 months, which suggests it will not disrupt the antibiotic’s potency if administered concurrently

•A 1995 study found DMSO combined with a tuberculosis antibiotic (which was washed away prior to applying other antibiotics) made multi-drug resistant tuberculosis (both in test tubes and within macrophages) much more susceptible to other tuberculosis antibiotics (isoniazid rifampicin and streptomycin). Specifically, non-lethal doses of ethambutol and 2-5% DMSO caused a 4-64 fold increase in the sensitivity to other antibiotics (4-16X for rifampicin, 16-33X for streptomycin and 4-16X for isoniazid), while isoniazid and 2.5% DMSO caused an 8 fold increase in susceptibility to other tuberculosis medications.

To quote those authors:

Our data indicate that the agents that modify cell wall permeability can enhance the susceptibility of multiple drug resistant strains to drugs to which they were originally resistant. This could provide a new approach to treating drug resistant tuberculosis.

Note: ethambutol works by inhibiting tuberculosis cell wall synthesis, thereby removing its barrier to other antibiotics entering.

•A 2013 study found 50% DMSO caused an approximately 50% decrease in mycobacterium tuberculosis growth.

Additionally, a 1982 study tested 27 antiobiotic resistant isolates of myobacterium avium-intracellulare, finding that 27% were resistant to rifampin and streptomycin, 81% resistant to isoniazid and ethambutol and 96% resistant to ethionamide. Once 2.5% DMSO was used as well, all the antibiotics affected 26-30% more cultures (except for ethionamide, which only had an 11% increase, going from 96% being resistant to 85% being resistant). Three isolates were inhibited only in the presence of DMSO plus a drug, six isolates demonstrated growth inhibition without any enhanced effect due to DMSO, while the remaining eighteen isolates were sensitive to at least one drug in the presence of DMSO and to different drugs in the absence of DMSO. Note: tuberculosis is also a mycobacterium, and the antibiotics tested in this study are also used to treat tuberculosis. Human Studies:

•A 1969 study of 32 patients with destructive pulmonary tuberculosis and endobronchial tuberculosis gave them nebulized streptomycin and penicillin mixed in 10% or 25% DMSO. Of the 32, 14 showed an absence of tuberculosis secretion and most showed improvement (e.g., reduced endobronchitis, perifocal infiltration and lung tissue destruction).

•A 1980 study used DMSO to treat children with pulmonary tuberculosis.

•A 1991 study found nebulized DMSO mixed with rifampin over 1-2 months was an effective treatment for 148 pulmonary tuberculosis and 18 obstructive bronchitis patients (e.g., it healed the destructive cavities caused by tuberculosis), that it could be used alone or to enhance the efficacy of conventional therapies and that DMSO significantly reduced the chronic liver toxicity of rifampin.

Additionally, one complication of the (live) tuberculosis vaccine is that it can cause recipients to form tuberculosis like abscesses (especially if the vaccine comes from a hot lot). A 1994 study of 287 children with either abscesses or regionally inflamed lymph nodes following tuberculosis vaccination who receiving isoniazid (a common antibiotic for tuberculosis) found that locally administering a rifampin DMSO mixture halved their recovery time, reduced the number of isoniazid injections and eliminated the need for other antibiotic therapies. Bacterial Toxins

One of the primary reasons bacterial infections sicken and kill is because of the toxins they release. DMSO in turn, has been repeatedly shown to mitigate this. For example:

•DMSO has been shown to protect the duodenum from H. pylori induced chronic ulcers.

•In rats, DMSO was shown to create a dose dependent reduction in the fluid secretion and mucosal permeability triggered by C. difficile’s toxin (with its maximum inhibition occurring at a 1% concentration). Given how common C. difficile colitis is and how low of a DMSO concentration was needed to create this effect, this application of DMSO has a great deal of promise.

•The shigella bacteria’s toxin causes severe diarrhea and bloody stools (and sometimes severe illness) by destroying the cells that line the colon. DMSO was shown to prevent cellular uptake of the toxin and partially reduce its cellular toxicity.

•Endotoxaemia occurs in response to bacterial lipopolysaccharide (LPS) entering the bloodstream and is one of the most severe and ubiquitous disease processes in horses. A 2008 study of 18 horses found DMSO reduced the fevers that followed artificially induced endotoxemia. This is highly relevant to humans as LPS is highly inflammatory and can create a variety of severe disease states (e.g., sepsis). Unlike many agents, DMSO can protect cells from the damage this toxin causes.

Note: one of the most important characteristics the early adopters of ultraviolet blood irradiation recognized about it was that UVBI could effectively neutralize toxins in the bloodstream (a property which saved a significant number of lives).