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Over the past few weeks I've amassed dozens of medical journal articles on Mycoplasma, and I'll try when I am feeling up to it, to sort through them for some that might be particularly helpful or to the point.

(BTW, Mycoplasma of course should not be confused with Mycobacterium, which is a different group of bacteria entirely and includes the infectious cause of tuberculosis, Mycobacterium tuberculosis).

From memory (fingers crossed I have this right) one of the more troubling things I've read that I see mentioned less often, is that Mycoplasma pneumoniae can have at least one nasty toxin (CARDS toxin) that is recognized as one of its virulence factors.
https://en.wikipedia.org/wiki/Mycoplasma_pneumoniae
(see CARDS toxin, under "Cytotoxicity and organismal effects")
"The CARDS toxin most likely aids in the colonization and pathogenic pathways of M. pneumoniae, leading to inflammation and airway dysfunction."

Mycoplasma pneumoniae may also interfere with the function of human lung surfactant (a sort of "detergent" that our lungs make and require for health) or with other components of healthy lung function.
https://en.wikipedia.org/wiki/Pulmonary_surfactant

One possible outcome of Mycoplasma's mischief is purported to be that "irritant receptors" in the lung may become exposed and therefore may begin reacting to various materials - hence the part under "Cytotoxicity and organismal effects" in Wikipedia that says

"The cytotoxic effects of M. pneumoniae infections translate into common symptoms like coughing and lung irritation that may persist for months after infection has subsided. Local inflammation and hyperresponsiveness by infection induced cytokine production has been associated with chronic conditions such as bronchial asthma and has also been linked to progression of symptoms in individuals with cystic fibrosis and COPD"

Wikipedia doesn't seem to have much on "irritant receptors" that I can find, although there is a little bit here
https://en.wikipedia.org/wiki/Cough_reflex

And more here
https://en.wikipedia.org/wiki/Asthma-related_microbes
"There is also a possibility that M. pneumoniae infection may destroy respiratory mucosal cells and facilitate the penetration of antigens into the mucosa.[9] A study done by Laitinen et al. (1976) suggests that M. pneumoniae infection denude the epithelial surface and expose irritant receptors.[10] On top of that, M. pneumoniae induces the activation of mast cells..."

Normally these irritant receptors might be shielded by substances like human lung surfactant
https://www.ncbi.nlm.nih.gov/pubmed/10971473
"Much indirect evidence has been put forward previously in support of the concept that surface-active phospholipid (SAPL) normally masks irritant receptors in the lungs and upper respiratory tract; but this physical barrier is deficient in asthmatics, imparting hyperresponsiveness of the bronchoconstrictor reflex."

I am absolutely amazed that I have heard so little about this bacterium before now, and even more amazed that I have never once heard my doctors even mention it, in spite of some of the symptoms I've had.

The Centers for Disease Control information on Mycoplasma pneumoniae
https://www.cdc.gov/pneumonia/atypical/mycoplasma/index.html

Notice the wide range of possible symptoms, from "cold-like" to pneumonia.

There are fourteen different species of Mycoplasma that can infect humans that are mentioned here
https://en.wikipedia.org/wiki/Mycoplasma_orale

They are listed here (there may be more).
https://en.wikipedia.org/wiki/Mycoplasma

Mycoplasma are purported to be the smallest bacteria that have been discovered. Some Mycoplasma infections may be sexually transmissible.

Some details about challenges in clinical diagnosis and therapy for Mycoplasma can be found here in the sections on Diagnosis and Treatment.
https://en.wikipedia.org/wiki/Mycoplasma_pneumoniae

Mycoplasma pneumoniae can use hydrogen peroxide as a weapon or virulence factor against the host.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3178575
"The major virulence determinant of M. pneumoniae is hydrogen peroxide that is generated during the utilization of glycerol-3-phosphate, which might be derived from free glycerol or from the degradation of phospholipids. "

This article contains further, if mostly technical, information about Mycoplasma pneumoniae's generation of peroxide and utilization of phospholipids.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3178575

This article cites Mycoplasma for interfering with another of the body's natural defenses against free radicals or smoke, and for therefore apparently sensitizing people to these influences
https://www.nationaljewish.org/about/news/press-releases/2008/infection-blocks-response

More information of Mycoplasma pneumoniae
https://www.sciencedirect.com/topics/medicine-and-dentistry/mycoplasma-pneumonia

Stumbled across this recently, which names Mycoplasma in association with a number of diseases which it might therefore be capable of contributing to the symptoms or severity of, in the event that it isn't likely for it to be a benign presence in these conditions.

http://www.lymepa.org/Nicolson_LabMedicine0508.pdf
https://academic.oup.com/labmed/article/39/5/291/2504709

I'm wondering whether to try talking to a doctor about what continues to be suggestive of a chronic Mycoplasma infection exacerbating a pulmonary disease diagnosis - yes, Mycoplasma probably could turn out to be part of the picture for many people with pulmonary disorders including COPD and asthma thus I presume all affected or at risk should be aware of it - and noticed that there are several important references still missing here

This one suggests that it's human lung surfactant's job to help get rid of Mycoplasma infections and a chronic Mycoplasma infection may imply that something may have gone wrong with the production or action of lung surfactants like "Surfactant protein A" (SP-A) or its close relatives

Surfactant protein A mediates mycoplasmacidal activity of alveolar ...
https://www.ncbi.nlm.nih.gov/pubmed/10220400
by J Hickman-Davis - ‎1999 - ‎Cited by 137 - ‎Related articles
Apr 27, 1999 - Surfactant protein A mediates mycoplasmacidal activity of alveolar macrophages by production of peroxynitrite. Hickman-Davis J(1), ...

And this one seems to flat-out accuse Mycoplasma's nasty CARDS (Community Acquired Respiratory Distress Syndrome) Toxin itself of binding directly to Surfactant Protein A, in addition to its ability to kill human cells

Structure of CARDS toxin, a unique ADP-ribosylating and ... - NCBI - NIH
https://www.ncbi.nlm.nih.gov/pubmed/25848012
by A Becker - ‎2015 - ‎Cited by 32 - ‎Related articles
Apr 6, 2015 - Structure of CARDS toxin, a unique ADP-ribosylating and ... CARDS TX binds to human surfactant protein A and annexin A2 on airway ...

It's very tempting to consider Mycoplasma as a cause of my troubles because putting these last pieces in place, we get a picture where damaging or interfering with lung surfactant proteins may expose or sensitize irritant receptors (pulmonary stretch receptors) to various stimuli, including cold air (which I am currently having TERRIBLE trouble with), smoke, steam, fragrances, dust...

I also learned a remarkable thing lately, that in spite of the number of papers that make up the case against Group A Strep as a potential cause or contributor to Tourette's, PANDAS or tics, there are some researchers who seem equally suspicious of Mycoplasma infection being eligible for the same role.

Perhaps not coincidentally, I'm informed that a standard test for Mycoplasma (the complement fixation assay) has fallen by the wayside due to its tendency to cross-react with other pathogens such as Strep, which perhaps is a clue. If Mycoplasma indeed shares this eligibility with Streptococcus, perhaps it may be because of a shared or very similar common antigen that is recognized by the same antibody that may also recognize a human target in order to produce or promote some of the symptoms of Tourette's, PANDAS or tic.

So I had planned to go to the doctor with Strep at the top of my priority list, but I'm wondering if Mycoplasma shouldn't go at the top of the list. My tics are terrible, blatantly breathing-related (I can stop them by pushing up the end of my nose oddly enough but I can't go through life holding up the end of my nose obviously) and nothing is setting them off anywhere near like breathing cold air.

Sadly, even though Mycoplasma infections may be trying to lay claim to representing the majority of pneumonia cases, I'm not sure if many doctors have been properly briefed about it yet, and between this and the difficulties of actually detecting it, a lot of cases might get written off as a cold or the flu (further confusion might arise if it's possible for a person to have both a cold or flu, and a Mycoplasma infection at the same time?) - which could result in patients not receiving antibiotic treatment even when it may be appropriate.

Here are some more references about or related to Mycoplasma's possible role in pulmonary diseases

The respiratory system: Anatomy, physiology, and adaptations to exercise and training
https://www.sciencedirect.com/topics/veterinary-science-and-veterinary-medicine/pulmonary-stretch-receptors
PIERRE LEKEUX, ... DAVID R. HODGSON, in The Athletic Horse (Second Edition), 2014
Pulmonary and airway receptors
Three kinds of receptors with vagal afferents are located in the lungs and play a role in ventilatory control. The pulmonary stretch receptors are nerves ending in the tracheal and bronchial smooth muscles. Their activity is enhanced by enlargement of airway cross-section, for example, when the lung volume increases, and results in an inhibition of further inspiratory activity. The stretch receptors could be responsible for the adjustment in the pattern of breathing to minimize the energy cost of breathing. They also could prevent lung overstretching when the ventilatory demand is high, that is, during heavy exercise.
Irritant receptors have a minor role in the control of breathing. They are located between and below the epithelial cells of the airways (larynx, trachea, bronchi, and intrapulmonary airways). They protect the lung against various aggressors or irritants by reacting to a variety of stimulations (such as inhalation of irritant gases, dust, release of histamine) and inducing tachypnea, bronchospasm, cough, and mucus secretion.

Mycoplasma pneumoniae: Current Knowledge on Macrolide ...
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4916212
by S Pereyre - ‎2016 - ‎Cited by 42 - ‎Related articles
Jun 22, 2016 - These infections occur both endemically and epidemically worldwide. M. pneumoniae lacks cell wall and is subsequently resistant to beta-lactams and to all antimicrobials targeting the cell wall. This mycoplasma is intrinsically susceptible to macrolides and related antibiotics, to tetracyclines and to fluoroquinolones.

http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1413-86702007000500012
Mycoplasma pneumoniae infections constitute 20%-40% of all community-acquired pneumonias; the severity is highly variable, and this condition may lead to severe sequelae. Mycoplasma pneumoniae frequency is underestimated in clinical practice because of the lack of specific features and a diagnosis that needs serology or PCR. Effective management of M. pneumoniae infections can usually be achieved with macrolides. In Brazil, epidemiological studies are needed in order to assess the incidence of this bacterium.

Mycoplasma pneumoniae and its role in asthma - NCBI - NIH
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2805928
by N Nisar - ‎2007 - ‎Cited by 144 - ‎Related articles
Mycoplasma pneumoniae (M pneumoniae), primarily recognised as a .... that such infection denuded the epithelial surface and exposed irritant receptors.
There is a possibility that mycoplasmal infection led to the destruction of respiratory mucosal cells and facilitated the penetration of antigens into the mucosa; the patient become atopic to other allergens, in addition to M pneumoniae allergen, after this infection.14 Laitinen et al,30 suggested that such infection denuded the epithelial surface and exposed irritant receptors. As mycoplasma are antigenic and can initiate an antibody response, it is possible that IgE attach to mast cells and then interact with M pneumoniae antigen, which in turn stimulates histamine release to cause airway obstruction.31

If anyone is versed in the possibility of Mycoplasma contributing to ME/CFS, I would love to hear more about it. I haven't had the chance to research the subject but I am getting suspicious since some of the "flus" that have gone around here may have been Mycoplama infections instead, and they've been known to leave people feeling badly fatigued and going to bed way early for weeks or even months.

Most of all, if anyone has heard of alternative or over-the-counter treatments for Mycoplasma infections, it would be wonderful to hear from you. Usually people on the Internet are just full of suggestions for home remedies but that may not be the case with Mycoplasma since it seems to have been particularly good at staying off the radar.

This might be an important work on Mycoplasma - it addresses a very good question about how Mycoplasmas are able to use peroxide as a weapon against us when they do not seem to have the enzyme catalase to protect themselves from it. (If I recall correctly, Mycoplasmas might also be able to steal certain antioxidants from us, such as glutathione, so it's possible they may have more than one way of surviving their own weaponry).

Relation of catalase to substrate utilization by Mycoplasma pneumoniae.
Low IE, Eaton MD, Proctor P.
J Bacteriol. 1968 Apr;95(4):1425-30.
No catalase activity was detected in four strains of glucose-grown Mycoplasma pneumoniae at any time during the replication of the organism. Exogenous catalase dramatically increased the O(2) uptake with glycerol, presumably by releasing inhibition caused by hydrogen peroxide. The effect of added catalase on the O(2) uptake of washed organisms with glucose as substrate was moderate and variable in degree. The production of hydrogen peroxide was demonstrated by the quantitative enzymatic assay for inorganic peroxide and by the fact that added pyruvate, which is non-enzymatically oxidized by H(2)O(2) to acetic acid and CO(2) could mimic the action of catalase.
PMID: 5646630 PMCID: PMC315103 [Indexed for MEDLINE] Free PMC Article

Another good question might be whether producing pyruvate as an antioxidant may help protect Mycoplasma from certain types of antibiotics that may have an underappreciated oxidative mechanism of microbicide - the prediction I could make on that basis generally seems to match what is reported as effective or not - so maybe following this lead would help us to be able to find ways (and hopefully some simple and down-to-earth ones) to get more antibiotics to work better against Mycoplasma infections.

Apologies because that's a little obscure, but I've been following the remarkable work of researchers like Dwyer, Jacob, Kohanski, Drlica and others into surprising ways that antibiotics may work such as though oxidation/free radicals, which our immune systems also use as weaponry. Some of these researchers have strengthened their argument for an oxidative microbe-killing mechanism for certain classes of antibiotics (microbicides) by demonstrating that antioxidants may be able to protect microbes from these very same antibiotics.

It's perhaps not terribly easy to sort out since Mycoplasmas may persist as intracellular pathogens, taking up residence in host cells - which according to some authors may also be a means by which certain microbes may be able to avoid antibiotics since the abilities of various antibiotics to get into infected cells may not all be created equal. Perhaps not surprisingly, when I had to address that question concerning a different diagnosis of mine, macrolide antibiotics seemed to have a very good reputation for getting into infected cells - that too makes them seems very promising but it may make it less clear exactly what gives antibiotics like macrolides the advantage.

Reactive oxygen species and the bacterial response to lethal stress.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4254325
Zhao X1, Drlica K2.
Curr Opin Microbiol. 2014 Oct;21:1-6. doi: 10.1016/j.mib.2014.06.008. Epub 2014 Jul 30.

At any rate, we may have some reasonable antibiotic recommendations for Mycoplasmas even if the details of the reasons they work may be surprising to many of us.

Some works referring to Mycoplasma as a possible contributor to Tourette's/tics:

Mycoplasma pneumoniae infection and Tourette's syndrome.
Müller N1, Riedel M, Blendinger C, Oberle K, Jacobs E, Abele-Horn M.
Psychiatry Res. 2004 Dec 15;129(2):119-25.
https://www.ncbi.nlm.nih.gov/pubmed/15590039
Antibody titers against M. pneumoniae were determined by microparticle agglutination (MAG) assay and confirmed by immunoblot. Elevated titers were found in significantly more TS patients than controls (17 vs. 1). Additionally, the number of IgA positive patients was significantly higher in the TS group than in the control group (9 vs. 1). A higher proportion of increased serum titers and especially of IgA antibodies suggests a role for M. pneumoniae in a subgroup of patients with TS and supports the finding of case reports implicating an acute or chronic infection with M. pneumoniae as one etiological agent for tics. An autoimmune reaction, however, has to be taken into account. In predisposed persons, infection with various agents including M. pneumoniae should be considered as at least an aggravating factor in TS.

Suppl 1: The Relationship between Tourette’s Syndrome and Infections
Daniela L Krause* and Norbert Müller
Open Neurol J. 2012; 6: 124–128.
Published online 2012 Nov 16. doi: 10.2174/1874205X01206010124
PMCID: PMC3514747 PMID: 23230453
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3514747
One hypothesis is that not only one particular infectious agent causes directly to the disease; instead different (chronic) infections influence the immune balance and are therefore involved in the pathology. In tic disorders, infections with group A streptococci, Borrelia burgdorferi or Mycoplasma pneumoniae seem to be associated with symptoms of the disease. Studies have shown that immunologic treatment improves and prevents the re-occurrence of clinical symptoms in Tourette’s syndrome.

Mycoplasma and autoimmunity

https://en.wikipedia.org/wiki/Mycoplasma_pneumoniae
The similarity between the compositions of M. pneumoniae and human cell membranes can also result in autoimmune responses in several organs and tissues.[2]

Mycoplasma pneumoniae and Its Role as a Human Pathogen
Ken B. Waites and Deborah F. Talkington
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC523564
Clin Microbiol Rev. 2004 Oct; 17(4): 697–728.doi: 10.1128/CMR.17.4.697-728.2004
PMCID: PMC523564 PMID: 15489344
In addition to M. pneumoniae-specific antibodies, a variety of cross-reactive antibodies may develop in association with M. pneumoniae infection. The extensive sequence homology of the M. pneumoniae adhesin proteins and glycolipids of the cell membrane with mammalian tissues is a well-known example of molecular mimicry that may trigger autoimmune disorders that involve multiple organ systems through formation of antibodies against substances such as myosin, keratin, fibrinogen, brain, liver, kidney, smooth muscle, and lung tissues (16). Mycoplasmal adhesins also exhibit amino acid sequence homologies with human CD4 and class II major histocompatibility complex lymphocyte proteins, which could generate autoreactive antibodies and trigger cell killing and immunosuppression (353)...

A property of many species of mycoplasmas that affects the immune responsiveness of the host is their propensity for mitogenic stimulation of B and T lymphocytes, thereby inducing autoimmune disease through the activation of anti-self T cells or polyclonal B lymphocytes (403)...

Extrapulmonary Manifestations
As many as 25% of persons infected with M. pneumoniae may experience extrapulmonary complications at variable time periods after onset of or even in the absence of respiratory illness. Autoimmune reactions have been suggested to be responsible for many of the extrapulmonary complications associated with mycoplasmal infection (403).

Several more general references on Mycoplasma that may be worthwhile

https://emedicine.medscape.com/article/1941994-medication
Medication Summary
In the treatment of mycoplasmal pneumonia, antimicrobials against M pneumoniae are bacteriostatic, not bactericidal. Tetracycline and erythromycin compounds are very effective. The second-generation tetracyclines (doxycycline) and macrolides are the drugs of choice. [52] Macrolide resistance has been reported in several areas of the world, but most experts agree that macrolides are the antibiotics of choice for treating M pneumoniae infections in adults and children. [53, 54, 55, 56, 57] If a patient does not respond appropriately to a macrolide, a fluoroquinolone should be added to the treatment regimen. [53, 54] Penicillins and cephalosporins are ineffective, because the organism lacks a cell wall.
Macrolide resistance has been increasing throughout the world, with 0-15% resistance in Europe and the United States, 30% in Israel, and 90-100% in Asia, [58] but macrolides remain the mainstay of treatment. If symptoms do not resolve, consider prescribing tetracyclines (doxycycline and minocycline) or fluoroquinolones (levofloxacin)
eMedicine Logo

http://antimicrobe.org/m05.asp
Drug of Choice
Macrolides usually are considered the first-line choice for the treatment of M. pneumoniae infection. Treatment of M. pneumoniae pneumonia with clarithromycin or azithromycin results in clinical benefit equal to that seen with erythromycin therapy (7, 8, 37, 38) and a three-day regimen of azithromycin appears to be as effective as five days (37). Microbiologic cure has not been carefully compared in these studies, but because the clinical significance of bacteriologic persistence is not known, eradication may not be an appropriate measure for effectiveness. Treatment of M. pneumoniae pneumonia with roxithromycin resulted in good to excellent results in 12 of 13 patients and eradication of the organism in 4 of the 6 patients cultured (24).
Early studies in adults indicated that both erythromycin and tetracycline were more effective than placebo (25) or penicillin (35, 39) in reducing duration of symptoms, hospitalization, and abnormal chest x-ray in young adults (military recruits and college students) with M. pneumoniae pneumonia. Etiology was documented by culture and/or paired anti-mycoplasmal antibody response in these studies. In children less impressive benefits from antibiotic therapy have been demonstrated (17, 36)

A Compendium for Mycoplasma pneumoniae
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4828434
Gretchen L. Parrott,* Takeshi Kinjo, and Jiro Fujita
Front Microbiol. 2016; 7: 513.
Published online 2016 Apr 12. doi: 10.3389/fmicb.2016.00513
PMCID: PMC4828434 PMID: 27148202
The incidence of M. pneumoniae pneumonia in adults is less than the burden experienced by children. Transmission rates among families indicate children may act as a reservoir and maintain contagiousness over a long period of time ranging from months to years. In adults, M. pneumoniae typically produces a mild, “walking” pneumonia and is considered to be one of the causes of persistent cough in patients. M. pneumoniae has also been shown to trigger the exacerbation of other lung diseases. It has been repeatedly detected in patients with bronchitis, asthma, chronic obstructive pulmonary disorder, and cystic fibrosis.

Mycoplasmas: Sophisticated, Reemerging, and Burdened by Their Notoriety
Joel B. Baseman and Joseph G. Tully
https://wwwnc.cdc.gov/eid/article/3/1/97-0103_article
Recently, mycoplasmas have been linked as a cofactor to AIDS pathogenesis and to malignant transformation, chromosomal aberrations, the Gulf War Syndrome, and other unexplained and complex illnesses, including chronic fatigue syndrome, Crohn's disease, and various arthritides (4-8). Even with mounting evidence of their pervasive and pathogenic potential, mycoplasmas still evoke the image of a group of obscure or impotent microorganisms. Yet they are evolutionarily advanced procaryotes (9-11), and their elite status as "next generation" bacterial pathogens necessitates new paradigms in fully understanding their disease potential...
This molecular mimicry is especially interesting since it has been suggested for decades that mycoplasmas provoke an antiself response that triggers immune disorders, although the basis for the induction has been elusive (65). Patients with documented M. pneumoniae respiratory infections demonstrate seroconversion to myosin, keratin, and fibrinogen (33)...
Antistreptococcal antibodies reactive against ahelical coiled-coil regions of the M protein crossreact with heart myosin, tropomyosin, and mycoplasmal adhesins (14,66). In the latter case, these mycoplasmal adhesins exhibit amino acid sequence homologies with human CD4 and class II major histocompatibility complex lymphocyte proteins, which could generate autoreactive antibodies and trigger cell killing and immunosuppression (67,68).

I think I am still lacking here an academic source that describes how when Mycoplasmas fuse with host cell membranes, they can acquire material from the host cell membrane, and any academic source that clarifies whether this curious property of Mycoplasmas could make further contributions to autoimmune diseases.

Mycoplasma as a contaminant in cell lines used in scientific experiments:

Out, Damned Mycoplasma!
Pointers for keeping your cell cultures free of mycoplasma contamination
Dec 1, 2013
KELLY RAE CHI
In the 1950s, when mycoplasma were first isolated from cell cultures, contamination was found in 57–92 percent of lab-grown cells. Because the organisms lack a cell wall, they are resistant to common antibiotics, such as streptomycin and penicillin, and they easily slip through filters.
Even though scientists are now more aware of mycoplasma as possible contaminants, it is estimated that as much as 35 percent of the cell cultures currently used in research may be infected. It remains a common problem—especially in university labs, where trainees come and go, and cell lines freely change hands—partly because the bacteria are impossible to see using conventional microscopy. They also produce indirect, subtle effects on eukaryotic cells.