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The Pathogenesis and Treatment of Mycoplasmal Infections


Quote:Summary
Pathogenic mycoplasmas have been found in the blood or other specimens of patients with a variety of chronic clinical conditions, including respiratory, oral cavity, genital and other
infections, autoimmune, inflammatory and immunosuppressive diseases and fatigue syndromes of unknown origin. ... Although they are not widely appreciated for their pathogenic properties, certain Mycoplasma species and certain other species of bacteria (Chlamydia, Borrelia, etc.) appear to play a role in disease progression or patient morbidity in rather large subsets of chronic illness patients.

Introduction
Certain Mycoplasma species, the smallest and simplest, free-living, bacteria that lack a rigid cell wall, are important pathogens in animal, plant and insect species. In humans mycoplasmal
infections have only recently been associated with certain acute and chronic illnesses where they  may function as causative agents, cofactors or opportunistic infections that cause patient
morbidity. .... certain species appear to cause morbidity when they penetrate into the blood and spread to and colonize various tissues. For example, M. fermentans can cause severe, fatal neurological and respiratory signs and symptoms after injection into the cerebral fluid of rats.
Although sometimes questioned, several pathogenic Mycoplasma species have been proposed  to be etiologic agents in various acute and chronic diseases in man. Less appreciated is the possibility that multiple chronic infections, including Mycoplasma species, play an important role  in various chronic illnesses and their progression.

Mycoplasma genomes are the smallest among bacteria The genomes of most Mycoplasma species encode about 600 proteins. ... Since they are cell wall-deficient bacteria, there is a major reduction in genetic information needed for cell wall biosynthesis. Although Mycoplasma species carry a minimal set of genes involved in energy metabolism and biosynthesis, they still have the essential genes for DNA replication, transcription, translation, and the minimal number of rRNA and tRNA genes. The reduction in mycoplasmal genomes explains their need for host nutritional molecules. A significant number of mycoplasmal genes appear to be devoted to cell adhesion and attachment organelles as well as variable membrane surface antigens to maintain parasitism and evade host immune and nonimmune surveillance systems.

Mycoplasma species variably express structurally heterogeneous cell surface antigens. Variations in the genes encoding cell surface adherence molecules reveal distinct patterns of  mutations capable of generating changes in mycoplasma cell surface molecular size and antigenic diversity. Variable surface antigenic structures and rapid changes in their expression are thought to play important roles in the pathogenesis of mycoplasmal infections by providing altered structures for escape from immune responses and protein structures that enhance cell and tissue colonization and penetration of the mucosal barrier.

Mycoplasma interactions with host immune systems Certain Mycoplasma species can either activate or suppress host immune systems, and they may use these activities to evade host immune responses. ... Moreover, it was also found that M. fermentans-derived lipids can interfere with the interferon (IFN)-g-dependent expression of MHC class II molecules on macrophages. This suppression results in impaired antigen presentation to helper T-cells in an experimental animal model.

Mycoplasma species are known to secrete immune-modulating substances.

As described above, mycoplasmas can evade immune recognition by undergoing surface antigenic variations thus rapidly altering their cell surface structures. Such antigenic variability, the ability to suppress host immune responses, slow growth rates and intracellular locations may explain the chronic nature of mycoplasmal infections and the common inability of a host to suppress mycoplasmal infections with host immune and nonimmune responses.

Mycoplasmas Can Induce Programmed Cell Death and Necrosis
Mycoplasmas can directly suppress host immune responses by initiating or enhancing apoptosis. For example, M. fermentans, an AIDS-associated mycoplasma, can initiate or enhance
concanavalin A-induced apoptosis of T-cells. Relatively large amounts of nucleases are also expressed by Mycoplasma species, and these can be released intracellularly to cause
degradation of host DNA. Mycoplasmal nucleases may also be involved in secondary necrosis seen in advanced mycoplasmal infections, as indicated by the occurrence of morphological characteristics of apoptosis (chromatin condensation) and necrosis (loss of membrane integrity  and organelle swelling). Although mycoplasmas can release activated oxygen species that may be involved in initiating apoptosis, some Mycoplasma species, such as M. fermentans, express a novel cytolytic activity in a nonlipid protein fraction that has a cytocidal effect not mediated by the known mycoplasmal cytokines like TNFa.

In addition to apoptosis, mycoplasmas can also release growth inhibitory molecules into their surroundings, such as arginine deaminase...

Clinical Testing for Mycoplasmal Infections
Until recently one of the most difficult problems in detecting mycoplasmal infections was that the available techniques, serological and culturing procedures, were relatively insensitive for
detecting intracellular infections. Mycoplasma culture techniques can be highly specific for detection of some mycoplasmal infections, but they are relatively insensitive because of difficulty culturing various Mycoplasma species. Conventional serological detection of mycoplasmal  infections is quite difficult due to the lack of humoral immune responses in most patients. Also, detection methods that use antibodies against mycoplasma antigens are not very reliable, because mycoplasmas are able to hide inside cells. This can result in rather normal antibody titers during active mycoplasmal infections.

The most reliable clinical testing for mycoplasmal infections uses whole blood, blood leukocytes or tissue biopsies and polymerase chain reaction (PCR). Even with this approach it is necessary to insure that intracellular Mycoplasma species are being detected at high sensitivity. Another research technique that has been used for intracellular infections is nucleoprotein gene tracking. This approach detects mycoplasmal genes directly in nucleoprotein complexes isolated  directly from cell nuclear fractions. Although highly specific, it is not as sensitive as PCR.

Persistence of Mycoplasmal Infections and Various Clinical Conditions
Mycoplasmas have been found at significantly higher incidence in blood and tissue specimens obtained from patients with various chronic illnesses compared to healthy controls. Since little is known about the involvement of mycoplasmas in the pathogenesis of chronic illnesses, it remains uncertain whether these findings indicate that some Mycoplasma species are causal
agents, cofactors, or opportunistic (superinfections) in patients with immundisturbances. ... The distinguishing characteristic in pathogenic infections may be the penetration of Mycoplasma species into the blood circulation and especially into cells in various tissues. ... Unless mycoplasmas penetrate into tissues and cells, it is unlikely that they can exert their pathogenic effects, but in some individuals the presence of mycoplasmas is not associated with any clinical condition.
[...]
Mycoplasmal Infections and Respiratory Illnesses
Various respiratory illnesses, such as chronic asthma, airway inflammation, chronic pneumonia and other respiratory diseases, are known to be associated with mycoplasmal infections. ... M. pneumoniae is a common cause of upper respiratory infections, and severe asthma is commonly associated with mycoplasmal infections. Recent evidence has shown that certain mycoplasmas, such as M. fermentans (incognitus strain), are unusually invasive and found within respiratory epithelial cells. Similar to certain Chlamydia species, pulmonary macrophages appear unable to kill pathogenic Mycoplasma species.
[...]
Mycoplasmal Infections in Immunosuppressive Diseases
Some Mycoplasma species, M. fermentans, M. penetrans, and M. pirum, have been implicated as infectious cofactors in HIV-AIDS. Using relatively insensitive techniques all three mycoplasmas have been detected in up to 20% of patients with HIV infections, and serological studies have suggested that the presence of M. penetrans is also associated with HIV infection. ... Also, the development of AIDS may increase the susceptibility of HIV-infected patients for coinfection with various Mycoplasma species, such as M. fermentans. This species is able to bind HIV capsid protein gp120 permitting adhesion of HIV virions to the mycoplasma surface. Subsequently the HIV viruses could be transported directly to cells expressing CD4 receptors. After binding to target cells, mycoplasmas can stimulate host cell activation by IL-1 and TNFa, which are known effectors for virus reproduction. In addition, oligosaccharides of the mycoplasmal glycocalyx may protect bound HIV-1 virons from host immune responses.

Antigen similarities between the surface components of mycoplasmas and HIV-1 have led to speculation that they use similar mechanisms for cell entry.

Mycoplasmal Infections in Rheumatic Diseases
Mycoplasmal Infections in Cardiac Diseases
Mycoplasmal Infections in Autoimmune Diseases

Mycoplasmal Infections in Fatigue Illnesses
Chronic fatigue is the most commonly reported medical complaint of all patients seeking medical care. However, the fatigue syndromes, such as chronic fatigue syndrome (CFS, sometimes called myalgic encephalomyelitis), fibromyalgia syndrome (FMS) and Gulf War illnesses (GWI) are distinguishable as separate syndromes that have muscle and overall fatigue as major characteristics, among many other multiorgan signs and symptoms, including immune system abnormalities. Because of the complex nature of these illnesses, many patients are often diagnosed with multiple syndromes. We and others have examined the presence of mycoplasal blood infections in CFS, FMS and GWI patients and have found that the majority
of patients have blood mycoplasmal infections.

Patients with CFS or FMS often have multiple mycoplasmal infections and probably other chronic infections as well. When we examined CFS/FMS patients for the presence of M. fermentans, M. pneumoniae, M. penetrans, M. hominis infections, multiple infections were found in over one-half of 93 patients. CFS/FMS patients had double (>30%) or triple (>20%) mycoplasmal infections, but only when one of the species was M. fermentans or M. pneumoniae (17). We also found higher score values for increases in the severity of signs and symptoms in CFS/FMS patients with multiple infections. CFS/FMS patients with multiple mycoplasmal  infections generally had a longer history of illness, suggesting that patients may have contracted additional infections during their chronic illnesses.

Antimicrobial Therapy for Mycoplasmal Infections
Once mycoplasmal infections have been identified in subsets of chronic illness patients, they can be successfully treated, if the therapy continues for some time to eliminate or suppress dormant  forms of the microorganism. Using this strategy appropriate treatment with antibiotics can result  in patient improvement and even recovery. The recommended treatments for diagnosed mycoplasmal blood infections require long-term antibiotic therapy, usually multiple 6-week cycles of doxycycline (200-300 mg/day), ciprofloxacin (1,500 mg/day), azithromycin (500 mg/day) or clarithromycin (750-1,000 mg/day). Multiple cycles are required, because few patients recover after only a few cycles, possibly because of the intracellular locations of mycoplasmas like M. fermentans and M. penetrans, the slow-growing nature of these microorganisms and their ability to exhibit persistence as dormant forms and their relative drug sensitivities. For example, of 87 GWI patients that tested positive for mycoplasmal infections, all patients relapsed after the first 6-week cycle of antibiotic therapy, but after up to 6 cycles of therapy 69/87 patients recovered and returned to active duty. The clinical responses that were seen were not due to placebo effects, because administration of some antibiotics, such as penicillins, resulted in patients becoming more not less symptomatic, and they were not due to immunosuppressive effects that can occur with some of the recommended antibiotics.

Chronic illness patients often have nutritional and vitamin deficiencies that must be corrected. These patients are often depleted in vitamins B, C and E and certain minerals. Unfortunately, patients with these chronic illnesses often have poor absorption. Therefore, high doses of some vitamins must be used, and others, such as vitamin B complex, must be given sublingual. Antibiotics that deplete normal gut bacteria can result in over-growth of less desirable flora, so Lactobacillus acidophillus supplementation is recommended. In addition, a number of natural remedies that boost the immune system are available and are potentially useful, especially during antibiotic therapy or after therapy has been completed. They appear to be useful during therapy to boost the immune system or after antibiotic therapy in a maintenance program to prevent relapses.

Additional Info

  • Type of Document: Scientific Study
  • ISBN-10: n/a
  • # of Pages: n/a
  • Author Name: Garth L. Nicolson, Marwan Y. Nasralla and Nancy L. Nicolson Antimicrobics and Infectious Disease Newsletter (Elsevier Science) 1999; 17(11):81-88
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Published in Biological Research
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