Welkom bij het Lymeforum

Mycoplasma, the Most Common Lyme Coinfection

Macroliden zijn een goed alternatief in geval van penicilline-allergie of falen van amoxicilline. De nieuwe macroliden zijn actief tegen het grootste deel van de respiratoire pathogenen. De gevoeligheid van Haemophilus influenzae is variabel.


•Macroliden zijn eerste keuze antibiotica bij vermoeden van een infectie door een atypische kiem zoals Mycoplasma pneumoniae, Chlamydia pneumoniae en Legionella pneumophila. De nieuwere macroliden zouden beter verdragen worden door patiënten die ongewenste gastro-intestinale effecten met erythromycine vertonen.

Mycoplasma pneumoniae en Chlamydia pneumoniae zijn de voornaamste oorzaken van atypische pneumopathie. Deze pathologieën zijn indicaties om tetracyclines te gebruiken. Deze stammen spelen eveneens een rol bij acute bronchitis, soms met een ernstigere hoest of meer persisterend karakter dan deze van virale oorsprong. Een behandeling met antibiotica (tetracyclines of macroliden) kan dan verantwoord zijn.

Sproetje schreef:
Ik weet niet welke klachten precies waar bij horen.
Maar ik heb wel last van mijn longen, ik denk dat het bij mycoplasma past.

Sproetje schreef:Hoi VGM,

Nee ik ben niet getest op Chlamydia Pneu
Het is wel voorgesteld om nog een paar co-infecties te testen.
Misschien ook die Chlamydia Pneu, goed dat je me eraan helpt herinneren.

Abstract


Mycoplasmas cause chronic inflammation and are implicated in asthma. Mast cells defend against mycoplasma infection and worsen allergic inflammation, which is mediated partly by histamine. To address the hypothesis that mycoplasma provokes histamine release, we exposed mice to Mycoplasma pulmonis, comparing responses in wild-type and mast cell–deficient KitW-sh/KitW-sh (W-sh) mice. Low histamine levels in uninfected W-sh mice confirmed the conventional wisdom that mast cells are principal sources of airway and serum histamine. Although mycoplasma did not release histamine acutely in wild-type airways, levels rose up to 50-fold above baseline 1 week after infection in mice heavily burdened with neutrophils. Surprisingly, histamine levels also rose profoundly in infected W-sh lungs, increasing in parallel with neutrophils and declining with neutrophil depletion. Furthermore, neutrophils from infected airway were highly enriched in histamine compared with naive neutrophils. In vitro, mycoplasma directly stimulated histamine production by naive neutrophils and strongly upregulated mRNA encoding histidine decarboxylase, the rate-limiting enzyme in histamine synthesis. In vivo, treatment with antihistamines pyrilamine or cimetidine decreased lung weight and severity of pneumonia and tracheobronchitis in infected W-sh mice. These findings suggest that neutrophils, provoked by mycoplasma, greatly expand their capacity to synthesize histamine, thereby contributing to lung and airway inflammation.

Abstract


Mycoplasma pneumoniae, which causes mycoplasmal pneumonia in human, mainly causes pneumonia in children, although it occasionally causes disease in infants and geriatrics. Some pathogenic factors produced by M. pneumoniae, such as hydrogen peroxide and Community-Acquired Respiratory Distress Syndrome (CARDS) toxin have been well studied. However, these factors alone cannot explain this predilection. The low incidence rate of mycoplasmal pneumonia in infants and geriatrics implies that the strong inflammatory responses induced by M. pneumoniae coordinate with the pathogenic factors to induce pneumonia. However, M. pneumoniae lacks a cell wall and does not possess an inflammation-inducing endotoxin, such as lipopolysaccharide (LPS). In M. pneumoniae, lipoproteins were identified as an inflammation-inducing factor. Lipoproteins induce inflammatory responses through Toll-like receptors (TLR) 2. Because Mycoplasma species lack a cell wall and lipoproteins anchored in the membrane are exposed, lipoproteins and TLR2 have been thought to be important for the pathogenesis of M. pneumoniae. However, recent reports suggest that M. pneumoniae also induces inflammatory responses also in a TLR2-independent manner. TLR4 and autophagy are involved in this TLR2-independent inflammation. In addition, the CARDS toxin or M. pneumoniae cytadherence induces inflammatory responses through an intracellular receptor protein complex called the inflammasome. In this review, the inflammation-inducing factors of M. pneumoniae are summarized.

Mycoplasma scavenge fats from the myelin sheath covering nerve tissue. Not surprisingly, mycoplasma (and other stealth microbes including chlamydia and borrelia) have been linked to multiple sclerosis. Mycoplasma has been closely linked to other neurodegenerative diseases including ALS (M. fermentans is most common) and Parkinson’s disease.
•Mycoplasma has been found in the bone marrow of children with leukemia.
•Mycoplasma has been found in cancer tissue, including cervical and ovarian cancer.

Abstract


We report the autopsy findings for a 45-year-old man with polyradiculoneuropathy and fatal acute disseminated encephalomyelitis after having Mycoplasma pneumoniae pneumonia. M. pneumoniae antigens were demonstrated by immunohistochemical analysis of brain tissue, indicating neuroinvasion as an additional pathogenetic mechanism in central neurologic complications of M. pneumoniae infection.
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