Neurological disease associated with Mycoplasma pneumoniae infection. PCR evidence against a direct invasive mechanism

Abstract

Aims-To investigate the pathology in patients presenting with sudden onset neurological illnesses associated with Mycoplasma pneumoniae infection. Methods-M pneumoniae infection was diagnosed by a highly rigorous interpretation of serological markers initially using complement fixation, agglutination and IgM antibodies. Confirmation of the serological diagnosis was achieved using indirect immunofluorescence for IgM, IgA, and IgG. Serum and cerebrospinal fluid (CSF) samples from these patients were examined using the polymerase chain reaction to look for evidence of M pneumoniae DNA. Results-No M pneumoniae DNA was found in any serum or CSF samples. Diagnosis of M pneumoniae infection by agglutination and complement fixation antibodies was not always confirmed by indirect immunofluorescence. Conclusion-The neurological lesions in these patients do not appear to be caused by the direct invasion of M pneumoniae into the nervous system. The lesions may be an immune response to infection. Serological diagnosis of M pneumoniae continues to be a laboratory problem. (Jr Clin Pathol: Mol Pathol 1995;48:M51-M54)

Mycoplasmal cerebral vasculopathy in a lymphoma patient: Presumptive evidence of Mycoplasma pneumoniae microvascular endothelial cell invasion in a brain biopsy

“…Resident microglial cells in the parenchyma have alterations no different than those found in the neocortex of normal elderly individuals [51] and astrocytosis is also no more than expected for age. Our patient's recovery without significant inflammation or ultrastructural evidence of fibrin or platelet thrombus formation is consistent with temporary vaso-occlusion, which has been suggested as a cause of resolving mycoplasmal encephalitis even when direct brain invasion may not occur [12]. However, thrombi could be missed in our case from sampling error.…”

“…Neurological symptoms typically arise 1 to 2 weeks after a respiratory infection and they may be treated empirically with macrolide antibiotics, even though most macrolides penetrate the blood-brain barrier poorly, as well as with tetracycline and quinolones. There is some controversy concerning the need for antibiotic therapy since many mycoplasmal infections resolve spontaneously [8,[12][13][14][15]. Mycoplasma pneumoniae is the best-studied and perhaps the most frequent mycoplasma in neurological disease [8,11].…”

“…Mycoplasmal encephalitis has long been considered to be immunemediated, perhaps through molecular mimicry involving the plasma membrane and lipoglycan capsule, while a hypercoagulable state may lead to stroke [10][11][12][13]. However, direct neuroinvasion has been increasingly suggested from the results of immunoglobulin G (IgG), RNA hybridization, and polymerase chain reaction (PCR) testing of cerebrospinal fluid (CSF) and brain tissue [10,[16][17][18].…”

Chronic Lyme Disease and Co-infections: Differential Diagnosis

“…However, the connection between Mycoplasma pneumoniae and neurological manifestations is not undisputed [203, 206]. …”

Exploring the pathogenetic mechanisms of Mycoplasma pneumoniae (Review)

“…A number of studies suggested that the recognition of M. pneumoniae by innate immune cells and the subsequent cell activation may play a pivotal role in causing severe M. pneumoniae complications ( 61 ). A previous study conducted by Fink et al ( 62 ) examining serum IgM, IgA, IgG and cerebrospinal fluid in individuals with sudden neurological manifestations, suggested that nervous system damage may not stem directly from M. pneumoniae invasion, but may likely result from an immune response to the infection. Immune-driven mechanisms play a key role in M. pneumoniae -associated extrapulmonary diseases (MpEPDs) ( 9 ).…”