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ment by Mycoplasma pneumoniae in children,2 despite the fact that their subjects were mainly children. When discussing CNS involvement by M pneumoniae, particularly in children, it is vital that patients with encephalitic episodes are examined as well. Recently, my research group studied CNS involvement byMpneumoniae using the polymerase chain reaction (PCR),3 and found that patients with encephalitis, in whom onset of neurological symptoms occurred within seven days of the onset of fever, exhibited a significantly higher incidence of mycoplasma DNA in cerebrospinal fluid (CSF) than patients with later onset of fever.4 Fink et al stated that six of seven patients with confirmed M pneumoniae infection reported a febrile illness or upper respiratory tract infection six to 14 days before the onset of neurological symptoms. Our data suggest that in most, but by no means all, of their patients mycoplasma DNA may not be detectable in the CSF. We are of the opinion that the presence of mycoplasma DNA in CSF is not evidence of a direct, invasive mechanism. Nevertheless, the clinical characteristics of illnesses involving the CNS or other factors, such as the interval between the onset offever and the onset ofthe neurological symptoms, should be taken into account before a conclusion is reached whether or not a direct invasive mechanism plays a role in CNS involvement byM pneumoniae.

molecular pathology

Quantitative analysis of silver stained nucleolar organiser regions: a reliable marker of cell proliferation and a promising prognostic parameter in tumour pathology