We appreciate the interest by Lanczik and colleagues in our article involving a patient diagnosed as having fulminant and fatal coxsackie-virus B4 meningoencephalitis. These authors describe a patient with apparent brainstem encephalitis who had meningism, lethargy, 4-limb weakness, and polymorphonuclear pleocytosis; serologic determination of M pneumoniae as a possible causative agent; and a good recovery after antibiotic treatment. Owing to the similarity of clinical manifestation and findings on magnetic resonance imaging scans, they suggest that M pneumoniae might have been the causative agent in our case. Although in rare cases this organism can cause neurological complications such as aseptic meningitis, meningoencephalitis, cranial nerve neuritis, Guillain-Barré syndrome, transverse myelitis, and psychosis,1 it is doubtful that M pneumoniaewas a coinfectious agent or responsible for rhomboencephalitis in our case. In our patient, coxsackievirus B4 was clearly identified in both the cerebrospinal fluid and on a rectal swab, indicating that the patient was still actively shedding the virus and that the time window was ideal for effective treatment (with pleconaril). We believe that the patient did not respond to therapy because of her preexisting immunocompromised state.2 Multiple sputum samples failed to identify M pneumoniae, although our patient was treated for several weeks with tobramycin, meropenem, and sulfamethoxazole with trimethoprim for hospital-acquired pneumonia. She developed the characteristic myocarditis, dilated cardiomyopathy, and heart block previously reported in patients with coxsackieviral infections.3 Taken together, these findings are typical clinical sequelae of coxsackievirus infection.
Bernardini GL, Cree BC, Hays AP, Lowe G. Mycoplasma pneumoniae Infection as a Treatable Cause of Brainstem Encephalitis—Reply. Arch Neurol. 2003;60(12):1813–1814. doi:10.1001/archneur.60.12.1813-a
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