Severe Mycoplasma Encephalitis in a Child: The Corticosteroid TreatmentSchwere Mycoplasma-Enzephalitis bei einem Kind: die Kortikosteroid-Behandlung
Mycoplasma pneumonia (M. pneumonia) is a common cause of respiratory tract illness in children (Waites & Talkington, Clinical Microbiology Reviews 2004; 17-4, 697–728). Central nervous system (CNS) complications are the most common of extrapulmonary manifestations of M. pneumonia infection. CNS involvement has been reported in up to 7% of the patients hospitalized with M. pneumonia (Bitnun et al., Pediatric Infectious Diseases, 2003; 14-2, 96–107; Koskiniemi, Clinical Infectious Diseases 1993; 17-1, 52–57; Pönkä, Scandinavian Journal of Infectious Diseases 1980; 12-3, 175–184). However, the incidence of CNS complications is less than 0.1% (Yesnick, L. AMA Arch Intern Med 1956; 97-1, 93–98). Encephalitis is the most recurrent neurological complication in children (Pönkä, Scandinavian Journal of Infectious Diseases 1980; 12-3, 175–184).
The pathogenesis of the CNS manifestation associated with M. pneumonia infection is unknown. Direct invasion of the CNS, autoimmunologic effects, vascular injury, and neurotoxin involvement are discussed (Pönkä, Scandinavian journal of infectious diseases 1980; 12-3, 175–184). The diagnosis is based on serological and chest radiographic findings in the majority of cases with a neurological disorder.
A previously healthy 13-year-old boy with a 9-day history of fever and cough was admitted to the emergency department due to clinical deterioration, abnormal speech, and hallucinations. He was treated for an upper respiratory tract infection with amoxicillin-clavulanate. He had no remarkable medical or drug history.
On examination, he was lethargic and Glasgow Coma Scale was 9. His vital signs and remainder of systemic and neurological examinations were normal. Neck stiffness was positive.
Laboratory investigations revealed normal biochemical parameters and blood count but positive CRP (52,7 mg/L; normal range <3 mg/L). Although he had symptoms of upper respiratory tract infection, chest X-ray was normal ([Fig. 1]). Brain computed tomography (CT) and an electroencephalogram (EEG) were reported as normal. A lumbar puncture performed on admission revealed 180 leukocytes, protein level of 49,4 mg/dl (15–45 mg/dl), and glucose level of 73 mg/dl (simultaneous blood glucose 120 mg/dl). Meningoencephalitis was suspected and the patient was initially treated with intravenous ceftriaxone and acyclovir. All bacterial and viral cultures of his blood, respiratory secretions, and cerebrospinal ﬂuid were negative. Polymerase chain reaction (PCR) for herpes simplex virus 1 and 2, varicella-zoster virus and enterovirus were negative in CSF. Serum antibodies against Cytomegalovirus, Epstein-Barr Virus Capsid Antigen, Herpes Simplex Virus were negative, but anti-M. Pneumonia IgM (titer>1:10) and IgG (titer>1:10) were positive, indicating an acute M. pneumonia infection. Clarithromycin was added to treatment.
Brain MRI demonstrated that T2 hyperintensity was seen in the bilateral thalamus, pontine tegmentum and periaqueductal area and also showed diffuse leptomeningeal enhancement ([Fig. 2]). These MR findings supported encephalitis and when evaluating with clinical and laboratory findings, the case was considered M. pneumonia associated encephalitis.
On the third day of hospitalization, methylprednisolone (MPZ) (30 mg/kg/day for 3 days) was added to treatment. He was fully conscious on the third day of MPZ treatment. His repeat anti-M. pneumonia IgG titer showed elevation. Follow-up MRI 2-weeks later showed the pathological hyperintense signals disappeared completely and no evidence of leptomeningeal enhancement ([Fig. 2]). He was discharged from the hospital with no neurological sequel on the 20th day.
27 April 2020 (online)
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