Central nervous system complications of Mycoplasma pneumoniae.

Abstract

phenicol and dexamethasone. The next morning his right upper limb was in a decorticate posture. His breathing was abnormal: there was a long and stertorous expiratory time and the patient tried to help himself by pressing his right hand on his sternum. Neurological examination revealed normal awareness, speech and intellectual function. There was a left central facial weakness and paralysis, hyperreflexia and spasticity of all four limbs. Sensory examination was normal. X-rays of the chest on admission revealed a patchy infiltrate at the base of the right lung. An electroencephalogram (EEG) showed theta-delta dysrhythmia on the right and irregular alpha rhythm on the left. A CT scan and bilateral carotid angiography were normal. Cerebrospinal fluid (CSF) was normal (table 1). Smears and cultures for bacteria, acid-fast bacteria, fungi and viruses were negative, as were cultures of blood, urine and pharyngeal secretions. The patient had a raised mean corpuscular volume due to cold-induced agglutination of the cells in the Coulter counter. As indicated in table 2, when the cold haemagglutinin level decreased, the mean corpuscular volume returned to a normal value. After the second day in hospital the diagnosis of acute disseminated encephalitis secondary to Mycoplasma pneumoniae infection was suspected; the patient was given 200 mg doxycycline daily, and the dexamethasone and chloramphenicol were gradually reduced.

Mycoplasma pneumoniae as an Under- Recognized Agent of Vasculitic Disorders

“…It has been reported in association with M. pneumoniae infection [Sakoulas, 2001;Saitoh et al, 1993;van Buiren & Uhl, 2003;Zambrino et al, 2000]. Chorea or choreiform movements may be a neurological consequence of striatal damage [Al-Mateen et al, 1988;Decaux et al, 1980;Zambrino et al, 2000]. Concerning its etiology, it has been reported that no patients with M. pneumoniae-associated striatal necrosis have also exhibited systemic hypercoagulative state.…”

“…Microthrombosis has also been identified as a possible contributing factor to disease progression [Knochel, 1993]. On an interesting related note, rhabdomyolysis due to M. pneumoniae infection has occasionally been accompanied by neurological manifestations, in one case with acute disseminated encephalomyelitis [Decaux et al, 1980] and in two cases with transverse myelitis [Rothstein & Kenny, 1979;Weng et al, 2009]; the etiology of both of these www.intechopen.com neurological manifestations are presumed to involve vasculopathy (see next section). Regardless of whether they have an etiological link with M. pneumoniae-associated rhabdomyolysis, these neurological manifestations deserve further study on the assumption that there are common pathogenetic factors leading to vascular damage.…”

“…Infections have been included in the panel of causes, and M. pneumoniae infection-associated rhabdomyolysis has not infrequently been reported [Berger & Wadowksy, 2000;Daxböck et al, 2002;Decaux et al, 1980;Minami et al, 2003, Rothstein & Kenny, 1979Weng et al, 2009]. A central role in the development of this disease condition has been assigned to tumor necrosis factor-, which can cause acute proteolysis [Knochel, 1993] and which can be induced by M. pneumoniae.…”

Mycoplasma pneumoniaeand Its Role as a Human Pathogen

“…Approximately 6 to 7% of hospitalized patients with serologically confirmed cases of M. pneumoniae pneumonia may experience neurological complications of varying severity (237,294,332,387). Such complications have included encephalitis, cerebellar syndrome and polyradiculitis, cranial nerve palsies, aseptic meningitis or meningoencephalitis, acute disseminated encephalomyelitis, coma, optic neuritis, diplopia, mental confusion, and acute psychosis secondary to encephalitis (39,98,159,226,264,331,386,392). A number of motor deficiencies have also been described, including cranial nerve palsy, brachial plexus neuropathy, ataxia, choreoathetosis, and ascending paralysis (Guillain-Barré Syndrome) (2,4,9,12,39,44,223,226,319).…”

Atypische Enzephalitis eines 20-jährigen Wehrpflichtigen

“…Hochwirksam dagegen sind mit der bakteriellen Proteinsynthese interferierende Antibiotika wie Makrolide oder Tetrazykline. Beim Vorliegen einer ZNS-Infektion durch Mykoplasmen wird aus theoretischen Überlegungen heraus empfohlen, bevorzugt Tetrazykline einzusetzen, da diese die Blut-Liquor-Schranke besser passieren können [8,20].Über den Spontanverlauf der Mykoplasmenenzephalitis gibt es keine zuverlässigen Informationen aus größeren Studien.Es wurden jedoch wiederholt Patienten beschrieben,bei denen es unbehandelt zu einer schweren Enzephalitis mit generalisiertem Hirnödem und Hirndrucksymptomatik kam,was gelegentlich sogar eine dekompressive Operation erforderlich machte [20,22].Dagegen ist unter adäquater antibiotischer Therapie die Prognose günstig; ungefähr 90% der Patienten überleben die Erkrankung bei guter funktioneller Restitution [9,17] -auch bei sehr ungünstigen klinischen Ausgangsbefunden, wie es bei unserem Patienten der Fall war.…”