[Clostridium tetani isolated from patients with systemic tetanus].

Clostridium tetani is widely distributed in ground or mud, especially in field and pond-shore surface layers. C. tetani is rarely isolated from specimens of patients with tetanus, and is generally diagnosed based on clinical symptoms such as trismus or general tonic spasms. This means that positive C. tetani infection is rarely diagnosed bacterially. Using gram straing, we identified C. tetani in specimens from patients suspected of C. tetani infection brought to the Kitasato University Hospital emergency center. Rapid gram staining information in the bacteriology laboratory is expected to improve recovery from C. tetani infection. It is therefore necessary to ensure clinical specimen quality control, and to keep standard strains of rare bacteria for isolation and identification.

Elevated S100B level in cerebrospinal fluid could predict poor outcome of carbon monoxide poisoning.

OBJECTIVE: S100B is a calcium-binding protein produced by astroglia in the brain and has been used as a marker of neuronal damage after brain trauma. We investigated the utility of S100B in cerebrospinal fluid (CSF) measured during the early phase of carbon monoxide (CO) poisoning in predicting the subsequent clinical course. METHODS: The study included 31 patients who were admitted to the hospital with loss of consciousness following CO poisoning. S100B levels were measured by enzyme-linked immunosorbent assay in CSF, and serum samples collected simultaneously within 24 hours and on the fourth day after CO exposure. All patients were followed for at least 3 months and divided into 3 groups based on the clinical course: persistent vegetative state (PVS), delayed encephalopathy (DE), and complete recovery with no complications (NC). RESULTS: During the 3-month period, 3 patients developed PVS, 5 developed DE, and 23 were classified as NC. The mean S100B levels in the CSF within 24 hours after CO exposure were higher in the PVS group (9.25 ng/mL) than in the DE (2.03 ng/mL) and NC groups (1.86 ng/mL). However, the mean serum S100B levels were not elevated in the 3 groups (0.21, 0.59, and 0.16 ng/mL, respectively). CONCLUSION: Early elevation of S100B in CSF after CO poisoning could be a suitable predictor of subsequent development of PVS.

Aseptic meningitis in association with glyphosate-surfactant herbicide poisoning.

INTRODUCTION: The mechanisms underlying early central nervous system (CNS) signs and symptoms of glyphosate-surfactant herbicide (GlySH) poisoning are unclear. CASE PRESENTATION: A 58-year-old woman ingested approximately 150 mL of GlySH containing 41% glyphosate and 15% polyoxyethyleneamine. Two days later, she was admitted in the Emergency Center in a semicomatose state. Acute respiratory distress syndrome, circulatory collapse, acute renal failure, and disseminated intravascular coagulopathy were diagnosed. Meningitis was also suspected as she demonstrated Kernig's sign and significant neck stiffness with rigidity of the extremities as well as consciousness disturbance and fever (38.4°C). Investigations of cerebrospinal fluid (CSF) revealed the presence of glyphosate (122.5 µg/mL), significant elevation of IL-6 (394 µg/mL), and pleocytosis (32 cells/µL) with monocyte dominance. All bacteriological and virological tests were later found to be negative. She recovered completely after responding to aggressive supportive care in the intensive care unit. All signs and symptoms suggesting meningitis resolved as the concentration of glyphosate in CSF decreased. She was discharged on day 39 of hospitalization. DISCUSSION: These findings suggest that the present case involved aseptic meningitis in association with GlySH poisoning. CONCLUSION: CNS signs and symptoms induced by aseptic meningitis should be considered in cases of glyphosate-surfactant herbicide poisoning.

Severe carbon monoxide poisoning complicated by hypothermia: a case report.

It is proposed that the significant elevation of interleukin-6 (>400 pg/mL) in cerebrospinal fluid during the early phase of carbon monoxide poisoning may be a predictive biomarker for the development of delayed encephalopathy. A 52-year-old man presented to the emergency department with severe carbon monoxide poisoning. On arrival, the patient was comatose with decorticate rigidity (Glasgow Coma Scale, E1V1M3). His core body temperature, measured in the urinary bladder, was 32.4°C. Laboratory blood analysis revealed elevated CO-Hb (36.0%) and metabolic acidosis with elevated lactate (pH 7.081; base excess [BE], -19.2 mmol/L; HCO3, -9.8 mmol/L; lactate, 168.8 mg/dL). After treatment with hyperbaric oxygen and several different rewarming techniques, he became alert and his core body temperature increased to normal. Interleukin-6 in cerebrospinal fluid at 5.5 hours after his last exposure to carbon monoxide was significantly elevated (752 pg/mL). However, he did not develop delayed encephalopathy. In this case, hypothermia in the range of therapeutic hypothermia (32°C to 34°C) may have suppressed formation of reactive oxygen species and subsequent lipid peroxydation, preventing the development of delayed encephalopathy. Therapeutic hypothermia initiated soon after the last exposure to carbon monoxide may be an effective prophylactic method for preventing the development of delayed encephalopathy.

The early elevation of interleukin 6 concentration in cerebrospinal fluid and delayed encephalopathy of carbon monoxide poisoning.

OBJECTIVE: This study was designed to investigate whether interleukin 6 (IL-6) in cerebrospinal fluid (CSF) in the early phase of carbon monoxide (CO) poisoning can be a predictive marker of delayed encephalopathy (DE). METHODS: Nine patients with CO poisoning were included in the study. Cerebrospinal fluid was sampled within 24 hours of the last exposure to CO, on hospital day 4, and once a week for at least 1 month to determine IL-6 and myelin basic protein concentrations. All patients were followed at least 3 months. RESULTS: Three patients demonstrated significant early IL-6 elevation in CSF, normal IL-6 level in CSF on day 4, and significant delayed myelin basic protein elevation in CSF. The 2 patients with the highest early IL-6 elevation in CSF developed DE. Interleukin 6 in serum was not related to DE. CONCLUSION: Interleukin 6 in CSF at the early phase of CO poisoning may be a predictive marker of DE.

Myelin basic protein in cerebrospinal fluid: a predictive marker of delayed encephalopathy from carbon monoxide poisoning.

This study was designed to investigate whether myelin basic protein (MBP) in cerebrospinal fluid (CSF) can be a predictive marker of delayed encephalopathy from carbon monoxide (CO) poisoning. Five patients with CO poisoning were included in the study. The CSF was serially sampled to determine the MBP concentration. All patients were classified into group DE or group non-DE according to whether delayed encephalopathy developed or not. In all 3 patients in group DE, the MBP levels in the CSF were markedly elevated preceding the clinical manifestations of delayed encephalopathy. In both group non-DE patients, the MBP concentrations in the CSF were never elevated. Elevated MBP concentrations in the CSF may represent a predictive marker of delayed encephalopathy from CO poisoning, leading to a more appropriate triage of patients with CO poisoning.

Regional cerebral blood flow and cerebrovascular reactivity during chronic stage of stroke-like episodes in MELAS -- implication of neurovascular cellular mechanism.

BACKGROUND: Ischemic vascular hypothesis as a causative role in the pathogenesis of stroke-like episodes in MELAS remains to be debated. METHODS: This study consisted of two parts. Part 1 is a clinicoradiological study during acute stage of 18 consecutive stroke-like episodes in six patients with MELAS. Part 2 is a SPECT study to assess the regional cerebrovascular reactivity (rCVR) to acetazolamide during chronic stage in five patients with MELAS. RESULTS: Headache and epileptic seizure were the most common presenting symptoms. Unique features of acute stroke-like lesions included progressive spread of cortical lesions with vasogenic edema, focal periodic epileptiform discharges, focal hyperperfusion, and cortical laminar necrosis during subacute stage. During chronic stage, SPECT showed hypoperfusion in non-affected occipital cortex in three patients as well as in previously affected regions in four. The rCVR was preserved in three patients, focally impaired in one, and extensively impaired in one, but relatively preserved in the occipital cortex in all patients. CONCLUSIONS: Stroke-like episodes could be non-ischemic neurovascular events initiated by neuronal hyperexcitability. Once neuronal hyperexcitability develops in a focal brain region, epileptic activities depolarize adjacent neurons, leading to a propagation of epileptic activities into the surrounding cortex, and resulting in energy imbalance. The mechanisms for neuronal hyperexcitability remain to be elucidated.