Multijurisdictional Outbreak of Enterohemorrhagic Escherichia coli O157 Caused by Consumption of Ready-to-Eat Grilled Skewered Meat in Niigata, Japan.

Enterohemorrhagic Escherichia coli O157 (EHEC) causes severe complications such as hemolytic uremic syndrome. Contaminated ready-to-eat (RTE) food is one of the vehicles of multijurisdictional outbreaks of foodborne disease worldwide. Multijurisdictional (covering cities, towns, and villages) outbreaks of EHEC are usually linked to an increase in cases, and here we describe such an outbreak involving 29 cases in October 2017 in the Niigata Prefecture. After prefecture-wide active case finding, we conducted a case-control study of 29 cases with eligible data who tested positive for EHEC. To determine the association of the outbreak with risk factors, we compared these cases with 38 controls selected from family and acquaintances who were both symptom free and tested negative for EHEC. The largest number of cases was in the 20-29-year age group (7/29; 24%) and most were women (20/29; 69%). All 29 cases had an identical or similar multilocus variable number tandem-repeat analysis (MLVA) profile. Of these, 76% (22/29) had consumed some type of grilled skewered meat. Also, 69% (20/29) had consumed grilled skewered meat produced by company X. EHEC infection was strongly associated with the consumption of grilled skewered meat produced by any food processing company (odds ratio [OR] = 11.8, confidence interval [95% CI]: 3.7-37.4) and by company X (OR = 9.8, 95% CI: 3.2-30.7). At company X, the skewered meat was grilled to 95°C and then removed from the grilling area to meat trays. The meat trays were not sufficiently washed and disinfected. Testing indicated that the facility was negative for EHEC but four asymptomatic employees tested positive for EHEC. Company X was temporarily closed and voluntarily recalled the foods. We recommend that all employees sufficiently wash and disinfect meat trays to prevent contamination of RTE food, avoid cross-contamination of grilled skewered meat through the environment by regularly cleaning the facility, and appropriately practice self-health care.

Surgical procedure and results of cisternal washing therapy for the prevention of cerebral vasospasm following SAH.

In 1994, we started cisternal washing therapy (CWT) using urokinase combined with head-shaking method in order to prevent cerebral vasospasm. In this paper, we showed the surgical procedure for CWT and reported the effect of this therapy in preventing vasospasm following SAH. A total of 332 consecutive cases with Fisher group 3 SAH since 1988 were analyzed. Of these patients, 118 cases (56 cases before 1994 and 62 cases after 1994) had not CWT, and, 214 cases after 1994 had this therapy. All of these patients had clipping surgery within 3 days following SAH, and had postoperative management both with normovolemia and normal to mild hypertension. In these two groups, the incidence of symptomatic vasospasm (transiently symptomatic vasospasm without infarction), cerebral infarction due to vasospasm on CT, and mortality and morbidity (M&M) due to vasospasm were analyzed. In the group without CWT, the incidences of symptomatic vasospasm, cerebral infarction on CT, and M&M due to vasospasm were 4.2%, 28.8%, and 17.8%, respectively. On the other hand, in the group with CWT, they were 3.7%, 6.5%, and 2.8%, respectively. In the patients with CWT, the incidence of cerebral infarction on CT due to vasospasm and M&M due to vasospasm were significantly (p < 0.05) decreased. CWT was effective in preventing cerebral vasospasm.

Association between symptom duration and cerebrospinal fluid pressure, protein concentration, and number of cells in patients with intracranial hypotension.

We sought to investigate the association between symptom duration and cerebrospinal fluid (CSF) pressure, protein concentration, and cell counts in patients with intracranial hypotension, in addition to examining differences between spontaneous and post-traumatic types. We investigated 115 consecutive patients with CSF leaks, demonstrated by radionuclide cisternography. In patients with spontaneous CSF leaks, a significant decrease in pressure and increase in protein concentration and number of cells were observed in patients with a symptom duration of 3 months. Symptom duration was not associated with those CSF parameters in patients with post-traumatic CSF leaks.

Symptom predictors of cerebrospinal fluid leaks.

BACKGROUND: Spinal cerebrospinal fluid (CSF) leaks, which are considered a cause of intracranial hypotension, generally do not cause any local symptoms. Although symptoms are key elements for further evaluation, few studies have examined symptom predictors of intracranial hypotension. The aim of this study was to determine what symptoms are predictors of CSF leaks in patients suspected of intracranial hypotension. METHODS: We performed radionuclide cisternography in 207 consecutive patients suspected of intracranial hypotension. Intracranial hypotension was suspected when a patient had a history of minor trauma and complained about uncontrolled headache, cranial nerve dysfunction, autonomic dysfunction, or higher brain dysfunction. The leakage of CSF was defined as direct signs of tracer leak into the spinal epidural space or early accumulation of the tracer in the urinary bladder. We obtained information on 16 symptoms commonly reported in previous studies. RESULTS: CSF leaks were observed in 154 cases (74%). Back pain, limb pain, and limb numbness were inversely associated with CSF leaks (p = 0.042, p = 0.045, and p = 0.006, respectively). In logistic regression analysis, diplopia was a positive predictor of CSF leaks (odds ratio [OR], 6.53; 95% confidence interval [CI], 1.49 to 28.51), whereas limb numbness was a negative predictor (OR, 0.38; 95% CI, 0.17 to 0.84). Of the 21 patients in whom diplopia was present and limb numbness was absent, 20 had CSF leaks (specificity, 98%; positive predictive value, 95%). CONCLUSION: Some symptoms may be helpful in the diagnosis of CSF leaks in patients suspected of intracranial hypotension.

[Acute onset of visual disturbance in a patient with arachnoid cyst in the middle cranial fossa].

Intracranial arachnoid cyst occurs most frequently in the middle fossa. Most of them are asymptomatic with or without neurological involvement. However some develop neurological deficits such as increased intracranial pressure, which manifests as headache, epilepsy and focal neurological deficits. Here we present an adult case of arachnoid cyst in the middle cranial fossa: the patient demonstrated rapidly deteriorating visual field defect and decreased visual acuity. The symptoms were improved by an emergency surgery. This is the first case report describing optic nerve compression due to an arachnoid cyst. Result of the coronal and sagittal magnetic resonance imaging (MRI) scans showed effective optic nerve compression. Long-standing asymptomatic arachnoid cysts might progress rapidly to cause cranial nerve deficits thus meticulous MRI follow-up are important in these patients.

Preservation of the lesser occipital nerve during microvascular decompression for hemifacial spasm. Technical note.

The authors report on their technique for preserving the lesser occipital nerve (LON) during lateral suboccipital craniotomy. In their technique, the LON, which runs along the surface of or just beneath the sternocleidomastoid muscle, is identified and preserved. Lesser occipital nerve preservation using their technique was attempted in 25 patients who underwent microvascular decompression for hemifacial spasm. The LON was successfully preserved in 16 of these patients, was impossible to preserve in two patients, and could not be identified in seven patients. Among the patients in whom LON preservation was successful, 87.5% were free of sensory disturbance 6 months after surgery, whereas both patients in whom the LON could not be preserved complained of sensory disturbances in the occipital area and the posterior part of the auricula. Fifty-seven percent of the patients whose LON could not be identified complained of sensory disturbance. Thus, this technique for preserving the LON reduces the incidence of sensory disturbance in the occipital region after suboccipital craniotomy for microvascular decompression for hemifacial spasm.

Pituitary cyst presenting with hyponatremia and increased secretion of brain natriuretic peptide. Case report.

In most cases of pituitary cyst there are no clinical symptoms and the lesions are found incidentally. The authors report the case of a 60-year-old man with a pituitary cyst causing visual disturbance and hyponatremia. The patient presented with appetite loss and general fatigue. On admission, blood workup showed severe hyponatremia (112 mEq/L), and bitemporal hemianopsia was observed on neurological examination. Magnetic resonance imaging revealed an intra- and suprasellar region cystic mass extending to the frontal base and hypothalamic area. The serum level of brain natriuretic peptide (BNP) was elevated (92 pg/ml) with polyuria and excessive Na excretion. Transsphenoidal surgery was performed to drain the cyst. The cyst wall was partially excised and the cystic fluid was aspirated. The secretion of BNP normalized postoperatively, and the hyponatremia and visual symptoms resolved. Histological examination, including an electron microscopy study, confirmed the diagnosis of a simple cyst. This appears to be the first reported case of a pituitary simple cyst associated with hyponatremia and an elevated BNP level.

[Body temperature in the super-acute phase of the cerebrovascular disorders: mainly focused on the subarachnoid hemorrhage].

BACKGROUNDS AND PURPOSE: Body temperature in the acute phase of cerebrovascular disorders(CVDs) may influence the outcome. However, the natural course of body temperature after CVDs has not yet been clarified. The purpose of this study was to elucidate the natural courses of body temperature after CVDs. PATIENTS AND METHODS: We retrospectively investigated 681 patients with CVDs(subarachnoid hemorrhage(SAH): 478, cerebral ischemia: 47, intracerebral hemorrhage(ICH): 156) who were admitted within 24 h after onset. The body temperature was measured with an electronic thermometer at the axilla on admission. The body temperatures of 73 patients with non-ruptured cerebral aneurysms on admission(admitted between 09:00 and 15:00) were used as normal control group. RESULTS: The body temperature in the control group was 36.49 +/- 0.45 degrees C. In comparison, the temperature in the SAH group was significantly lower(35.88 +/- 1.00 degrees C, n = 338, p < 0.001) when the patients were admitted within 4 h after onset, and significantly higher (36.80 +/- 0.85 degrees C, n = 140, p < 0.05) when they were admitted after 4 h and up to 24 h. There was a significant negative correlation between the severity of the SAH and body temperature within 4 h and a significant positive correlation beyond 4 h. Body temperature in the cerebral ishcemia group was significantly lower than in the control group(36.09 +/- 0.59 degrees C, n = 17, p < 0.05) when the patients were admitted within 2 h, but was close to that in the control group when they were admitted beyond 2 h and up to 24 h after onset (36.45 +/- 0.58 degrees C, n = 30). The falls of body temperature in the super-acute phase in the SAH and the cerebral ischemia groups were observed in patients admitted between 09:00 and 15:00. Although body temperature in the ICH group was slightly lower when the patients were admitted within 4 h and slightly higher when admitted beyond 4 h and up to 24 hours after onset, no significant differences were observed in comparison with the control group. In the super-acute phase of the cerebral ischemia and the ICH, body temperature tended to be lower in the patients with worse condition. CONCLUSION: This study clearly demonstrated that body temperatures in patients with CVDs changed rapidly within 24 h after onset. Body temperature in the SAH group within 4 h and that in the cerebral ischemia group within 2 h after onset was significantly lower than in the control group. These temperature falls were not the products of circadian rhythm. The temperature in the SAH group beyond 4 h and up to 24 h after onset rose significantly. Comparison with normal controls and consideration of the circadian rhythm are important when studying changes of body temperature in patients with CVDs.