Multistate outbreak of listeriosis associated with cantaloupe.

BACKGROUND: Although new pathogen-vehicle combinations are increasingly being identified in produce-related disease outbreaks, fresh produce is a rarely recognized vehicle for listeriosis. We investigated a nationwide listeriosis outbreak that occurred in the United States during 2011. METHODS: We defined an outbreak-related case as a laboratory-confirmed infection with any of five outbreak-related subtypes of Listeria monocytogenes isolated during the period from August 1 through October 31, 2011. Multistate epidemiologic, trace-back, and environmental investigations were conducted, and outbreak-related cases were compared with sporadic cases reported previously to the Listeria Initiative, an enhanced surveillance system that routinely collects detailed information about U.S. cases of listeriosis. RESULTS: We identified 147 outbreak-related cases in 28 states. The majority of patients (127 of 147, 86%) were 60 years of age or older. Seven infections among pregnant women and newborns and one related miscarriage were reported. Of 145 patients for whom information about hospitalization was available, 143 (99%) were hospitalized. Thirty-three of the 147 patients (22%) died. Patients with outbreak-related illness were significantly more likely to have eaten cantaloupe than were patients 60 years of age or older with sporadic illness (odds ratio, 8.5; 95% confidence interval, 1.3 to ∞). Cantaloupe and environmental samples collected during the investigation yielded isolates matching all five outbreak-related subtypes, confirming that whole cantaloupe produced by a single Colorado farm was the outbreak source. Unsanitary conditions identified in the processing facility operated by the farm probably resulted in contamination of cantaloupes with L. monocytogenes. CONCLUSIONS: Raw produce, including cantaloupe, can serve as a vehicle for listeriosis. This outbreak highlights the importance of preventing produce contamination within farm and processing environments.

Rapid assessment of Ebola infection prevention and control needs--six districts, Sierra Leone, October 2014.

As of October 31, 2014, the Sierra Leone Ministry of Health and Sanitation had reported 3,854 laboratory-confirmed cases of Ebola virus disease (Ebola) since the outbreak began in May 2014; 199 (5.2%) of these cases were among health care workers. Ebola infection prevention and control (IPC) measures are essential to interrupt Ebola virus transmission and protect the health workforce, a population that is disproportionately affected by Ebola because of its increased risk of exposure yet is essential to patient care required for outbreak control and maintenance of the country's health system at large. To rapidly identify existing IPC resources and high priority outbreak response needs, an assessment by CDC Ebola Response Team members was conducted in six of the 14 districts in Sierra Leone, consisting of health facility observations and structured interviews with key informants in facilities and government district health management offices. Health system gaps were identified in all six districts, including shortages or absence of trained health care staff, personal protective equipment (PPE), safe patient transport, and standardized IPC protocols. Based on rapid assessment findings and key stakeholder input, priority IPC actions were recommended. Progress has since been made in developing standard operating procedures, increasing laboratory and Ebola treatment capacity and training the health workforce. However, further system strengthening is needed. In particular, a successful Ebola outbreak response in Sierra Leone will require an increase in coordinated and comprehensive district-level IPC support to prevent ongoing Ebola virus transmission in household, patient transport, and health facility settings.

Risk factors early in the 2010 cholera epidemic, Haiti.

During the early weeks of the cholera outbreak that began in Haiti in October 2010, we conducted a case-control study to identify risk factors. Drinking treated water was strongly protective against illness. Our results highlight the effectiveness of safe water in cholera control.

Effect of diazepam and yohimbine on neuronal activity in sham and hemiparkinsonian rats.

The prefrontal cortex and the amygdala are critical for the emotional guidance of behavior and are believed to be a site of action for many anxiolytics and anxiogenics. Despite extensive studies examining how these drugs affect behavior, there is little information regarding their effects on neuronal activity. Additionally, with recent recognition of anxiety as a non-motor symptom of Parkinson's disease, it is unknown if activity in the cortex and the amygdala is altered. Previously, we reported that hemiparkinsonian rats had higher baseline anxiety-like behavior and diminished responsiveness to the acute anxiolytic, diazepam. In contrast, sham-lesioned rats exhibited anxiolytic behavior to diazepam. In this study, we monitored in vivo single-unit spiking activity simultaneously from the anterior cingulate cortex (ACC) and the basolateral amygdala (BLA) in anesthetized sham-lesioned and hemiparkinsonian rats to unmask neuro-circuits underpinning the difference in diazepam responsiveness. We found that baseline spiking activity in the ACC was the same in both sham and hemiparkinsonian rats. We also noted a similar phenomenon for baseline activity in the BLA between sham and hemiparkinsonian rats. However, neuronal spiking activity after diazepam administration (1.5mg/kg, SubQ) was lower than in controls in the ACC of sham-lesioned rats whereas no difference was noted after diazepam treatment in hemiparkinsonian rats. BLA neuronal spiking activity was unaffected by diazepam administration in either animal group. On the other hand, yohimbine treatment (5mg/kg, SubQ) coincided with lower neuronal spiking activity compared to controls in the BLA of sham-lesioned rats, but was unchanged from controls in hemiparkinsonian rats. Yohimbine did not affect ACC neuronal spiking activity in either group. Overall, the lack of ACC responsiveness to diazepam in hemiparkinsonian, but not sham-lesioned rats underscores a plausible fundamental difference in anxiety-related neural signaling between animal groups.

Investigation of diazepam efficacy on anxiety-like behavior in hemiparkinsonian rats.

There is growing recognition that anxiety disorders have a greater impact on quality of life in Parkinson's disease than motor symptoms. Yet, little is known about the pathophysiology underlying this non-motor symptom in Parkinson's disease which poses a considerable barrier in developing effective treatment strategies. Here, we administered diazepam to hemiparkinsonian and non-parkinsonian rats and assessed its efficacy in three anxiety behavioral tests. At present, no information about this exists in preclinical research with sparse data in the clinical literature. Moreover, diazepam is an acute anxiolytic which makes this drug a suitable research tool to unmask differences in anxiety-like behavior. Using the unilateral, medial forebrain bundle 6-hydroxydopamine rat model of Parkinson's disease, we noted that hemiparkinsonian rats had more baseline anxiety-like behavior with 60% of them exhibiting high anxiety (HA) behavior in the elevated plus maze. In contrast, 41% of sham-lesioned rats and 8% of naïve rats exhibited HA behavior. Next, we employed the elevated plus maze and noted that diazepam (1.5mg/kg) was anxiolytic in low anxiety (LA) sham-lesioned (p=0.006) and HA sham-lesioned rats (p=0.016). Interestingly, diazepam was anxiolytic for LA hemiparkinsonian rats (p=0.017), but not for HA hemiparkinsonian rats (p=0.174) despite both groups having similar motor impairment and parkinsonian phenotype. Overall, diazepam administration unmasked differences in anxiolytic efficacy between HA hemiparkinsonian rats, LA hemiparkinsonian rats and non-parkinsonian rats. Our data suggests that neuro-circuits involved in anxiety-like behavior may differ within these groups and posits that diazepam may have reduced efficacy in certain individuals with PD anxiety disorders.

Stimulation of the subthalamic nucleus engages the cerebellum for motor function in parkinsonian rats.

Deep brain stimulation (DBS) is effective in managing motor symptoms of Parkinson's disease in well-selected individuals. Recently, research has shown that DBS in the basal ganglia (BG) can alter neural circuits beyond the traditional basal ganglia-thalamus-cortical (BG-TH-CX) loop. For instance, functional imaging showed alterations in cerebellar activity with DBS in the subthalamic nucleus (STN). However, these imaging studies revealed very little about how cell-specific cerebellar activity responds to STN stimulation or if these changes contribute to its efficacy. In this study, we assess whether STN-DBS provides efficacy in managing motor symptoms in Parkinson's disease by recruiting cerebellar activity. We do this by applying STN-DBS in hemiparkinsonian rats and simultaneously recording neuronal activity from the STN, brainstem and cerebellum. We found that STN neurons decreased spiking activity by 55% during DBS (P = 0.038), which coincided with a decrease in most pedunculopontine tegmental nucleus and Purkinje neurons by 29% (P < 0.001) and 28% (P = 0.003), respectively. In contrast, spike activity in the deep cerebellar nuclei increased 45% during DBS (P < 0.001), which was likely from reduced afferent activity of Purkinje cells. Then, we applied STN-DBS at sub-therapeutic current along with stimulation of the deep cerebellar nuclei and found similar improvement in forelimb akinesia as with therapeutic STN-DBS alone. This suggests that STN-DBS can engage cerebellar activity to improve parkinsonian motor symptoms. Our study is the first to describe how STN-DBS in Parkinson's disease alters cerebellar activity using electrophysiology in vivo and reveal a potential for stimulating the cerebellum to potentiate deep brain stimulation of the subthalamic nucleus.

Gap junction blockers attenuate beta oscillations and improve forelimb function in hemiparkinsonian rats.

Parkinson's disease (PD) is a neurodegenerative disease characterized by akinesia, bradykinesia, resting tremors and postural instability. Although various models have been developed to explain basal ganglia (BG) pathophysiology in PD, the recent reports that dominant beta (ß) oscillations (12-30Hz) in BG nuclei of PD patients and parkinsonian animals coincide with motor dysfunction has led to an emerging idea that these oscillations may be a characteristic of PD. Due to the recent realization of these oscillations, the cellular and network mechanism(s) that underlie this process remain ill-defined. Here, we postulate that gap junctions (GJs) can contribute to ß oscillations in the BG of hemiparkinsonian rats and inhibiting their activity will disrupt neuronal synchrony, diminish these oscillations and improve motor function. To test this, we injected the GJ blockers carbenoxolone (CBX) or octanol in the right globus pallidus externa (GPe) of anesthetized hemiparkinsonian rats and noted whether subsequent changes in ß oscillatory activity occurred using in vivo electrophysiology. We found that systemic treatment of 200mg/kg CBX attenuated normalized GPe ß oscillatory activity from 6.10±1.29 arbitrary units (A.U.) (pre-CBX) to 2.48±0.87 A.U. (post-CBX) with maximal attenuation occurring 90.0±20.5min after injection. The systemic treatment of octanol (350mg/kg) also decreased ß oscillatory activity in a similar manner to CBX treatment with ß oscillatory activity decreasing from 3.58±0.89 (pre-octanol) to 2.57±1.08 after octanol injection. Next, 1µl CBX (200mg/kg) was directly injected into the GPe of anesthetized hemiparkinsonian rats; 59.2±19.0min after injection, ß oscillations in this BG nucleus decreased from 3.62±1.17 A.U. to 1.67±0.62 A.U. Interestingly, we were able to elicit ß oscillations in the GPe of naive non-parkinsonian rats by increasing GJ activity with 1µl trimethylamine (TMA, 500nM). Finally, we systemically injected CBX (200mg/kg) into hemiparkinsonian rats which attenuated dominant ß oscillations in the right GPe and also improved left forepaw akinesia in the step test. Conversely, direct injection of TMA into the right GPe of naive rats induced contralateral left forelimb akinesia. Overall, our results suggest that GJs contribute to ß oscillations in the GPe of hemiparkinsonian rats.

Force and pressure distribution beneath a conventional dressage saddle and a treeless dressage saddle with panels.

The objective of this study was to compare forces and pressure profiles beneath a conventional dressage saddle with a beechwood spring tree and a treeless dressage saddle without a rigid internal support and incorporating large panels and a gullet. The null hypothesis was that there is no difference in the force and pressure variables for the two saddles. Six horses were ridden by the same rider using the conventional dressage saddle and the treeless dressage saddle in random order and pressure data were recorded using an electronic pressure mat as the horses trotted in a straight line. The data strings were divided into strides with ten strides analyzed per horse-saddle combination. Variables describing the loaded area, total force, force distribution and pressure distribution were calculated and compared between saddles using a three-factor ANOVA (P<0.05). Contact area and force variables did not differ between saddles but maximal pressure, mean pressure and area with pressure >11kPa were higher for the treeless dressage saddle. The panels of the treeless dressage saddle provided contact area and force distribution comparable to a conventional treed saddle but high pressure areas were a consequence of a narrow gullet and highly-sloped panels. It was concluded that, even with a treeless saddle, the size, shape, angulation, and position of the panels must fit the individual horse.