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A 21-year-old girl with recurrent abdominal pain after a robbery.
Selva-O'Callaghan A, Gomez-Acha J, Munne P, Vilardell-Tarres M.
Department of Internal Medicine, Vall d'Hebron Hospital, Passeig Vall d'Hebron, 119-129 08035 Barcelona, Spain. aselva@vhebron.net
Publication Types:
PMID: 16182903 [PubMed - indexed for MEDLINE]
Outbreak of Vibrio parahaemolyticus gastroenteritis associated with Alaskan oysters.
McLaughlin JB, DePaola A, Bopp CA, Martinek KA, Napolilli NP, Allison CG, Murray SL, Thompson EC, Bird MM, Middaugh JP.
Division of Public Health, Alaska Department of Health and Social Services, Anchorage, AK 99503, USA. joe_mclaughlin@health.state.ak.us
BACKGROUND: Vibrio parahaemolyticus, the leading cause of seafood-associated gastroenteritis in the United States, typically is associated with the consumption of raw oysters gathered from warm-water estuaries. We describe a recognized outbreak of V. parahaemolyticus infection associated with the consumption of seafood from Alaska. METHODS: After we received reports of the occurrence of gastroenteritis on a cruise ship, we conducted a retrospective cohort study among passengers, as well as active surveillance throughout Alaska to identify additional cases, and an environmental study to identify sources of V. parahaemolyticus and contributors to the outbreak. RESULTS: Of 189 passengers, 132 (70 percent) were interviewed; 22 of the interviewees (17 percent) met our case definition of gastroenteritis. In our multiple logistic-regression analysis, consumption of raw oysters was the only significant predictor of illness; the attack rate among people who consumed oysters was 29 percent. Active surveillance identified a total of 62 patients with gastroenteritis. V. parahaemolyticus serotype O6:K18 was isolated from the majority of patients tested and from environmental samples of oysters. Patterns on pulsed-field gel electrophoresis were highly related across clinical and oyster isolates. All oysters associated with the outbreak were harvested when mean daily water temperatures exceeded 15.0 degrees C (the theorized threshold for the risk of V. parahaemolyticus illness from the consumption of raw oysters). Since 1997, mean water temperatures in July and August at the implicated oyster farm increased 0.21 degrees C per year (P<0.001 by linear regression); 2004 was the only year during which mean daily temperatures in July and August at the shellfish farm did not drop below 15.0 degrees C. CONCLUSIONS: This investigation extends by 1000 km the northernmost documented source of oysters that caused illness due to V. parahaemolyticus. Rising temperatures of ocean water seem to have contributed to one of the largest known outbreaks of V. parahaemolyticus in the United States. Copyright 2005 Massachusetts Medical Society.
PMID: 16207848 [PubMed - indexed for MEDLINE]
Acute pancreatitis due to erythromycin overdose.
Tenenbein MS, Tenenbein M.
Department of Pediatrics and Child Health, University of Manitoba, Canada.
BACKGROUND: Antibiotic overdose is typically regarded as a benign event. We report a 15-year-old girl who developed pancreatitis after an overdose of erythromycin. CASE: A 15-year-old girl presented for care because of severe epigastric pain after an overdose of 5.3 g (16 x 333 mg tablets) of erythromycin base. Her physical examination was normal except for epigastric tenderness. Her serum lipase was 2024 U/L (normal, <60). She was treated with intravenous fluids and an opiate analgesic. Her serum lipase declined to 1834 and 73 U/L at 17 and 36 hours, respectively, after the initial measurement at which time she was asymptomatic. CONCLUSION: Our case supports transient pancreatitis as a potential consequence of erythromycin overdose.
PMID: 16215473 [PubMed - in process]
Protein adduct formation as a molecular mechanism in neurotoxicity.
Lopachin RM, Decaprio AP.
Department of Anesthesiology, Albert Einstein College of Medicine, Montefiore Medical Center, Bronx, New York 10467-2490, USA. lopachin@aecom.yu.edu
Chemicals that cause nerve injury and neurological deficits are a structurally diverse group. For the majority, the corresponding molecular mechanisms of neurotoxicity are poorly understood. Many toxicants (e.g., hepatotoxicants) of other organ systems and/or their oxidative metabolites have been identified as electrophiles and will react with cellular proteins by covalently binding nucleophilic amino acid residues. Cellular toxicity occurs when adduct formation disrupts protein structure and/or function, which secondarily causes damage to submembrane organelles, metabolic pathways, or cytological processes. Since many neurotoxicants are also electrophiles, the corresponding pathophysiological mechanism might involve protein adduction. In this review, we will summarize the principles of covalent bond formation that govern reactions between xenobiotic electrophiles and biological nucleophiles. Because a neurotoxicant can form adducts with multiple nucleophilic residues on proteins, the challenge is to identify the mechanistically important adduct. In this regard, it is now recognized that despite widespread chemical adduction of tissue proteins, neurotoxicity can be mediated through binding of specific target nucleophiles in key neuronal proteins. Acrylamide and 2,5-hexanedione are prototypical neurotoxicants that presumably act through the formation of protein adducts. To illustrate both the promise and the difficulty of adduct research, these electrophilic chemicals will be discussed with respect to covalent bond formation, suspected protein sites of adduction, and proposed mechanisms of neurotoxicity. The goals of future investigations are to identify and quantify specific protein adducts that play a causal role in the generation of neurotoxicity induced by electrophilic neurotoxicants. This is a challenging but critical objective that will be facilitated by recent advances in proteomic methodologies.
Publication Types:
PMID: 15901921 [PubMed - indexed for MEDLINE]
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Neurobehavioral effects of chronic dietary and repeated high-level spike exposure to chlorpyrifos in rats.
Moser VC, Phillips PM, McDaniel KL, Marshall RS, Hunter DL, Padilla S.
Neurotoxicology Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, US Environmental Protection Agency, Research Triangle Park, North Carolina 27711, USA.
This study aimed to model long-term subtoxic human exposure to an organophosphorus pesticide, chlorpyrifos, and to examine the influence of that exposure on the response to intermittent high-dose acute challenges. Adult Long-Evans male rats were maintained at 350 g body weight by limited access to a chlorpyrifos-containing diet to produce an intake of 0, 1, or 5 mg/kg/day chlorpyrifos. During the year-long exposure, half of the rats in each dose group received bi-monthly challenges (spikes) of chlorpyrifos, and the other half received vehicle. Rats were periodically tested using a neurological battery of evaluations and motor activity to evaluate the magnitude of the acute response (spike days) as well as recovery and ongoing chronic effects (non-spike days). Effects of the spikes differed as a function of dietary level for several endpoints (e.g., tremor, lacrimation), and in general, the high-dose feed groups showed greater effects of the spike doses. Animals receiving the spikes also showed some neurobehavioral differences among treatment groups (e.g., hypothermia, sensory and neuromotor differences) in the intervening months. During the eleventh month, rats were tested in a Morris water maze. There were some cognitive deficits observed, demonstrated by slightly longer latency during spatial training, and decreased preference for the correct quadrant on probe trials. A consistent finding in the water maze was one of altered swim patterning, or search strategy. The high-dose feed groups showed more tendency to swim in the outer annulus or to swim very close to the walls of the tank (thigmotaxic behavior). Overall, dietary exposure to chlorpyrifos produced long-lasting neurobehavioral changes and also altered the response to acute challenges.
PMID: 15901919 [PubMed - indexed for MEDLINE]
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