scholarly journals Multiple episodes of 1080 (sodium monofluoroacetate) intoxication in a California calf-raising operation

2018 ◽  
Vol 30 (5) ◽  
pp. 747-751 ◽  
Author(s):  
John M. Adaska ◽  
Guillermo Rimoldi ◽  
Patricia C. Blanchard ◽  
John Champagne ◽  
Robert H. Poppenga ◽  
...  

Over a 1-y period, a California calf-raising operation experienced 4 separate episodes of sudden death in 4–6-mo-old steers. Each episode occurred in 1–3 contiguous pens on 1 of 3 properties owned by the operation, but eventually all 3 properties were involved. In each episode, animals appeared normal at the evening feeding but at the subsequent morning feeding were found dead or dying. Remaining live calves had a stiff gait and were often dribbling urine, but did not show respiratory signs until they were down and agonal. At postmortem examination, calves consistently had moderate-to-large numbers of ecchymotic and suffusive hemorrhages on the epicardial surface and moderate-to-large amounts of fluid in the pericardial sac. Pulmonary edema and/or moderate amounts of watery fluid in the thoracic and abdominal cavities were present in a smaller percentage. On histologic examination, the myocardium had variable myofiber degeneration characterized by hypereosinophilia and fragmentation with mild interstitial infiltrates. Testing of heart and liver samples for monensin found levels lower than in previous cases of monensin toxicity. Rumen content was negative for oleandrin and grayanotoxins. Sodium monofluoroacetate (trade name: 1080) was consistently detected at ⩾10 ppb in kidney and liver, and was concluded to be the cause of the intoxication.

2006 ◽  
Vol preprint (2007) ◽  
pp. 1
Author(s):  
Henry Krous ◽  
Amy Chadwick ◽  
Douglas Miller ◽  
Laura Crandall ◽  
Hannah Kinney

PEDIATRICS ◽  
1956 ◽  
Vol 17 (5) ◽  
pp. 663-699 ◽  
Author(s):  
Lester Adelson ◽  
Eleanor Roberts Kinney

One hundred twenty-six consecutive cases of sudden and unexpected death in children between the ages of 10 days and 2 years were studied. Anatomic and microbiologic studies were carried out and an investigation was made at the home in each case. Both sexes were equally vulnerable. Eighty-five per cent of the children were less than 6 months old. The peak incidence was at 2 months. Ninety-nine children were found dead and 27 were observed to die. The same variety and severity of anatomic lesions were found in both categories. Sixteen children in the same age range who died rapidly following known lethal voilence were studied as a control group. Of the nontraumatic sudden death ("unexplained") series 106 (84 per cent) revealed microscopic inflammatory changes in 1 or more sites of the respiratory tract, and histologic evidence of inflammatory disease in other organs was seen in many cases. Acute hemorrhagic pulmonary edema was a common anatomic finding (82 per cent). It was usually accompanied by visceral and cerebral congestion and hemorrhages. Special investigative procedures including staining of the liver for glycogen, determination of the glucose level of the cerebrospinal fluid and study of the adrenals for sudanophilia and birefringence indicated that these factors are without significance in sudden death in early life. A variety of congenital and acquired abnormalities, the presence of which had been unsuspected, was demonstrated at necropsy. Eleven per cent of the 126 cases showed no anatomic abnormalities other than the circulatory phenomena. No single bacterial organism or group of organisms was isolated with any degree of consistency from any site. All attempts to isolate viruses were negative. Ante-mortem symptomatology, circumstances of death, history of contact with infectious disease, and past history of repeated respiratory infection were without prognostic significance and were not pathognomic as to the cause of death. Eighty children had histories of mild illness for 48 hours or less prior to death. Fifty-three children had received some form of treatment during this interval. Sixty-nine children had histories of contact with infectious diseases. Forty-one children had past histories of repeated respiratory infections. The cases came from every social level. Sixty-five per cent had received good care while 35 per cent had received poor care. Many of the control cases showed inflamatory disease in the respiratory tract similar to that seen in the natural death group as well as anatomic evidence of lethal trauma. The inflammatory lesions are thus not incompatible with life. Several hypotheses are offered in an effort to link microscopic inflammatory respiratory tract changes with hemorrhagic pulmonary edema and sudden death. Anatomic and anamnestic evidence exclude mechanical suffocation by bedding. No statement as to the cause of death of an infant who has died suddenly and unexpectedly should be made without complete gross and microscopic studies and thorough investigation of the scene and circumstances of death.


2013 ◽  
Vol 2013 ◽  
pp. 1-3
Author(s):  
Guillermo M. Rimoldi ◽  
Robert B. Moeller

An adult Angus cow developed hyperthermia, prostration, and respiratory distress, dying 36 hours after the onset of clinical signs. The main finding during postmortem examination was a severe focally extensive pneumonia. Icterus and a chronic mastitis were also noticed. Histologic examination of the lungs detected fibrinonecrotic pneumonia, with large number of oat cells and intralesional Gram-negative bacterial colonies. Samples from lung lesions were collected, and a pure growth of Escherichia fergusonii was obtained. E. fergusonii is a member of Enterobacteriaceae, related to Escherichia coli and Salmonella sp. In veterinary medicine, E. fergusonii has been reported in calves and sheep with clinical cases suggestive of salmonellosis; in a horse and a goat with enteritis and septicemia; and in ostriches with fibrinonecrotic typhlitis. To our knowledge, this report represents the first description of E. fergusonii associated with an acute pneumonia in cattle.


2020 ◽  
Vol 30 (3) ◽  
Author(s):  
Samuel Anu Olowookere ◽  
Adegboyega Adeleke Abiodun ◽  
Joseph Gbenga Omole ◽  
Akinwumi Oluwole Komolafe ◽  
Akintunde Julius Olowookere ◽  
...  

BACKGROUND: Postmortem examination is necessary to diagnose the cause of sudden death, and family caregivers are expected to consent to this examination. This study assessed knowledge, attitude, practices and willingness of family caregivers to consent to postmortem examination of their relative if they die suddenly in a Nigerian tertiary hospital.METHODS: Descriptive cross-sectional study of family caregivers of our patients that completed an interviewer administered semistructured questionnaire assessing their knowledge, attitude, practices and willingness to consent to postmortem examination of their relative if they die suddenly. Data were analyzed using descriptive and inferential statistics.RESULTS: A total of 224 caregivers were interviewed. The mean age (SD) was 34.95 (11.74), ranging 22-75 years. They were parents (32.6%), siblings (37.9%), spouses (11.2%) and other relatives (18.3%). Only 17% had adequate knowledge, 44.6% positive attitude and 11.2% good practices to postmortem examination of sudden death. The majority (75.9%) would consent to postmortem examination of their relatives if they die suddenly. Sociodemographic variables associated with willingness to consent to postmortem examination after relative’s sudden death include being male (AOR 3.61; 95%CI 3.09-8.92; p=0.001), having tertiary education (AOR 4.83; 95%CI 1.01-8.29; p=0.034), Christianity (AOR 2.59; 95%CI 1.25-5.35; p=0.010) and skilled worker (AOR 1.43; 95%CI 1.33-3.80; p=0.020).CONCLUSION: Some family caregivers would not consent to postmortem examination of their relatives when they die suddenly. Sensitization programs targeting family caregivers are necessary to increase knowledge and enhance prevention of sudden death as well as improve willingness to consent to postmortem examination when their relatives die suddenly.


2017 ◽  
Vol 56 (2) ◽  
pp. 143-145 ◽  
Author(s):  
Hideyuki Maeda ◽  
Ruri Kikura-Hanajiri ◽  
Maiko Kawamura ◽  
Erika Nagashima ◽  
Ken-Ichi Yoshida

2017 ◽  
Vol 29 (4) ◽  
pp. 457-464 ◽  
Author(s):  
Josepha DeLay

Postmortem lesions and cause of death were evaluated retrospectively for 963 horses examined as part of the Ontario Racing Commission Death Registry over a 13-y period. The Death Registry was established in 2003 to identify factors leading to death or euthanasia of racehorses in this Canadian province. Postmortem examination was carried out on 56% of horses reported to the Death Registry and included Standardbred, Thoroughbred, and American Quarter Horses. Musculoskeletal injury was the most common reason for death associated with racing or training among all racehorses and involved 68% of horses. A history of sudden death during or immediately following exercise was described for 31% of racing- or training-associated deaths, and in 16% of all horses in the study. Sudden death occurred in horses of all breeds, and our report describes lesions associated with sudden death in a series of Standardbreds. The cause of death in these cases was most frequently attributed to cardiopulmonary lesions. The cause of death was undetermined in 20% of sudden death cases, and it is speculated that cardiac arrhythmia may have contributed to these deaths. Injection-associated death was documented in 4% of the study population. Lesions among horses whose death was not associated with exercise were similar to those in other equine populations, and lesions involving the gastrointestinal system were most common. Standardization of pathology reporting of pulmonary and other lesions in racehorse postmortem cases would allow direct comparison of results among racehorse populations.


1983 ◽  
Vol 20 (4) ◽  
pp. 440-449 ◽  
Author(s):  
J. A. Johnson ◽  
J. F. Prescott ◽  
R. J. F. Markham

Six foals were inoculated intrabronchially with a suspension of Corynebacterium equi. Six weeks before this challenge, three foals were vaccinated with a C. equi bacterin. Three foals were unvaccinated controls. All foals developed a severe bronchopneumonia in the inoculated lung, indicating that vaccination was not protective. Three foals (two vaccinated, one control) were killed eight to nine days after infection. One control died on day 9 with lesions of disseminated intravascular coagulation. The remaining two foals (one vaccinated, one control) were killed on day 17. C. equi was cultured in large numbers from affected lung and bronchial lymph nodes, and in smaller numbers from unaffected lung. spleen, and liver in all foals. In the 8- to 9-day-old lung lesions, the alveoli were filled with macrophages, neutrophils, and multinucleate giant cells and most contained numerous C. equi. The few foci of alveolar necrosis were associated with groups of bacteria-laden macrophages undergoing degeneration. In the lesions of 17-day duration. there was extensive parenchymal destruction with little fibrous tissue reaction. Lesions common to both groups included hyperplastic bronchiolitis, pulmonary edema, and perivascular lymphocytic cuffs and a pyogranulomatous lymphadenitis in bronchial nodes. One vaccinated foal had a microscopic pyogranulomatous colitis. The lesions in the experimentally infected foals are compared with those in naturally infected foals and discussed in terms of likely pathogenetic mechanisms involved in C. equi pneumonia in foals.


1937 ◽  
Vol 66 (4) ◽  
pp. 397-404 ◽  
Author(s):  
Sidney Farber

1. Bilateral cervical vagotomy in rabbits soon leads to death, usually within 8 to 24 hours. 2. Gradually increasing dyspnea, crises with expulsion of frothy, serous or sanguineous fluid from the mouth and nose, and terminal asphyxia are the important clinical features. 3. Postmortem examination reveals severe acute pulmonary edema and congestion, variable amounts of bronchopneumonia, and evidences of aspiration of food and secretions. This picture is similar to that found in the lungs in the bulbar form of poliomyelitis. 4. These changes are brought about by a combination of factors secondary to bilateral vagotomy: laryngeal paralysis (aspiration of food, slow asphyxia); loss of the vagal innervation of the lungs. 5. Laryngeal paralysis is not an essential factor in the production of severe pulmonary edema and death following bilateral cervical vagotomy. 6. To denote the pathogenesis of this type of edema, the term neuropathic pulmonary edema is employed.


2017 ◽  
Vol 29 (4) ◽  
pp. 442-449 ◽  
Author(s):  
Santiago S. Diab ◽  
Robert Poppenga ◽  
Francisco A. Uzal

In racehorses, sudden death (SD) associated with exercise poses a serious risk to jockeys and adversely affects racehorse welfare and the public perception of horse racing. In a majority of cases of exercise-associated sudden death (EASD), there are no gross lesions to explain the cause of death, and an examination of the cardiovascular system and a toxicologic screen are warranted. Cases of EASD without gross lesions are often presumed to be sudden cardiac deaths (SCD). We describe an equine SD autopsy protocol, with emphasis on histologic examination of the heart (“cardiac histology protocol”) and a description of the toxicologic screen performed in racehorses in California. By consistently utilizing this standardized autopsy and cardiac histology protocol, the results and conclusions from postmortem examinations will be easier to compare within and across institutions over time. The generation of consistent, reliable, and comparable multi-institutional data is essential to improving the understanding of the cause(s) and pathogenesis of equine SD, including EASD and SCD.


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