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A large outbreak of haemorrhagic fever (subsequently named Ebola haemorrhagic fever) occurred in southern Sudan between June and November 1976. There was a total of 284 cases; 67 in the source town of Nzara, 213 in Maridi, 3 in Tembura, and 1 in Juba. The outbreak in Nzara appears to have originated in the workers of a cotton factory. The disease in Maridi was amplified by transmission in a large, active hospital. Transmission of the disease required close contact with an acute case and was usually associated with the act of nursing a patient. The incubation period was between 7 and 14 days. Although the link was not well established, it appears that Nzara could have been the source of infection for a similar outbreak in the Bumba Zone of Zaire.In this outbreak Ebola haemorrhagic fever was a unique clinical disease with a high mortality rate (53% overall) and a prolonged recovery period in those who survived. Beginning with an influenza-like syndrome, including fever, headache, and joint and muscle pains, the disease soon caused diarrhoea (81%), vomiting (59%), chest pain (83%), pain and dryness of the throat (63%), and rash (52%). Haemorrhagic manifestations were common (71%), being present in half of the recovered cases and in almost all the fatal cases.Two post mortems were carried out on patients in November 1976. The histopathological findings resembled those of an acute viral infection and although the features were characteristic they were not exclusively diagnostic. They closely resembled the features described in Marburg virus infection, with focal eosinophilic necrosis in the liver and destruction of lymphocytes and their replacement by plasma cells. One case had evidence of renal tubular necrosis.Two strains of Ebola virus were isolated from acute phase sera collected from acutely ill patients in Maridi hospital during the investigation in November 1976. Antibodies to Ebola virus were detected by immunofluorescence in 42 of 48 patients in Maridi who had been diagnosed clinically, but in only 6 of 31 patients in Nzara. The possibility of the indirect immunofluorescent test not being sufficiently sensitive is discussed.Of Maridi case contacts, in hospital and in the local community, 19% had antibodies. Very few of them gave any history of illness, indicating that Ebola virus can cause mild or even subclinical infections. Of the cloth room workers in the Nzara cotton factory, 37% appeared to have been infected, suggesting that the factory may have been the prime source of infection.
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PMID:Ebola haemorrhagic fever in Sudan, 1976. Report of a WHO/International Study Team. 30 55

Twelve patients with otherwise uncomplicated acute viral hepatitis (two were HBsAg-positive) developed renal failure. Apart from dehydration due to repeated vomiting in one patient, no factor responsible for precipitating renal failure could be identified. The clinical course was characterised by renal failure with plasma urea concentrations reaching maximum values of 26-69 mmol/l (175-416 mg/100 ml). Ten patients needed dialysis for up to two weeks. Seven patients recovered completely, while the other five died from sepsis. The types of renal failure were similar to those described in fulminant hepatic failure and cirrhosis--namely, functional renal failure in five patients and acute tubular necrosis in seven. Two of the patients with functional renal failure later developed tubular necrosis. The mechanism responsible for renal failure in acute viral hepatitis is uncertain, though endotoxaemia may contribute.
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PMID:Renal failure in otherwise uncomplicated acute viral hepatitis. 68 5

Seven patients, 4 girls and 3 boys, aged 3 to 12 years /X = 7.14/ affected by haemorrhagic fever with renal syndrome /HFRS/., were hospitalized at the University Children's Hospital in Belgrade during the last two years /January 1988-January 1990/. The diagnosis was established on the basis of clinical features, epidemiological data and autopsy findings in one patient while in the others the diagnosis of HFRS was confirmed serologically by indirect immunoflorescence tests on Vero E 6 cells. A significant increase in antibody titre against Hantaan virus was found in all serologically tested patients. Three of them had also significant increase of antibody titre against Soeul and one against Puumale virus. In four patients the disease appeared as family outbreak at the end of January 1988 while the others were sporadical cases. All patients but one mentioned contact with rodents at home or in fields. The predominant slynical symptom were: sudden onset of febrile condition with headache, generalized malaise, myalgia, abdominal pain, vomiting, diarrhoea, oliguria and oedema. All patients had haematuria and only one had other severe haemorrhagic manifestations. Four patients were hypertensive. Two patients had renal insufficiency, but only one required haemodialysis. Five patients recovered after 2 to 8 weeks without sequellae, one patient was still /7 months after the beginning of the disease/ in mild renal insufficiency and one patient died. Autopsy findings showed tubular necrosis in the kidney, myocarditis, massive pneumonia with hydrothorax and jejunal haemorrhagia.
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PMID:[Hemorrhagic fever with renal syndrome in children]. 168 34

The effect of meropenem on animal kidneys has been assessed in rats (5 of each sex/group), rabbits (3 of each sex/group) and monkeys (3 of each sex/group) in comparative iv studies with ceftazidime, cefotaxime, cephaloridine and imipenem (without cilastatin). Diarrhoea occurred in rabbits and monkeys dosed with imipenem or meropenem. Emesis occurred only after the administration of imipenem to monkeys. After 14 days administration to rats evidence of nephrotoxicity was seen only in males dosed with cephaloridine (850 mg/kg); no changes were seen with ceftazidime, cefotaxime or meropenem (all at 1000 mg/kg). Four days after a single dose to rabbits renal tubular necrosis was seen in all animals receiving imipenem (150 mg/kg) and cephaloridine (250 mg/kg). Minimal histopathological changes to the kidneys were seen with cefotaxime, ceftazidime and meropenem (all at 400 mg/kg). After seven days' administration to cynomolgus monkeys imipenem (180 mg/kg) caused moderate to severe tubular necrosis. No tubular damage was seen with meropenem at 180 mg/kg or with cefotaxime or ceftazidime (both at 500 mg/kg). At 500 mg/kg meropenem caused mild tubular regeneration and/or fat accumulation in 3/6 animals, with mild tubular necrosis in one of these. The data from these three species indicate that meropenem has a low nephrotoxic potential in these animal models.
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PMID:Safety evaluation of meropenem in animals: studies on the kidney. 268 Nov 27

Because of a projected pilot study with EDHPA in Cooley's anemia patients, animal studies with emphasis on reversibility of potential toxic signs were performed. Young dogs were treated iv with 6-18 mg/kg or orally with 30-240 mg/kg for 14 days followed by a 16-day recovery period. Drug-induced emesis, elevated BUN changes in kidney, spleen, and thymus weights diminished during recovery. One deceased dog exhibited nephrotoxicity consisting of tubular necrosis and deposition of the iron-EDHPA complex. The latter was observed in the excreta of survivors but kidney damage was not evident. Atrophy of the spleen and thymus in the deceased dog was consistent with less intense organ weight changes in recovered survivors. In the absence of morphologic changes after recovery, the precise effect on the immune system is unknown. The iv LD50 was 53 mg/kg for rats and mice. No rodent deaths occurred at an oral dose of 6000 mg/kg. An elevated BUN and changes in kidney, spleen, and thymus weights were confirmed in rodents given iv doses of 5-20 mg/kg or oral doses of 150-600 mg/kg for 5 days. It is cautioned that during the use of EDHPA derivatives that the functions of the renal and immune systems be monitored.
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PMID:Preliminary toxicity findings in dogs and rodents given the iron chelator ethylenediamine-N,N'-bis(2-hydroxyphenylacetic acid) (EDHPA). 369 19

25 Patients with metastatic non-seminomatous testicular neoplasms were treated by surgery and cytostatic therapy using a combination consisting of Velban, Bleomycin, Cis-Platinum and/or Ifosfamid. In 22 patients this procedure induced a persistant complete remission with a mean observation time of 23 months. 2 patients died because of post-surgical complications after a second-look-lymphadenectomy. They suffered from rapidly progressive tumor disease. One patient died in a septicemia during chemotherapy. Our experience is that morbidity of an effective chemotherapy should not be underestimated. Transient bone marrow suppression, anorexia, alopecia and hyperpigmentation are unavoidable. However, severe vomiting, disturbed electrolyte metabolism, hemorrhagic cystitis, anemia and septicemia can well be managed by respective supportive care. Septicemia, for instance, may be treated with appropriate antibiotics without inducing tubular necrosis. Supportive measures also will avoid severe chronic defects of ear and kidney function.
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PMID:[Side-effects of polychemotherapy in metastatic testicular neoplasms (author's transl)]. 617 53

We confirmed a cerebral lesion due to sodium bromate intoxication on MRI, SPECT, auditory brainstem response (ABR) and sensory evoked potential (SEP). The patient was 34 years old, and ingested sodium bromate (14 g) to commit suicide. Vomiting, epigastralgia, watery diarrhea and anuria appeared after 30 minutes and he became deaf within 12 hours. Renal function recovered after hemodialysis. Renal biopsy revealed acute renal tubular necrosis. After one month, burning pain appeared in bilateral lower extremities. Sporadic, clear and small high intensity spots were observed in the deep white matter of the right occipitotemporal border zone and bilateral centrum semiovale on T2 and proton weighted images of brain MRI. IMP-SPECT disclosed partial low perfusion in the left parietal gray matter. Central conduction time was delayed on ABR and SEP. The clinical symptoms and course together with laboratory studies suggest that the cerebral lesion was due to direct sodium bromate intoxication.
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PMID:[A case of sodium bromate intoxication with cerebral lesion]. 836 61

We present a case of acute lethal poisoning by oil of "epazote" (oil of chenopodium), in a 2 y 9 m female. The volatile oil was administered according to the advice of a "curandera" (female healer), in a total quantity of 40 ml. Clinical features of the poisoning were: vomiting, deep coma, seizures, mydriasis, apnea, metabolic acidosis, neurogenic shock and death. The EEG suggested a diffuse encephalopathy, the CT scan with an image of severe brain edema and ventricular collapse. Relevant postmortem findings were brain edema and neuronal necrosis, pneumonia, enteritis, pericholangitis, mild pancreatitis and tubular necrosis. The phytochemical analysis of volatile oil identified ascaridol, the main active compound of the chenopodium herbs, in a quantity of 39 mg/ml (1,560 mg in the dose administered), and Chenopodium graveolens as the plant employed to prepare it. According to the age of the patient, 60 mg of ascaridol would be the recommended dose formerly used in the treatment of parasitic disease. Thus 1,560 mg was 26 times higher than the recommended dose, and exceeded by 56% the dose of 1,000 mg reported as lethal in humans.
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PMID:[Fatal poisoning caused by oil of epazote, Chenopodium graveolens]. 896 84

The use of zinc in metal alloys and medicinal lotions dates back before the time of Christ. Currently, most of the commercial production of zinc involves the galvanizing of iron and the manufacture of brass. Some studies support the use of zinc gluconate lozenges to treat the common cold, but there are insufficient data at this time to recommend the routine use of these lozenges. Zinc is an essential co-factor in a variety of cellular processes including DNA synthesis, behavioral responses, reproduction, bone formation, growth, and wound healing. Zinc is a relatively common metal with an average concentration of 50 mg/kg soil and a range of 10-300 mg/kg soil. Meat, seafood, dairy products, nuts, legumes, and whole grains contain relatively high concentrations of zinc. The mobility of zinc in anaerobic environments is poor and therefore severe zinc contamination occurs primarily near points sources of zinc release. The recommended daily allowance for adults is 15 mg zinc. The ingestion of 1-2 g zinc sulfate produces emesis. Zinc compounds can produce irritation and corrosion of the gastrointestinal tract, along with acute renal tubular necrosis and interstitial nephritis. Inhalation of high concentrations of zinc chloride from smoke bombs detonated in closed spaces may cause chemical pneumonitis and adult respiratory distress syndrome. In the occupational setting inhalation of fumes from zinc oxide is the most common cause of metal fume fever (fatigue, chills, fever, myalgias, cough, dyspnea, leukocytosis, thirst, metallic taste, salivation). Zinc compounds are not suspected carcinogens. Treatment of zinc toxicity is supportive. Calcium disodium ethylenediaminetetraacetate (CaNa2EDTA) is the chelator of choice based on case reports that demonstrate normalization of zinc concentrations, but there are few clinical data to confirm the efficacy of this agent.
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PMID:Zinc. 1038 62

This report describes the clinical and pathological findings in a case of acute zinc poisoning in a young dog. The puppy suffered four days of progressively more severe vomiting and diarrhoea. Jaundice and pale mucous membranes, severe haematemesis and haemoglobinuria were other findings. Despite intensive therapy, the dog died a few hours after hospitalisation. Postmortem examination revealed a metallic foreign body in the stomach, catarrhal gastritis, hepatomegaly and enlarged, dark kidneys. Histology showed hepatic centrilobular vacuolar degeneration, haemoglobinuric nephrosis with early tubular necrosis, haemosiderosis and extramedullary haematopoiesis, as well as neuronal damage. The foreign body was mainly composed of zinc. Plasma zinc values were markedly raised (34.5 microg/ml; normal range 0.8 to 1.0 microg/ml). Pathophysiological mechanisms of zinc poisoning are discussed.
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PMID:Clinical and pathological findings of acute zinc intoxication in a puppy. 1248 42


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