Peracute Death Research Articles

Chlamydiosis in a Captive Group of Houbara Bustards (Chlamydotis undulata)

A chlamydiosis outbreak occurred in a Houbara bustard (Chlamydotis undulata) captive breeding group in Saudi Arabia, inducing peracute deaths, highly variable clinical signs, and pathological and histological lesions. Typical inclusion bodies in stained impression smears of spleen and prevalence (80%) of antibodies against Chlamydia, detected by a competitive enzyme immunoassay test, provided the bases for the diagnosis. This is the first report on a chlamydiosis outbreak in birds of the family Otididae.

Mechanism of pruritus and peracute death in mice induced by pseudorabies virus (PRV) infection.

Mechanisms of postinfectious pruritus and peracute death in mice by pseudorabies virus (PRV) were investigated by inoculating the Yamagata-S81 strain of PRV peripherally or intracerebrally into 4-week-old ICR and BALB/c mice. Clinical signs developed most rapidly in mice inoculated intracerebrally, with intermediate speed in mice inoculated intraocularly, and slowly in mice inoculated subcutaneously. Since intraocularly inoculated mice showed an acute reaction and this is considered a peripheral route, the distribution of viral antigens in the nervous system of intraocularly inoculated mice was examined immunohistologically. Viral antigens were mainly detected along the trigeminal and the oculomotor nerves, but neither necrosis nor an inflammatory response was observed in these areas. The infectious virus was efficiently recovered from the viral antigen-positive tissues. In the pruritic skin lesions, viral antigens were not observed. These findings indicate that the main route of viral spread in intraocularly inoculated mice is the trigeminal and oculomotor nerves and that the virus in the trigeminal nerve may trigger pruritus.

Enhanced cardiotoxicity in rabbits treated with verapamil and adriamycin.

Verapamil, a calcium channel blocker, reduces resistance of some tumors to Adriamycin by inhibiting Adriamycin efflux from resistant cells. This study shows that rabbits given 7 mg/kg of Adriamycin and 0.8 mg/kg of verapamil died earlier with functional and morphological cardiac abnormalities than rabbits given Adriamycin alone. Rabbits that were given verapamil and died peracutely had higher concentrations of Adriamycin in the myocardium. The relatively high dose of Adriamycin was expected to produce cardiotoxicity in rabbits within a matter of days. However, peracute death (within hours) in rabbits given the same dose of Adriamycin but with verapamil treatment was unexpected. These results suggest that combining Adriamycin with verapamil increases early cardiac toxicity. Therefore, clinical use of this combination should be approached cautiously until the interactions, including the possibility for enhanced normal tissue damage, are fully understood.

Salt Poisoning in Turkey Poults

A 4% mortality in 5-to-11-day-old turkey poults was attributed to 1.85% sodium chloride in the feed. The syndrome included peracute respiratory distress, ascites, and sudden death that resembled peracute heart failure. Clinical signs were observed only in the final phase of the toxicity, but progressive histologic lesions were found. Live, apparently unaffected poults showed increases in intracellular glycogen and cytoplasmic granularity, loss of striation, and early mild intercellular myocardial edema; similar but more severe histologic lesions were seen in live, ascites-affected poults. The ascites-affected poults had hydropericardium and hydrothorax which seemed to develop just minutes before death. Ultrastructurally, focal areas of myocardial cells exhibited myofibrillar disarray, lysis of myofilaments, widened Z-bands, and dilation of sarcoplasmic reticulum.

Investigation by the Ames test of urine samples from rats exposed to methyl isocyanate.

There is limited toxicological information on methyl isocyanate (MIC) which was the causal agent in the Bhopal disaster in December 1984 when several thou sand people were killed or injured. Kimmerle and Eben established that MIC was highly irritant to skin and mucosae and caused pulmonary oedema.1 Nemery etal suggested that at high concentrations MIC probably caused peracute death through reflex inhibition of breathing and rats surviving exposure exhibited narrowing of the airways and haemorrhagic pulmonary oedema.2 The lesions were repaired rap idly but residual peribronchal fibrosis and signs of renewed inflammation were apparent. Nemery etal also showed that sodium thiosulphate does not pro tect rats from the acute and subacute effects of MIC and that cyanide intoxication is not concerned in the clinical syndrome seen after exposure to MIC.3 There is little information on the genotoxic poten tial of this compound but MIC has been reported to be non-mutagenic in the standard Ames assay.4 Com pounds that are negative in the standard plate incor poration assay, however, may show positive results when urine from animals treated with the compound are tested.5

Effects of methyl isocyanate on the respiratory tract of rats.

Static exposure of rats to methyl isocyanate, for one hour, led to respiratory impairment during and after exposure. The resultant changes in breathing pattern suggest that this compound is both a sensory and a pulmonary irritant. Low concentrations resulted in extensive necrosis and loss of epithelial cells in the proximal airways but widespread alveolar damage was found only after exposure to high, lethal concentrations. At high concentrations methyl isocyanate probably caused peracute death through reflex inhibition of breathing. Animals surviving the exposure exhibited signs of airway narrowing and development of (haemorrhagic) pulmonary oedema. The epithelial lesions were repaired rapidly, but residual peribronchial fibrosis and signs of renewed injury/inflammation were apparent.

豚の増殖性出血性腸炎の発生について

Proliferative hemorrhagic enteritis (PHE) has been prevailing on two collective hog farms and a comprehensive farm in Okayama Prefecture since May, 1978, when 2 pigs died suddenly of it. Up to May, 1980, 309 hogs and young breeding pigs were affected. Of them, 112 died an acute death and the others recovered after treatment with several antibiotics or were condemned.Characteristic findings were extreme anemia, stinking tar-like feces, and acute or peracute death after a course of 1-2 days. Autopsy revealed plicate mucosal thickening of the ileum and deposition of bloody feces. Histologically, adenomatous proliferation of the mucosal epithelium led to the formation of irregular crypts and marked thickening of the mucosa. A number of Campylobacter organisms were found in the cytoplasm of hyperplastic epithelial cells. An attempt was made to isolate these organism by culture, but in vain.

Peracute and acute death from ischaemic heart disease within 4 days of onset of symptoms

Post-mortem examination was made of 136 patients who died of ischaemic heart disease from within a few minutes to 4 days after the onset to symptoms. Acute myocardial infarction was detected by means of the histochemistry of dehydrogenases in 102 cases (75%); in 34 cases(25%) no infarction was found, but the presence of coronary obstruction together with clinical symptoms justified the diagnosis of acute coronary insufficiency. Fifty-six of the infarctions occurred within 2--3 h after the onset of ischaemia, 24 within 4--5 h, 12 within 6--24 h, and 10 within 1--4 days. The chances of recovery increased if the patients survived for 24 h. The period of 5 h after the onset of ischaemia appeared especially important; 80 of 102 patients with acute myocardial infarction died during that period. Thirty-one of 34 patients with acute coronary insufficiency and 60 of 102 patients with acute myocardial infarction died peracutely, i.e. within a few minutes to 2 h after the onset of symptoms. In the patients of the latter group the onset of symptoms must have been delayed, otherwise none of these patients could have appeared in the category of peracute death. This delay was more obvious in the patients with acute myocardial infarction localized in the area supplied by the left descending artery. The occurrence of peracute deaths could not be correlated witha particular localization of area of infarction. The causes of coronary obstructions and the role of dynamic disturbances of coronary perfusion in the pathogenesis of coronary insufficiency and myocardial infarction and discussed.

Hepato- and pneumotoxicity of pyrrolizidine alkaloids and derivatives in relation to molecular structure

62 pyrrolizidine alkaloids and derivatives have been screened for acute and chronic hepato- and pneumotoxicity by the single dose method previously described. This procedure is satisfactory for the compounds of medium to high hepatotoxicity but failed to detect toxicity in certain other compounds of known, low hepatotoxicity. New findings significant in relation to hepatotoxicity are as follows: (i) On a molar basis, diesters of heliotridine and retronecine are about 4 times as toxic as the respective mono-esters and heliotridine esters are 2–4 times as toxic as retronecine esters. (ii) Crotanecine esters are less toxic than retronecine esters, and the 6,9-diester madurensine, 2–4 times less toxic than the 7,9-diester anacrotine (the difference being ascribed to there being only one reactive alkylating centre in the toxic metabolite from madurensine). (iii) Hepatotoxicity was confirmed for 7-angelylheliotridine but not observed for 9-angelylheliotridine and 7- and 9-angelylretronecine. (iv) Other significant compounds failing to induce hepatotoxicity were 9-pivalyl- and 7,9-dipivalylheliotridine, the α- and β-epoxides of monocrotaline, 7-angelyl-1-methylenepyrrolizidine and the methiodides of monocrotaline and senecionine. The following compounds are readily converted by rat liver microsomes in vitro into dehydroheliotridine (or dehydroretronecine): 7- and 9-angelylheliotridine, 7- and 9-angelylretronecine, 7,9-dipivalylheliotridine and otosenine. 7,9-Divalerylheliotridine, the α- and β-epoxides of monocrotaline, and retusamine yield pyrrolic metabolites more slowly. The preparation and characterisation of several alkaloid derivatives are described.Chronic lung lesions were produced by most compounds which gave chronic liver lesions, although a higher dose was required in some instances. This requirement may sometimes mean that chronic lung lesions cannot be induced because of the intervention of acute or peracute deaths. Apart from this factor, structure activity requirements for pneumotoxicity are the same as for hepatotoxicity, consistent with their being both caused by the same toxic metabolites.