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Extract Between November 1972 and February 1973, severe outbreaks of a disease in broilers, characterized by congestive heart failure,, hydropericardium, liver shrinkage, ascites, and sometimes subcutaneous oedema were observed in the North Island. The disease resembled enzootic fatal syncope (toxic heart degeneration) described earlier in laying hens in New Zealand (Fischel, 1946), chick edema disease seen in the U.S.A. (Schmittle et al., 1958; Sanger et al., 1958), possible fat intoxication in chickens reported from Britain (Wannop and Chubb, 1961), and alimentary toxaemia or water belly ascites experienced in Australia (Sinkovic, 1961).

INTRODUCTION FOR the most part, studies of the chick edema disease have been short-term, that is, of four weeks duration or less (Brew et al., 1959; Douglass and Flick, 1961; Flick et al., 1962, 1963a,b, 1965a,b; and Alexander et al., 1962. A few long-term or chronic studies have been reported (Allen, 1961. A few long-term or chronic studies have been reported (Allen, 1964; and Allen and Lalich, 1962. The studies in this report were made to extend our knowledge of the chick edema disease to include the chronic effects of feeding fat containing the chick edema factor (CEF) at low levels for twelve weeks. EXPERIMENTAL Day-old S. C. White Leghorn cockerels were used for these studies. On the day of receipt from the hatchery, the chicks were randomized in the shipping carton, wing-banded, weighed, and placed in cages with raised wire-mesh floors. Ten or eleven birds were placed in each cage and were fed and watered ad libitum. Room temperature …

Feeding and injection studies have been performed with synthetic compounds which produce edema and pathological changes in S.C. White Leghorn chicks. Polychlorinated derivatives of dibenzo-p-dioxin were prepared either by chlorination of dibenzo-p-dioxin or by pyrolysis of 2,3,4,6-tetrachlorophenol and pentachlorophenol. The compounds prepared were administered to chicks by either oral feedings, oral intubation or intra-abdominal injection. Results of the feeding studies indicated that the hexachloro derivatives of dibenzo-p-dioxin most readily elicited the edema aspect of the chick edema disease but had low lethality, whereas the derivatives containing 3 and 4 chlorine atoms per molecule also caused edema but were the most lethal of the compounds tested. Hepta-and octachloro-dioxins, although capable of producing evidence of disease, were less toxic than the other polychlorinated derivatives. The pyrolytic product of 2,3,4,6-tetrachlorophenol, a mixture of predominantly hexa- and heptachlorodibenzo-p dioxins, was toxic when administered in single doses by way of oral intubation or by intra-abdominal injection.

PREVIOUS studies have shown that various oral diuretics incorporated into diets containing the chick edema factor (CEF) are selectively beneficial in the prevention of edema associated with the development of the chick edema disease (Flick and O’Dell, 1968a). Further, by carefully grading the dietary level of diuretics fed concomitantly with a fixed level of toxic fatty material (TFM) containing CEF, the diuretic activity of the compounds can be assayed (Flick and O’Dell, 1968b). This report is a confirmation and extension of our previous studies and deals with the effects of the oral diuretic, hydrochlorothiazide, at various dietary levels. MATERIALS AND METHODS Day-old S. C. White Leghorn cockerels were used for these studies. On the day of receipt from the hatchery, the chicks were randomized in the shipping carton, wing-banded, weighed, and placed in battery brooders (10 chicks/cage) with raised wire-mesh floors. Feed and water were accessible at all times. Room . . .

DURING the fall of 1957 severe outbreaks of an edema condition resulted in the death of millions of broilers in Central and Eastern United States. The pathology of this condition, termed chick edema disease, water belly, or hydropericardium (HP) syndrome, has been described by Schmittle et al. (1958), Sanger et al. (1958), and Hathaway et al. (1959). Wilder and Dugan (1958), Friedman et al. (1959), Machlin et al. (1959), Ames et al. (1960), and Harman et al. (1960) have also reported studies with the unknown factor. The source of the HP factor was traced to specific lots of feed grade fats containing a residue from some fat processing operations. It is believed that the residue contained either a contaminant, or in the course of the fat processing, a new and toxic compound for chicks was formed. The toxic principle appeared as a minor constituent in the unsaponifiable fraction of the …

Chick edema disease first came to the attention of the Food and Drug Administration in December, 1957, when it was learned that millions of broilers died in the eastern and Midwestern parts of the United States. Several groups in industry and government quickly determined that the disease was due to toxic components in certain feed fats (1-3), and that toxicity was associated with the unsaponifiable portion of the fat. Characteristic symptoms included the presence of excessive fluid in the heart sac and in the abdominal cavity of chicks fed toxic fat (2, 4, 5). These and other symptoms such as subcutaneous edema and liver necrosis were accompanied by high mortality beginning approximately in the third week. Allen (6, 7) suggested several years later that the accumulation of large quantities of extravascular fluid in chickens might be due to altered permeability of the vascular bed as well as cardiac decompensation and liver necrosis.

INTRODUCTION THE chick edema disease is a relatively new pathological entity first reported in 1957. The early reports of the syndrome, Anonymous (1957, 1958a, b, c), presented no analytical data on the body changes characteristic of the condition. Schmittle, Edwards and Morris (1958) reported that the disease resulted from feeding various rations and was not caused by a bacterial or viral agent. These workers were the first to describe the gross pathological appearance of chicks with the syndrome. Various workers, Ames et al. (1959), Brew et al. (1959), Friedman et al. (1959), Wooten and Alexander (1959), Harman et al. (1960) and Yartzoff et al. (1960), have attempted to chemically separate, purify and characterize the toxic agent. The first comprehensive study of the anatomical, biochemical and histological changes of the chick edema disease was reported by Allen (1961). He found that feeding a fat containing the toxic principle resulted in reduced…

The chick edema disease factor was found to be present in a number of distillates and residues that were obtained during the production of commercial fatty acids. The raw materials from which the toxic samples were produced included inedible animal tallows, acidulated vegetable oil foots, and oils recovered from tin plate manufacture. The chick edema factor was found to be present in several oleic acids and in a triolein. Twenty stearic acid samples which were examined were nontoxic.

Based on recently obtained analytical information, calculations were made to ascertain the toxic effects of chick edema factor (CEF) preparations for the intact day-old chick, the developing chick embryo, and the monkey. Results indicate that CEF, principally polychlorodibenzo-p-dioxins, elicits toxic responses in these experimental animals. For the intact chick, approximately 9 μ g./chick of total dioxins containing 2–8 chlorine atoms/molecule are detectable. For the fertile chicken egg, less than 1.0 ng. is detectable. For the monkey, as little as 2.15 mg. ingested for 445 days, or less, elicits obvious adverse effects. It is postulated that ingestion of these types of compounds may be toxic for man.

Summary Iranian strains of foot-and-mouth disease virus of Types A, O, and SAT 1 were attenuated for cattle by serial passage in different kinds of cells of hamster, cattle and sheep origin. Fully attenuated strains immunized cattle poorly and elicited a poor antibody response. Concentration by adsorption on aluminum hydroxyde increased the immunizing effect slightly, but the immunity produced was partial only. Intralingual challenge caused primary tongue vesicles without generalization. Saponin (1: 10,000) was without effect. Partly attenuated strains were immunogenic but cannot be used prophylactically. The possibility is discussed of using such strains as interfering agents in herds where FMD has just appeared and possibly also on adjacent farms directly menaced by the disease. Zusammenfassung Verhalten von iranischen Maul- und Klauenseuche-Virusstammen bei Rindern nach serienweiser Passage uber verschiedene Zellarten Iranische Maul- und Klauenseuche-Virusstamme der Typen A, O und SAT 1 wurden fur Rinder durch reihenweise Passagen auf verschiedenen Zellarten von Hamster, Rind und Schaf abgeschwacht. Voll abgeschwachte Stamme immunisierten Rinder nur schlecht und riefen auch kaum Antikorperbildung hervor. Eine Konzentrationssteigerung durch Adsorption an Aluminiumhydroxyd verbesserte den Immunisierungseffekt zwar etwas, doch bildete sich auch nur eine teilweise Immunitat. Intralinguale Verimpfung rief auf der Zunge Primarblaschen ohne Generalisation hervor. Saponin (1/10 000) hatte keine Wirkung. Nur teilweise abgeschwachte Stamme waren immunogen, doch lassen sie sich nicht prophylaktisch verwenden. Es wird die Moglichkeit diskutiert, solche Stamme als interferierende Agentien in Herden zu verwenden, in denen die Maul- und Klauenseuche gerade ausgebrochen ist, und moglicherweise auch auf den angrenzenden Farmen, die von der Seuche unmittelbar bedroht sind. Resume Comportement de souches iraniennes du virus de la fievre aphteuse chez les boeufs apres passages series sur differentes especes cellulaires Des souches iraniennes du virus de la fievre aphteuse des types A, O et SAT 1 sont attenuees pour les boeufs par des passages successifs sur differentes especes cellulaires du hamster, du boeuf et du mounton. 18 Tiere starben und 16 wurden pathologisch-histologisch untersucht. Klinische, pathologische und patho-histologische Befunde standen einheitlich in Beziehung zu gesteigerter Kapillardurchlassigkeit und allgemeiner Kreislaufstorung. Die Veranderungen glichen im wesentlichen denen der odemkrankheit der Schweine. Resume Donnees experimentales sur la pathogenie de la maladie de l'oedeme du porc: image clinique, modifications macroscopiques et microscopiques en relation avec un choc d'endotoxine On produit un choc d'endotoxine chez 52 porcs, en leur administrant des lipopolysaccharides de souches de E. coli O 9, O 89 et O 141. 18 animaux perissent et 16 sont examines sous l'aspect histo-pathologique. Les resultats cliniques, pathologiques et histo-pathologiques se trouvent en etroite relation avec l'augmentation de la permeabilite capillaire et les troubles generalises de la circulation. Les modifications s'apparentent pour l'essentiel a celles de la maladie de l'oedeme du porc. Resumen Datos experimentales sobre la patogenia de la enfermedad de los edemas del cerdo; cuadro clinico, alteraciones macro y microscopicas en relacion con el choque endotoxinico Con endotoxina lipoeolisacaarida de las estirpes E. coli O 9, O 89 y O 141, se produjo un choque endotoxinico en un total de 52 cerdos. 18 animales murieron y 16 fueron examinados histopatologicamnete. Los hallazgos clinicos, patologicos e histopatologicos se hallaban relacionados de manere armoniosa con la aumentada permeabilidad capilar y la alteracion general de la circulacion sanguinea. Los desarreglos se asemejaban en esencia a los de la enfermedad de los edemas del cerdo.

1959年,岩手県盛岡市を中心とする豚浮腫病発生例につき病理学的研究を行い,その病理像を確立した即ち,病理組織学的には全身における血栓形成,浮腫,及び血管壁変化が主体をなす.又退行性変化として全身各所,例えばリンパ節,心筋,骨賂筋,脳神経細胞,神経線維,副腎髄質細胞,皮j{=]・=7,舌等の変性乃至壊死が認められた.特に筋線維及び脳神経細胞の変化は重視さるべきものであった.又骨閤における特徴的好酸球増生,全身組織にみられる好酸球浸潤,或はアレルギー性炎類似の皮膚及び舌病変が注目された.これら自己所見を基礎とし,本症の病理発生を論じ,浮腫に関しては血液性状の変化に基く全身性表現の一環であるとする考え2重視した.最後に本症の病理発生とアレルギーとの関連についていささか考察を加えた.