Studies of the Chick Edema Disease

Flick, D. F.; Douglass, Carl D.; Gallo, Linda A.

doi:10.3382/ps.0420855

Cited by 22 publications

(5 citation statements)

References 12 publications

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“…The order of appearance of edema in this chronic study was the same as reported previously in a short-term study (Flick et al, 1963b). The frequency distribution of grossly observed edema was as follows; first, hydropericar-dium; second, abdominal; and third, subcutaneous.…”

Section: Resultssupporting

confidence: 79%

Studies of the Chick Edema Disease

1967

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Section: Resultssupporting

confidence: 79%

Studies of the Chick Edema Disease

1967

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“…As we previously reported (Flick et al, 1963b), the hematocrits reveal that birds with the disease have decreased levels of blood cells (Table 3). With hydrochlorothiazide fed at 25, 50 or 100 mg./kg.…”

Section: Resultssupporting

confidence: 51%

“…These data show that the lower dietary levels of the diuretic partially prevent an increased ESR and that the higher levels (500 and 1,000 mg./kg., groups 6 and 7) are markedly effective in preventing an increased sedimentation rate. These studies reveal that hydrochlorothiazide, a potent diuretic in man and other animals (De Stevens, 1963;Hutcheon, 1965), has a beneficial effect in the prevention of the anemia, manifested by low hematocrit and hemoglobin values previously found to accompany the disease (Flick et al, 1963b), in addition to the marked preventive effect on the formation of edema.…”

Section: Resultsmentioning

confidence: 95%

Studies of the Chick Edema Disease

Flick

O'Dell

1968

Poultry Science

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“…When fats containing the chick-edema factor were incorporated into the feed of S.C. white leghorn cockerels the following signs were seen (Flick et al, 1963): growth depression, dose-dependent accumulation of fluid in the pericardial sac, accumulation of fluid in the abdomen and in the subcutaneous region and other body cavities including the air sacs. Early in the search for the chick-edema factor, PCBs were tested (McCune et al, 1962) and Aroclor 1242 incorporated in the diet of Vantress x White Rock chicks caused the following signs: labored respiration with rales, distention of the abdominal cavity with fluid, hydropericardium, blood in the crop, swollen and pale kidneys, enlarged and mottled liver, hydropic lungs, and a yellow, fibrin-containing, jellylike fluid under the skin and in the body cavities.…”

Section: Biologymentioning

confidence: 98%

“…The increased permeability of the cardiac vascular bed results in cardiac congestion leading to secondary pulmonary stress. Fluid accumulation in lungs can flow by gravity to the air sacs of the abdominal cavity and of the subcutaneous alar and abdominal regions (Flick et al, 1963). It is possible that the high incidence of "pipped and died" chicks observed at hatching in Great Lakes fish-eating bird colonies may be mediated by the reduced cardiovascular capacity caused by the external pressure in the pericardial sac.…”

Section: Biologymentioning

confidence: 99%

Great lakes embryo mortality, edema, and deformities syndrome (GLEMEDS) in colonial fish‐eating birds: Similarity to chick‐edema disease

Gilbertson¹,

Kubiak

Ludwig³

et al. 1991

Journal of Toxicology and Environmental Health

342

150

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Several species of colonial fish-eating birds nesting in the Great Lakes basin, including herring gulls, common terns and double-crested cormorants, have exhibited chronic impairment of reproduction. In addition to eggshell thinning caused by high levels of DDT and metabolites, the reproductive impairment is characterized by high embryonic and chick mortality, edema, growth retardation, and deformities, hence the name Great Lakes embryo mortality, edema, and deformities syndrome (GLEMEDS). The hypothesis has been advanced that GLEMEDS in colonial fish-eating birds resembles chick-edema disease of poultry and has been caused by exposure to chick-edema active compounds that have a common mode of action through the cytochrome P-448 system. Detailed evidence has been collected from the following three groups of studies on herring gulls in the lower Great Lakes during the early 1970s; Forster's terns in Green Bay, Wisconsin in 1983; and double-crested cormorants and Caspian terns in various locations in the upper Great Lakes from 1986 onwards. It has proved difficult to establish not only the onset of the disease in the various species at various locations but also the period in which chick-edema active compounds were released. Anecdotal evidence suggested that serious egg mortality in Lake Ontario herring gulls first occurred in 1966, through the signs of chick-edema disease were not looked for until 1974. Only indirect evidence is available on the date of the release of one of the presumed causal agents, 2,3,7,8-tetrachlorodibenzo-p-dioxin, but highest levels may have occurred in the early to mid 1960s. More reliable data show that the onset of the improvement of reproduction of Lake Ontario herring gulls coincided with the declines in organochlorine compounds and particularly 2,3,7,8-TCDD and PCB. Similarly, information on the onset of the disease and exposures in the Forster's tern and double-crested cormorants in Green Bay is uncertain but bird banders did not observe deformities until the 1970s, which corresponds with the onset of high levels of PCB. If the disappearance of the Caspian tern from Saginaw Bay in the mid 1960s corresponds with the onset of GLEMEDS at that location, then there is a close temporal relationship to the onset of high PCB levels. Chick-edema disease is difficult to diagnose because there is no specific lesion, but rather there is a suite of lesions.(ABSTRACT TRUNCATED AT 400 WORDS)

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Studies of the Chick Edema Disease

Cited by 22 publications

References 12 publications

Studies of the Chick Edema Disease

Studies of the Chick Edema Disease

Studies of the Chick Edema Disease

Great lakes embryo mortality, edema, and deformities syndrome (GLEMEDS) in colonial fish‐eating birds: Similarity to chick‐edema disease

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