Bokt.nl

Jannepauli schreef:

Zolang hier nog geen wetenschappelijke gepubliceerde documenten en peer-reviewed reacties op zijn, neem ik dit verhaal nog maar even met een korrel zout.

Jannepauli schreef:

Zolang hier nog geen wetenschappelijke gepubliceerde documenten en peer-reviewed reacties op zijn, neem ik dit verhaal nog maar even met een korrel zout.

Citaat:

The earliest written report of selenium poisoning is thought to be the description by Marco Polo of a necrotic hoof disease of horses that occurred in China in 13. century. However recognition of Se as toxic principle come in the early 1930s. Severity of Se poisoning depends on chemical forms of the element, species of animals and routes of administration. The soluble Se salts (Na2SeO3 and Na2SeO4) appear to be among the more toxic compounds; the Se inherent in grains and selenoamino acids (selenomethionine and selenocystine) appear to have relative moderate toxicity; the poorly soluble forms (e.g., elemental Se, Na2Se, SeS2 and diphenyl selenide) are among the least toxic of the Se compounds. In general, toxicity of Se compounds are substantially less when they are administered orally than when they are given parenterally. Rosenfeld and Beath described three clinical types of Se intoxication: acute selenosis, subacute selenosis (i.e., blind staggers type), and chronic selenosis (i.e., alkali disease type). Acute poisoning occurs when high Se content plants are consumed in large quantities within short period. Accidental acute poisoning occurs as consequence of errors in formulation of a Se supplemented diet. The most characteristic sign of acute selenosis is garlic breath due to the pulmonary excretion of volatile Se metabolites. Other signs include lethargy, excessive salivation, vomiting, dyspnea, muscle tremors and respiratory distress. Pathological findings are: congestion of the liver and kidney, fatty degeneration and focal necrosis of the liver, endocarditis and myocarditis. Subacute selenosis ("blind staggers") occurs as a consequence of exposure to large doses of Se over a longer period of time and manifests with neurological signs (e.g., blindness, ataxia, disorientation) and respiratory distress. This form of selenosis is most frequently observed in grazing animals that have consumed Se-accumulated plants. Chronic selenosis ("alkali disease") comes about when animals consume moderate levels of Se (more than 5 mg/kg and less than 40 mg/kg) for period of weeks or months. The usual clinical signs of chronic selenosis in horses, cattle and swine are: loss of hair (horses and cattle lose long hair from the mane and tails), emaciation, hoof lesions and lameness. In advanced cases liver cirrhosis, atrophy of the heart and anemia occur. In swine symmetrical poliomyclomalacia of cervical and lumbal/sacral spinal cord segment has been seen. Sheep seen to be more tolerant and get milder form of the disease. They lose appetite and have reduced gain. In growing chicks reduced gain and feed intake, rough feathers, and characteristics of nervousness has been observed. Reduced egg production, embryonic deformations and reduced hatchability has been observed in hens.

lailapri schreef:

Misschien dat daarom al mijn oudjes zo weinig cushing symptomen hebben. Ik voer redelijk sober.

Dees schreef:

Ach, er gaan ook paarden dood aan juist een SE-tekort.

Wellicht is het beste advies daarom gewoon: mensen, blijf toch gewoon normale brok van een A-merk voeren. Dat moderne gesleutel met toevoegingen en weglatingen levert alleen maar onbalans op en dus zieke paarden.

lailapri schreef:

[naam verwijderd] schreef:

Ach, er gaan ook paarden dood aan juist een SE-tekort.

Wellicht is het beste advies daarom gewoon: mensen, blijf toch gewoon normale brok van een A-merk voeren. Dat moderne gesleutel met toevoegingen en weglatingen levert alleen maar onbalans op en dus zieke paarden.

Dan vraag ik me af, hoe gezond is die brok van dat a merk... Ik heb alleen maar ellende gezien bij mijn dieren en kan me zo even geen uitzondering bedenken.