Defatted rice bran poisoning in cattle

Rice processing produces a series of by-products, including brown rice, from which defatted rice bran (DRB) is obtained after hexane solvent extraction of the oil. The main advantage of DRB is that it does not go rancid, which allows the product to be stored for a prolonged period [[1], [2], [3]]. The average dry matter composition of samples of DRB from Brazil and Uruguay is: crude protein 17.7 %, neutral detergent fibre 52.4 %, acid detergent fibre 14.6 %, hemicellulose 39.8 %, fat 1.3 %, ash 11.3 %, Ca 0.04 %, P 2.24 %, Zn 92 ppm and Cu 10 ppm [4].

Cases of poisoning by DRB have been described in both dairy and beef cattle in Brazil [[5], [6], [7]] and in Uruguay [4,8,9]. The first report was from Uruguay when a condition characterized by dermatitis with lesions located primarily in the distal hindlimbs was described [4]. This report documented spontaneous outbreaks of the condition on eight farms in Uruguay, all feeding cattle with DRB, which led to the suspicion that this feed ingredient was the cause. Epidemiological studies carried out on these farms revealed that the condition developed 10–60 days after the start of DRB administration [4]. Cows, heifers, calves, bulls and steers were affected, with morbidity ranging from 10 % to 100 % [4]. A subsequent study was conducted on 12 farms to confirm the cause and pathogenesis of the condition and found that the disease can appear up to 90–120 days after the start of DRB feeding, with an average morbidity rate of 13 % in cattle up to 1 year old and 39 % in older cattle [9]. Age and dietary inclusion of DRB without prior adaptation were important risk factors for occurrence of the condition. In these outbreaks, the cattle had ingested DRB at inclusion rates of 0.4 % to more than 1 % of bodyweight (BW) daily over 10–60 days [8].

Initial lesions of DRB poisoning are characterized by erythema and oedema of the coronary band, metatarsus and fetlock. These changes evolve into ulceration with the development of 0.5–1 cm thick crusts formed by matted hair and exudate. Some animals present with heat, swelling and itching in the affected area and, in some cases, lameness [9,10]. In severe cases, the lesions can extend to the tarsus, inner thigh region, scrotum and udder. However, this severe form only occurs in adult animals such as dairy cows and fattening steers [9]. Histologically, these lesions are characterized by a perivascular dermatitis comprising lymphocyte, histiocyte and eosinophil infiltration and epidermal hyperplasia with ortho- or parakeratotic hyperkeratosis [6,8,10].

In studies carried out in Uruguay, it was concluded that the pathogenesis of DRB toxicity involved type I hypersensitivity, mediated by IgE, and also cell-mediated type IV hypersensitivity (T lymphocytes) [8]. That author performed intradermal inoculation (caudal fold) with a DRB extract on cattle that had been ingesting DRB for 4 months and on negative control cattle. Increased caudal fold thickness was observed 1–2 h after inoculation of the cattle that had ingested DRB, and these cattle developed mild skin lesions 10 days after challenge. In a passive intradermal test to detect the presence of serum IgE, serum from animals that had ingested DRB was injected into five cattle that had never ingested DRB followed, 72 h later, by injection of DRB extract. In this experiment, all five tested cattle developed an IgE-mediated immune response characteristic of type I hypersensitivity. Control cattle were negative [8]. Immunodiffusion tests for IgG and IgM were negative in all cattle. These negative results suggested that the hypersensitivity could also be type IV, which supports the histopathological findings associated with food allergies [8,11].

The objectives of the present work were: (1) to experimentally reproduce DRB poisoning to confirm its allergic nature; (2) to carry out a retrospective study of outbreaks investigated by the Regional Diagnostic Laboratory of the Veterinary School, Federal University of Pelotas (LRD/UFPel) in order to document the epidemiology, pathology and pathogenesis; and (3) to identify a maximum safe dietary inclusion level for cattle.

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