Jatropha has been highlighted as an oleaginous potential for the production of biofuel. The cake, produced by oil extraction, could be used in animal feed. However, some varieties of jatropha are toxic by limiting their incorporation into animal diets. The objective of this study was to evaluate the hepatotoxicity of diets added with jatropha cake – JC (Jatropha curcas) in rats. Thirty-five (35) male Wistar adults rats (Rattus norvegicus) with initial weight of 352.1 ± 26.8 g were used. The animals were fed for 21 days with the diets: control, 10, 25, 40 and 50% JC. In the feeding with 50% JC the animals presented themselves prostrate and with piloerection. Development and survival decreased, since the inclusion of JC in diets increased. In rats submitted to 10 and 25% JC there was an increase of 17.52% in the hepatosomatic index in relation to the control group. Increase of JC in the rat diet promoted an increase in the activity of ALT and AST enzymes. Anatomic-histopathological evaluation demonstrated that, regardless of the levels tested, JC in rat diet causes hypertrophy of the hepatocytes, with a reduction in energy reserves. This study demonstrated that the use of JC resulted in decreased food intake, associated with weight loss due to the clinical pattern of toxicity, demonstrated by biochemical and histopathological changes in the liver. It was concluded that the inclusion of jatropha cake in rat feeding presents high hepatotoxic potential leading to lesions in the liver parenchyma. | O pinhão-manso tem se destacado como oleaginosa potencial para a produção de biocombustível. A torta, coproduto da extração do óleo, poderia ser utilizada na alimentação animal. No entanto, algumas variedades de pinhão-manso são tóxicas, limitando sua incorporação em dietas animais. Objetivou-se neste estudo avaliar a hepatotoxicidade de dietas acrescidas de torta de pinhão-manso (Jatropha curcas) em ratos. Foram utilizados trinta e cinco (35) ratos Wistar (Rattus norvergicus) machos adultos com peso inicial de 352,1 ± 26,8 g. Os animais foram alimentados por 21 dias com as dietas: controle, 10, 25, 40 e 50% TPM. Na alimentação com 50% TPM os animais apresentaram-se prostrados e com piloereção. O desenvolvimento e a sobrevivência apresentaram diminuição conforme o aumento da inclusão de TPM nas dietas. Em ratos submetidos a 10 e 25% TPM houve aumento de 17,52% no índice hepatossomático em relação ao grupo controle. O aumento de TPM na dieta de ratos promoveu aumento da atividade das enzimas ALT e AST. A avaliação anatomo-histopatológica revelou que, independentemente dos níveis testados, a TPM na alimentação de ratos provoca hipertrofia dos hepatócitos, com redução das reservas energéticas. Este estudo demonstrou que a utilização de TPM resultou em diminuição do consumo de alimento associado à perda de peso devido ao quadro clínico de toxicidade demonstrado pelas alterações bioquímica e histopatológica no fígado. Conclui-se que a inclusão de torta de pinhão-manso na alimentação de ratos apresenta alto potencial hepatotóxico levando a lesões no parênquima hepático.

Objective-To evaluate time-dependent alterations in gene expression of chemokines in bronchial epithelium of recurrent airway obstruction (RAO)-affected horses and whether alterations resulted from increases in gene expression of interleukin (IL)-17 in cells isolated from bronchoalveolar lavage fluid (BALF). Animals-8 RAO-susceptible horses and 9 control horses. Procedure-In 2 experiments, both groups of horses were evaluated after being maintained on pasture and after being stabled and fed dusty hay for 1, 14, 35, and 49 days (experiment 1) or 14 and 28 days (experiment 2). In experiment 1, gene expression of IL-8, chemokine (C-X-C motif) ligand 1 (CXCL1), granulocyte-macrophage colony-stimulating factor (GM-CSF), granulocyte colony-stimulating factor (G-CSF), and Toll-like receptor 4 (TLR4) in epithelium and IL-8, IL-17, and TLR4 in BALF cells was measured. In experiment 2, bronchial biopsy specimens were evaluated for IL-8 immunoreactivity. Results-In RAO-susceptible horses after 14 days of challenge exposure, there was a 3- and 10-fold increase in gene expression of IL-8 for epithelial and BALF cells and an increase in IL-8 immunoreactivity in epithelial cells. Challenge exposure failed to alter gene expression of CXCL1, GM-CSF, G-CSF, and TLR4 in epithelial cells of any horses at any time point. During challenge exposure, gene expression of BALF cell IL-17 was downregulated in control horses (day 1) and upregulated in RAO-affected horses (day 35). Conclusions and Clinical Relevance-Epithelial-derived IL-8 may promote airway neutrophilia, but the inciting stimulus is unlikely to be IL-17 because upregulation of this gene is subsequent to that of IL-8 in epithelial cells.

A longitudinal survey of 820 cats in 73 households was conducted over a period of 6 years to establish the fate of pet cats that were seropositive after natural exposure to feline coronavirus (FCoV). In particular, their risk of developing feline infectious peritonitis (FIP) was determined. The seropositive cats were assigned to 1 of 3 groups: cats from households in which FIP had recently been diagnosed; cats from households in which FIP had not been diagnosed, but from which kittens had been relocated and subsequently died of FIP; and cats from households in which FIP had not been diagnosed. Cats in the first group were not at greater risk of developing FIP than were cats in the other 2 groups. Consequently, any household in which seropositive cats live must be considered a potential source of FCoV that can cause FIP. There was no evidence that the enhanced disease, which has been described after experimentally induced infection of seropositive cats, exists in nature. Thus, analysis of the survival of the seropositive cats over periods of up to 36 months indicated that their risk of developing FIP decreased with time, suggesting the development of immunity rather than increased susceptibility to disease. In addition, of 56 cats deemed to have been naturally reinfected because their anti-FCoV antibody titers decreased and subsequently increased, only 3 developed FIP.

Effects of selenium (Se) deficiency and supplementation on production of colostral immunoglobulins by beef cows and transfer of antigen-specific and nonspecific immunoglobulins to their calves were examined. Eighty beef cows, with marginal to deficient Se status (blood Se concentration, 50 micrograms/L), were allotted by breed and age to 1 of 4 Se treatment groups (n = 20/group): no supplemental Se; parenteral administration of 0.1 mg of Se and 1 mg of vitamin E/kg of body weight; ad libitum consumption of 120 mg of Se/kg of salt-mineral mix (SMM); and parenteral administration of 0.1 mg of Se and 1 mg of vitamin E/kg plus ad libitum consumption of 120 mg of Se/kg of SMM. All cows were inoculated IM with lysozyme. Cows consumed Se-deficient pastures or hay (21 to 62 micrograms/kg) during the study that began at mid-gestation and ended at postpartum hour 24. Although the concentration of specific lysozyme antibodies was not affected, cows given 120 mg of Se/kg of SMM (treatments 3 and 4) had higher colostral IgG concentration (P < 0.002) than did Se-deficient cows (treatments 1 and 2). Calves from cows in treatments 3 and 4 had higher postsuckle serum concentrations of IgG (P < 0.01) than did calves from cows in treatments 1 and 2. Colostral IgM and calf serum IgM concentrations did not differ among treatments.

Reduced prevalence of diarrhea and mortality has been reported after dietary supplementation with zinc compounds in swine with naturally acquired colibacillosis and those challenge-exposed with Serpulina hyodysenteriae; however, the usefulness of this approach for control of enteric diseases of swine remains to be determined. To examine the effect of dietary zinc-containing compounds on the colonization and development of cecal lesions associated with S hyodysenteriae infection, a defined diet alone or with added ZnO, ZnSO4, or Zn-methionine complex to a final concentration of approximately 6,000 mg of Zn2+/kg of complete feed was fed ad libitum to 156 female mice (strain C3H/HeN) for 10 days prior to oral inoculation either with S hyodysenteriae or sterile trypticase soy broth. Rations were continued for 42 days, while at weekly intervals, 3 mice/group were necropsied for determination of body weight, cecal weight, liver zinc concentration, presence of S hyodysenteriae in the cecum, and gross and histologic assessments of cecal lesions. From postinoculation day 0 to 42, the liver zinc concentration of mice fed the zinc-supplemented diets was approximately twice that of mice fed the basal diet, irrespective of the source of zinc. From postinoculation day 7 through 42, the overall recovery rate of S hyodysenteriae in infected mice fed the basal diet was 77.8%. In contrast, recovery rates of S hyodysenteriae from S hyodysenteriae-inoculated mice fed the zinc-supplemented diets were 0% for Zn-methionine and ZnO and 16.7% for ZnSO4. Mice fed the basal diet had significantly (P < 0.05) higher weight gain than mice fed the zinc-supplemented diets. However, the severity of cecal lesions, as determined by histologic examination and quantitative determination of longitudinal crypt length of the cecum was significantly (P < 0.05) less in mice fed the zinc-supplemented diets than in mice fed the basal diet. Data from this study indicate that dietary supplementation with 6,000 mg of zinc/kg of feed significantly reduced the recovery rate of S hyodysenteriae and provided partial protection against development of cecal lesions in mice inoculated with S hyodysenteriae. However, at this concentration, zinc had a deleterious effect on growth of the mice.

Aflatoxin (AF)-contaminated and fumonisin B1 (FB1)-contaminated (culture material from Fusarium moniliforme) diets were fed singly and in combination to growing cross-bred barrows. Six barrows (3 replicates of 2 each; mean body weight, 17.5 kg) per group were fed: 0 mg of AF and 0 mg of FB1/kg of feed (control); 2.5 mg of AF/kg of feed; 100 mg of FB1/kg of feed; or 2.5 mg of AF plus 100 mg of FB1/kg of feed for 35 days. The effects on production performance, serum biochemical, hematologic, immunologic, and pathologic measurements were evaluated. Body weight, gain, and feed consumption were significantly (P < 0.05) decreased by AF and AF plus FB1 diets. The FB1 diet decreased feed consumption, and although body weight was numerically decreased, it was not statistically significant. Aflatoxin increased serum gamma-glutamyltransferase (GGT) activity and total iron concentration and decreased urea nitrogen concentration and unsaturated iron-binding capacity. The FB1-alone diet increased serum GGT activity, whereas the AF plus FB1 diet increased serum aspartate transaminase, cholinesterase, alkaline phosphatase, and GGT activities, increased RBC count, triglycerides, and total iron concentrations, and decreased unsaturated iron-binding capacity and urea nitrogen concentration. For the most part, the effects of the AF plus FB1 diet on body weight and hematologic measurements could be considered additive. However, the effect of the AF plus FB1 diet on cholinesterase and alkaline phosphatase activities was greater than additive and was a synergistic response. One pig in the FB1-diet group and 2 pigs in the combination-diet group died. Postmortem lesions in pigs of the FB1-diet group consisted of ascites and increased liver weight. Observations at necropsy for pigs of the AF plus FB1-diet group consisted of hydrothorax, ascites, pulmonary edema, gastric erosions and ulceration, and increased liver and spleen weights. The AF diet increased relative liver weight and resulted in liver that was pale, rubbery, and resistant to cutting. Histologic lesions consisted of hepatic necrosis or degeneration, or both, with variable degrees of bile duct proliferation in barrows of the AF-diet groups. Renal tubular nephrosis was observed in barrows of the FB1 diet group, but this was not consistent in the AF plus FB1-diet group. Cell-mediated immunity, as measured by mitogen-induced lymphoblastogenic stimulation index, was decreased in barrows of the AF and FB1-diet groups, and values in barrows given the combination diet were significantly decreased from those in barrows given the single toxin diets. It was concluded that AF and FB1 (from culture material), singly or in combination, can adversely affect clinical performance, serum biochemical, hematologic, and immunologic values and induce lesions in growing barrows. For most of the variables we evaluated under our study conditions and dosages of toxins, measurements were affected more by the combination diet than by either single toxin diet, and the toxic responses could be described as additive or more than additive, particularly for induction of liver disease.

Consumption of chlortetracycline (CTC) at concentration of 220 mg/kg of feed for 4 weeks in experiment 1 and at concentrations of 110 and 220 mg/kg for 3 weeks and 440 mg/kg for 2 weeks in experiment 2 failed to eliminate streptococci-induced lymphadenitis from swine referred to as principals. Abscesses, mostly in the head and neck, developed in at least a third of all swine in the various groups fed these CTC concentrations. Feeding of 220 mg of CTC/kg of feed in experiment 1 began 12 weeks after exposure of principals to an untypeable group E streptococci (GES; isolate 3X29A). In experiment 2, feeding of 110 and 220 mg of CTC/kg of feed began 5 weeks after exposure of principals to GES and feeding of 440 mg of CTC/kg of feed began 6 weeks after exposure. One or more cohabitating sentinel swine of experiment 1 and one or more sentinels in all groups of principals of experiment 2, except group 2, developed abscesses that were mostly in the head and neck. In experiment 2, correlation between serum GES antibody titer and development of one or more abscesses in the principals was highly significant (P < 0.01); however, correlation between antibody titer and abscesses in the sentinels only approached significance (P < 0.10).

Observations were made on development of diarrhea in special-fed calves (n = 460) on 8 commercial facilities during 2 successive 16-week production cycles at weeks 0, 2, 4, 8, 12, and 16. A total of 23% were affected, with peak number of calves with diarrhea observed at week 0. Suspected enteropathogens were identified in 86% of these calves, most commonly cryptosporidia, coronavirus, and rotavirus. Identified potential zoonotic pathogens included Giardia and Salmonella spp and verotoxigenic Escherichia coli. Noncytopathic bovine viral diarrhea virus was isolated from 6 calves that had repeated bouts of illness. Only 22% of calves entering the veal facilities had adequate transfer of passive immunity. At week 0, serum IgG concentration in calves that subsequently died or had diarrhea was lower (P < 0.001) than that in healthy calves. All calves that died (n = 6) during the first 4 weeks of production had complete failure of transfer of passive immunity.

Drug-metabolizing enzyme activities were measured in livers from calves fed commercial milk replacer (nonfunctioning rumen [veal]), and those fed milk replacer supplemented with whole grain and hay from the first week of age (functioning rumen [ruminating calves]). After birth, cytochrome P450 and its NADPH-dependent reductase activities remained unchanged in veal calves; in ruminating calves they increased almost 50%. Cytochrome P450-mediated reactions, such as aniline hydroxylase activity, tripled in ruminating calves, but remained unchanged in veal calves. In both groups of calves, coumarin hydroxylase and 7-ethoxycoumarin 0-deethylase activities increased after birth, but maturation rates and activity values in ruminating calves were considerably greater than those of veal calves. The aminopyrine N-demethylase activity for veal calves was equal to that of calves with functioning rumen. Uridine diphosphoglucuronic acid glucuronyl transferase and glutathione-S-transferase activities also were higher in calves with functioning rumen than in veal calves. This increased activity in calves with functioning rumen probably represents a response to environmental exposure to xenobiotics. Compared with rumen-functional calves, bob veal (0 to 3 weeks old) and fancy veal (15 to 19 weeks old) calves fed commercial milk replacer have a significantly (P = 0.05) diminished capacity for metabolizing drugs and other xenobiotics. From a regulatory perspective, the variance in drug-metabolizing enzyme activities within these different market classes of calves suggests that specific studies designed to determine drug residue-depletion times in veal calves may be needed.

Sixteen IgA-deficient German Shepherd Dogs with small intestinal bacterial overgrowth were randomized into 2 groups. One group was fed a chicken-based kibble diet; the other was fed the same diet, but with 1% fructo-oligosaccharides supplemented at the expense of cornstarch. After being exposed to the diets for 46 to 51 days, the group that ate the supplemented diet had significantly (P = 0.04) fewer aerobic/facultative anaerobic bacterial colony-forming units in fluid from the duodenum/proximal part of the jejunum, as well as in the duodenal mucosa. We could not detect significant differences in the species of bacteria found in the intestine of these 2 groups of dogs. We conclude that at least some dietary carbohydrates can affect small intestinal bacterial populations in dogs with small intestinal bacterial overgrowth.