Lipid and colour stability of beef from grazing heifers supplemented with sunflower oil alone or with fish oil.

The effect of sunflower and fish oil supplementation of grazing heifers on lipid oxidation and colour stability in beef was investigated. For 150 days, heifers were assigned unsupplemented grazing (G) or restricted grazing with 2.5kg concentrates containing 1250I.U. α-tocopheryl acetate and 290g sunflower oil (S1), 415g sunflower oil (S2), 290g sunflower+85g fish oil (FS1) or 415g sunflower+85g fish oil (FS2). Longissimus dorsi muscle was excised 24h post-mortem and stored at -30°C prior to analysis. Muscle α-tocopherol in the oil-supplemented groups was higher (P<0.05) than the G group. Lipid oxidation in refrigerated, minced raw or cooked beef was not significantly affected by diet but metmyoglobin was higher (P<0.05) in raw beef from oil-supplemented groups compared to the G group. Lipid oxidation and metmyoglobin formation increased (P<0.001) during refrigerated storage. Vitamin E supplementation together with pasture grazing appeared to offset any potential deleterious effect of oil supplementation on lipid and colour stability.

Trapping and immobilization of Nippostrongylus brasiliensis larvae at the site of inoculation in primary infections of interleukin-5 transgenic mice.

Interleukin-5 (IL-5) transgenic mice are highly resistant to primary infections with the intestinal nematode Nippostrongylus brasiliensis; few parasites are found in the intestines of infected animals, and egg production is minimal. While adult worms may be damaged in the intestine, larval migration, development, and viability may also be impaired in other tissues. This study addresses the migration of N. brasiliensis larvae through the skin and lungs and associated cellular responses in primary infections of IL-5 transgenic mice. Although some larvae may have been trapped and killed in the lungs of IL-5 transgenic mice, most apparently failed to reach this site. Two or more hours after infection of IL-5 transgenic mice, eosinophils were a major component of the cellular infiltrate at the subcutaneous site of injection, and localized eosinophil degranulation was extensive. Seventy-five to ninety-five percent of the larvae injected into subcutaneous air pouches in IL-5 transgenic mice were retained there for at least 24 h. In contrast, in nontransgenic mice, less than 20% of larvae could be recovered from the skin 2 or more h postinjection, and eosinophil activity was modest at all times. The data strongly suggest that eosinophils can restrict the movement of N. brasiliensis larvae in the first few hours of a primary infection and that this has profound effects on later stages of parasite development. Preexisting eosinophilia, due either to allergy or to infection with tissue-invasive helminth species, may therefore confer some degree of immediate and nonspecific resistance in primary infections with parasitic worms.

Interleukin-5 transgenic mice show enhanced resistance to primary infections with Nippostrongylus brasiliensis but not primary infections with Toxocara canis.

In this study, interleukin-5 (IL-5) transgenic mice with lifelong eosinophilia were assessed for resistance to primary infections with two tissue-invading nematodes, Nippostrongylus brasiliensis and Toxocara canis. Relative to nontransgenic littermates, three lines of IL-5 transgenic mice with varying degrees of eosinophilia all displayed enhanced resistance to N. brasiliensis. Although the timing of final worm expulsion was similar in transgenic and nontransgenic hosts, intestinal worms in transgenic mice were fewer in number throughout infection, failed to increase in size over the course of the infection, and were much less fecund. In contrast, T. canis larvae were recovered in similar numbers from tissues of transgenic mice with "low" or "high" eosinophilia and from nontransgenic mice. These results and other data suggest that eosinophils can contribute to host resistance to some parasite species. Parasite transit time through the host may correlate with relative sensitivity to eosinophils.

Evaluation of non-radioactive trivalent DNA probe (LT, ST1a, ST1b) for detecting enterotoxigenic Escherichia coli.

AIMS: To evaluate a digoxigenin-labelled trivalent DNA probe (LT, ST1a, ST1b) for detecting enterotoxigenic Escherichia coli (ETEC), by comparison with a cell culture assay for detecting LT, individual DNA probes for LT, ST1a and ST1b, and an enzyme immunoassay for detecting ST1. METHODS: A 1268 base pair DNA fragment, containing parts of the genes for E coli heat labile enterotoxin (LT) and heat stable enterotoxins (ST1a and ST1b), was random prime labelled with digoxigenin-dUTP. The labelled DNA was used as a probe in colony hybridisation reactions to examine 180 E coli strains of which 92 had previously been shown by a cell culture assay to produce LT. Six LT negative ST1 positive E coli, 34 Verotoxin producing E coli (VTEC), and 84 organisms from other genera were also examined. All organisms other than VTEC were isolated from travellers returning from abroad with diarrhoea. All E coli strains were retested by cell culture for LT, and were tested by enzyme immunoassay (EIA) for ST1, and by the trivalent and individual DNA probes. RESULTS: All 81 isolates, that on retesting by cell culture were positive for LT, also hybridised with the trivalent and LT probes; 27 of these were also enzyme immunoassay (EIA) positive for ST1 of which 24 hybridised with the ST1b probe and three with the ST1a probe. Of 99 isolates, that on retesting by cell culture were negative for LT, all were negative by LT probe and only three were EIA positive for ST1; these three were positive by both trivalent and ST1b probes. Four isolates were positive by the trivalent probe but negative by cell culture and EIA; all four were positive by ST1b probe. Compared with the cell culture assay for LT, the probe had a sensitivity and specificity both of 100%; compared with the EIA for ST1, the probe had a sensitivity of 100% and specificity of 88%. CONCLUSIONS: The trivalent DNA probe is a sensitive, specific, and reliable method for detecting ETEC that should be considered for use by diagnostic microbiology laboratories.

Comparison of Y1 mouse adrenal cell and coagglutination assays for detection of Escherichia coli heat labile enterotoxin.

A commercial coagglutination assay (COA; Phadebact LT-ETEC) was compared with a Y1 mouse adrenal cell assay for detecting the heat labile enterotoxin of Escherichia coli. Of four different media evaluated for use with the COA, only one (modified blood agar) gave a positive result with all strains known to produce heat labile enterotoxin. With modified blood agar, the COA detected 74 (85%) of 87 such strains. Eighty six strains negative by cell culture assay were also negative by COA, and one strain positive by COA could not be confirmed by cell culture. The Phadebact LT-ETEC kit provides a simple, sensitive, and economical method for detecting E coli heat labile enterotoxin.