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This study evaluated the effect of feeding pelleted or mash ergot contaminated grain fed continuously or intermittently on the growth performance, blood serum variables, and carcass quality of finishing beef steers. Sixty black angus steers (442 ± 36.7 kg) were used in a complete randomized finishing (90% concentrate:10% barley silage DM basis) 126-d study. Steers were randomly assigned to 4 different treatments and individually housed. Treatments included: 1) control ration [CON; no added ergot alkaloids (EA)], 2) continuous ergot mash (CEM; fed continuously at 2 ppm total EA), 3) intermittent ergot mash (IEM; fed at 2 ppm EA during the first week of each 21-d period and control diet for the remaining 2 weeks), and 4) intermittent ergot pellet (IEP; fed at 2 ppm EA incorporated into a pelleted supplement during the first week of each 21-d period and control diet for the other 2 weeks). Steers were weighed every 21 d and blood samples were collected on day 0, 42, 84, and 126. Steer DMI (P <0.01, 9.95 vs. 11.05 kg/day) and ADG (P= 0.04) decreased for all EA treatments compared with the CON. Total shrunk BW gain (P= 0.03, 202.5 vs. 225.2 kg), final BW (P = 0.03, 617.9 vs. 662.2 kg), and carcass weight (P= 0.06) decreased for all EA steers compared with the CON steers. No treatment effects (P> 0.05) were observed for carcass dressing percentage, ribeye area, marbling score, or liver abscess. The percent of carcasses graded AAA decreased for all EA steers compared CON steers (P <0.01, 46.7 vs. 93.3%). Steers fed EA had increased rectal temperature compared with CON steers (P <0.01, 39.8 vs. 39.4 °C). Hair cortisol concentrations were less in steers fed IEP (P= 0.05, 1.23 vs. 1.76 pg/mg) than CON. No treatment effects (P> 0.05) were observed for complete blood count, and serum prolactin, haptoglobin, albumin, alkaline phosphatase, alanine transaminase, amylase, calcium, creatine, glucose, lipase, total bilirubin, total protein, or globulin. Blood urea nitrogen was less for EA steers compared with CON (P= 0.01, 3.48 vs. 4.10 mmol/L). The IEM steers had decreased concentrations of serum gamma-glutamyl transferase compared with IEP steers (P= 0.04, 23.4 vs. 28.5 IU). Pelleting ergot contaminated grain did not reduce the impact of ergot alkaloids on any of the measured parameters. Results suggest that continuously or intermittently feeding an ergot contaminated diet (2 ppm EA) can significantly reduce intake, growth performance, and carcass weight, with minimal impact on blood serum variables in finishing steers. Pelleting was not an effective method of reducing ergot toxicity.

This study evaluated the effect of feeding ergot contaminated grain continuously or intermittently through backgrounding (BG) and finishing (FN) in a mash or pelleted supplement on the growth performance, health and welfare parameters, and carcass characteristics of feedlot beef steers. Sixty black Angus steers (300 ± 29.4 kg BW) were used in a complete randomized 238-d study. Steers were stratified by weight and randomly assigned to four different diets (15 steers/treatment) and individually housed. Treatments included: (1) control [CON; no added ergot alkaloids (EA)], (2) continuous ergot mash (CEM; fed continuously at 2 mg total EA/kg of DM), (3) intermittent ergot mash (IEM; fed at 2 mg total EA/kg of DM, during the first week of each 21-d period and CON for the remaining 2 wk, this feeding pattern was repeated in each period), and (4) intermittent ergot pellet (IEP; fed at 2 mg of total EA/kg of DM as a pellet during the first week of each 21-d period and CON for the remaining 2 wk as described for IEM). Steers were fed barley based BG diets containing 40% concentrate:60% silage (DM basis) for 84 d (four 21-d periods), transitioned over 28 d (no ergot fed) to an FN diet (90% concentrate:10% silage DM basis) and fed for 126 d (six 21-d periods) before slaughter. In the BG phase, steer DMI (P< 0.01, 7.45 vs. 8.05 kg/d) and ADG (P< 0.01) were reduced for all EA diets compared to CON. The CEM fed steers had lower ADG (P< 0.01, 0.735 vs. 0.980 kg) and shrunk final BW (P< 0.01, 350 vs. 366 kg) than CON. CEM had lower gain:feed (P< 0.07, 0.130 vs. 0.142) than CON. In the FN phase, steer DMI (P< 0.01, 9.95 vs. 11.05 kg/d) and ADG (P= 0.04) were also decreased for all EA fed steers compared to CON. Total shrunk BW gain (P = 0.03, 202.5 vs. 225.2 kg), final BW (P= 0.03, 617.9 vs. 662.2 kg), and carcass weight (P= 0.06) decreased for all EA fed steers compared to CON. The percentage of AAA carcasses decreased for all EA fed steers (P< 0.01, 46.7 vs. 93.3%) compared to CON. EA fed steers had increased rectal temperatures (P< 0.01, 39.8 vs. 39.4 °C) compared to CON. Pelleting ergot contaminated grain did not reduce the impact of ergot alkaloids on any of the measured parameters during BG or FN. Continuously or intermittently feeding ergot contaminated diets (2 mg total EA/kg of DM) significantly reduced intake, growth performance, and carcass weight, with minimal impact on blood parameters in feedlot steers. Pelleting was not an effective method of reducing ergot toxicity.This study evaluated the effect of continuous or intermittent feeding EA in a mash or pelleted form on growth performance, health and welfare parameters, and carcass characteristics of feedlot beef steers. Continuously or intermittently feeding an ergot contaminated diet (2 ppm EA) both reduced intake, growth performance, and carcass weight, but pelleting did not reduce the toxicities of EA.Produced by the fungus Claviceps purpurea, ergot alkaloids (EA) are toxic to beef cattle when consumed and can lead to reduction in feed intake and growth performance, vasoconstriction of the blood vessels, hyperthermia, damage to extremities (ears, tails, and hooves) and in severe cases, death. Grain is often cleaned to meet quality standards, and the resulting screenings are often utilized for feeding livestock and can have high concentrations of EA. The application of heat during pelleting of EA contaminated grain has been suggested to reduce its toxicity. Backgrounding and finishing beef cattle feeding experiments were conducted to assess the effect of continuously or intermittently feeding EA contaminated grain (2 mg/kg of diet DM) either as a pellet or as mash on growth performance, health, and animal welfare. Feeding EA grain continuously or intermittently either as a mash or pellet drastically reduced growth performance of steers, with no difference between treatments.

This study was designed to evaluate the effects of feeding increasing dietary concentrations of ergot alkaloids from cereal grains (EA; 0, 0.75, 1.5, 3.0 mg/kg of dietary DM) to feedlot cattle over backgrounding (BG) and finishing (FS) phases on health, welfare, and growth performance. Two hundred and forty commercial steers (280 ± 32 kg BW) were stratified by weight and randomly allocated to 16 pens (15 steers/pen), 4 of which were equipped with the GrowSafe system (1 pen/treatment) to measure individual feed intake. Each pen was randomly assigned to a treatment (n= 4/treatment). Treatments included 1) control (CTRL), no added EA; 2) CTRL + 0.75 mg/kg EA (EA075); 3) CTRL + 1.5 mg/kg EA (EA150); and 4) CTRL + 3.0 mg/kg EA (EA300). Steers were fed barley-based BG diets containing 40% concentrate: 60% silage (DM basis) for 84 d. Steers were then transitioned over 28 d to an FS diet (90% concentrate: 10% silage DM basis) and fed for 119 d before slaughter. The diet fed to EA300 steers was replaced with the CTRL diet after 190 d on feed (DOF), due to EA-induced hyperthermia starting at 165 DOF. In the BG phase, average meal length (P= 0.01) and size (P= 0.02), daily feeding duration (P= 0.03), final body weight (BW; P= 0.03), and total BW gain (P= 0.02) linearly decreased with increasing EA levels, while gain to feed (G:F) responded quadratically (P= 0.04), with EA150 having the poorest value. Increasing concentrations of EA in the diet linearly increased rectal temperature (P< 0.01) throughout the trial. Over the full FS phase, a quadratic response was observed for ADG (P= 0.05), final BW (P= 0.05), total BW gain (P= 0.02), and carcass weight (P= 0.05) with steers fed EA150 having the lowest performance, as EA300 steers were transferred to CTRL diet after 190 DOF. Dressing percentage (P= 0.02) also responded quadratically, with the lowest values observed for EA300. Thus, EA reduced ADG during BG and FS phases, although more prominently in FS, likely due to increased ambient temperatures and high-energy diet in FS triggering hyperthermia. When EA300 steers were transferred to the CTRL diet, compensatory gain promoted higher hot carcass weight (HCW) when compared with steers fed EA150. In conclusion, feeding feedlot steers diets with > 0.75 mg/kg EA caused reductions in performance and welfare concerns, although this breakpoint may be affected by duration of feeding, environmental temperatures, and EA profiles in the feed.The maximum concentration of cereal ergot alkaloid (EA) in the diet that do not affect health and performance of feedlot cattle is poorly defined. Hence, this study was conducted to better understand the impact of increasing levels of cereal EA, on the performance, health, and the welfare of feedlot steers.Ergot alkaloids (EA) are produced by a parasitic fungus (Claviceps purpurea) during the cereal grain growth cycle. Feeding cereal grain containing EA to beef cattle can cause constriction of blood vessels, hyperthermia, gangrene of extremities (ears, hoof, and tail), reduced feed intake and growth, and even death. Feed cleaning and processing technologies have been developed to remove EA from the human food chain, thus diverting contaminated feed for livestock use. We performed a beef cattle feedlot experiment to evaluate the impact of increasing levels of EA (0, 0.75, 1.50, 3.00 mg/kg of diet DM) on performance, health, and welfare. Steers fed 3.0 mg/kg of EA were transferred to the control diet (without EA) in the last half of finishing due to toxicity (hyperthermia). As EA levels increased, growth rate throughout the backgrounding and finishing phases decreased, while rectal temperatures increased and altered feeding behaviors occurred. Steers removed from 3 mg/kg EA diet exhibited compensatory gain, but their respiratory rate remained elevated 50 d after EA were last consumed.

The rumen simulation technique (RUSITEC) was used to investigate the effect of ergot alkaloids (EA) and a mycotoxin deactivating product (Biomin AA; MDP) on nutrient digestion, ruminal fermentation parameters, total gas, methane, and microbial nitrogen production. Ruminal fermentation vessels received a feedlot finishing diet of 90:10 concentrate:barley silage (DM basis). Using a randomized complete block design, treatments were assigned (n= 4 vessels/treatment) within two RUSITEC apparatuses in a 2 × 2 factorial arrangement. Treatments included: (1) control (CON) diet (no EA and no MDP); (2) CON diet + 1 g/d MDP; (3) CON diet + 20 mg/kg EA; and (4) CON diet + 20 mg/kg EA + 1 g/d MDP. The study was conducted over 14 d with 7 d of adaptation and 7 d of sample collection. Data were analyzed in SAS using PROC MIXED including fixed effects of EA, MDP, and the EA×MDP interaction. Random effects included RUSITEC apparatus and cow rumen inoculum (n= 4). Ergot alkaloids decreased dry matter (DMD) (P= 0.01; 87.9 vs. 87.2%) and organic matter disappearance (OMD) (P= 0.02; 88.8 vs. 88.4%). Inclusion of MDP increased OMD (P= 0.01; 88.3 vs. 88.9%). Neutral detergent fiber disappearance (NDFD) was improved with MDP; however, an EA×MDP interaction was observed with MDP increasing (P< 0.001) NDFD more with EA diet compared to CON. Acetate proportion decreased (P= 0.01) and isovalerate increased (P= 0.03) with EA. Consequently, acetate:propionate was reduced (P= 0.03) with EA. Inclusion of MDP increased total volatile fatty acid (VFA) production (P< 0.001), and proportions of acetate (P= 0.03) and propionate (P= 0.03), and decreased valerate (P< 0.001), isovalerate (P= 0.04), and caproate (P= 0.002). Treatments did not affect (P≥ 0.17) ammonia, total gas, or methane production (mg/d or mg/g of organic matter fermented). The inclusion of MDP reduced (P< 0.001) microbial nitrogen (MN) production in the effluent and increased (P= 0.01) feed particle-bound MN. Consequently, total MN decreased (P= 0.001) with MDP. In all treatments, the dominant microbial phyla were Firmicutes, Bacteroidota, and Proteobacteria, and the major microbial genus was Prevotella. Inclusion of MDP further increased the abundance of Bacteroidota (P= 0.04) as it increased both Prevotella(P= 0.04) and Prevotellaceae_UCG-003 (P= 0.001). In conclusion, EA reduced OMD and acetate production due to impaired rumen function, these responses were successfully reversed by the addition of MDP.Ergot alkaloids can affect ruminal metabolism of cattle, which can have large impacts on production, welfare, and health. Mycotoxin deactivators can alleviate some of the negative impacts that dietary ergot has on cattle.Ergot formed from a parasitic fungus (Claviceps purpurea) affects various types of grains (rye, wheat, or oats) and may contain several toxic ergot alkaloids (EA). Individual EA may impact the rumen microorganisms, and cattle feed intake, digestibility, health, and overall performance. A common method to alleviate toxicity in mycotoxin-contaminated feed is through the addition of mycotoxin binders (MDP); however, their efficacy against EA is unknown. To better understand the effect of EA in cattle, we performed an in vitroexperiment to examine the impact of EA on the ruminal microbial populations and fermentation of a finishing feedlot diet using an artificial rumen (RUSITEC). Additionally, an MDP was added to test if it could reduce the detrimental effects of EA on rumen fermentation. MDP increased total volatile fatty acids (VFA) and reduced total microbial protein synthesis. Furthermore, EA reduced microbial diversity and the acetate:propionate ratio. Although EA reduced organic matter digestibility and acetate production, these negative effects were reversed by the addition of the MDP.

Vasoconstriction is a known effect associated with ergot alkaloid consumption. The vascular contractile responses are often sustained for an extended period after exposure. Ergot alkaloids exist in two molecular configurations, the C-8-(R)-isomer (R-epimer) and the C-8-(S)-isomer (S-epimer). The sustained vascular contractile response to the R-epimers has been studied previously, unlike the S-epimers which are thought to be biologically inactive. Additionally, antagonists have been utilized to attenuate the vascular contraction associated with the R-epimers of ergot alkaloids utilizing ex vivo techniques. This study utilized an arterial tissue bath to examine and compare the sustained vascular contractile response attributed to ergocristine (R) and ergocristinine (S) using dissected bovine metatarsal arteries. The contractile blocking effect of a noncompetitive alpha-adrenergic antagonist, phenoxybenzamine (POB), was also investigated in precontracted arteries. Arteries (n= 6/epimer) were exposed to a single dose of ergocristine or ergocristinine (1 × 10−6M in buffer). Each of the epimer doses was followed by a POB (1 × 10−3M) or methanol (control) treatment at 90 min and the response was observed for another 90 min. Both epimers produced a sustained contractile response over the 180-min incubation period in the control groups. The R-epimer caused a greater sustained contractile response from 60 to 180 min post epimer exposure, compared to the S-epimer (P< 0.05, generalized estimating equations, independent t-test). Phenoxybenzamine caused a decrease in the contractile response induced by ergocristine and ergocristinine from 105 to 180 min, compared to the control (P< 0.05, generalized estimating equations, paired t-test). Overall, these results demonstrate the presence of a sustained vascular contractile response attributed to the R-and S-epimer of an ergot alkaloid with differences in contractile response between the epimers, suggesting differences in receptor binding mechanisms. Furthermore, this study demonstrated that a noncompetitive antagonist could attenuate the sustained arterial contractile effects of both ergot configurations ex vivo. Additional investigation into S-epimers of ergot alkaloids is needed. This research contributes to the understanding of the ergot epimer-vascular receptor binding mechanisms, which may support the investigation of different approaches of minimizing ergot toxicity in livestock.The R-and S-epimer of an ergot alkaloid, ergocristine, and ergocristinine, produced a sustained vascular contractile response. A noncompetitive antagonist, phenoxybenzamine, alleviated vascular contraction during the sustained contractile response.Ergot alkaloids cause blood vessels to contract when contaminated feed is consumed by animals. Vascular contraction often remains for a prolonged period and involves the binding of ergot to specific receptors in the blood vessels. This study assessed and compared the sustained contraction of cow arteries after exposure to two forms of an ergot alkaloid, namely, ergocristine and ergocristinine. The effects of a specific receptor blocker, phenoxybenzamine, on the vascular contraction induced by these forms were also examined. This study showed that both forms of ergot caused a sustained contraction of cow arteries but to different magnitudes. Differences in contraction could be related to differences in how each form of ergot binds to receptors. The receptor blocker decreased the sustained contractile response of both forms of ergot. Further understanding of how the different forms of ergot bind to receptors, and how to decrease the adverse effects, may help mitigate the toxic effects of ergotism.

The primary objective of the current study was to describe micronutrient concentrations in livers collected during postmortem examination from 501 beef calves and fetuses in western Canada. The most frequently identified deficiencies based on reported ranges for aborted fetuses were magnesium, copper, and vitamin E. For stillborn, neonatal, and postnatal calves, the most common deficiencies were magnesium, vitamin A, and vitamin E. However, for calves that died after 3 days of age, selenium deficiency was also very likely. Concentrations of all micronutrients examined in the study except zinc (P= 0.85) were different among fetuses, stillbirths, and neonatal and postnatal losses. This included liver selenium, copper, manganese, molybdenum, iron, magnesium, vitamin A, and vitamin E (P< 0.01). The percentiles of micronutrient concentrations for each age group, empirical prediction intervals for individual calves, and model predicted confidence intervals to compare with average concentrations from groups of calves were summarized for each age group. Information on cow, calf, and herd management attributes were available for 221 samples from 106 herds collected as part of study 1. Cow age, supplementation history, water quality, and herd location were associated with the concentration of iron, zinc, and molybdenum. The current study is unique in the number of samples included from young calves that were submitted as part of routine surveillance and not based on suspicion of either deficiency or toxicity. Most previous studies have been focused on older animals or fetuses and have contained a mix of beef and dairy animals with little or no information on their supplementation history.

Detoxification of ergot-contaminated feed by ammonia would be a practical application, given that ammonia is routinely used in the agriculture industry. To assess the effects of ammonia on ergot alkaloids, natural ergot-contaminated wheat was ammoniated. The total concentration of ergot alkaloids (R-and S-epimers) decreased after exposure to ammonia (8–29%). Separately, the total R-epimers decreased in concentration (40–66%), whereas the total S-epimers increased (21–81%). Specific ergot alkaloids demonstrated degradation and/or epimerization after exposure to ammonia, potentially associated with structural differences, and influenced the total concentrations observed. Ammonization of ergot standards resulted in potential degradation products and epimerization, supporting the above results. The use of ultrahigh-performance liquid chromatography–tandem mass spectrometry provides an updated assessment of the detoxification potential of ammonia for ergot alkaloids and the quantification of the S-epimers. Ammonia alters the R-and S-epimers of ergot alkaloids, which may lead to a potential practical detoxification process of ergot-contaminated feed.

A rumen simulation technique (RUSITEC) investigated effects of ergot alkaloids (E) and a mycotoxin deactivating product (Biomin® AA; B) on nutrient digestion, rumen fermentation, total gas and methane emissions. Fermenters received a finishing diet of 90:10 concentrate:barley silage. Using a randomized complete block design, treatments were assigned (4 vessels/treatment) within two RUSITECs in a 2 × 2 factorial. Treatments included: 1) control diet, 2) control + 1 g B, 3) control + 20 ppm E, and 4) control + 20 ppm E + 1 g B. The study had a 14-d experimental period, with 7-d adaptation and 7-d sample collection. Data were analyzed in SAS using PROC mixed including fixed effects of E, B, and E×B interaction. Random effects included RUSITEC apparatus and cow rumen inoculum (n = 4). Ergot decreased dry matter disappearance (DMD) (P < 0.05; 87.9 vs. 87.2%) and organic matter disappearance (OMD) (P < 0.05; 88.8 vs. 88.4%). Adding B increased OMD (P < 0.05; 88.3 vs. 88.9%) and neutral detergent fiber disappearance (NDFD) (P < 0.01); however, an E×B interaction was observed for NDFD (P < 0.01) with B promoting greater increases with E. Ergot decreased acetate proportions (P < 0.01) and increased isovalerate (P < 0.05). Consequently, acetate:propionate was reduced (P < 0.05) with E. Inclusion of B increased total volatile fatty acids (P < 0.01), and proportions of acetate (P < 0.05) and propionate (P < 0.05), and decreased valerate (P < 0.01), isovalerate (P < 0.01), and caproate (P < 0.01). Treatments did not affect (P ≥ 0.17) ammonia-N, total gas, or methane production (mg/d or mg/g of OM fermented). In conclusion, E reduced OMD and acetate production, but these responses were reversed by the addition of B.

Lead poisoning is commonly diagnosed in cattle. In this study, 3 groups of cattle from different herds accidentally exposed to discarded lead batteries on pasture were intensively studied to determine the extent and severity of exposure. The losses from acute death due to lead toxicity were substantial in all the 3 study groups at 12%, 17%, and 4%. Blood samples were taken from all cattle around the time of the first diagnosis and then later in 2 of the 3 herds to monitor the change in lead concentrations over time. Asymptomatic lead toxicosis was observed in these herds. In these 3 groups, between 4% and 12% of asymptomatic cattle had blood lead concentrations consistent with acute lead poisoning (>0.35 ppm), and between 7% and 40% of these asymptomatic animals were in the high-normal range (0.1–0.35 ppm). Because of the consistently high number of asymptomatic cattle with elevated lead levels, all cattle potentially exposed to a lead source should be tested before sale or slaughter to minimize the entry of lead into the food chain. The blood lead concentrations, which were monitored for months after the initial diagnosis, decreased slowly after the cattle were removed from the lead source. The prolonged retention of lead may be due to continued release and absorption of lead from metal particles in the reticulum or rumen. The mean reduction in the lead level was 0.046 ppm (95% CI, 0.017–0.075 ppm) every 30 days for these 2 herds. Using a single-component exponential model, the half-life of lead in the animals retested from Herds 1 and 2 was highly variable. The median half-life was 63 days (interquartile range, 34–107 days). One out of 8 pregnant heifers with high blood levels had a stillborn calf. There were no abortions or calf mortalities in this group. Blood samples were collected from the calves around the time of birth. The concentrations of lead in the blood of the calves exposed in utero were low (0.010–0.095 ppm).

Lesions of heart failure, specifically cardiac dilation or hypertrophy along with a nodular liver (chronic passive congestion) and ascites, have been found in 4-5% of aborted bovine fetuses. In this study, a group of 22 such fetuses was compared with groups of aborted fetuses without lesions of heart failure and with nonaborted fetuses obtained from a slaughterhouse. The fetuses were necropsied, tissues were taken for histopathology, and samples were collected for routine bacteriologic and virologic examinations. Liver and kidney tissue was saved for selenium analysis. Histopathologic examinations of myocardium of fetuses with cardiac failure revealed myocardial necrosis and mineralization in 7 fetuses, lymphocytic myocarditis in 5 fetuses, myocardial fibrosis in 5 fetuses, or no microscopic lesions in 5 fetuses. Mean liver selenium levels were 5.5 (μmol/kg in the fetuses with heart lesions, 6.5 μmol/kg in the fetuses without heart lesions and 7.5 μmol/kg in fetuses from the slaughterhouse; these differences were statistically significant. The results suggest that selenium deficiency in bovine fetuses may cause myocardial necrosis and heart failure. This study also provides data on normal liver and kidney selenium levels in bovine fetuses from the analyses of 19 nonaborted fetuses.

1Weanling male CD-1 mice were fed 120 (control), 5000 and 8000 mg of iron kg-1for seven weeks. The haematocrit (P=0.265), water consumption (P=0.170) and percentage body weight ratios of kidney, spleen and heart were not affected by iron supplementation.2Iron supplementation reduced weight gain (P=0.023), increased weight of liver (P=0.0001), the iron deposition index and concentration of iron in the liver (P<0.01). A strong correlation between liver iron concentration and level of iron in the diet (r=0.989) was observed. Histologically, the deposition of iron was restricted to the hepatocytes, Kupffer cells and splenic macrophages.3Consumption of 5000 and 8000 mg of iron kg-1resulted in hepatic damage, as judged by elevated serum alkaline phosphatase and alanine aminotransferase activities (P<0.05).4This study indicates that prolonged feeding of excess dietary iron has the potential to cause hepatic accumulation of iron with resultant liver toxicity, and that mice may be a suitable model to study the mechanisms of dietary iron overload.

The humoral immune response was evaluated in male CD-1 mice fed the iron deficient (7 ppm Fe), iron sufficient (120 ppm Fe), and high-iron diets (3000 or 5000 ppm Fe) for 54 d. The IgM and IgG antibody responses against sheep erythrocytes (SRBC) determined by hemolytic plaque assay were suppressed by 65.4 and 51.2%, respectively, in the iron deficient mice. Subclinical iron deficiency was manifested by a marked reduction in hepatic iron concentration without any changes in hematocrit or body weight gain. In contrast, consumption of high-iron diets caused a marked accumulation of iron in the liver and a twofold reduction in the IgM antibody response without alteration in the IgG response. The suppression of the IgG antibody response in the iron deficient mice, however, did not result in a compensatory increase in delayed type hypersensitivity response.

In the present paper, we are reviewing experimental evidence demonstrating that phagocytic cells, such as macrophages, may be used as a biomarker of immunotoxicity in wildlife studies. We will first present data obtained after exposure in vitro with selected chemicals showing the comparative sensitivity of phagocytic cells from different species. These results demonstrate that, at least for metals, each species produce a similar shaped dose-response curve, although considerate interspecies sensitivity is evident. These results also demonstrate the sensitivity of the phagocytic activity, suggesting indeed that this function could be used to monitor exposure to chemicals. The similar shaped dose-response curves imply that mechanisms of action may also be similar. Furthermore, based on the relative speices sensitivity, sentinel species could be selected for field monitoring. Such an approach may also be useful to establish correction factors required to extrapolate results between species. This sensitivity of the phagocytic activity of macrophages will be further under controlled conditions in laboratory animal models. Finally, the reliability of this approach will be demonstrated using case studies with wildlife species.