Sex hormones, reproductive status, and pathogen load all affect stress. Together with stress, these factors can modulate the immune system and affect disease incidence. Thus, it is important to concurrently measure these factors, along with their seasonal fluctuations, to better understand their complex interactions. Using steroid hormone metabolites from fecal samples, we examined seasonal correlations among zebra and springbok stress, reproduction, gastrointestinal (GI) parasite infections, and anthrax infection signatures in zebra and springbok in Etosha National Park (ENP), Namibia, and found strong seasonal effects. Infection intensities of all three GI macroparasites examined (strongyle helminths, Strongyloides helminths, and Eimeria coccidia) were highest in the wet season, concurrent with the timing of anthrax outbreaks. Parasites also declined with increased acquired immune responses. We found hormonal evidence that both mares and ewes are overwhelmingly seasonal breeders in ENP, and that reproductive hormones are correlated with immunosuppression and higher susceptibility to GI parasite infections. Stress hormones largely peak in the dry season, particularly in zebra, when parasite infection intensities are lowest, and are most strongly correlated with host mid-gestation rather than with parasite infection intensity. Given the evidence that GI parasites can cause host pathology, immunomodulation, and immunosuppression, their persistence in ENP hosts without inducing chronic stress responses supports the hypothesis that hosts are tolerant of their parasites. Such tolerance would help to explain the ubiquity of these organisms in ENP herbivores, even in the face of their potential immunomodulatory trade-offs with anti-anthrax immunity.
The male reproductive system is sensitive to endocrine disrupting chemicals (EDCs) during critical developmental windows. Male Sprague-Dawley rats were exposed in utero-, during lactation-and directly to 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT), 1,1,-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE) and a mixture of DDT, deltamethrin (DM), pnonylphenol (p-NP) and phytoestrogens, at concentrations found in a malaria-area. After dosing for 104 days, histological assessments and reproductive-endpoints were assessed.The anogenital distance (AGD) (P = 0.005) was shorter in the mixture-exposed group, while the prostate mass (P = 0.018) was higher in the DDT-exposed group. A higher testicular mass and abnormal histology was observed in the DDT-(P = 0.019), DDE-(P = 0.047) and mixture-exposed (P < 0.005) groups. This study shows that in utero-, lactational-and direct exposure to EDCs present in a malaria-area negatively affects male reproductive parameters in rats. These findings raise concerns to EDC-exposures to mothers living in malaria-areas and the reproductive health of their male offspring. 1
The composition of blood from veld and boma (enclosure)-kept impala, obtained immediately after the animals were manually restrained, was compared to control values. Statistically significant differences existed between the values for hematocrit, lactate, glucose, and osmolarity of veld and boma-kept animals compared to control data. Cortisol values were significantly greater (P less than .05) in boma-kept animals (93 +/- 21 nmol/liter) but not in veld impala (11 +/- 3 nmol/liter). It is suggested that the high cortisol and other values measured in boma-kept impala were due to an anticipatory conditioned response in these animals which occurred prior to them actually being caught. Repeated capture and handling, over a period of several months, of boma-kept impala resulted in statistically insignificant decreases in the mean values of several variables. Although this is indicative of adaptation it is doubtful whether the animals would ever fully adapt to the procedures involved.
The plasma concentration of the neuromuscular blocking drug, succinylcholine, is difficult to measure. We have measured concentrations of the breakdown product of succinylcholine, choline, to assess whether choline concentration gives an accurate measure of succinylcholine concentration. Choline concentration was measured by HPLC and electrochemical detection in two blood or plasma samples, one in which succinylcholine hydrolysis was inhibited by 10(-5) M physostigmine and another in which succinylcholine was completely hydrolysed in 20 min by 200 mU butyrylcholinesterase at 37 degrees C. The difference in choline content between the two samples gives the succinylcholine concentration. Ninety-five per cent recovery of choline was achieved. Choline standard curves were linear from 156 pmol ml-1 to 200 nmol ml-1. Within-day and between-day mean coefficients of variation for succinylcholine hydrolysis were small (mean (SD) 3.7% (1.2%) and 3.8% (1.6%), respectively). We conclude that this method of measuring succinylcholine concentration in blood is accurate, repeatable and relatively easy.
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