Interspecific competition and rarity in mudsnails: feeding interactions between and within Hydrobia acuta neglecta and sympatric Hydrobia species

• 1. Using production of faecal pellets as a proxy for feeding rate, possible reciprocal effects of the widespread and abundant mudsnails Hydrobia ulvae and Hydrobia ventrosa on the rare Hydrobia acuta neglecta were investigated under the sea‐water salinity conditions in which all three species occur naturally in East Anglia, UK.
• 2. Over a density range equivalent to 1000–34 000 m^?2, H. acuta and H. ventrosa (though not H. ulvae) at some point displayed an intraspecific reduction in egestion with increase in density. For H. acuta, every 5000 extra snails above a threshold of 16 000 m^?2 reduced egestion by up to 8%; and for H. ventrosa, every 5000 extra snails above a threshold of 8000 m^?2 reduced egestion by an average 7%.
• 3. Keeping the density of one test species constant at 4000 m^?2 whilst varying that of a sympatric one from 0 up to 30 000 m^?2 indicates that H. ulvae has a marked effect on H. acuta at all densities, decreasing its egestion by 10% for every 5000 m^?2 H. ulvae also present, but that H. acuta has no such reciprocal effect on H. ulvae. H. ventrosa had no effect on egestion in H. acuta, although H. acuta did have some minor effect on H. ventrosa, on average decreasing its egestion by 3% for every 5000 m^?2 H. acuta present.
• 4. The intensity of intraspecific competition within H. acuta, therefore, exceeds that exerted on H. acuta by H. ventrosa, and likewise intraspecific effects within H. ventrosa generally outweigh any interspecific effect from H. acuta. The effect of H. ulvae on H. acuta, however, exceeds that intraspecifically within H. acuta.
• 5. These results are discussed in relation to the rarity of H. acuta neglecta.

Copyright © 2005 John Wiley & Sons, Ltd.     

Venereal colibacillosis (acute vaginitis) in turkey breeder hens

Two flocks of turkey breeders experienced an increased mortality and high culling rate in the first weeks of egg production. The majority of dead and culled hens had cheesy core in the cloaca and vagina. Postmortem examination revealed fibrinous pseudomembranes in the vagina and cloaca. The thickness of these membranes posed an obstruction to egg passage leading to internal laying and egg peritonitis. Swabs from cloaca and vagina produced numerous colonies of only E. coli. Investigations of this unusual vaginitis showed that these two flocks had a higher number of immature hens with present hymens, and insemination crews mistakenly inseminated all hens in which they were able to evert the cloaca. Breaking the hymen with an insemination pipette created a wound and developed extensive infection with E. coli bacteria.     

Enhancement of enteropathogenic Escherichia coli pathogenicity in young turkeys by concurrent turkey coronavirus infection

In a previous study, turkey coronavirus (TCV) and enteropathogenic Escherichia coli (EPEC) were shown to synergistically interact in young turkeys coinfected with these agents. In that study, inapparent or mild disease was observed in turkeys inoculated with only TCV or EPEC, whereas severe growth depression and high mortality were observed in dually inoculated turkeys. The purpose of the present study was to further evaluate the pathogenesis of combined TCV/EPEC infection in young turkeys and determine the role of these agents in the observed synergistic interaction. Experiments were conducted to determine 1) effect of EPEC dose, with and without concurrent TCV infection, and 2) effect of TCV exposure, before and after EPEC exposure, on development of clinical disease. Additionally, the effect of combined infection on TCV and EPEC shedding was determined. No clinical sign of disease and no attaching and effacing (AE) lesions characteristic of EPEC were observed in turkeys inoculated with only EPEC isolate R98/5, even when turkeys were inoculated with 10(10) colony forming units (CFU) EPEC (high dose exposure). Only mild growth depression was observed in turkeys inoculated with only TCV; however, turkeys inoculated with both TCV and 10(4) CFU EPEC (low dose exposure) developed severe disease characterized by high mortality, marked growth depression, and AE lesions. Inoculation of turkeys with TCV 7 days prior to EPEC inoculation produced more severe disease (numerically greater mortality, significantly lower survival probability [P < 0.05], increased frequency of AE lesions) than that observed in turkeys inoculated with EPEC prior to TCV or simultaneously inoculated with these agents. Coinfection of turkeys with TCV and EPEC resulted in significantly increased (P < 0.05) shedding of EPEC, but not TCV, in intestinal contents of turkeys. These findings indicate that TCV infection predisposes young turkeys to secondary EPEC infection and potentiates the expression of EPEC pathogenicity in young turkeys.     

Effects of racing on lymphocyte proliferation in horses

OBJECTIVE: To measure the lymphocyte proliferation response in horses 12 to 16 hours after completion of a race. ANIMALS: 8 Thoroughbreds that competed in 14 races and 3 control Thoroughbreds that did not race. PROCEDURE: Horses participated in races during the late afternoon or evening. Venous blood samples were collected on a morning before a race (1 or 2 days before the race or on the day of the race), on the afternoon of a race (40 to 60 minutes after the race), and on the morning of the day after a race (12 to 16 hours after the race). Lymphocyte proliferation responses and WBC count were measured in samples obtained in the mornings. Plasma cortisol was measured in all samples. RESULTS: Lymphocyte proliferation responses were significantly reduced and WBC counts significantly increased 12 to 16 hours after a race. Plasma cortisol concentrations were significantly increased 40 to 60 minutes after a race. In samples from the control horses, lymphocyte proliferation responses, WBC counts, or plasma cortisol concentrations did not differ significantly among time periods. CONCLUSIONS AND CLINICAL RELEVANCE: A decrease in proliferative responses of circulating lymphocytes can be found as late as 12 to 16 hours after a horse participates in a race. Although the clinical consequences of these exercise-related alterations of the immune response are not yet known, managers of horses should take into account that the immune system of a horse may be affected by racing.     

The effect of storage temperature on the shelf‐life of eviscerated air‐chilled Turkeys

1. Eviscerated air‐chilled turkeys (weighing about 5.5 kg) were stored in groups of 10 at temperatures between 5 and — 2 °C. Slight “off” odour was detected in an average time of 7.2 d at 5 °C, 13.9 d at 2 °C, 22.6 d at 0 °G and about 38 d at ‐2 °C.

2. The microbiological condition of the carcasses was determined initially and after storage at — 2 ^oC for 28, 35 and 42 d. It was found that, whilst pseudomonads (pigmented and non‐pigmented) were present at 10⁸/cm² after 35 and 42‐d storage, yeasts were also present at 10⁷/cm² and probably accounted for the unusual fusty “off” odours.     

The relationship between brain levels of cismethrin and bioresmethrin in female rats and neurotoxic effects

The oral toxicity of 5-benzyl-3-furylmethyl-(1R, cis)-chrysanthemate (cismethrin) to female rats decreased as their environmental temperature was raised. Acute oral LD₅₀ values increased from 157 mg/kg at 4°C to 197 mg/kg at 20°C and to > 1000 mg/kg at 30°C. Cismethrin was much more toxic given intravenously when the LD₅₀ was 4.5 mg/kg. This value did not change at different environmental temperatures. Irrespective of the environmental temperature, or route of adminstration, following the respective LD₅₀'s cismethrin caused tremors in rats when brain levels of 0.5–1.0 μg/g were reached and, at death, brain concentrations were 3.9–5.1 μg/g. These results suggested that the accumulation of cismethrin by the brain could be used as a model for the nervous system as a whole. The isomeric 5-benzyl-3-furylmethyl-(1R, trans)-chrysanthemate (bioresmethrin) was about 50 times less toxic to rats than cismethrin. After an intravenous LD₅₀, tremors started when brain concentrations were 4–5 μg/g. At death, brain levels were 25–35 μg/g. Plasma esterases were about equally active in hydrolysing cismethrin and bioresmethrin, whereas liver microsomal esterases hydrolyzed bioresmethrin over 10 times more rapidly than cismethrin. It is suggested that the lower toxicity of bioresmethrin is not only due to its faster metabolism but to an intrinsically lower toxicity at the critical site of action in the nervous system.     

Prevalence of tetracycline-resistant Campylobacter in organic broilers during a production cycle

Tetracycline (tet) resistance in Campylobacter isolated from organically raised broilers was investigated in this study. Two hundred forty-five samples from an organic broiler farm were collected weekly from the first week to the end of the production cycle, and they were cultured for thermophilic Campylobacter. Tetracycline resistance of these Campylobacter isolates was identified by the agar dilution method, whereas DNA fingerprinting profiles of tet-susceptible and tet-resistant strains were determined by pulsed-field gel electrophoresis (PFGE). None of the Campylobacter isolates from the third and the fourth week of the production period were resistant to tetracycline, whereas 66.7% of the isolates from the fifth week were resistant to this antibiotic. Although the prevalence of tetracycline resistance reached 100.0% during the sixth and seventh week, less than 34.0% of the isolates from the 10th week were resistant to this antimicrobial agent. In addition, only 13.8% of Campylobacter isolates from the intestinal tracts of these organically raised broilers were resistant to tetracycline. The presence of the tet(O) gene was detected in 98.9% of tet-resistant Campylobacter isolates, and tet-susceptible and tet-resistant Campylobacter strains showed distinct PFGE genotypes. The results suggest that the Campylobacter strains isolated from the early stage of the production were susceptible to tetracycline, but they were subsequently displaced by tet-resistant Campylobacter.