Origins of coccidiosis research in the fowl--the first fifty years

In 1910, H. B. Fantham described the life cycle of a coccidian parasite in birds. Fantham was a parasitologist at Cambridge University in the United Kingdom working for an enquiry into diseases affecting the red grouse. Despite the growing importance of the poultry industry and the realization that coccidiosis was an important disease of the fowl, little further work was carried out in the United Kingdom until coccidiosis research was initiated at the Veterinary Laboratory, Weybridge almost 30 yr later. Further progress depended upon research carried out at academic and agricultural institutions in the United States. E. E. Tyzzer at Harvard University provided the solid foundation upon which our present knowledge of coccidiosis, and the species of Eimeria involved in the disease, is based. Agricultural experiment stations (AESs) throughout the nation played an important role in communicating advances to the agricultural community. W. T. Johnson at Western Washington and, subsequently, Oregon AES made significant contributions to our understanding of the disease, as did C. A. Herrick and coworkers at Wisconsin AES, J. P. Delaplane and coworkers at Rhode Island AES, and P. P. Levine at Cornell University.     

Acid-base balance of cats with chronic renal failure: effect of deterioration in renal function

In a previous cross-sectional study of feline chronic renal failure (CRF), metabolic acidosis was identified in 52.6 per cent of animals with severe renal failure (plasma creatinine concentration >400 micromol/litre). The aim of this longitudinal study was to determine whether metabolic acidosis preceded or accompanied a deterioration in renal function in cats with CRF. Data were analysed from 55 cats with CRF that had been followed longitudinally for at least four months. Twenty-one cases showed deterioration in renal function over the period of the study, as evidenced by significant rises in their plasma creatinine concentrations and decreases in bodyweight. In five of the 21 cases, acidaemia accompanied the deterioration in renal function. Only one of these cats had evidence of metabolic acidosis before renal function deterioration. One other case developed metabolic acidosis without a rise in plasma creatinine concentration. These data suggest that biochemical evidence of metabolic acidosis does not generally occur until late in the course of feline CRF.     

Assessing the agreement of Western blot test results for paired serum and cerebrospinal fluid samples from horses tested for antibodies to Sarcocystis neuronaf

Equine protozoal myeloencephalitis (EPM) is a neurological disease of equids that is caused by infection of the central nervous system with Sarcocystis neurona. Veterinarians diagnose EPM by performing a neurological examination and by ordering Western blot tests for antibodies to S. neurona in the blood and/or cerebrospinal fluid (CSF). The negative predictive value of the Western blot test is generally accepted to be high for both serum and CSF. If the agreement between serum and CSF test results is strong, serum tests could be used to substitute for CSF tests in some cases. The purpose of this study was to assess the agreement of the results of 181 paired serum and CSF Western blot antibody tests on equine samples submitted to the Michigan State University Animal Health Diagnostic Laboratory. The agreement of the paired serum and CSF results was assessed for three possible test outcomes--negative, positive or suspect. An additional analysis was performed in which samples reported as suspect were reclassified as negative. The kappa statistic for negative, positive and suspect samples was 0.469. The kappa statistic for the analysis in which the suspect results were reclassified as negative was 0.474. In addition, 29% (33/112) CSF samples from seropositive horses were negative. Our results demonstrate that the level of agreement is only moderate in diagnostic samples. This supports the practice of testing CSF of seropositive horses suspected of having EPM.     

A rat model for the energetic regulation of gonadotropin secretion: role of the glucose-sensing mechanism in the brain

Energy availability has been considered to regulate gonadal activity by modulating the release of gonadotropin-releasing hormone (GnRH)/luteinizing hormone (LH) at various reproductive phases, such as lactation and puberty in domestic as well as wild animals. Experimental models with rats and sheep have demonstrated that fasting or glucoprivation suppresses pulsatile LH release. From those experiments, the information on energy deficiency is considered to be detected by specific central sensors and conveyed to the hypothalamus to regulate LH release as well as food intake. Noradrenergic neurons, originating in the medulla oblongata and projecting to the hypothalamic paraventricular nucleus (PVN), is reported to be one of the pathways mediating the response of LH release to energy deficiency. The other component is considered to be an energy-sensing mechanism in the brain. Glucose or other oxidizable fuels may function as a metabolic signal to regulate LH release. Previous studies suggest the presence of a glucose-sensing mechanism in the rat hindbrain. From our previous results in the rat, the ependymocytes lining the wall of the cerebroventricle could possibly serve as a glucose sensor to regulate GnRH/LH release. Greater understanding of the nature of the energy-sensing mechanism in the brain will contribute to the nutritional manipulation of reproductive performance in domestic animals in various conditions.     

Occurrence of Arcobacter in Iranian poultry and slaughterhouse samples implicates contamination by processing equipment and procedures

1. The occurrence of Arcobacter spp. and three pathogenic species of Arcobacter from Iranian poultry carcasses was investigated at different steps of broiler processing to determine critical control points for reducing carcass contamination.

2. Samples were collected from (a) cloaca immediately before processing, (b) different points during processing and (c) at different stations in a processing plant of a slaughterhouse in southern Iran.

3. After enrichment steps in Arcobacter selective broth, DNA of the samples was extracted and three significant pathogen species of Arcobacter were identified based on polymerase chain reaction (PCR) detection of 16S rRNA and specific species PCR.

4. Out of a total of 540 samples, 244 (45%) were positive for Arcobacter spp. Arcobacter butzleri was more frequently detected (73% ± 13.9%) than A. cryaeophilus (9% ± 13.9%) and A. skirrowii (4.1%). In addition, co-colonisation (A. butzleri and A. cryaerophilus) occurred in 13.9% of the positive samples.

5. The results indicate a high prevalence of Arcobacter in the investigated slaughterhouse and broiler carcasses and that Arcobacter is not a normal flora of the broilers. Evidence for the presence of Arcobacter in the environment and water of processing plants suggests that these are sources of contamination of poultry carcasses. In addition, contamination of the poultry carcasses can spread between poultry meats in different parts and processes of the slaughterhouse (pre-scalding to after evisceration).     

Efficacy of Omeprazole Powder Paste or Enteric‐Coated Formulation in Healing of Gastric Ulcers in Horses

Background

GastroGard, an omeprazole powder paste formulation, is considered the standard treatment for gastric ulcers in horses and is highly effective. Gastrozol, an enteric‐coated omeprazole formulation for horses, has recently become available, but efficacy data are controversial and sparse.

Objectives

To investigate the efficacy of GastroGard and Gastrozol at labeled doses (4 and 1 mg of omeprazole per kg bwt, respectively, PO q24h) in healing of gastric ulcers.

Animals

40 horses; 9.5 ± 4.6 years; 491 ± 135 kg.

Methods

Prospective, randomized, blinded study. Horses with an ulcer score ≥1 (Equine Gastric Ulcer Council) were randomly divided into 2 groups and treated for 2 weeks each with GastroGard followed by Gastrozol (A) or vice versa (B). After 2 and 4 weeks, scoring was repeated and compared with baseline. Plasma omeprazole concentrations were measured on the first day of treatment after administration of GastroGard (n = 5) or Gastrozol (n = 5).

Results

Compared with baseline (squamous score (A) 1.65 ± 0.11, (B) 1.98 ± 0.11), ulcer scores at 2 weeks ((A) 0.89 ± 0.11, (B) 1.01 ± 0.11) and 4 weeks ((A) 1.10 ± 0.12, (B) 0.80 ± 0.12) had significantly decreased in both groups (P < .001), independent of treatment (P = .7). Plasma omeprazole concentrations were significantly higher after GastroGard compared with Gastrozol administration (AUC_GG = 2856 (1405‐4576) ng/mL × h, AUC_GZ = 604 (430‐1609) ng/mL × h; P = .03). The bioavailability for Gastrozol was 1.26 (95% CI 0.56–2.81) times higher than for GastroGard.

Conclusions and Clinical Importance

Both Gastrozol and GastroGard, combined with appropriate environmental changes, promote healing of gastric ulcers in horses. However, despite enteric coating of Gastrozol, plasma omeprazole concentrations after single labeled doses were significantly higher with GastroGard.