Interactions between different media and follicle‐stimulating hormone supplementation on in vitro culture of preantral follicles enclosed in ovarian tissue derived from collared peccaries (Pecari tajacu Linneaus, 1758)

The aim was to verify the effect of follicle‐stimulating hormone (FSH) supplementation to α‐MEM+ or TCM199+ media on the in vitro development of ovarian preantral follicles (PFs) derived from collared peccaries. Ovaries (n = 5 pairs) were collected and divided into fragments destined to control group (non‐cultured) or treatments that were cultured for 7 days. The PFs morphology, growth and activation were evaluated by classical histology. The immunohistochemistry markers Ag‐NOR and PCNA were used for nuclear proliferation analysis, and the picrosirius red labelling was used for ovarian extracellular matrix (ECM) evaluation. After 7‐day culture, only the TCM199+ treatment maintained the proportion of intact PFs similar to day 1 (63.2%), but no differences were found among treatments (p > .05). In addition, a significant increase in the growing follicles proportion was verified for all the treatments, indicating follicular activation (p > .05). By the Ag‐NOR analysis, only the TCM199+/FSH maintained the nuclear proliferation similar to the first day (p > .05). The picrosirius red staining revealed that the ECM remained intact in all the treatments (p > .05). We suggest the use of TCM199+ medium supplemented of FSH for the in vitro development of peccaries PFs under 7‐day culturing conditions.     

Disseminated Aspergillus flavus infection in broiler breeder pullets

Increased morbidity and mortality occurred in a 5-wk-old broiler breeder replacement pullet flock. The affected broiler pullet flock was housed on the first floor of a two-story confinement building. Mortality increased to 0.1%/day compared to the flock on the second floor, which had mortality levels of less than 0.01%/day. Clinical signs in the affected chickens included inactivity, decreased response to stimuli, and anorexia. No respiratory or neurologic signs were observed. On necropsy, affected pullets were dehydrated and emaciated and had disseminated variably sized single or multiple heterophilic granulomas that contained intralesional septate and branching fungal hyphae. Lesions were extensive around the base of the heart in the thoracic inlet and in the kidneys. Other affected organs included eyelid, muscle, proventriculus, ventriculus, intestine, liver, spleen, lung, and heart. Aspergillus flavus was cultured from the visceral granulomas. The source of flock exposure to the organism was not determined.     

Streptococcus iniae: an aquatic pathogen of global veterinary significance and a challenging candidate for reliable vaccination

Streptococcus iniae has become one the most serious aquatic pathogens in the last decade causing high losses in farmed marine and freshwater finfish in warmer regions. Although first identified in 1976 from a captive Amazon freshwater dolphin, from which it derives its name, disease outbreaks had most likely been occurring for several decades in marine aquaculture in Japan. S. iniae is globally distributed throughout warm water finfish aquaculture. In common with other encapsulated beta-haemolytic streptococci and in direct contradiction to the phenomenal success story of bacterial vaccines in finfish aquaculture, control of S. iniae by vaccination has met with limited success. Thus, antibiotic usage is the current practice for reducing mortality and consequent economic loss. Vaccine failure appears to result in part from serotypic variation and, whilst 2 serotypes have been named, variation would appear to be more complex. S. iniae also has zoonotic potential, with human infections identified in the USA, Canada, and throughout Asia. In humans, infection is clearly opportunistic with all cases to date associated with direct infection of puncture wounds during preparation of contaminated fish, and generally in elderly or immunocompromised individuals. Significant progress has been made in terms of research into pathogenic mechanisms of S. iniae, with recent research elucidating the role of capsule in virulence for fish through antiopsonic activity. In light of this recent coverage in the literature, the present review centres on areas of direct veterinary interest including identification, epidemiology, therapy and prevention in farmed finfish. Clearly as the prevalence of S. iniae and associated economic losses continue to increase, further work towards developing a reliable vaccine is essential. This would appear to require a much better understanding of cell-surface variability amongst S. iniae isolates.     

The effect of pressure on turkey breast skin

In an attempt to experimentally reproduce focal ulcerative dermatitis (FUD) in turkeys, pressures of 94, 136, and 240 mmHg were applied for 2, 4, or 6 hr daily for 4 consecutive days to unfeathered breast skin of six 9-week-old toms. No gross lesions occurred either immediately after treatment or during a 10-day post-treatment period, and no microscopic changes were present in the skin at the conclusion of the trial. These findings suggest that avian skin is resistant to pressure-induced decubital ulceration and that pressure is unlikely to be either the cause of or a significant contributor to FUD.     

The effect of processing and marketing procedures on the bacteriological condition and shelf life of eviscerated turkeys

Experiments carried out in a turkey processing plant showed that there was a fivefold increase in the number of psychrophilic bacteria present after holding eviscerated carcasses in static slush ice tanks for 24 hr. The predominant bacteria in the 24 hr chill tanks were strains of Flavobacterium, Cytophaga and Pseudomonas.

The carcasses were wrapped in heat‐shrunk‐oxygen‐impermeable film and after freezing packed in individual boxes and held at ‐20° C. The storage life at 1°, 10° and 20° C. was determined together with the time taken for the frozen carcasses to equilibrate to these temperatures. It was found that at 1° C. the carcasses kept for about 3 weeks, but at 10° C. they spoiled within 7 days and at 20° G. within 3 days.

An analysis of the spoilage flora showed that although Pseudomonas strains predominated on the turkeys stored at 1° C. fewer were isolated from turkeys stored at 10° C. and 20° C. At these two temperatures an organism identified as Enterobacter liquefaciens predominated together with atypical lactobacilli resembling unidentified strains previously described by Thornley and Sharpe (1959).     

Prevalence of enteropathogenic Escherichia coli in naturally occurring cases of poult enteritis-mortality syndrome

Enteropathogenic Escherichia coli (EPEC) previously were identified in poult enteritis-mortality syndrome (PEMS)-affected turkeys and associated as a cause of this disease. In the present study, the prevalence of EPEC in PEMS-affected turkeys was examined retrospectively with archived tissues and intestinal contents collected from 12 PEMS-affected turkey flocks in 1998. Formalin-fixed intestinal tissues were examined by light and electron microscopy for attaching and effacing (AE) lesions characteristic of EPEC, and frozen (-75 C) intestinal contents were examined for presence of EPEC. Escherichia coli isolates were characterized on the basis of epithelial cell attachment, fluorescent actin staining (FAS) test, and presence of E. coli attaching/effacing (EAE), shigalike toxin (SLT) type I, SLT II, and bundle-forming pilus (BFP) genes by polymerase chain reaction procedures. EPEC isolates were examined for pathogenicity and ability to induce AE lesions in experimentally inoculated young turkeys. AE lesions were identified by light microscopy in Giemsa-stained intestines from 7 of 12 PEMS-affected turkey flocks. Lesions consisted of bacterial microcolonies attached to epithelial surfaces with epithelial degeneration at sites of attachment and inflammatory infiltration of the lamina propria. Electron microscopy confirmed the identity of AE lesions in six of seven flocks determined to have AE lesions by light microscopy. EPEC were identified in 4 of 12 flocks on the basis of the presence of EAE genes a nd absence of SLT I and SLT II genes; all isolates lacked BFP genes. EPEC isolates produced AE lesions and variable mortality in turkeys coinfected with turkey coronavirus. In total, EPEC were associated with 10 of 12 (83%) naturally occurring PEMS cases on the basis of identification of AE lesions and/or EPEC isolates. These findings provide additional evidence suggesting a possible role for EPEC in the pathogenesis of PEMS.