Infection with Basidiobolus ranarum in two dogs

Basidiobolus ranarum is a saprophytic fungus in the environment that also is a part of the endogenous microflora in the gastrointestinal tract of several vertebrates. These organisms may penetrate skin or muscosa of humans and other animals, causing granulomatous inflammation. Two dogs infected with B. ranarum had prolonged or repeated exposure to water or soil in their environment. One dog had progressive subcutaneous infection of all the limbs, and the other dog had recurrent coughing and dyspnea caused by tracheobronchitis. In both dogs, secondary bacterial infection of the lesions was evident. Treatment of the dog with subcutaneous infection involved cutaneous dressings and sequential use of enrofloxacin and itraconazole; however, this resulted in suspected liver damage without clinical improvement. Subsequent treatment with potassium iodide and a lipid formulation of amphotericin B was also unsuccessful, and the dog was euthanatized. The other dog was treated alternately with enrofloxacin and itraconazole. When the clinical signs and infection returned, combination treatment with both drugs was more effective; however, the dog developed liver damage. Subsequent treatment with enrofloxacin on an intermittent basis controlled the dog's coughing during a 3-year period.     

Is Change in Electrical Potential or pH a Hatching Signal for Heterodera glycines?

ABSTRACT This study explored the possibilities that changes in the egg shell/lipid layer electrical potential or pH communicate external hatching conditions to the Heterodera glycines second-stage juvenile (J2) within the mature egg and that electrophysiology could measure effects of chemicals on emergence. Potentials were measured following application of the emergence inducers (ZnSO(4) and ZnCl(2)), ions that do not affect emergence, or synthetic emergence inhibitors. Results were compared with pH measurements and emergence bioassays. Healthy appearing eggs had negative resting potentials. Application of ZnSO(4) caused a smooth depolarization. However, eggs containing J2 and immature eggs depolarized to a similar degree when ZnSO(4) was added. In addition, ZnSO(4), synthetic emergence inhibitors, and CaCl(2) caused similar depolarization, and some depolarization was measured in dye-permeable eggs and empty shells. Results suggest that change in cation surface charge contributed to depolarization and that Cl penetrated the egg shell/lipid layer without causing potential changes. In bioassays, zinc consistently stimulated emergence to a greater degree than H(2)O, other cations, or buffers, and counteracted emergence inhibitors. Zinc-caused emergence stimulation was independent of pH. In summary, it is concluded that depolarization and pH are not emergence signals and electrophysiology is unlikely to measure effectiveness of emergence stimulators or inhibitors.     

Multiple digital tumours in a rottweiler

An eight-and-a-half-year-old rottweiler bitch was examined on four separate occasions over a period of 32 months for lameness caused by a mass on a digit. On each occasion the mass and affected digit were amputated. Three different neoplasms were diagnosed: two squamous cell carcinomas, a melanocytoma and an intracutaneous cornifying epithelioma. There was no recurrence following surgical excision.     

Energy and nitrogen metabolism and oxygen use by broilers susceptible to ascites and grown at three environmental temperatures

1. An experiment using respiration calorimetry was performed to examine the energy and nitrogen metabolism of 2 strains of male broilers grown at 3 environmental temperatures; the results were then related to the susceptibility of the strains to the ascites syndrome.

2. Broilers selected for food conversion efficiency were less responsive to environmental temperature than were broilers selected principally for increased weight gain.

3. The susceptibility to ascites of broilers selected for food conversion efficiency may be the result not of a genetic incapacity to use oxygen but of the ability of the bird to maintain growth rate in adverse thermal environments.     

Herpesvirus that caused epizootic mortality in 1995 and 1998 in pilchard, Sardinops sagax neopilchardus (Steindachner), in Australia is now endemic

Propagating epizootics due to Pilchard herpesvirus (PHV) occurred in the Australian population of pilchard, Sardinops sagax neopilchardus (Steindachner) (Clupeidae), in 1995 and 1998-99, with up to 60% losses. No mortality events have been evident in the ensuing 7 years, one reason for which could be that PHV is now endemic. During 2004, a survey was conducted to establish if PHV was present in pilchards in Australia. The pilchard is a highly active, pelagic schooling fish which is found in subpopulations, creating difficulties for the conduct of surveys. It occurs in Australian coastal waters and embayments below about 25 degrees S latitude, feeds on plankton and is predated by birds, mammals and larger fish. It reaches sexual maturity at 2 years of age, spawns at sea, enters embayments when about 5 months old and returns to sea when about 1 year old. It may live for 6-9 years, reaching a maximum length of 200 mm. It forms schools and may travel up to 30 km per day. Pilchards aggregate in mobile shoals of fish containing large highly mobile schools, which interact randomly and exchange individuals. Four subpopulations were defined for the purposes of this survey based on differences in biological characteristics: south-eastern Queensland/northern New South Wales (NSW), Victoria/South Australia (SA), south coast Western Australia (SWA) and west coast Western Australia (WWA). Specimens were obtained from the catch of commercial fishermen using random sampling where possible. Polymerase chain reaction (PCR) for the detection of PHV was performed after appraising the suitability of all available tests according to their impact on sample size requirements, total survey costs and logistical constraints. In the analysis, estimates of true prevalence (TP) of infection and 95% confidence limits were adjusted from the apparent prevalence estimates provided by PCR results. Percentage TP of PHV and corresponding 95% confidence intervals for the four subpopulations: NSW, SA, SWA and WWA were thus estimated as 0 (0-1.5), 31 (22-43), 42 (31-55) and 29 (20-41), respectively. PHV is now endemic in Australian populations of pilchard. Implications of the findings for fisheries management are discussed.