Severity and persistence of footrot in Merino sheep experimentally infected with a protease thermostable strain of Dichelobacter nodosus at five sites

Objective To test the hypothesis that ovine footrot associated with a thermostable protease strain of Dichelobacter nodosus undergoes self cure or is sustained as an annually recurring disease, depending on the environment.
Design and procedure Forty Merino sheep from a single blood line were infected with a protease thermostable strain of D nodosus a t each of five sites in Western Australia. Footrot lesions and microscopic evidence of D nodosus were recorded every fortnight for 2.5 years, supplemented by laboratory culture. Rainfall, soil and air temperature, pasture quantity and composition and soil types were also recorded. Flocks that apparently self cured were relocated to a more favourable site for footrot in the final spring season.
Results The maximum prevalence of feet with clinical footrot lesions was 80.6, 1.3, 14.4, 3.8 and 88.1% at the five sites. Severe footrot occurred for three consecutive spring seasons at one site that had clay loam soil and at least 3500 kg/ha total pasture dry matter annually. However, the infection was asymptomatic for up to 10 weeks between outbreaks. D nodosus was isolated from flocks for 2.5 years at only two sites, although there was microscopic evidence of the organism at other sites in the final year. A thermolabile variant (strain U6) of D nodosus was isolated from the two sites where footrot persisted.
Conclusion Depending on time and location, ovine footrot induced by a protease thermostable strain of D nodosus either self cured or persisted as annual outbreaks interspersed with periods of asymptomatic infection.     

von Willebrand's disease in Scottish Terriers in Australia

SUMMARY Over a 5-year period (1988–92), von Willebrand factor antigen (vWf:Ag) assays were performed on plasma samples from 207 Scottish Terriers. Based on these tests, 47 dogs (23%) had vWf:Ag concentrations < 50 canine units (CU)/dL and were classified as heterozygous carriers of the von Willebrand's disease (vWD) gene, while 9 (4%) had concentrations below the sensitivity of the assays and were classified as homozygous. There was thus an overall prevalence of 27% for the vWD gene in the Scottish Terriers tested. The homozygous dogs (median age 0.6 years at diagnosis) consisted of 7 males and 2 females. Eight of these had haemorrhage attributable to the disease, mostly spontaneous and from the oral mucosa. Other signs included haemorrhage induced by trauma or surgery, easy bruising and epistaxis. Many haemorrhagic episodes were severe enough to warrant therapeutic intervention and there was a single fatality. Pedigree analysis, possible in 7 of the dogs, revealed that each was the progeny of a mating between dogs with vWf:Ag concentrations < 50 CU/dL, which supported an autosomal recessive mode of inheritance. A single heterozygous carrier suffered haemorrhage after surgery that, in contrast to the homozygotes, was mild and did not require therapy. The data indicate that vWD is a significant problem in Scottish Terriers in Australia. Accordingly, we recommend that steps be taken to reduce the prevalence of the disease and thereby the number of clinically affected dogs, such as the establishment of a national testing scheme to determine the vWD status of all breeding dogs.     

Transendoscopic injection of poly-L-lactic acid into the soft palate in horses: A new therapy for dorsal displacement of the soft palate?

The purpose of this study was to establish a minimal invasive, transendoscopic technique for injection of poly-L-lactic acid into the free edge of the soft palate that can be performed on the standing sedated horse. Furthermore, whether the implant material induces an increase in fibrous tissue at the injection site, resulting in a greater rigidity of the soft palate, was determined.In 4 horses, the injection was performed bilaterally along the caudal margin of the soft palate, and the influence of the treatment on the soft palate function was determined. Clinical, radiographic and endoscopic examinations at rest were performed before and up to 168 days after injection according to a standardized examination protocol.In 6 horses, the implant material was injected unilaterally into the right half of the caudal margin of the soft palate. After clinical and endoscopic follow-up examinations, 2 horses each were killed 28, 84, and 168 days after the implantation procedure. At necropsy, macroscopic comparison of the treated and the untreated halves of the soft palate showed the influence on the size of the ostium intrapharyngeum and on the soft palate thickness. The localization of the implant material in the soft palate and the tissue response to the poly-L-lactic acid were evaluated histologically.Transendoscopic injection into the soft palate requires neither general anesthesia nor wound management, and it is noted for minimal tissue trauma. After injection, no alteration of the soft palate function was observed in horses with normal upper airway mechanics. One horse with intermittent dorsal displacement of the soft palate showed an improvement of the soft palate function for 112 days after implantation. No significant alteration in the size of the ostium intrapharyngeum was evident in any horse. Histologic assessment indicated the presence of implant material during the entire observation period of 168 days. The implant was accompanied by a granulomatous inflammation, and it was encapsulated by fibrous tissue. This may result in an increase in stiffness, and subsequent a greater rigidity of the soft palate, preventing it from displacement. The injection may therefore be considered an alternative to established therapies in horses showing dorsal displacement of the soft palate because of its unstable free edge.     

Chediak-Higashi syndrome: hereditary gigantism of cytoplasmic organelles

In the Chediak-Higashi syndrome, an anomalous hypopigmentation is associated with large lysosomal granules in the blood leukocytes. Since the inheritance pattern is that of an autosomal recessive trait, we postulated a common mechanism for these two primary features of the disease. Electron microscopy of melanocytes revealed that the pigmentary anomaly is indeed based on giant melanosomes. Since both types of granules, leukocytic and melanosomal, are characterized by limiting membranes, Chediak-Higashi disease may be a genetic disease of membranes.     

Targeting malaria virulence and remodeling proteins to the host erythrocyte

To establish infection in the host, malaria parasites export remodeling and virulence proteins into the erythrocyte. These proteins can traverse a series of membranes, including the parasite membrane, the parasitophorous vacuole membrane, and the erythrocyte membrane. We show that a conserved pentameric sequence plays a central role in protein export into the host cell and predict the exported proteome in Plasmodium falciparum. We identified 400 putative erythrocyte-targeted proteins corresponding to approximately 8% of all predicted genes, with 225 virulence proteins and a further 160 proteins likely to be involved in remodeling of the host erythrocyte. The conservation of this signal across Plasmodium species has implications for the development of new antimalarials.