Cherry picking by pseudomonads: After a century of research on canker,genomics provides insights into the evolution of pathogenicity towards stone fruits

Bacterial canker disease is a major limiting factor in the growing of cherry and other Prunus species worldwide. At least five distinct clades within the bacterial species complex Pseudomonas syringae are known to be causal agents of the disease. The different pathogens commonly coexist in the field. Reducing canker is a challenging prospect as the efficacy of chemical controls and host resistance may vary against each of the diverse clades involved. Genomic analysis has revealed that the pathogens use a variable repertoire of virulence factors to cause the disease. Significantly, strains of P. syringae pv. syringae possess more genes for toxin biosynthesis and fewer encoding type III effector proteins. There is also a shared pool of key effector genes present on mobile elements such as plasmids and prophages that may have roles in virulence. By contrast, there is evidence that absence or truncation of certain effector genes, such as hopAB, is characteristic of cherry pathogens. Here we highlight how recent research, underpinned by the earlier epidemiological studies, is allowing significant progress in our understanding of the canker pathogens. This fundamental knowledge, combined with emerging insights into host genetics, provides the groundwork for development of precise control measures and informed approaches to breed for disease resistance.     

Ocular and encephalic toxoplasmosis in canaries

In this report we describe the lesions produced by the protozoal organism, Toxoplasma gondii, in the eyes and brain of the common yellow canary (Serinus canaria). Nine of 15 birds in a flock were affected with blindness, which developed over a 3-mo span, and two birds developed torticollis. Microscopic alterations within the eye consisted of a nonsuppurative chorioretinitis with large numbers of macrophages that contained the tachyzoite form of T. gondii in the subretinal space, and aggregates of tachyzoites were found in the nerve fiber layer of the retina with and without necrosis. Tissue cysts with bradyzoites were scattered throughout the meninges and neuropil of the cerebrum and cerebellum. Both forms were confirmed by transmission electron microscopy in the eye and brain. Frozen brain samples reacted with T. gondii-specific cat sera in indirect fluorescent antibody tests. The source of infection was hypothesized to be from a stray cat the owner kept that had access to some of the bird feed. Treatment (trimethoprim 0.08 g/ml H2O and sulfadiazine 0.04 g/ml in water for 2 wk) was instituted by the referring veterinarian on the remaining birds. A second treatment regime was given for 3 wk. The owner of the canaries did not return for further treatment.     

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.