Newcastle Disease Strain F. Virus — A Review

Strain F Newcastle disease virus is a virus of low virulence originally reported by Asplin (1952) in England. Since that date, the use of this virus as an immunizing agent in the form of a live vaccine, has been studied. As a result, Strain F Newcastle disease vaccine has been used in national and experimental control programs in several countries in Europe, Africa and Asia. The published literature is reviewed under the following headings: properties, viability, clinical effects of vaccination, duration of immunity and a simultaneous Newcastle disease fowl pox vaccination. This review includes 24 reports published outside North America.     

Effect of focused and radial extracorporeal shock wave therapy on equine bone microdamage

OBJECTIVES : To determine whether bone microcracks are altered after application of focused and radial extracorporeal shock wave therapy (ESWT) to the equine distal limb. STUDY DESIGN : An ex vivo experimental model. SAMPLE POPULATION : A contralateral limb specimen was obtained from 11 Thoroughbred racehorses with a unilateral catastrophic injury. Distal limb specimens were also obtained from 5 non-racing horses. METHODS : Three separate skin-covered bone segments were obtained from the mid-diaphysis of the metacarpus (MC3) or metatarsus (MT3). Focused (9,000 shockwaves, 0.15 mJ/mm2, 4 Hz) and radial (9,000 shockwaves, 0.175 mJ/mm2, 4 Hz) ESWT treatments were randomized to the proximal and distal segments and the middle segment was used as a treatment control for pre-existing microcracks. After treatment, bone specimens were bulk-stained with basic fuchsin and microcracks were quantified in transverse calcified bone sections. RESULTS : ESWT had small but significant effects on microcracks. Microcrack density (Cr.Dn) and microcrack surface density (Cr.S.Dn) were increased after focused ESWT, whereas Cr.Le was increased after radial ESWT. In racing Thoroughbreds, Cr.Le increased with increased number of races undertaken. Cr.Dn and Cr.S.Dn were not significantly influenced by the number of races undertaken. CONCLUSION : ESWT has small but significant effects on bone microcracking ex vivo. CLINICAL RELEVANCE : These preliminary data suggest that ESWT has the potential to increase bone microcracking in equine distal limb bone in vivo. Such effects may be more pronounced in Thoroughbreds that are actively being raced, because in vivo microcracking increases with increased number of races undertaken.     

Seroprevalence of Bartonella infection in American free-ranging and captive pumas (Felis concolor) and bobcats (Lynx rufus)

Bartonella henselae is the main agent of cat scratch disease in humans and domestic cats are the main reservoir of this bacterium. We conducted a serosurvey to investigate the role of American wild felids as a potential reservoir of Bartonella species. A total of 479 samples (439 serum samples and 40 Nobuto strips) collected between 1984 and 1999 from pumas (Felis concolor) and 91 samples (58 serum samples and 33 Nobuto strips) collected from bobcats (Lynx rufus) in North America, Central America and South America were screened for B. henselae antibodies. The overall prevalence of B. henselae antibodies was respectively 19.4% in pumas and 23.1% in bobcats, with regional variations. In the USA, pumas from the southwestern states were more likely to be seropositive for B. henselae (prevalence ratio (PR) = 2.82, 95% confidence interval (CI) = 1.55, 5.11) than pumas from the Northwest and Mountain states. Similarly, adults were more likely to be B. henselae seropositive than juveniles and kittens (PR = 1.77, 95% CI = 1.07, 2.93). Adult pumas were more likely to have higher B. henselae antibody titers than juveniles and kittens (p = 0.026). B. henselae antibody prevalence was 22.4% (19/85) in bobcats from the USA and 33.3% (2/6) in the Mexican bobcats. In the USA, antibody prevalence varied depending on the geographical origin of the bobcats. In California, the highest prevalence was in bobcats from the coastal range (37.5%). These results suggest a potential role of wild felids in the epidemiological cycle of Bartonella henselae or closely related Bartonella species.     

In vivo characterization of inflammatory biomarkers in swine and the impact of flunixin meglumine administration

Non-steroidal anti-inflammatory drugs (NSAID) are a family of chemicals that function to reduce pain, fever, and inflammation, and they are commonly used in people and animals for this purpose. Currently there are no NSAIDs approved for the management of inflammation in swine due to a lack of validated animal models and suitable biomarkers to assess efficacy. A previous in vitro study examining biomarkers of inflammation identified fourteen genes that were significantly altered in response to Escherichia coli lipopolysaccharide (LPS)-induced inflammation. In the present study, five of those fourteen genes were tested in vivo to determine if the same effects observed in vitro were also observed in vivo. Plasma levels of prostaglandin E(2) (PGE(2)), an essential mediator of fever and inflammation, were also determined. Two groups of swine were stimulated with LPS with the second group also treated with flunixin meglumine. Blood was collected at 0, 1, 3, 6, 8, 24, and 48h post LPS-stimulation. The RNA was extracted from the blood and quantitative real-time-PCR (qRT-PCR) was utilized to determine the expression patterns of CD1, CD4, serum amyloid A2 (SAA2), Caspase 1, and monocyte chemoattractant protein 1 (MCP-1). The LPS-stimulated animals demonstrated a statistically significant alteration in expression of SAA2 and CD1 at 3h post-stimulation. Flunixin meglumine treated animals' demonstrated reduced expression of CD1 in comparison to the LPS-stimulated swine at 24 and 48h post LPS-stimulation. Flunixin meglumine treated animals exhibited reduced expression of SAA2 at 48h post-stimulation compared to LPS-stimulated swine. Swine treated with LPS demonstrated statistically significant increases in plasma PGE(2) at 1h post-stimulation. Swine treated with flunixin meglumine had no increase in plasma PGE(2) levels at any time. These results demonstrate that PGE(2) production, along with two out of five genes (SAA2 and CD1) have the potential to serve as early biomarkers of inflammation as well as indicators of NSAID efficacy.