Inorganic arsenic toxicosis in a beef herd

Over a 44-day period, 4 of 5 affected calves in a 170-head herd of beef cattle died after exhibiting clinical signs of lethargy, ataxia, anorexia, and diarrhea. Histopathological examination of tissues and toxicological analysis of a suspicious powder discovered in the pasture confirmed arsenic trioxide toxicosis.     

Flow alteration and thermal pollution depress modelled growth rates of an iconic riverine fish,the Murray cod Maccullochella peelii

The serial discontinuity concept (SDC) proposes that hypolimnetic‐releasing impoundments cause major disruptions to the naturally occurring physical, chemical and biological gradients of rivers but that this impact diminishes with distance downstream. Such a gradient in discharge, flow velocity and temperature regime occurs below a large hypolimnetic‐releasing impoundment, the Hume Dam, on the River Murray in south‐eastern Australia. To examine the effects of this disturbance gradient on a warm‐water large‐bodied freshwater fish, the Murray cod (Maccullochella peelii), a bioenergetics model was developed and calibrated to explore energy expended under differing water velocities and temperature regimes. Model simulations predicted negative growth of juveniles directly downstream of the impoundment, due largely to the energetic costs associated with active and, to a lesser extent, standard metabolism outweighing the achievable energetic gains through food consumption. As flow velocity and temperature regimes became more favourable downstream, so did the simulated growth of the species. It was not until +239 km downstream of the impoundment that the model predicted that flow velocity and temperature regimes were suitable for greater weight gains. The modelled growth responses of juvenile Murray cod are consistent with the predictions of the SDC, emphasising that changes in the bioenergetics of individuals are likely to be reflected in reduced growth rates under the changed flow velocity and temperature regimes imposed by disturbance gradients. This research represents a valuable step in the biological understanding of Murray cod within variable riverine environments and emphasises the urgency required to mitigate impacts associated with hypolimnetic impoundments.     

Predation on native sculpin by exotic brown trout exceeds that by native cutthroat trout within a mountain watershed (Logan,UT, USA)

We explored potential negative effects of exotic brown trout (Salmo trutta) on native sculpin (Cottus sp.) on the Logan River, Utah, USA by (i) examining factors most strongly correlated with sculpin abundance (e.g., abiotic conditions or piscivory?), (ii) contrasting the extent of brown trout predation on sculpin with that by native cutthroat trout (Oncorhynchus clarkii utah) and (iii) estimating the number of sculpin consumed by brown trout along an elevational gradient using bioenergetics. Abundance of sculpin across reaches showed a strong (r ≥ 0.40) and significant (P < 0.05) correlation with physical variables describing width (positive) and gradient (negative), but not with abundance of piscivorous brown trout or cutthroat trout. In mainstem reaches containing sculpin, we found fish in 0% of age‐1, 10% of age‐2 and 33% of age‐3 and older brown trout diets. Approximately 81% of fish consumed by brown trout were sculpin. Despite a similar length–gape relationship for native cutthroat trout, we found only two fish (one sculpin and one unknown) in the diets of native cutthroat trout similar in size to age‐3 brown trout. Based on bioenergetics, we estimate that an average large (> 260 mm) brown trout consumes as many as 34 sculpin per year. Nevertheless, results suggest that sculpin abundance in this system is controlled by abiotic factors and not brown trout predation. Additional research is needed to better understand how piscivory influences brown trout invasion success, including in‐stream experiments exploring trophic dynamics and interactions between brown trout and native prey under different environmental conditions.     

Equilibrative nucleoside transporter 3 deficiency perturbs lysosome function and macrophage homeostasis

Lysosomal storage diseases (LSDs) are a group of heterogeneous disorders caused by defects in lysosomal enzymes or transporters, resulting in accumulation of undegraded macromolecules or metabolites. Macrophage numbers are expanded in several LSDs, leading to histiocytosis of unknown pathophysiology. Here, we found that mice lacking the equilibrative nucleoside transporter 3 (ENT3) developed a spontaneous and progressive macrophage-dominated histiocytosis. In the absence of ENT3, defective apoptotic cell clearance led to lysosomal nucleoside buildup, elevated intralysosomal pH, and altered macrophage function. The macrophage accumulation was partly due to increased macrophage colony-stimulating factor and receptor expression and signaling secondary to the lysosomal defects. These studies suggest a cellular and molecular basis for the development of histiocytosis in several human syndromes associated with ENT3 mutations and potentially other LSDs.     

A survey of needle handling practices and needlestick injuries in veterinary technicians

A survey of veterinary technicians identified that needlestick injuries are very common, with 210/226 (93%) technicians reporting at least one needlestick injury over the course of their career. One hundred sixty-seven (74%) had experienced a needlestick injury during the preceding year. Exposure to animal blood and various drugs was common. It was particularly concerning that needlestick injuries involving chemotherapeutic agents and prostaglandin were reported. Eight (3.5%) technicians had required medical care for a needlestick injury and 2 (0.8%) had lost time at work. The approach to sharps handling and needlestick injury avoidance was poor and most needlestick injuries had not been reported to employers. Measures need to be undertaken to improve sharps handling practices to reduce the number of needlestick injuries among veterinary technicians.     

Genetic determinants of pathogenesis by feline infectious peritonitis virus

Feline infectious peritonitis (FIP) is a fatal, immune-augmented, and progressive viral disease of cats associated with feline coronavirus (FCoV). Viral genetic determinants specifically associated with FIPV pathogenesis have not yet been discovered. Viral gene signatures in the spike, non-structural protein 3c, and membrane of the coronavirus genome have been shown to often correlate with disease manifestation. An "in vivo mutation transition hypothesis" is widely accepted and postulates that de novo virus mutation occurs in vivo giving rise to virulence. The existence of "distinct circulating avirulent and virulent strains" is an alternative hypothesis of viral pathogenesis. It may be possible that viral dynamics from both hypotheses are at play in the occurrence of FIP. Epidemiologic data suggests that the genetic background of the cat contributes to the manifestation of FIP. Further studies exploring both viral and host genetic determinants of disease in FIP offer specific opportunities for the management of this disease.