Changes in wild pig (Sus scrofa) relative abundance,crop damage,and environmental impacts in response to control efforts

BACKGROUND

As the population and range of wild pigs (Sus scrofa) continue to grow across North America, there has been an increase in environmental and economic damages caused by this invasive species, and control efforts to reduce damages have increased concomitantly. Despite the expanding impacts and costs associated with population control of wild pigs, the extent to which wild pig control reduces populations and diminishes environmental and agricultural damages are rarely quantified. The goal of this study is to quantify changes in wild pig relative abundance and subsequent changes in damages caused by invasive wild pigs in response to control.

RESULTS

Using a combination of wild pig population surveys, agricultural damage assessments, and environmental rooting surveys across 19 mixed forest-agricultural properties in South Carolina, USA, we quantified changes in wild pig relative abundance and associated damages over a 3-year period following implementation of a professional control program. Following implementation of control efforts, both the number of wild pig detections and estimated abundance decreased markedly. Within 24 months relative abundance was reduced by an average of ~70%, which resulted in a corresponding decline in environmental rooting damage by ~99%.

CONCLUSION

Our findings suggest that sustained wild pig control efforts can substantially reduce wild pig relative abundance, which in turn resulted in a reduction in environmental rooting damage by wild pigs. Ultimately this study will help fill critical knowledge gaps regarding the efficacy of wild pig control programs and the effort needed to reduce impacts to native ecosystems, livestock, and crops. © 2023 The Authors. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.     

Cottonseed meal (gossypol) toxicosis in a swine herd

Cottonseed meal (CSM) that contained a high concentration of free gossypol was inadvertently used as a protein supplement, without appropriate iron supplementation, for a swine herd in Illinois. Fifty percent of 300 grower and finishing swine died, and an additional 20% became ill during a 4- to 6-week period. Clinical signs included respiratory distress and abdominal distention. At necropsy, the hearts were diffusely pale, flaccid, and rounded because of dilatation of all 4 chambers, the livers were large and congested, and hydropericardium, hydrothorax, and ascites were evident. Histologic changes consisted of diffuse myocardial fiber atropy with perinuclear vacuolation, and multifocal myocardial and skeletal muscle necrosis. Changes in the liver included marked centrilobular congestion, loss of hepatocytes, and fatty degeneration. Differential diagnoses included monensin, selenium, and gossypol toxicoses, and vitamin E/selenium deficiency. Analyzed feed samples did not contain monensin. Feed selenium concentrations ranged from 428 to 1,513 micrograms/kg, and iron concentrations from 160 to 180 mg/kg. Cottonseed meal (3 to 10%) was detected by feed microscopy. A sample of the 40% protein supplement contained 19% CSM and 1,300 mg of free gossypol/kg, whereas feed samples contained 200 to 400 mg of free gossypol/kg. The history, clinical signs, pathologic findings, and feed analyses were compatible with a diagnosis of gossypol toxicosis. Cottonseed meal, a high-protein supplement used widely in southern United States, may contain gossypol (a polyphenolic binaphthalene pigment), which in its free form is especially toxic to simple-stomached animals. If CSM is used, supplementation with ferrous sulfate is recommended at a 1:1 weight ratio with free gossypol, up to 400 mg of FeSO4/kg.     

Dominant expression of interleukin-8 vs interleukin-1β and tumour necrosis factor alpha in lungs of lambs experimentally infected with Mannheimia haemolytica

Abstract

AIMS: To quantify the number of cells infected with Mannheimia haemolytica and expressing interleukin (IL)-1β, tumour necrosis factor alpha (TNFα) and IL-8 using immunohistochemistry, and to measure the immunoreactivity of cytokines in pulmonary tissue extracts using ELISA, in the lung of lambs experimentally infected with M. haemolytica, and to compare the patterns of expression of cytokines in airways at different times post-infection (p.i.).

METHODS: Twenty 3-month-old lambs of both sexes were randomly assigned to two groups, viz infected (n=15), and uninfected controls (n=5). Each lamb in the infected group was inoculated with 1.5 x 10⁹ cfu M. haemolytica in 5 mL sterile nutrient broth, control lambs were inoculated with 5 mL sterile nutrient broth and clinical signs were monitored. Infected and control animals were killed at 1, 3, 5, 7, and 15 days p.i. Histopathology and immunohistochemistry were conducted to determine the number of immunolabelled cells in pneumonic lungs, and study the pattern of expression of IL-1β, TNFα and IL-8 in lung extracts using ELISA.

RESULTS: Lesions in bronchi and bronchioles ranged from epithelial desquamation to bronchiolitis obliterans and necrosis. The alveoli had areas of seroproteinaceous fluid, fibrin and bacterial aggregates that evolved to foci of pyogranulomatous inflammation with clustered inflammatory cells, referred to as ‘oat cells’. M. haemolytica antigen was observed in the cytoplasm of inflammatory cells. Labelling of IL-1β, TNFα and IL-8 was observed in bronchial and bronchiolar epithelial cells, alveolar exudate, and in interstitial inflammatory infiltrate, with increased expression on 1 and 3 days p.i. for IL-1β and TNFα, and 1, 3, and 5 days p.i. for IL-8. In lung tissue extracts, peak concentrations of IL-1β (55 (SD 5) ng/mL), TNFα (92 (SD 6) pg/mL) and IL-8 (8 [SD 2] μg/mL) occurred at 3 days p.i.

CONCLUSIONS: The results of this study suggested that the inflammatory cytokines IL-1β, TNFα and IL-8 may play an important role in enhancing the biological response to M. haemolytica, and contribute to the development of lesions in the lung in pulmonary pasteurellosis in sheep. Given that the expression of IL-8 in lung was much greater than that of IL-1β and TNFα, anti-cytokine agents directed at this mediator could be useful in the prevention and treatment of this disease.     

Exertional heat illness: a review of the syndrome affecting racing Thoroughbreds in hot and humid climates

Metabolic heat produced by Thoroughbred racehorses during racing can rapidly elevate core body temperature (1°C/min). When environmental conditions are hot and humid, the normal physiological cooling mechanisms become ineffective. The heat accumulated may exceed a critical thermal maximum (estimated to be 42°C), which may trigger a complex pathophysiological cascade with potentially lethal consequences. This syndrome has been labelled exertional heat illness (EHI). EHI is described in humans, but has not been well documented in Thoroughbred racehorses. The clinical signs described in racehorses would suggest that the pathophysiological events affecting the central nervous (CNS) and gastrointestinal systems are similar to those described in humans. Clinical signs are progressive and include signs of endotoxaemia and increasing levels of CNS dysfunction. Initially, horses that may be mildly irritable (agitated, randomly kicking out) may progress to unmanageable (disorientation, severe ataxia, falling) and ultimately convulsions, coma and death. Currently, the approach to treatment is largely empirical and involves rapid and effective cooling, administration of drugs to provide sedation, administration of non‐steroidal anti‐inflammatory drugs to ameliorate the effects of endotoxaemia and glucocorticoids to stabilise cell membranes and reduce the effects of inflammation on the CNS. This review provides an overview of the current knowledge about EHI in Thoroughbred racehorses, suggests a likely pathophysiology of the syndrome in horses based on the current literature on heat illness in humans and horses, and outlines current treatment strategies being used to treat racehorses with clinical signs of EHI.