The 2007 outbreak of equine influenza in Australia: lessons learned for international trade in horses

In August 2007 Australia experienced its first outbreak of equine influenza. The disease occurred first in a quarantine station for imported horses near Sydney and subsequently escaped into the general horse population. After an extensive campaign the disease was eradicated and Australia is again recognised as free of this disease. Equine influenza was then, and is now, recognised to be the major disease risk associated with live horse imports into Australia and measures designed to mitigate this risk formed the basis of the quarantine protocols then in place. Subsequent investigations into the cause of the outbreak identified failures in compliance with these quarantine requirements as a contributing factor. It is also likely that the immunity of horses vaccinated as part of the import protocol was less than optimal, and that this had a significant role to play in the escape of the disease from quarantine.

Atopic disease and breastfeeding - cause or consequence?

Background

A number of studies have observed an association between breast-feeding and increased risk of development of asthma and eczema. It has been proposed that these results might be due to early signs of atopic disease in the infant causing mothers to prolong breast-feeding.

Objective

We sought to determine whether early symptoms of atopic disease (eczema, food reaction, or asthma) or positive skin prick test responses reduce the likelihood of ceasing breast-feeding.

Methods

A prospective birth cohort of 620 infants from Melbourne, Australia, was used. Telephone interviews every 4 weeks were conducted until 64 weeks and then again at 78 and 104 weeks to determine duration of breast-feeding (both exclusive and total) and evidence of atopic disease. Because of the varying time of onset of atopic symptoms, they were modeled as time-varying covariates in Cox models.
Results

Only 52 (8.4%) infants did not establish breast-feeding, whereas an additional 103 (25.0%) did not establish exclusive breast-feeding. Early signs of atopic disease or sensitization were independently associated with an approximately 28% reduction in risk of ceasing exclusive breast-feeding (adjusted hazard ratio, 0.72; 95% CI, 0.53-0.97); P = .029), but there was no evidence for a relationship with risk of ceasing breast-feeding completely (adjusted hazard ratio, 1.12; 95% CI, 0.92-1.37; P = .262).
Conclusion

Early signs of atopic disease might prolong the duration of exclusive breast-feeding. This could mask a protective effect of breast-feeding or even result in breast-feeding appearing to be a risk factor for the development of atopic diseases. Future investigation of the relationship between breast-feeding and atopic diseases should consider this possibility.

Comorbidity between depression and inflammatory bowel disease explained by immune-inflammatory, oxidative, and nitrosative stress; tryptophan catabolite; and gut–brain pathways

The nature of depression has recently been reconceptualized, being conceived as the clinical expression of activated immune-inflammatory, oxidative, and nitrosative stress (IO&NS) pathways, including tryptophan catabolite (TRYCAT), autoimmune, and gut–brain pathways. IO&NS pathways are similarly integral to the pathogenesis of inflammatory bowel disease (IBD). The increased depression prevalence in IBD associates with a lower quality of life and increased morbidity in IBD, highlighting the role of depression in modulating the pathophysiology of IBD.This review covers data within such a wider conceptualization that better explains the heightened co-occurrence of IBD and depression. Common IO&NS underpinning between both disorders is evidenced by increased pro-inflammatory cytokine levels, eg, interleukin-1 (IL-1) and tumor necrosis factor-α, IL-6 trans-signalling; Th-1- and Th-17-like responses; neopterin and soluble IL-2 receptor levels; positive acute phase reactants (haptoglobin and C-reactive protein); lowered levels of negative acute phase reactants (albumin, transferrin, zinc) and anti-inflammatory cytokines (IL-10 and transforming growth factor-β); increased O&NS with damage to lipids, proteinsm and DNA; increased production of nitric oxide (NO) and inducible NO synthase; lowered plasma tryptophan but increased TRYCAT levels; autoimmune responses; and increased bacterial translocation. As such, heightened IO&NS processes in depression overlap with the biological underpinnings of IBD, potentially explaining their increased co-occurrence. This supports the perspective that there is a spectrum of IO&NS disorders that includes depression, both as an emergent comorbidity and as a contributor to IO&NS processes. Such a frame of reference has treatment implications for IBD when “comorbid” with depression.