Until recently, my go to book for parasites was Paul Schmid-Hempel's monograph on Parasites in Social Insects, 1998, Princeton University Press. Realizing that parasites shape the biology of social insects: ants, wasps, bees, termites; by broadening the database he found insights not always recognized when focusing on honey bees alone. I particularly like his Breaking into the Fortress analogy.
Recently, I was provided an interesting and useful 2015 (first edition) book: Nicolas Vidal-Naquet's Honeybee Veterinary Medicine: Apis millifera L. For those looking to produce a Best Practices Management data collection and reporting, take note of the "Veterinary Beekeeping Sanitary Audit Guide, Appendix 4, Diseases Notifiable to the OIE and European Countries (Appendix 2), and the Sampling, Testing and Diagnosis Guide (Appendix 3).
In both of these review texts, I looked for dysentery versus diarrhea - Schmid-Hempel talks about bees becoming dysenteric; while the more recent book by Vidal-Naquet uses both terms, seemingly interchangeably. So, I'll simply call the two terms the Big D.
What I find interesting - in my own experience, I've seldom seen the Big D in the absence of N. apis, and I've never seen it in the presence of N. ceranae alone.
In work with Robert Cramer, we've seen N. apis in conjunction with N. ceranae, but if we only see one Nosema, it's always been shown by PCR to be N. ceranae. I don't agree with the hypothesis that N. ceranae is displacing N. apis. If we look in the locations and at the times of the year when we used to see N. apis, we still find it. On the other hand, from 2006-2010, we hardly ever found a sample of bees without some presence of N. ceranae at any time of the year; but that's not true anymore. Just as N. apis typically appeared in the spring and then disappeared in strong colonies in summer, we now have trouble finding N. ceranae in the summer in northwestern states. But as I have said before, our N. ceranae tends to peak here in MT in fall-winter, which is inconsistent with the reports from South Eastern areas from Richard Fell.
As per the notion that the Big D is not associated with N. apis, the older book talking about microsporidia, says of N. apis that infected bees show no signs of disease, but are shorter lived and have less well developed, vacuolated hypophyaryngeal glands and fat bodies, show an accelerated age-related schedule of tasks, a reduction of pollen collecting, and reduced life span that can be partially offset by pollen feeding. And then it says: "infected bees become dysenteric, which may serve the spread of the disease within the colony".
But, it's an older book - maybe its out of date. Turning to the 2015 book and N. apis pathogenesis, I found that the description of the pathogenesis of N. apis to include:
1) inflammation of the digestive tract with diarrhea or constipation caused by obstruction by the numerous released spores (Kilani, 1999),
2) Digestive function becomes disorganized and nutrient uptake impaired,
3) Epithelial cells degenerate with large vacuoles and glycogen deposits, leading to lesions,
4) Ribosomes aggregate leading to a reduction in RNA synthesis that alters protein and enzyme secretion (Kilani, 1999 again),
5) The consequence is negative effect on fat bodies, protein metabolism, and protein levels in haemolymph.
6) Lesions in the digestive tract may be an entry point for other pathogens.
The newer book notes that wintering with forest honey containing melezitose can crystalize, causing midgut lesions contributing to development of N. apis,
runny syrup may contribute to diarrhea and soiled combs, and protein starvation as well as inadequate preparation and management of wintering bees as beekeeping practices affecting nosemosis.
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