Nosema Disease in Honey Bees

Impacts of Nosema apis & Nosema cerana on Honey Bee Colonies

The Nosema disease is caused by microsporidian fungi that infect the digestive systems of adult bees. The two primary species of microsporidian fungi are Nosema apis and Nosema ceranae, with the latter being more common. Infected bees show symptoms of general weakness, poor digestion (and at times, dysentery) and have an overall shortened lifespan. Infections are confirmed with a laboratory diagnosis, or by sheer confidence that the bee diarrhea is in fact, a Nosema infection.

Treatments for Nosema begin with good beekeeping practices (strong colonies, well ventilated hives and adequate nutrition), with the antibiotic fumagillin begin available for control (however this use is fading out of practice).

Identifying Signs of Nosemosis

Nosema is the name of the disease and Nosemosis are the groups of symptoms associated with it (Reviewed in Galajda et al., 2021). During inspections, a beekeeper may find fecal streaks on the outside (and inside) of the hive, which is a defining characteristic of this disease. From there, more general symptoms occur such as:

• Reduced energy and vigour in infected bees,
• A shortened lifespan of adult honey bees (for those tracking it),
  • Although the 2014 work of Milbrath and colleagues reported no significant decreases in infected bee lifespan.
• Reduced honey production at high infection rates,
• Colony decline and collapse, in severe cases.

If in doubt, a laboratory diagnosis can confirm infections. Observing diarrhoea around the hive and a reduced bee vigour is a likely indicator of Nosema infections.

Nosema apis vs Nosema ceranae

Originally, N. apis was the primary Nosema species affecting European honey bees; N. ceranae was associated with the Asian honey bees, Apis cerana. As with other honey bee diseases, N. ceranae has now spread globally, also affecting the European honey bee colonies.

Visibly, both diseases are similar, in that they cause dysentery. This is less common in N. ceranae infections, yet still can still lead to colony decline. The work of Cox-Foster & colleagues (2007) showed that N. ceranae is more abundant than N. apis, in both healthy and diseased colonies (in this case, those afflicted with colony collapse disorder). This could suggest that N. ceranae spores are opportunistic, awaiting for a colony to be stressed or weakened so that the infection can take hold.

Under microscopic examination, the two species are distinguished by the number of turns in their polar tubes¹. In mature N. ceranae spores, this number was 20 – 23, whereas N. apis had over 30 mature spores with larger filaments (Fries et al., 1996).

Comparing the two cryptosporidians, N. ceranae has a higher tolerance for warmer temperatures compared to N. apis (Gisder et al., 2010). This allows it to be prevalent throughout the year, as opposed to the outbreaks of N. apis; limited to the early spring and autumn.

Laboratory Diagnosis of Nosema

When a suspected sample is sent to a lab, the technician performs microscopic examinations of whole bees or their crushed abdomen. This method looks for the presence of Nosema spores, and will not differentiate between N. apis or N. ceranae. Should the beekeeper want more accurate results, they can request molecular techniques like PCR testing (I’m sure you know what this acronym is by now), which differentiates the two strains on the basis of their genetics.

For those academic researchers, or people with (too much) time and money on their hands, consider transmission electron microscopy. This visualization method shows you the 20-30 polar tubes of N. ceranae, compared to the over 30 coils in N. apis (Fries et al., 1996). It’s a costly method (these microscopes are huge), and involves intensive preparation methods, and usually reserved for the academic audience.

Nosema neumanni From Africa

Sidenote: A third Nosema species, N. neumanni, causes nosemosis in Ugandan honey bees (Chemurot et al., 2017). First discovered in 2017, it produces spores of a relatively small size compared to N. apis and N. ceranae, and was distinguished from the other two species using PCR testing. The study found that the occurrence of N. neumanni-infected colonies was higher compared to the other two strains. The authors suggested that this an endemic Ugandan species, and so the local honey bee populations were able to reach an equilibrium and maintain low levels of infections.

As of writing, this is the only study that describes N. neumanni in honey bees. Stay tuned for what the future holds!

Nosema Treatments

Historically, the antibiotic fumagilin was used for Nosema treatment (yes, microsporidians are closer to fungi then they are to bacteria). Fumagilin works by inhibiting the enzyme methionine aminopeptidase-2, which is used in spore development (Huang et al., 2013). Beekeepers would dissolve the drug in sugar syrup in the early spring/late autumn and feed it to the infected colonies. The 2013 study of Huang & colleagues, the degradation of fumagilin reduced its potency, and enabled N. ceranae spores to proliferate, rendering the antibiotic ineffective. This was also observed by Klassen and colleagues in 2021.

Further, fumagilin residues can be found in honey for up to 8 months after application (van den Heever et al., 2015)

How to Treat Nosema Infestation Naturally

In the absence of commercial treatments, it is up to the beekeeper to maintain optimal honey bee health, whether through supplemental feeding, requeening or the “shook swarm” method of rehoming bees.

The basis of good hive management lies in removal of old combs (which can harbour spores), proper ventilation (keeps the hive clean), and providing adequate nutrition. These practices reduce the stress on bees and lower the incidence of Nosema, or assists them in recovering in already-infected hives.

At times, requeening is used to treat a colony for diseases by replacing the current queen bee with one containing superior genetics (or is of young age²). Some queen breeds are more resistant to diseases, including Nosema, and these genetics are passed onto the adult worker bees, which improves the overall resilience of the colony. Other breeds have better hygienic behaviour, whereby the worker bees can spot and remove diseased bees/infectious matter early before it accumulates and spreads.

Probiotics and Essential Oils

The aforementioned 2021 study by Klassen and colleagues fed bees with the probiotic Protexin, and found it effective at controlling springtime N. ceranae infections. The authors suggest that the component bacteria, Enterococcus faecium, produces antimicrobial compounds and lactic acid to prevent Nosema spores from establishing themselves. The authors also found prebiotics like Naringenin (a flavinoid compound found in grapefruits) but not Chitosan (a sugar extracted from the exoskeleton of shellfish) reduced the number of N. ceranae spores in infected colonies. But that is a topic for another time

Probiotics can maintain and restore the natural honey bee gut bacteria. They work by competing with pathogens like Nosema for nutrition and space in the gut, reducing the chances of Nosema (or any other pathogen) from reaching infective levels. They are administered in sugar syrups or pollen patties during the spring (to support colony buildup) or autumn (to prepare bees for overwintering). As in the above study, these are the critical times for colony health, where the bees are more vulnerable to Nosema infections.

Glavinic and associates (2022), found the essential oil such thymol (extracted from thyme) effective in reducing the disease burden of N. ceranae³. However, they note that in the uninfected (control) colonies, thymol had a reduced immune-related gene expression, which is a net negative impact. The overall study was positive, suggesting to only use essential oils when required, and not as a preventative probiotic like the Protexin mentioned above.

Preventing Nosema infections

Nosema infections depend on external conditions (i.e. it’s more about what happens in the hive rather than what happens in the bee). One major factor is hive temperature, increasing the infection risk as lowers from the optimal ~35°C. This is why the incidence of Nosema is lower in the summer, and why beekeepers (like yours truly) should take care before opening hives on cold or rainy days.

In regions where bees form a winter cluster, the overcrowding of bees inside the hive increasing the risk of a Nosema epidemic. This can be managed by overwintering hives indoors and taking them outside on warmer days for the bees to perform cleansing flights. Given the time and money requirements, this isn’t feasible for the average beekeeper.

“Keeping strong hives” is a preventive method repeated over and over again. In a strong colony, the bees withstand Nosema infections by spreading the disease burden amongst several bees. This process goes on until the spring arrives, or daytime temperatures increase, and so the bees can fly out and defecate, eventually curing themselves.

Of course, beekeepers should keep clean equipment and disinfect tools after use; basic hygienic beekeeping principles. After infection, the spores on the hive entrance and walls should be destroyed by either scorching with a blowtorch, or with chemicals such as formic acid evaporator plates (commonly used in the treatment of bee mites like Varroa; the vapors reduce the spores’ overall health).

Transmission of Nosema Infection in Honey Bees

In strong hives, Nosema infections can occur as a result of robber bees returning with contaminated hive products. The spores can also be introduced to the hive from the environment, contaminated equipment, infected wax foundations and bad beekeeping practices, such as:

• Using the same tools for every hive (not an issue for urban beekeepers, more so for those hives used in commercial pollination),
• Requeening hives with an infected queen (if in doubt, obtain queens from reputable sources),
• Splitting or combining infected hives.

For example, when a foraging bee makes contact with a Nosema-contaminated source, the spores are placed onto the bee’s body. The bee ingests them as she grooms herself, or from receives them from other bees during trophallaxis feeding. The spores germinate inside the infected bee, and around five days following infection, die from septicaemia.

This fatal infection is due to disruption of intestinal barrier by Nosema spores, which enables the otherwise normal gut bacteria to pass through it and into the bee haemolymph (blood). The circulatory system is full of nutrients, and these bacteria treat it as any other source of nutrition, thereby consuming the nutrients in the blood and spreading (Vidau et al., 2014).

Infected bees continue conducting their normal foraging duties, leading to the contamination of flowers and water sources (such as those provided by the beekeeper). As the infected hive weakens, it becomes a target for robber bees, who take the contaminated loot back to their hive. If the robber colony is strong, the risk of fatal colony infection is low, however it will reduce their strength and subsequent honey production.

Why do Bees Eat their Poop?

A very juvenile heading, I know. The aforementioned disruption to the intestinal barrier weakens the gut lining, leading to an impaired digestive function. This results in partially-digested foods (i.e. nectar and pollen) being excreted in the waste, giving it a sweeter taste. When combined with the hygienic behaviour of bees, a Nosema infection can quickly overrun a weak hive as a result of normal functions by the worker bees.

Lifecycle of Nosema species

I conclude with a technical note. In N. ceranae, the base form of the Nosema spores are “sporonts”, which grow into round-ish “sporoblasts” possessing a thickened cell membrane. As the sporoblasts matures, it develops its polar tubes, whereby it can pierce the target cell membrane and inject the spore contents (“sporoplasm”) into the host cell. The sporoplasm begins as a small spherical body that developed into a spindle shaped tissue (“meront”), that divides and grows in pairs, eventually separating as oval sporonts, thereby completing the cycle (adapted from Gisder et al., 2011).

This cycle takes around 96 hours, and the infected cell releases a high number of spores into the environment for host reinfection. Interestingly, in N. apis, the meronts are a round/oval shaped and do not form pairs when dividing, unlike the spindly meronts in N. cerana described above (Fries et al., 1996)

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Footnotes

1. Along with the posterior posterior vacuole, the polar tubes are necessary for infecting the host cell. Under ideal conditions, this tube rapidly expands out of the spore to produce a hollow tube between the target cell, enabling the material inside the spore to infect the cell (Lv et al., 2020). ↩︎
2. Queen age matters. Replacing an old queen (say, older than two years) with a new one can revitalize the colony, increasing brood production and subsequently hive population. A larger hive is a stronger hive, and better handles infections. ↩︎
3. In fungi like our microspordian musketeers, thymol disrupts the cell membranes, leading to the death or inhibited growth of spores. Essential oils are generally added to sugar syrup rather than patties and then fed to hives during the autumn or spring. ↩︎