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The Seasonality and Effects of Nosema


Requisites for nosema to gain a foothold. 2

The importance of pollen to Nosema transmission and reproduction. 4

The connection between nosema and dysentery. 6

putting it all together. 7

Coming. 8

citations and notes. 8


The Seasonality and Effects of Nosema

Randy Oliver

First Published in ABJ in Aug. 2019

Nosema apis had long been considered to be of concern only in the spring and fall; but once N. ceranae showed up, there are reports of it appearing even in summer.  An understanding of the reasons for the seasonality of nosema may help us to better understand the parasite as a whole.

Nosema apis was not named until 1909, and was not on U.S. beekeepers’ radar until it was well described by G.F. White [I believe E.B. specialized in spiders] in his seminal publication in 1919 [[1]].  Ingemar Fries reviewed what we knew about N. apis in 1993 [[2]], and described the typical seasonality of nosemosis (disease that may be the result of serious infection by nosema):

The level of infection found in a colony is highly variable. The seasonal trend of typical infections exhibits low levels during the summer, a small peak in the autumn and a slow rise of infection during the winter. In the spring, the level of infection increases rapidly as brood rearing starts and while flight possibilities are limited still.  The pattern is similar in both the northern and the southern hemisphere.

But in the early 2000s, in both North America and Europe, bee disease labs recorded a new trend — nosema prevalence in samples sent to diagnostic labs suddenly started to climb, and might be found at any time of the year [[3],[4]].  By 2005, nosema was being detected even in summer — retrospectively indicating that there had been an invasion by N. ceranae.  Unfortunately, the graph of prevalence in samples from Spain was widely misinterpreted as indicating intensity [[5]], suggesting that N. ceranae lacked the seasonality of N. apis.  This was actually not the case at all, as shown by the same researchers in a subsequent paper [[6]].

Since then, other researchers (including myself [[7]]) have documented that the epidemiology of N. ceranae rather closely follows that of N. apis, but since ceranae’s original host was the tropical Apis cerana, it’s not surprising that ceranae is somewhat better adapted to warmer temperatures, and may occasionally flare up during summer [[8]].

Practical application: During the invasive wave of N. ceranae, it was easy for me to find infected colonies at any time of the year in my apiaries.  But by 2012 it was difficult for me to find an infected hive in summer.  I suspect that a new host-parasite relationship had developed over that period of time.

Requisites for nosema to gain a foothold

The question of interest is why nosema has a seasonal pattern.  As elaborated by White, nosema transmits from one bee to another by the transfer of infective spores via the fecal-oral route.  Some observations of interest by White relate to the fact that simply exposing a colony to spores does not necessarily result in an epizootic of nosema within the hive:

Although wintering bees on soiled comb greatly increases the risk of detectable nosema disease the following spring, a detectable disease level does not always result. Thus, spore availability is not sufficient to create an epizootic disease in the honey bee colony [boldface mine].

He also noted that other beekeeper practices may contribute to the transmission of spores:

Other factors that contribute to the spread of N. apis spores within the honey bee colony include all management where bees are crushed. The liquid remains of crushed bees are readily ingested by other bees.  [Australian beekeepers have long been cautioned to avoid the crushing bees in hives during winter manipulations [[9]] (Fig. 1).]

Figure 1.  One way in which beekeepers can contribute to nosema spore transmission within the hive is by the inadvertent crushing of bees.  The workers in the photo above are lapping up the body fluids of a bee crushed moments ago.

Practical application: Don’t contribute to nosema spore transmission.  Avoid crushing bees within the hive, especially during winter [[10]].  The stress and confinement involved in the trucking of colonies — again, especially during winter — may also contribute to defecation within the hive [[11]].

But the observations by White that most caught my eye were:

The fact that a colony may contain a small percentage of Nosema-infected bees throughout the year and not become heavily infected at any time furnishes further evidence that Nosema infection does not always spread with rapidity within the hive. [As does his finding that a colony experimentally infected during summer will typically clear itself of infection within six weeks.]

Since merely exposing a colony to nosema spores does not necessarily result in the parasite going epizootic in the hive, to explain the seasonality of nosemosis, we need to look a little deeper.  At this writing, it appears to me that the seasonal pattern of nosemosis is largely about two things: (1) the parasite’s success at reproduction in individual bees, and then (2) achieving adequate bee-to-bee transmission of spores within the hive.  And then the overall effect of nosema upon colony performance is largely about the percentage of the colony’s bees that are infected (“prevalence”), the impact of that upon both broodrearing, and the shift in the survivorship of those infected workers.  To summarize in advance, we need to look at:


  1. The involvement of pollen with nosema reproduction in the bee midgut, and
  2. The seasonal availability of pollen.

Transmission in the Hive

  1. The transmission of nosema spores via consumption of pollen,
  2. The causes of dysentery, and
  3. The hours per day suitable for defecation flights.

Effect upon Colony Performance

  1. The percentage of bees infected,
  2. The effects of infection upon the nurse bees, and
  3. The effect of nosema-induced acceleration of worker transition to foraging.

I will be covering some of the above in subsequent articles, but first let’s focus upon pollen.

The importance of pollen to Nosema transmission and reproduction

The seasonal peaks of nosema in spring and fall certainly suggest an association with what are commonly heavy pollen flows at those times of the season.  It appears that there are at least three reasons for this:

  1. Within-colony transfer of nosema spores via the pollen loads brought back by the foragers.
  2. Between-colony transfer of spores at the flowers.
  3. The greater amount of nosema infectivity and reproduction in the gut when pollen is present.

So let’s take a look at the above one at a time.  When a bee defecates in flight, any post-defecation hygiene consists of it grooming itself with its hind legs — the same legs used to pack pollen into its corbicula.  Higes [[12]] found infective nosema spores in the pollen loads brought back to the hive — the very pollen that the nurse bees would soon consume.  Such transmission of spores could allow a single infected forager to spread the infection to the next generation of young bees in the same hive.

Graystock [[13]] showed that nosema could be surprisingly effectively transferred via the spores left on flowers by visiting foragers, and that bumblebees could vector honey bee parasites without getting infected themselves.  The implication is that parasite spores can be readily transmitted from colony to colony via flower visitation (Fig. 2).

Figure 2.  This freshly-returned forager may be bringing back a load of nutritious pollen, but that pollen could possibly be contaminated with nosema spores from its own gut, or picked up from a flower.

Practical application: Nosema transmission appears to easily take place via floral visits, and the transfer of spores via incoming pollen loads.

The importance of pollen doesn’t end there. Reproduction of both nosema species appears to be largely dependent upon pollen being present in the bee midgut [[14],[15],[16],[17],[18]] — the more pollen in the diet, the greater the number of spores produced.

In northerly climes, strong pollen flows typically occur in spring and fall, with perhaps some midsummer spikes.  In Mediterranean climes, nosema tends to disappear during the late-summer pollen dearth.  In tropical Mexico, N. ceranae levels correlate with the rainy season from April through December [[19]].

A couple of very nice studies [[20], [21]] have shown a strong correlation between pollen or pollen sub in the diet, and the number of nosema spores produced.  Of interest is that at least in cage trials, it appears that although the consumption of pollen increases nosema reproduction in a bee, that pollen in the diet largely offsets the reduction in bee longevity (provided that those bees don’t engage in precocious foraging) [please explain—do you mean “precocious foraging”?] due to being parasitized by nosema.

Practical application: The reproduction and transmission of nosema in a colony appears to be largely dependent upon the bees foraging upon, and consuming, pollen.  Expect nosema spore counts to go up if there’s a pollen flow on, or if you’re feeding pollen sub. 

The connection between nosema and dysentery

It would make complete sense to expect that nosema would cause diarrhea (dysentery) in infected bees; but I’ve yet to see any evidence in support of that premise.  But that doesn’t mean that dysentery is not a critical component for understanding the seasonality of nosema.

Workers typically become infected as nurse bees, likely due to their ravenous consumption of pollen.  The parasite then rapidly reproduces within their midgut epithelial cells during times of heavy pollen consumption (via “vegetative spores”), and then later produces the “environmental spores” found in the hindgut and feces.  It is thus the mid-age bees, and especially the foragers, that exhibit the highest spore counts [[22]].

Practical application: Although I’ve found no supportive evidence that nosema causes dysentery in bees, that discharged fecal matter can clearly act as a transmitting vehicle (fomite) of nosema spores within the hive.  And that doesn’t mean that you need to see signs of dysentery all over the face of your hive.  We like to think that bees never poop in the hive, but if you’ve spent much time watching an observation hive, you’ve likely noticed that occasionally a bee does (Fig. 3) and that other workers then immediately “clean it up” with their tongues.

Figure 3.  The occasional defecation “accident” in the hive may be enough to ensure low-level transmission from the older workers to younger ones.  The droplets on the top bars above have obviously not yet been ingested by the janitors, but it’s safe to assume that any accidents on the faces of the combs would have been “cleaned up” immediately by ingestion.

Practical application: The occasional “accident” within the hive may be enough to ensure the continued transmission of nosema from one generation of bees to the next.  This could explain how a  low-level prevalence could continue even during summer — especially during confinement due to rain, or if hives get trucked.

putting it all together

As best that I can tell, the reason that nosema peaks in fall, may slowly climb during winter, and then spike again in spring, is that reproduction and transmission of the parasite strongly correlate with two factors: flight hours and pollen availability.  And this then brings us back to dysentery and in-hive defecation.

The fewer warm days in which nosema-infected bees can freely fly for cleansing flights, the greater the chance that some of them are going to slip up and defecate within the hive.  Such in-hive defecation is a highly effective basis for the fecal-oral route of transmission, and may largely explain why nosemosis is more likely to occur when cool weather prevents bees from freely flying outside the hive to defecate, and why infection tends to disappear during the summer months.

During winter, nosema can persist in the long-lived winter bees, but doesn’t appear to correlate with winter colony mortality [[23]].  It is only when the colony begins to rear brood again (often in mid-winter) that nosema again begins to increase— likely due to the combination of the consumption of nosema-contaminated stored beebread, or of honey or honeydew stores that cause dysentery, or increased in-hive defecation due to water balance issues coupled with lack of opportunity for defecation flights (I’ll cover the causes of dysentery in a following article).

Once springtime comes, then nosema is most effectively transmitted and infective due to the colony actively gathering pollen and rearing brood [[24]].  All colonies likely get exposed to nosema spores via colony-to-colony transmission of spores when the foragers of different hives visit the same flowers.  And then the nurse bees would tend to get infected from the consumption of nosema spores inadvertently added to pollen loads by infected foragers.  The nurses’ hindguts, which are often packed full of the remains of digested pollen, may contain very large numbers of infective spores — young workers defecate during their first orientation flights, before they begin foraging, and they then “wipe themselves” with their hind legs before they come back to the hive.  And when the weather does not allow those bees to take cleansing flights, there is even more chance for in-hive transmission of spores via accidental defecation.  I’ve seen little research on whether highly-infected forager bees defecate within the hive, but even if they defecate on the wing, they would still be expected to inadvertently transfer at least some spores to their pollen loads.

Once the weather warms, in-hive defecation rarely occurs, and the colony can then again break the infection cycle and largely purge itself of the parasite — which in the case of N. apis, largely disappears other than for dormant spores hidden in the combs, and in the case of the more heat-tolerant N. ceranae, smolders along in only a few bees in the hive.


The effects of nosema infection upon the colony, the causes of dysentery, sampling for nosema, how concerned you should actually be about this parasite, and what you can do about it.


citations and notes

[1] White, GF (1919) Nosema disease. U.S. Dept Agric Bulletin 780, 59 pp. Available in Google Books.

[2] Fries, I (1993) Nosema apis—A parasite in the honey bee colony. Bee World, 74(1): 5-19.

[3] Martín-Hernández, R, et al (2007) The outcome of the colonization of Apis mellifera by Nosema ceranae.  Applied and Environmental Microbiology http://aem.asm.org/cgi/content/abstract/AEM.00270-07v1

[4] http://scientificbeekeeping.com/sick-bees-17a-nosema-the-smoldering-epizootic/

[5] The study documented only whether nosema was present in a sample, not the intensity of the infection.  N. apis tends to completely disappear during the summer, whereas N. ceranae may often be found at a very low level during the warm months.

[6] Higes, M, et al (2008) How natural infection by Nosema ceranae causes honeybee colony.  Environmental Microbiology 10(10): 2659–2669.

[7] http://scientificbeekeeping.com/the-seasonality-of-nosema-ceranae/

[8] Traver, B.E., Fell, R.D., Prevalence and infection intensity of nosema in honey bee (Apis mellifera L.) Colonies in Virginia, Journal of Invertebrate Pathology (2011), doi: 10.1016/j.jip.2011.02.003

[9] Hornitzky, M (2005) Nosema disease: Literature review and survey of beekeepers.  RIRDC Publication No 05/055

Hornitzky, M (2008) Nosema Disease: Literature review and three year survey of beekeepers, Part 2.  RIRDC Publication No 08/006.

The two above reviews are worth reading; both are free downloads.

[10] http://scientificbeekeeping.com/does-the-crushing-of-bees-affect-colony-health/

[11] Bailey, L (1955) The epidemiology and control of nosema disease of the honey-bee. Annals of Applied Biology 43(3): 379-389.

[12] Higes, M, et al (2008) Detection of infective Nosema ceranae (Microsporidia) spores in corbicular pollen of forager honeybees. Journal of Invertebrate Pathology 97: 76–78.

[13] Graystock, P, et al (2015) Parasites in bloom: flowers aid dispersal and transmission of pollinator parasites within and between bee species. Proc. R. Soc. B 282: 20151371.

[14] Rinderer TE, Dell Elliott K (1977) Worker honey bee response to infection with Nosema apis: influence of diet. J Econ Entomol 70: 431–433.

[15] Porrini, MP, et al. (2011) Nosema ceranae development in Apis mellifera: influence of diet and infective inoculum. J Apicult Res 50: 35–41.

[16] Stevanovic J, et al (2013): Characteristics of Nosema ceranae infection in Serbian honey bee colonies. Apidologie 44: 522-536.

[17] Mendoza, Y, et al (2012) Incidence of Nosema ceranae during winter in honey bees colonies removed from Eucaliptus grandis plantations.  Veterinaria (Montevideo) 48(188): 13-19.  In Spanish.

[18] Fleming JC, et al (2015) Characterizing the impact of commercial pollen substitute diets on the level of Nosema spp. in honey bees (Apis mellifera L.). PLoS ONE 10(7):e0132014.

[19] Guerrero-Molina  (2016) op. cit.

[20] Porrini, MP, et al (2011) Nosema ceranae development in Apis mellifera: influence of diet and infective inoculum.  Journal of Apicultural Research 50(1): 35-41.

[21] Jack C, et al (2016) Effects of pollen dilution on infection of Nosema ceranae in honey bees. J Ins Physiol. 87:12–19.

[22] Jack, C, ibid.

[23] Even in Manitoba, Canada; Les Eccles, pers comm.

[24] Dr. Shimanuki, in his coverage of nosema in the 1992 edition of The Hive and the Honey Bee, notes that European researchers  had pointed out the connection between active broodrearing and nosema.

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