Source: Strobl et al, 2019

Susceptibility to infection in Hymenoptera

Several regions of the world have reported adecline in wild bee species. A contributing factor may be pathogen spillover from managed honeybees, and a variety of pathogens so far exclusively linked to honeybees have been detected in several wild bee species.

However, the detection of a pathogen does not necessarily mean the infection is spreadingper se. Pathogens may behave differently within a novel host, where a species may not serve as a suitable host or the parasite does not replicate. Disease progression and symptom intensity can also differ both between and within species.

Several factors influence host susceptibility to pathogens and infection, such as life history traits (e.g. reproductive strategies and sociality), environmental traits, nutrition and the genetics of the host and pathogen. For example, greater infection resistance is typically observed in hosts with geneticheterozygosityand in social groups with higher genetic diversity. Thehaploid susceptibility hypothesispredicts inHymenopterathe haploid males from unfertilized eggs should have higher susceptibility (compared to diploid females) as they lack heterozygosity.

Are bee parasites picky parasites?

Trypanosomatids单细胞真核鞭毛虫寄生虫,是吗nd some species colonize the hindgut of bees. They damage intestinal cells through formation of hemidesmosomes, and these lesions can reduce host health at the individual and colony level. In bumblebees, parasite cells multiply after oral ingestion and are transmitted to novel bumblebee hosts via fecal-oral transmission.

The trypanosomatid parasiteCrithidia mellificaeinfects honeybees. While little is known about the effects of infection, there are positive correlations betweenC. mellificae感染水平和何neybee colony winter mortality. Two common solitary bee species,Osmia cornutaandOsmia bicornishave also recently been suggested as novel hosts ofC. mellificae.

In a recent paper,Strobl and colleaguestested whether this parasite could infect a solitary bee by challenging male and femaleO. cornutawithC. mellificae. The authors also employed honeybee workers as positive controls to assess infection parameters in a known host. Bee body mass, survival and pathogen infection levels were evaluated as measures of susceptibility.

The experiment

O. cornutawere randomly allocated to treatment (exposed toC. mellificaecells) or uninfected controls, and the males and females separated (control: n = 2 cages,C. mellificaeexposure: n = 4 cages). Honeybee workers were randomly allocated to eight cages (control: n = 3,C. mellificaeexposure: n = 5), and all cages were maintained for 19 days.

Each cage was provided with aC. mellificae-infected sucrose solution or with sucrose (controls). Survival was recorded every 24 hours and dead individuals were removed. Bees were investigated for livingC. mellificaecells before inoculation withC. mellificae(day 0) and on days 6, 10, 15 and 19 post inoculation (p.i.). Bees were individually weighed to assess body mass and anesthetized with CO_2,before quantifyingC. mellificaecells. DNA sampled on day 0, 15 and 19 was analyzed by PCR and parasite loads were quantified by qPCR.

Results

In all groups of bees, body mass did not significantly change over time p.i. (all P> 0.05) or differ between control andC. mellificae–exposed individuals.

After 19 days p.i., 75.5% of the 83 control honeybees and 63.2% of the 128C. mellificae-exposed honeybees were alive, with significantly reduced survival in parasite-exposed individuals. Of the 80 honeybees sampled forC. mellificaecounting, 32.5% of the bees were infected. Parasite cell counts increased 6.6 fold in infected honeybees between days 6 and 19 p.i. and significantly reduced survival.

C. mellificaeexposure did not significantly affect survival ofO. cornutafemales. Of the 25 controlO. cornutafemales 80.7% survived compared to 68.1% of the 56C. mellificae-exposed females. However, maleO. cornutahad the lowest survival of all bee groups. After 19 days p.i., 39% of the 43 controls and none of the 81C. mellificae-exposed male bees were alive. Of the 41O. cornutafemales sampled over the entire p.i period, 68.3% showedC. mellificaecells, whereas 90% of the 30 males sampled showed parasite cell counts.

InO. cornutabees,C. mellificaenumbers increased 2–3.6 fold within cages but did not significantly change between days 6 and 19 p.i. in individual females or males. In both female and maleO. cornuta, the proportion of infected individuals increased over time p.i.

A significant positive correlation betweenC. mellificaecell counts andC. mellificaegenomic equivalent copies per bee was also observed in all groups of bees.

A walk on the wild side for trypanosomatids

Strobl and colleaguesdemonstrate that the solitary wild beeO. cornutacan host the honeybee parasiteC. mellificae,and that males are more susceptible. The proportion of infected hosts also increased inO. cornutacages with feces, but not in honeybee cages without feces. This indicates a fecal-oral transmission route forC. mellificae, as withCrithidiaspecies infecting bumblebees.

The reduced survival of infected honeybee workers provides some causal evidence for the correlation between overwintering colony mortality andC. mellificaeinfection levels. With evidence of a negative effect on managed honeybee species and male wild solitary bee species, field studies are required to evaluate spillover potential from managed to wild bees and vice versa.