# Nosemosis in Honeybees: A Review Guide on Biology and Diagnostic Methods
## Course of Infection
### Type C Nosemosis  
Cells attacked by _N. ceranae_ (which causes nosemosis type \"C\"), similar to type A nosemosis, are lysed and degenerated [15]. During the infection, the midgut and basal cells are severely damaged. Atrophy of the hypopharyngeal glands is observed (less royal jelly). Additionally, the secretion of hormones becomes impaired. Decreased levels of vitellogenin (Vg, a protein important in reproduction and the social life of bees) and increased levels of juvenile hormone (JH, regulation of vitellogenesis) in nurse bees [38] have an extremely negative impact on brood rearing. Changes in the Vg-JH feedback loop cause infected bees to foraging significantly earlier than the non-infected ones (fewer nurse bees). Decreased secretion of Vg results in oxidative stress [38], which causes unrestrained hunger (energetic stress) [39]. That hunger causes an increase in the occurrence of trophallaxis events and probably leads to the shortened lifespan of the bees [39]. Infected bees die more often in the field while foraging, likely due to altered flight ability and impaired memory [35]. In cage trials, the lifespan was no longer than 8 days post infection, independently of the dose of spores [15]. Additionally, all of the above processes cause immunosuppression [18]. The disease caused by _N. ceranae_ is called dry nosemosis because, during the course of infection, diarrhea is not observed [6; 15]. _N. ceranae_ infection is more widespread in foragers than in hive bees, but, in fact, the queen is also exposed. In highly infected colonies, supersedure is reported more often than in healthy colonies [35]. There are no characteristic symptoms that may be simple to notice by the beekeeper. The four phases of the _N. ceranae_ infection in the colony were described in [6; 40]. The first phase is from spring to early autumn. It is entirely symptomless, and the number of spores per bee is lower than \(10^{6}\). In autumn and winter, a normalization of strength in the colony is observed (phase 2). The queen continues to lay eggs and to hold the number of bees at appropriate levels. The percentage of infected foragers increases (\(\geq\)65%) because the majority of bees in the cluster are adult (the parasite has had time to reproduce). In the next season (the following spring), we observe the so-called \"false recovery\", phase 3. The colony looks as if it is very strong as the number of bees is very high, and almost all frames are full of brood, but still, there is usually no swarming. The percentage of infected foragers is \(<\)65% because a lot of young bees that are not yet infected are present. The fourth phase is depopulation. It occurs in autumn or early winter. Sometimes colony death occurs in early spring. Only a handful of bees, with the queen, some food, and brood remain in the hive. In that phase, the percentage of infected bees is again \(\geq\)65% [6; 40]. \begin{table}
\begin{tabular}{c c c} \hline \hline
**Type of** _Nosema_ **spp.** & **Symptoms** & **Time of the Season** \\ \hline \multicolumn{3}{c}{Fecal streaks present on combs and} \\  & \multicolumn{1}{c}{hive exterior} \\ _Nosema apis_ & \multicolumn{1}{c}{Dead bees at the hive entrance} \\  & \multicolumn{1}{c}{Swollen abdomens in adult bees} \\  & \multicolumn{1}{c}{Diarrhea in adult bees} \\  & \multicolumn{1}{c}{Crawling bees} \\ \hline \multicolumn{3}{c}{Symptomless (“silent killer”): 4 phases of} \\ _Nosema ceranae_ & \multicolumn{1}{c}{infection (see Section 3.2)} \\  & \multicolumn{1}{c}{Death of the colony (handful of bees with the queen)} \\ \hline \hline \end{tabular}
\end{table} 
Table 1: Symptoms of both type of nosemosis which can be observed in the colony. It is worth mentioning that _N. ceranae_ infection becomes more severe when the bees are simultaneously exposed to neonicotinoids [2]. Black queen cell virus, which often co-occurs with _N. ceranae_, also significantly aggravates nosemosis \"C\" [25; 41].