Beekeeping/Acute Bee Paralysis

Acute Bee Paralysis virus
Acute bee paralysis virus (ABPV) was originally discovered during laboratory experiments as a cause of asymptomatic infections of adult bees (Benjeddou et al., 2001). This virus is a common infective agent of honeybees, frequently detected in apparently healthy colonies from several countries worldwide (Allen and Ball, 1996; Békési et al., 1999; Benjeddou et al., 2001; Farkas et al., 2001; Bakonyi et al., 2002a, 2002b; Tentcheva et al., 2004; Antúnez et al., 2005; Ellis and Munn, 2005; Berényi et al., 2006; Forgach et al., 2007; Sanpa and Chantawannakul, 2009). These infections are sometimes exacerbated and activated by stressful environmental factors such as mite infestations, bacterial infections, pollution and the usual utilization of chemicals and insecticides in agricultural technology (Bakonyi et al., 2002a, 2002b). The overt infection of ABPV is characterized by rapid death of adults; previously the lethally infected adults show a rapidly progressing paralysis, including trembling, inability to fly and the gradual darkening and loss of hair from the thorax and abdomen (Bailey et al., 1963; Maori et al., 2007a; Ribière et al., 2008; de Miranda et al., 2010a).

ABPV could attack all stages of honeybees, but the most favourable hosts for virus multiplication were the pupae (Chen et al., 2005a; Sanpa and Chantawannakul, 2009). Either the accumulation of viral particles in the brain and especially in the hypopharyngeal glands (de Miranda et al., 2010) and the readily detection of ABPV in the faeces (Hung, 2000; Ribière et al., 2008; de Miranda et al., 2010a), prove the foodborne transmission of virus through the salivary gland secretions of infected adult bees used to feed the young larvae or mixed in the pollen (Benjeddou et al., 2001). Infected larvae either die before they are sealed in brood cells if large amounts of virus particles were ingested, or survive to emerge as healthy infected adult bees (Bailey and Ball, 1991). The detection of ABPV sequences in semen of apparently healthy drones (Yue et al., 2006) suggests the possibility of venereal transmission of this virus. Further studies will be necessary to clarify this crucial aspect and to analyse the impact of the consequent vertical transmission of the virus through the eggs.

ABPV has been indicated as the major factor contributing to the mortality of honeybees infested with V. destructor (Faucon, 1992; Nordstrom, 2000; Bakonyi et al., 2002a, 2002b; Antúnez et al., 2005) and it was detected to be a primary cause of mortality in weakened colonies from Germany, Yugoslavia, France, Hungary (Forgàch et al., 2007) and USA (Bakonyi et al., 2002a, 2002b). Moreover several studies have also detected the presence of ABPV in Varroa mites (Allen et al., 1986; Bakonyi et al., 2002a, 2002b; Tentcheva et al., 2004; Chantawannakul et al., 2006). The term bee parasitic mite syndrome has been used for the disease complex observed in infested colonies simultaneously infected by viruses, characterized by high mortality (Shimanuky et al., 1994; Hung et al., 1995). Due to the spread of the Varroa mite in the European apiaries during the last decade, ABPV has gained relevance (Berènyi et al., 2006). Indeed, the parasitic mite plays a crucial role in spreading this virus both as a vector and as an activator of viral infection weakening the honeybees (Bakonyi et al., 2002a, 2002b; Berènyi et al., 2006).