Diamphidia or Bushman arrow-poison beetle, is an African genus of beetles belonging to the Colorado potato beetle family of Chrysomelidae, the larvae and pupae of which hold a toxic principle used by Bushmen as an arrow poison.[1][2]
Discovery
The Swedish explorer, Hendrik Jacob Wikar who travelled in Southern Africa in 1773-1779 seems to have been the first to report on the "poisonous worms", but Hans Schinz was the first scientist to give a detailed description of the process by which poison was used by the Bushmen.
Species
Species in the genus Diamphidia include:
- Diamphidia nigro-ornata Stål
- Diamphidia femoralis Gerstaecker
- Diamphidia vittatipennis
Ecology
Feeding habits
The adults and larvae of Diamphidia nigro-ornata feed on Commiphora angolensis Engler, while Diamphidia vittatipennis use Commiphora africana (A.Rich.) Engler as a food plant.
Life cycle
Adult females of Diamphidia femoralis Gerstaecker and Diamphidia nigro-ornata Stål lay their eggs on the stems of Commiphora species and coat the eggs with their faeces which harden into a protective covering. As the larval instars develop, the pellets of their own faeces remain attached to their backs and posteriors.[3] The final instar sheds this faecal coat when entering the soil to pupate. The same behaviour is found in Blepharida, a Flea Beetle and Polyclada, the African Leaf Beetle.[3] The Diamphidia larvae burrow down for a depth of up to 1 metre in the sand under the food plant, where they may lie dormant for several years before going through a very rapid pupal phase.
Parasites
Diamphidia is parasitised by a carabid Lebistina beetle, the larva of which attaches itself to a mature Diamphidia larva, clinging to it until the Diamphidia has formed its cocoon, enclosing both host and parasite, and then feeding on its host's soft tissue.
Toxicology
The Lebistina larvae are more toxic than their hosts and are preferred by San hunters for arrow poison.[1]
Diamphotoxin, the poisonous principle in Diamphidia is a highly labile, low molecular weight compound which is bound to a protein protecting it from inactivation. It causes an increased permeability of cell walls, which, while not affecting normal ionic flow between cells, allows easy access to all small ions, thereby fatally disrupting normal cellular ionic levels.Although it has no neurotoxic effect, it produces a lethal haemolytic effect, and may reduce haemoglobin levels by as much as 75%, leading to haemoglobinuria.