ABSTRACT
An intricate network of crevices adorns the skin surface of the African bush elephant, Loxodonta africana. These micrometre-wide channels enhance the effectiveness of thermal regulation (by water retention) as well as protection against parasites and intense solar radiation (by mud adherence). While the adaptive value of these structures is well established, their morphological characterisation and generative mechanism are unknown. Using microscopy, computed tomography and a custom physics-based lattice model, we show that African elephant skin channels are fractures of the animal brittle and desquamation-deficient skin outermost layer. We suggest that the progressive thickening of the hyperkeratinised stratum corneum causes its fracture due to local bending mechanical stress in the troughs of a lattice of skin millimetric elevations. The African elephant skin channels are therefore generated by thickening of a brittle material on a locally-curved substrate rather than by a canonical tensile cracking process caused by frustrated shrinkage.
Subject(s)
Elephants/physiology , Skin Physiological Phenomena , Skin/anatomy & histology , Animals , Elephants/anatomy & histologyABSTRACT
Alcelaphine herpesvirus 1 (AlHV-1) is a gammaherpesvirus carried asymptomatically by wildebeests (Connochaetes sp.) in sub-Saharan Africa. Although asymptomatic in wildebeest, AlHV-1 infection in a number of other ruminant species causes a severe and fatal lymphoproliferative disease named wildebeest-derived malignant catarrhal fever (WD-MCF). Several endangered species of captive ruminants are highly susceptible to developing WD-MCF if infected by AlHV-1, which is a critical concern in zoos, game reserves and wildlife parks where wildebeests are also kept in captivity. Here, we investigated the seroprevalence of AlHV-1 in 52 captive wildebeests randomly sampled from five different zoos in France. We found 46% (24/52) seropositive animals and detected AlHV-1 DNA in one of them, demonstrating that AlHV-1 infection is present in captive wildebeests in France. In an interesting manner, the repartition of seropositive wildebeests was not homogenous between zoos with 100% (20/20) of seronegative animals in three parks. These results further highlight the importance of considering WD-MCF as a threat for clinically susceptible species and encourage for testing AlHV-1 infection in captive wildebeests as a management control strategy.