Hepatogenous photosensitization
Hepatogenous photosensitization syndrome has been reported in cattle, sheep, goats and buffalo grazing Brachiaria decumbens in Africa, South-East Asia and South America (FAO, 2010; Lascano et al., 1996). This toxicity is caused by the presence, in the bile ducts and liver, of crystals of insoluble salts of sapogenin glucuronides originating from steroidal saponins present in signal grass. The sapogenin content varies in the same Brachiaria species, due to environmental stress, plant age and the stage of growth. Animals develop skin lesions, facial oedema, liver damage and rumen stasis that result in severe drops in weight gain (down to 40%) and in some cases death (17% of cases) if the animals are not removed from the pasture (Gracindo et al., 2014; Fagliari et al., 2003). The disease occurs within the first 30 days after grazing signal grass or until 60 to 90 days after (Riet-Correa et al., 2011). Outbreaks of Brachiaria spp. poisoning in central Western Brazil are frequently observed in pastures left ungrazed for more than 30 days. They also occur during the growing stage of the pasture at the onset of the rainy season (Brum et al., 2009).
Sheep are more susceptible than other species, and lambs are more susceptible than adults. Differences of susceptibility existing among animals might be genetically inherited (Riet-Correa et al., 2011). Some buffalo and sheep might be resilient to hepatogenous photosensitization: poisoned animals showed histological lesions and high GGT serum concentrations but no clinical signs of disease. Selection of resistant or resilient animals as well as breeding signal grass varieties with low saponin content could prevent poisoning (Riet-Correa et al., 2011).