Abstract. Nile crocodile (Crocodilus niloticus) mass mortality events in the Olifants River between the Letaba River confluence in South Africa and Lake Massingir in Mozambique have been attributed to pansteatitis: a disease that affects fat depots of the animals. The disease is also found in sharptooth catfish (Clarias gariepinus) in the same area, and the cause of the disease is attributed to pollution. Although the Olifants River Valley is polluted, the impact of interventions such as dam construction on biodiversity receives little attention. We show that the onset of the pansteatitis epidemic in crocodiles and sharptooth catfish at the Olifants/Letaba confluence coincided with back-flooding of Lake Massingir that changed the Olifants River from a rock and sand substrate river to a clay substrate lake. Isotopic analysis shows that sharptooth catfish shifted from a predominantly vegetarian to a piscivorous diet that is highly correlated with pansteatitis prevalence, and crocodiles and tiger fish (Hydrocynus vittatus) show coincident trophic level increases. The evidence suggests that the ecosystem change altered the structure of the lotic foodweb and that an exotic or extralimital fish has invaded the confluence and is the vector of the pansteatitis epidemic. The invasive fish species is yet to be identified. The pansteatitis epidemic is an unintended ecological consequence of damming this river.

In late 2006 an unusual ulcerative condition in wild fish was reported for the first time in Africa from the Chobe and upper Zambezi Rivers in Botswana and Namibia. Concern increased with subsistence fishermen reporting large numbers of ulcerated fish in their catches. In April 2007 the condition was confirmed as an outbreak of epizootic ulcerative syndrome (EUS). The causative agent, Aphanomyces invadans, is a pathogenic water mould of fish that shows little host specificity. Ulcers follow infection of tissues by oomycete zoospores, resulting in a granulomatous inflammation associated with invading oomycete hyphae. Granulomatous tracts surrounding oomycete hyphae within the necrotic tissues characterise the diagnostic histological picture. The upper Zambezi floodplain at the confluence with the Chobe River spans the four countries of Botswana, Namibia, Zambia and Zimbabwe, making disease control a challenge. The floodplain ecosystem supports a high fish diversity of around 80 species, and is an important breeding and nursery ground. The annual cycle of flooding brings about changes in water quality that are thought to favour the infectivity of A. invadans, with diseased fish appearing soon after the plains become flooded. Since 2006 the disease has spread rapidly upstream along the upper Zambezi and its tributaries. By 2010 the disease was reported from the Okavango Delta in Botswana and in 2011 from the Western Cape Province of South Africa. EUS has the potential to disrupt floodplain ecosystems elsewhere in Africa where high fish diversity forms the basis of subsistence fisheries and local economies, and is a direct threat to freshwater fish culture.

Large numbers of adult Nile crocodiles

This study compares the aetiology of pansteatitis in Lake Loskop, relative to two other impoundments along the Olifants River. Macroscopic and microscopic pathology, age determination and analysis of stomach content, fatty acids and stable isotopes explain the high prevalence of pansteatitis in Oreochromis mossambicus (Peters) and several other species in Lake Loskop. All the dietary indicator comparisons between pansteatitis-affected and healthy fish fail to support a systemic cause. Pansteatitis in Lake Loskop was linked to size and weight of O. mossambicus, but not to ontogenic age. Fish in Lake Loskop showed abnormally high omega-3 to omega-6 fatty acid ratios normally only found in marine fish with no significant difference in degree of assimilation of these fatty acids between pansteatitis-affected and healthy fish. This explains the vulnerability to, but not the occurrence of, pansteatitis. As a cause for the pansteatitis, these results point towards sporadic vitamin E-depleting trigger events, known sporadic fish die-off occurrences that provide surviving fish with a rich source of rancid fats on which to scavenge. The mechanism ties pansteatitis to eutrophication and trophic cascade effects, the intrinsic drivers of the disease and suggests an adaptive management strategy that might be applied by relevant conservation authorities.