Summary Ceratocystis albifundus causes the disease known as wattle wilt of non‐native Acacia mearnsii trees in South Africa, Uganda and Kenya. Infection results in rapid wilt and death of susceptible trees and stem cankers on more tolerant trees. It has been suggested that C. albifundus is indigenous to southern Africa, possibly having spread from native Protea spp. to non‐native A. mearnsii and A. decurrens trees. Although C. albifundus has been collected from Protea spp., these reports are based on limited records for which only aged herbarium specimens exist. During surveys of wound‐infecting fungi on native tree species in South Africa, a fungus resembling C. albifundus was collected from Protea gaguedi, Acacia caffra, Burkea africana, Combretum molle, C. zeyheri, Faurea saligna, Ochna pulchra, Ozoroa paniculosa and Terminalia sericea. The identity of the fungus was confirmed as C. albifundus, using comparisons of DNA sequence data for the ITS and 5.8S gene of the rRNA operon. In pathogenicity trials, lesions were produced on C. molle and A. caffra, with some trees beginning to die at the termination of the experiment. This study represents the first report of C. albifundus from native tree species in South Africa and provides unequivocal evidence that the fungus occurs naturally on native Protea spp. The wide host range of C. albifundus, as well as its abundance on these indigenous hosts lends further support to the view that it is a native African pathogen.

This study was designed to confirm the toxicity of a plant implicated in an outbreak of poisoning of stock in Frankfort, Free State Province, South Africa. Cows died acutely after being introduced into a camp, where an abundant, green shrublet was noted to be heavily grazed. This plant was subsequently identified as Senecio inaequidens DC. (Asteraceae) by the South African National Biodiversity Institute (SANBI). Extraction and chemical analyses for pyrrolizidine alkaloids (PAs) in Senecio inaequidens revealed the presence of 4 different compounds, namely retrorsine and senecionine (known to be hepatotoxic) and 2 unidentified compounds. The average total PA (free base plus N-oxide) concentration in plant parts of S. inaequidens collected at Frankfort during the outbreak was 0.81 %, compared with the total alkaloid content in the dried, milled S. inaequidens plant material, collected 7 weeks after the outbreak, of only 0.18 %. Male Sprague-Dawley rats (n=4), aged 8-9 weeks, were dosed per os. Each rat received a different dose of the crude Senecio inaequidens extract, ranging from 0.049 mg/g body weight (b.w.) to 0.25 mg/g b.w. No clinical signs were observed in the rat receiving the lowest dose. Rats receiving higher doses showed depression, an unsteady gait, pilo-erection and jaundice, which was particularly noticeable in the ears. Clinical chemistry evaluation revealed an increase in the activities of ALP (except Rat 4), AST and GGT in all animals. Total serum bilirubin, creatinine and urea concentrations were also elevated. All rats had low serum globulin concentrations with an A/G ratio above 1.2. Post mortem examination of the rats revealed marked hepatic lesions. Histopathologically, these changes were characterised by necrosis (variable in extent) of the centrilobular and midzonal hepatocytes (but sparing the portal hepatocytes), with extensive haemorrhage and congestion. Proliferation of the bile ducts, fibrosis and oedema were also present. Ultrastructural changes in affected rats were characterised by margination of chromatin, the presence of numerous autolysosomes in necrotic hepatocytes, intramitochondrial woolly inclusions and changes in the endoplasmic reticulum. A sheep, also dosed with the crude extract, failed to exhibit clinical signs, clinical chemistry aberrations or macroscopic lesions; however, examination of the liver of this sheep revealed histopathological and ultrastructural changes similar, though milder, to those displayed by the rats. Pyrrolizidine alkaloids were extracted from the liver and kidneys of the rats and the sheep. In the case of the sheep, retrorsine was also detected in the lungs, urine and bile

During a six-year period (from January 2009 to December 2014), specimens collected from 344 cases of suspected organophosphorus and carbamate pesticide poisonings in wildlife, including birds, were submitted to the Toxicology Laboratory (ARC-OVI) for analysis. A positive diagnosis was made in 135 (39%) of these cases. The majority of cases were from birds, which included Cape vultures (Gyps coprotheres) and African white-backed vultures (Gyps africanus) and bateleur eagles (Terathopius ecaudatus). In one incident 49 vultures were killed when a farmer intentionally laced carcasses with carbofuran in an attempt to control jackal predation. There were 22 incidents of poisoning in helmeted guineafowl (Numida meleagris). On nine different occasions blue cranes (Anthropoides paradiseus) were poisoned, in one incident 14 birds were reported to have been killed. Over the period of investigation, there were 20 cases of poisoning involving mammalian species, the majority being vervet monkeys (Chlorocebus pygerythrus). The carbamate pesticides were responsible for 57 incidents of poisoning. Aldicarb, carbofuran and methomyl were detected in 26, 18 and 12 cases respectively. The majority of organophosphorus pesticide poisonings were caused by diazinon (n = 19), monocrotophos (n = 13) and methamidophos (n = 10).

Based on previous necropsy results, Microcystis blooms in constructed water impoundments in the Kruger National Park (KNP) have been identified as a cause of wildlife mortality. In response to wildlife mortality during 2007, water samples, containing algal bloom material, were collected during February 2007 and July 2007 from four dams (Nhlanganzwani, Mpanamana, Makhohlola, and Sunset) in the southeastern part of the KNP as part of the follow-up investigation. The toxicity of the Microcystis blooms was determined using the enzyme-linked immunosorbent assay (ELISA), protein phosphatase inhibition (PPI) assay, mouse bioassay, and African sharptooth catfish (Clarias gariepinus) primary hepatocytes. Both the ELISA and PPI assays indicated that the water sample collected during February 2007 from the Nhlanganzwani Dam, and samples collected from the Nhlanganzwani and Sunset dams in June 2007, were toxic. These dams, exhibiting the toxic Microcystis blooms, were also associated with the wildlife mortality. Mice injected intraperitoneally with water samples from Nhlanganzwani Dam (February 2007) induced hepatotoxicity and mortality within 1 hr. Primary hepatocytes from the sharptooth catfish exposed to samples from these dams gave similar results. This laboratory investigation and results strongly incriminate the toxic Microcystis blooms as the cause of the wildlife mortality. Eutrophication and bloom formation appear to have been the consequence of the high numbers of hippopotami (Hippopotamus amphibius) in specific dams.