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History and Background of the Study
The crocodile mortality events
The Olifants River Gorge and Lower Letaba River, at the confluence with the Olifants River, in the Kruger National Park (KNP), are home to one of the densest populations of large Nile crocodile, Crocodylus niloticusLaurenti, in South Africa. During 2007, the rising level of Lake Massingir,in Mozambique, flooded many of the rapids and pools in the Olifants Gorge. Altered hydrodynamics have resulted in the deposition of clay-rich sediments within the aquatic habitat of the area. During the autumn and winter of 2008 and 2009, large numbers of adult crocodiles were found dead in this area. Some 180 specimens out of a known population of at least 600 were found dead in 2008 alone. Autopsies performed by KNP veterinarians revealed exceptionally fat carcasses with an abnormal hardening of the fat.
Histological examination of tissue specimens by Drs E. Lane (National Zoological Gardens, Pretoria, South Africa), J. Steyl and F.W. Huchzermeyer (Faculty of Veterinary Science, University of Pretoria, Onderstepoort, South Africa) confirmed an inflammation of the fat typical of pansteatitis.
Organisational response to the crocodile mortality
In response to the crocodile deaths in 2008, the Consortium for the Restoration of the Olifants Catchment (CROC) was founded as a multidisciplinary initiative. CROC provides the following preamble: “Crocodile catastrophe – implications for mankind
• It is increasingly clear that the crocodile deaths in the Olifants Basin are symptomatic of a serious and growing environmental problem in which a tipping point has been reached /crossed with dramatic unexpected effects.
• Such a top predator collapse indicates prolonged and cumulative ecosystem stress caused by human activities in which the implementation of our legislated environmental controls and monitoring response proved inadequate.
• There are serious implications for human health and well-being if the situation continues and river health is not restored.”
A collaborative team effort was initiated, including KNP researchers, various universities, government departments and private sector consultants, to investigate various aspects,including fish pathology, that may have played a role leading to the development of pansteatitis in the crocodiles.
A fish survey in the Olifants Gorge conducted by the author during August 2008, at the request of South African National Parks (SANParks), indicated that some sharptooth catfish, Clarias gariepinus (Burchell),carried large stores of fat that appeared to be affected by steatitis. Other fish species appeared to be healthy. The author subsequently confirmed pansteatitis in these catfish by histological examination of affected adipose tissues. This finding by the author formed the basis for the research that led to this PhD study. As catfish are known to form part of the diet of large crocodiles, the investigation was focussed on a study of the pathology in catfish inhabiting the Olifants Gorge. On 8 July 2009, for the first time, a large fish mortality event was observed within the Olifants Gorge. Affected fish were almost exclusively large sharptooth catfish and were found in the area overlying the clay-rich deposits at the point where the gorge widens into the dam. Fish carcasses were observed to be very fat. The fish kill remained localized in space and time, and no mortalities were observed in either the Olifants or Letaba rivers up-stream of the gorge, and fish in Lake Massingir appeared unaffected. Pansteatitis was confirmed by the author in live catfish sampled from the Olifants Gorge around this time by SANParks scientists.
It was assumed that pansteatitis in catfish and crocodiles in the Olifants Gorge was linked and associated with pollution. This studywas based on the assumption that pollution-associated pathology in fish in the Olifants River in the KNP preceded the pansteatitis syndrome that caused the deaths of crocodiles during the winter of 2008 and that certain pathological indicators may be used to monitor the incidence of pansteatitisin catfish along the river. This information may indirectly reflect the risk that pansteatitis poses to crocodiles in the same section of the river.
CHAPTER ONE: INTRODUCTION
1.1. History and Background of the Study
1.1.1. The crocodile mortality event
1.1.2. Organisational response to the crocodile mortality
1.2. The Olifants River Catchment and Crocodile Mortalities
1.3. Justification for the study
1.4. Objective
CHAPTER TWO: LITERATURE REVIEW
2.1. Introduction
2.2. Pansteatitis
2.2.1. Pathology
2.3. Vitamin E
2.4. Oxidative Stress and in vivo Lipid Peroxidation
2.4.1. Free radical attack
2.4.2. Xenobiotics as pro-oxidants
2.5. Bio-monitoring
CHAPTER THREE: FIELD STUDY
3.1. Materials and Method
3.1.1. Introduction to the fieldwork
3.1.2. Description of the study area
3.1.3. Specimen collection
3.1.4. Sampling and fish dissections
3.1.5. Gross and histological examinations
3.1.6. Laboratory work
3.1.7. Statistical analysis
3.2. Results
3.2.1. Prevalence of pansteatitis
3.2.1.1. Prevalence in free living catfish
3.2.1.2. Stomach content relative to prevalence
3.2.1.3. Prevalence in a captive farmed population of catfish
3.2.1.4. Discussion of prevalence
3.2.2. Pathology of pansteatitis in catfish
3.2.4. Pathology in other fish species
CHAPTER FOUR: PERSISTENCE OF PANSTEATITIS AFTER REMOVAL OF THE INCITING DIETARY CAUSE
4.1. Introduction
4.2. Hypothesis
4.3. Objectiv
4.4. Materials and Method
4.4.1. Experimental design
4.4.2. Experimental facility
4.4.3. Experimental animal procedures
4.5. Results
4.6. Discussion
4.7. Conclusion
CHAPTER FIVE: EXPOSURE OF FISH TO SEDIMENTS FROM SITES WHERE PANSTEATITIS HAS OCCURRED
5.1. Introduction
5.2. Objective
5.3. Materials and Method
5.4. Results
5.5. Discussion
CHAPTER SIX: GENERAL DISCUSSION
6.1. Introduction
6.2. Prevalence of Pansteatitis
6.3. Pathology
6.4. Haematology, Blood Chemistry and Bio-monitoring
6.5. Xenobiotics as Possible Cause of Pansteatitis
6.6. Dietary Change and Pansteatitis in the KNP
6.7. Pansteatitis in Catfish and the Crocodile Mortality
6.8. Conclusion and Recommendations
REFERENCES
