7.1 `Paratuberculosis', or Johne's disease, has been described as "one of the most complex and interesting of the world's emerging animal diseases".1In describing the `science' of OJD, the Committee has made considerable use of a Scientific Review prepared for the Victorian Government by Dr Stephen Prowse of the CSIRO.
7.2 Some witnesses to the Inquiry were critical of the Prowse Report. They included people associated with the Mackinnon Project (at Melbourne University),2private veterinarians,3as well as individual producers.4 Criticisms included use of selective sources and absence of detailed referencing, use of personal communications, usage of terms such as `control', poor data in mortality rates and use of speculative hypotheses.
7.3 The Committee has used many primary sources of evidence and found that they essentially substantiated the evidence in the Prowse Report. A key reference that was referred to by others had not been published at the time Prowse wrote his report.5 The Committee understands that Dr Prowse was instructed to write his report in a style that is appropriate for an intelligent, non-scientific readership rather than as a learned paper and so detailed referencing throughout the text might have appeared inappropriate. The Committee also understands that results of scientific research usually take two or more years to be published in refereed journals and most recent research results can only be obtained as personal communications with the researchers involved. The Committee considers that the use of personal communications is appropriate and has indeed itself made a point of obtaining information on the most up-to-date research and developments by communicating directly with researchers in relevant fields.
7.4 The Committee found that terms like `control' were not used in a consistent way in the animal health literature - an issue of concern to the Committee but an issue not considered to devalue the Prowse Report. Poor mortality data is an issue of concern, but this is an area of ongoing research. Hypotheses made in the report are clearly identified as hypotheses.
7.5 Finally, the Committee sought comment on the Prowse Report by several of the leading Australian scientists involved in OJD research. They indicated that they were satisfied with the scientific evidence contained in the Report.6
7.6 That is not to say that the Prowse Report is perfect or the last word. It raises issues that are unresolved by current research. In any case, the Committee has not restricted its Inquiry to material provided in Prowse's Scientific Review. It has obtained evidence on scientific aspects of OJD from a wide range of sources, including the Mackinnon Project, written submissions, evidence provided at Public Hearings by research institutions and individuals, as well as scientific papers and reports.
7.7 Scientific knowledge concerning any disease is always incomplete.7 Indeed every new discovery almost always uncovers a need for additional knowledge. Many of the submissions received by the Committee referred to gaps in knowledge about OJD. Gaps mentioned included much of the detailed information on which disease management at the property level depends - the prevalence and epidemiology of the disease. 8 When the Committee examined available scientific knowledge it found that there is a substantial body of information on OJD and Johne's disease more generally, though there is also a need for additional information
7.8 At the Sixth International Colloquium on Paratuberculosis held in Melbourne in 1999 there were 123 papers presented, all of which contained reports of substantial scientific research. Thirty-seven papers dealt with the epidemiology and control of Johne's disease. Seven papers looked at fundamental issues of the molecular biology of M. paratuberculosis, including differences between strains. Forty papers dealt with an array of diagnostic techniques. Countries represented at the Colloquium included the United States of America, Britain, New Zealand, Iceland and several other nations from Europe, and Australia. Many of the papers described Australian research and field investigations.
7.9 According to noted United States animal health expert, Schnurrenberger, past experience indicates that those who strongly desire a particular program are likely to urge moving quickly, on the assumption that technical difficulties can be solved along the way. Those who are opposed to the program will advocate no action until there is more research.9 The risk in waiting until perfect knowledge is available is that the infection may spread to such an extent that it would be difficult to control. The mounting of an effective control program need not await perfect knowledge, but the available knowledge does need to be sufficient for the task.
7.10 Mycobacterium paratuberculosis, the bacterium that causes OJD, is also known as Mycobacterium avium, subspecies paratuberculosis.10 Various strains of M. paratuberculosis cause Johne's disease in many species.
7.11 In spite of its name, M. paratuberculosis is not closely related to the bacterium that causes tuberculosis. It does have similarities to many other benign Mycobacterium bacteria that are found naturally in the environment.11The ovine strain of M. paratuberculosis has proved to be much more difficult to culture than the bovine strain.12 In fact it was some years after Johne's disease was first discovered in sheep in Australia, in 1998, that the bacterium was successfully isolated and cultured from sheep tissue. This delayed the identification of OJD as a new disease in Australia, although the difference in the ease of culturing the ovine and bovine forms of M. paratuberculosis is now taken as evidence that they are indeed separate strains.13It is a bacillus (or rod) that can only grow and multiply inside animal cells except when artificially cultured. Such pathogens can be difficult to treat because they are protected from therapeutic drugs by the cells they have invaded.14 Though it cannot grow outside a host except when cultured, it can survive for months, and possibly as much as two years in damp environments. Its survival is due, at least in part, to a tough waxy coat that allows it to resist desiccation.15
7.12 Different strains of M. paratuberculosis occur in various species and in different geographical locations.16 The strain that causes OJD in Australia is different from the strain that causes Johne's disease in cattle and most other species in Australia.17 This has been confirmed by genetic fingerprinting.18 It is also likely that the strain which caused OJD in Iceland is a different strain again. Unlike the Australian strains, it has not been cultured successfully. It has been suggested that the strain infecting sheep in Scotland may be different from the Australian strain as well.19 Australian research, however, confirms that the ovine strain of M. paratuberculosis found in Australia is like that found in New Zealand.20DISEASE CHARACTERISTICS
7.13 M. paratuberculosis does not produce a strong immediate response in its host, nor does it kill its host quickly. These very factors allow the bacterium to be disseminated widely so that it can invade new hosts. This makes it a very successful parasite and a difficult infection to control.21
7.14 The primary site of M. paratuberculosis infection is the lining of the lower part of the small intestine - the ileum.22 Secondary infection of lymph nodes draining the small intestine is normal. There may also be tertiary infection of other tissue, including the liver and spleen. The milk of lactating animals can also be invaded by the bacterium, particularly when the disease is advanced.23 The small intestines and the surrounding lymph nodes are the sites where most changes are usually seen.
7.15 Well before symptoms of disease develop, the immune system of the host animal responds to the presence of infection. The first response, known as a cell-mediated immune reaction, is via specialised cells (macrophages and lymphocytes) that normally protect the body from invading micro-organisms by engulfing and destroying them.24 Chemicals released by these cells provide an early sign that infection has occurred. These chemicals include one known as gamma interferon. This chemical is used as the basis of tests discussed in the next chapter. The cell-mediated immune response decreases as clinical symptoms develop.25
7.16 Later the animal produces antibodies to the infection, but this is not effective in controlling multiplication of M. paratuberculosis.26 In fact, the presence of antibodies in the blood serum of an animal is an indication that shedding of bacteria in the animal's faeces will already have commenced and onset of clinical disease will soon follow.
7.17 Shedding of bacteria starts before disease symptoms are evident. Shedding does not normally occur from animals less than twelve months of age, although research at Sydney University and by the Victorian Department of Natural Resources and Environment has identified shedding from slightly younger animals that have become infected from very heavily contaminated pastures.27
7.18 Early symptoms of disease are changes to cells in the walls of the intestines producing areas of thickening (lesions). At this stage there may be only a few M. paratuberculosis bacteria in these cells.28 As the disease progresses, more of the intestine becomes inflamed and thickened. Lymph nodes enlarge and may feel `gritty'. Infected cells may now contain large numbers of the distinctive bacteria.
7.19 Damage to the walls of the intestine progresses until it prevents the animal from absorbing nutrients. The result is that the animal effectively starves to death. In many species, though not commonly in sheep, damage to the intestines also leads to diarrhoea. With sheep, the primary symptom is weight loss. This may be hard to observe until the disease is very advanced, because of the sheep's fleece. By the time the disease is obvious the animal can be very weak and emaciated.29 Shedding of bacteria will have greatly increased with the onset of disease symptoms.30
7.20 OJD is a slow-developing disease. In Australia sheep may be infected as lambs but have seldom shown symptoms at less than two years of age.31 Once an animal shows signs of wasting it invariably dies within six months and usually in half this time.32 Mortalities caused by OJD generally occur throughout the year, rather than in restricted seasons as with some wasting diseases.33
7.21 Treatment may effect a cure of some animal diseases. For many infections the animal's natural defence mechanisms may overcome the disease. This commonly occurs with infected wounds. There are a number of ways of treating animals to help them to overcome and recover from disease caused by infection. The main ones are:
a) minimising stress by ensuring a high standard of nutrition and avoidance of such factors as extremes of temperature;34providing booster vaccination to promote a strong antibody reaction;35administering antibiotics or other drugs to suppress and ultimately kill the infective organism, if effective drugs are available;36using chemical disinfectants for infections of the skin and superficial tissue (as for footrot);
b) drenching with chemicals that are toxic to intestinal parasites
7.22 According to Dr Britton, Veterinary Service Manager, CSL Ltd, there is tentative evidence in a Spanish study that vaccination may limit the progression of clinical symptoms of OJD in sheep that are already showing early symptoms.37 There are also drugs that can sometimes achieve a short remission in the disease. 38 However, the Committee has found no evidence of any available treatment that is able to free animals of infection once this has been contracted, or cure them of the disease. All available evidence supports work by British researcher Hermon-Taylor, which indicates that OJD cannot be cured by any techniques currently available.39Losses Caused by OJD
7.23 Prevalence of disease in a flock, and particularly mortality, can have a large influence on the economic impact of OJD.40 It is important for sheep farmers to know what mortality rates to expect if appropriate management is implemented on their properties.41
7.24 Evidence obtained by the Committee indicates that, to date, mortality rates in most infected Australian flocks are low - from 0 to 4 per cent - and occur mainly in older sheep. However, much higher mortality rates have been attributed to OJD - with 5 to 7 per cent mortality seen in a quarter of infected flocks and a few flocks having higher mortalities.42
7.25 Mortalities can increase as pastures become more heavily infected and rates of 20 per cent have been reported in NSW.43 Although it is unusual, in heavily infected flocks, animals that are less than two years old have died due to OJD. In New Zealand mortality was found to increase with greater average age of the flock.44
7.26 In Victoria, there are few flocks where the infection in a flock has progressed to a level where clinical symptoms have been observed and mortality recorded. This includes those flocks involved in the original outbreak of disease in Ensay. One affected owner reported losses in older sheep of about 20 per cent,45another reported mortality rates of 10 per cent in two-year-old wethers.46In the Bathurst area of NSW, owners of infected flocks have estimated losses due to OJD. This was done on the basis of increases in mortalities after the disease was identified in their flocks (that is, over and above their normal flock mortality rates from other causes) and the typical appearance of sheep killed by OJD. The results are summarised in Table 7.1.47 Mortalities, as indicated by these estimates, tended to increase over time. Estimated losses of 10 per cent on one property that was studied in detail were verified. These estimated losses are also consistent with considerable anecdotal evidence from the Bathurst region. For example, one farmer reported losses in yearling lambs of 40 per cent. Another farmer, who was said to be `irate' when initially advised that his flock was infected in the mid-1990s, because his losses were low, is now reporting 20 per cent losses of young sheep.48
7.27 The data in Table 7.1 suggest not only that mortalities in a flock can increase with time, but also that rates vary a great deal from flock to flock.49Table 7.1: Estimated mortalities reported by a sample of owners of OJD-infected properties in New South Wales
|
Years since diagnosis |
Number of properties |
Percentage annual mortalities |
|
|
Mean |
Range |
||
|
0-2 |
70 |
2.4 |
0-13 |
|
3-5 |
54 |
4.3 |
0-20 |
|
6-9 |
19 |
5.4 |
0-18 |
|
10+ |
12 |
5.9 |
1-20 |
|
Total |
155 |
3.7 |
0-20 |
Source: Eppleston, O,Neill, Thornberry, Lugton, Taylor and Hall (2000).
7.28 One possible complicating factor in determining mortality rates from OJD is the apparent interaction between stress and development of symptoms of disease. If stress, as appears evident, is a factor that can precipitate mortality from OJD, it is difficult to separate deaths from other causes, such as drought or parasites, from those caused by OJD.50 The Committee appreciates that there are often such interacting factors in animal health. On the other hand, the Committee received evidence during its field inspections of flocks that have not succumbed to droughts had subsequently had high mortality from OJD. Further research and surveillance currently being undertaken will help to determine more accurately the impacts of OJD on sheep mortalities.51
Mortality rates from OJD are not generally high in Australian flocks - but the mortality rates of infected farms appear to increase over time and can reach significant levels.
7.29 The Committee was provided with evidence that, in early stages of M. paratuberculosis infection, there may be little effect of the disease on the host animal.52 However, research at Sydney University has demonstrated that sheep infected with OJD that were showing no conspicuous signs of disease in fact gained less weight than non-infected sheep. This work corroborates other limited evidence that productivity can be affected before disease is obvious.53 Other production losses reported include reduced reproductive performance of breeding animals, lighter wool clips and a reduced capacity to achieve market specification for lambs.54 In late stages of the disease, wool becomes weak and breaks occur.55Dramatic falls in lambing rates in flocks heavily infected with OJD in the Ensay area in the late 1990s were reported to the Committee.56
7.30 Development of OJD depends on an animal first becoming infected and then the infection leading to symptoms of disease.
7.31 The Committee was presented with differences of opinion as to whether infection will, given sufficient time, inevitably lead to disease.57 There were claims that a sheep may carry M. paratuberculosis infection, and even be shedding bacteria, without ever developing clinical symptoms of the disease.58 The contention is that an external trigger is needed to convert infection to disease. Others argue that, if the sheep is not slaughtered or killed by other causes, progression to clinical disease is inevitable.59The Committee was not given any evidence to show that an external trigger is needed to convert infection to disease.60 It is clear, however, that animals may be infected for lengthy periods before any symptoms develop. This makes it very difficult for producers to protect themselves against the risk of buying infected animals. The diseases long incubation period also makes it difficult to research and to manage.
7.32 It is also evident that there may be a number of factors that can influence or hasten the transition from infection to clinical disease.
7.33 Evidence gathered by the Committee indicates that OJD is not highly infectious.61 Contact with the disease organism does not necessarily lead to infection. Animals, particularly older ones, need to come in contact with a considerable number of bacteria over a period of time for infection to become established.
7.34 Infection occurs only when the bacterial load is sufficient to defeat the primary defence mechanisms of the host, enter cells in the wall of the intestines and start to multiply. For M. paratuberculosis the number of bacteria needed to cause infection is usually substantial - that is, a considerable load of bacteria needs to be ingested.62 Consequently, the more contaminated the pastures and the longer an animal grazes them, the more likely the animal is to become infected. By implication, any factor that reduces the contamination of pastures (and drinking water) will lower the likelihood of individual animals becoming infected.
7.35 Age appears to affect the vulnerability of animals to infection.63 Sheep, as well as goats and deer, show some susceptibility to infection at any age, although lambs are the most vulnerable animals.64 This is unlike bovine Johne's disease, where generally only young calves become infected.65
7.36 All breeds of sheep are susceptible to infection but there is some evidence to suggest that British breeds are less vulnerable than merinos.66 In Victoria, it certainly seems that the greater majority of flocks infected by OJD are merino flocks. The Committee has heard evidence that one Poll Dorset breeder had his flock diagnosed as OJD infected,67one Corriedale stud was affected,68and that it is not a major problem in the goat industry of Victoria.69 Such evidence is not, however, conclusive as to breed susceptibility, as it is confounded by the fact that the different breeds are run under different management systems that may influence exposure to the bacterium. However, even within one flock there appear to be some animals that are more susceptible to infection than others.70Whether because of different vulnerability or different extent of exposure to the bacteria, there are usually many sheep within a flock that are not infected. There is also considerable variation in the prevalence of infection between different flocks. Staff of the Department of Natural Resources and Environment report that, within five flocks that were studied, the average level of infection was 25 per cent, but one flock had 2 per cent infection while the level in another flock was 50 per cent.71The Department of Natural Resources and Environment has studied prevalence in five of the flocks diagnosed with OJD early in the Victorian OJD Control Program. This provides information on the potential prevalence of OJD in flocks.72 Unlike most infected flocks in Victoria, these are likely to have been exposed to infection for a lengthy period. The results are presented in Table 7.2 and they show that prevalence can be high after prolonged exposure to infection.
Table 7.2: Distribution and prevalence of infection in five infected flocks (expressed as a percentage)
|
OJD prevalence* |
Farm 1 |
Farm 2 |
Farm 3 |
Farm 4 |
Farm 5 |
Across all farms |
|
In mob |
8 |
1 |
37 |
21 |
23 |
19.3 |
|
In `tail'of mob** |
57 |
4 |
86 |
59 |
67 |
51.5 |
|
Overall prevalence |
19 |
2 |
47 |
29 |
28 |
25 |
Source: Department of Natural Resources and Environment (2000), Written Submissions, OJD 087.
* Based on slaughter and full post-mortem examination. ** These were sheep with the lowest body condition.
7.37 Expression of disease in infected flocks can be variable, so some producers experience significant clinical disease in their flocks while others see little if any obvious effect.73 The reasons why this is so are only partly known. The Department of Natural Resources and Environment, in its submission, summarised factors that affect clinical expression of disease as:
a) length of time since the flock was infected;
b) breed of sheep;
c) property management;
d) enterprise mix;
e) climate; and
f) flock structure - that is, the proportion of animals at different ages.74
7.38 The NSW experience is that self-replacing merino flocks that have been infected for a substantial period are the ones likely to have the most disease.75The greater the exposure to infection the more rapidly the disease is likely to develop.76 This is probably a major reason for the build-up of symptoms that has been observed in some self-replacing flocks where a cycle of infection, pasture contamination and further infection can lead to heavily polluted pastures.77
7.39 Stress has also been shown to have an important influence on development of disease symptoms. Producers who provided evidence to the Committee at Public Hearings demonstrated this.78 Any stress, such as periods of cold weather, poor nutrition or parasite load may hasten onset of the disease.79 This is at least in part a consequence of the effects of stress on the immune system of the animal. 80 The condition of the immune system plays a part, not only in whether the animal is able to resist infection, but also on how quickly an infected animal develops symptoms of disease.
7.40 Several submissions suggested that soil nutrients might play a part in the development of disease symptoms. 81 The Committee was not able to find any evidence to suggest a direct link between OJD and the nutrient status of the pastures on which sheep are grazed.82 In fact, a proposition that there is a close link between copper deficiency and OJD seems unlikely, given the very different symptoms of the two diseases - copper deficiency is characterised by `steely wool' but specifically by no weight loss.83
7.41 Furthermore, eminent soil chemist and soil surveyor Dr. I. Sargeant has indicated that there is no relationship between the known distribution of OJD and that of localities known to be deficient in copper.
7.42 However, as stress can increase or bring on disease symptoms, it is reasonable to suppose that deficiencies in any aspect of an animal's nutrition could be a factor in the expression of OJD. Further, if animals were in a condition of early deficiency in any nutrient, damage to the gut could well further the problems of deficiency. A program of liming to encourage better pasture growth and dosing stock with trace minerals was described to the Committee by a Kangaroo Island producer.84 The locality is noted for `tender wool', a typical symptom of some nutrient deficiencies. In the two years since OJD was diagnosed on the property, there have been no deaths that can be attributed to OJD. While this time is too short to indicate that losses will not occur, efforts to avoid nutritional stress seem to have paid off so far.
7.43 The likelihood that susceptibility to disease, as well as to infection, is partly genetically determined was also suggested to the Committee.85 This seems supported by the evidence, as noted above, of differences in susceptibility between breeds.86 Though selecting for resistance to such an insidious and slow-developing disease would be a very long-term project, it is possible that some natural selection is responsible, at least in part, for variation in observed incidence of OJD in countries that have had the disease for many years.
Many factors appear to affect the infection rate, but the risk of infection increases where high numbers of bacteria are present and stress levels in sheep are high.
7.44 An indication of the rate of spread of the disease is shown in Figure 7.1. The rate of spread has increased over time.
7.45 Once infection builds up to a sufficient level in an animal, the M.
paratuberculosis bacteria are shed by the animal in its faeces.87
Very large numbers of bacteria may be shed this way, especially from sheep
showing symptoms of the disease - up to 1012 bacteria per
millilitre of faeces.88
As the faeces disperses, the bacteria contaminate pasture, soil and water.
Sheep then ingest the bacteria as they graze. Infection can be passed from
ewes to lambs in milk.89
Figure
7.1: Actual and forecast spread of Johne's disease in sheep in New Zealand
Source: West (1997), as recorded in Prowse (2000a).
7.46 Evidence presented to the Committee indicates that by far the most common way that infection is spread is by the addition of an infected animal to a flock.90 Road verges and laneways can also be sources of infection where these are shared by flocks including an infected flock. Shearing sheds that have been shared between farmers or properties have been implicated in the spread of the infection and indeed any shared area where high levels of faecal matter may accumulate - such as holding-yard areas or trucks used to transport infected sheep may offer risk of infection.
7.47 According to Professors A. Egan and W. Malcolm, sheep trading in Australia often follows traditional patterns.91 These need not be confined to a region and include considerable interstate trade. South Australian sheep farmers are often the source of supply of replacement sheep for farms in the Western District and north-western Victoria, while farmers in East Gippsland and northern Victoria will obtain replacement sheep from sources in NSW. Prime-lamb producers in southern and central Victoria will often get replacement first-cross ewes from the Riverina and the North-Central, Wimmera and Mallee regions of Victoria. Many of these traditional trading areas are not areas known to be affected with OJD.92The Department of Natural Resources and Environment indicated that these trading patterns are not always followed, however, and there is an increasing trend to obtain new genetic material from non-traditional sources.93 In addition to movement through deliberate trade, `sheep are prone to stray within their local district from farm to farm'.94 Consequently there is considerable movement of sheep within and into Victoria. This increases the risk of introducing an infected animal to a flock.
7.48 The risk of introducing the disease through trade is considerably increased by the fact that an animal may be shedding bacteria for years before it develops disease symptoms.95 It can also be infected for months before it produces detectable immune responses in the blood serum (antibodies).96 As a result, apparently `clean' sheep can be infected. The difficulty of detecting early infection can contribute to the spread of the disease.
7.49 The Department of Natural Resources and Environment also provided tentative evidence that there is a potential for the spread of infection by infected faeces being washed from paddock to paddock in periods of high rainfall and flooding.97 This appears to be a factor in the spread of infection in the Woodside area of Victoria.
7.50 Infection by way of faeces that finds its way into permanent running water would be greatly diluted. As a consequence, it is thought that spread from property to property by this means is most unlikely.98
7.51 Spread by movement of large quantities of faecal material or contaminated offal is possible.99 The Committee received in-camera evidence that composted offal and waste from saleyards was being used as manure on pastures. Such offal may include OJD-affected material and thus be spreading the disease to pasture and any animal that may be put out to graze on such pasture. This is of great concern to the Committee.
7.52 The potential for other species to be involved is discussed in a later section. Though there are a number of possible ways that infection may be spread, it is generally accepted that stock movement is the main source of infection.100
7.53 In both NSW and Victoria it has been found that OJD often occurs in a cluster of farms, presumably introduced to one property and then spreading to neighbours by one means or another.101 This does not imply that the infection spread from the first identified property. OJD is such an insidious disease that it is often very difficult to be sure of the source of infection.102
Spread of the disease appears to be caused mostly by sheep that have been infected for some time infecting pasture by shedding bacteria through their faeces.
7.54 The disease appears to progress slowly through a flock - it takes time after an infected animal is introduced into a flock for infection to spread to other animals. Dr Prowse put the likely time lags as 6 to 12 months from initial exposure of the flock for it to be positively infected - that is, for any animals in a previously uninfected flock to become infected as a result of ingesting bacteria shed by the introduced animal. It will be a few months after this before these newly infected animals will start to shed bacteria and contamination of the pasture start to build up so that more animals become infected.103The Committee could not find any conclusive research data on the rate of infection, although what limited data are available indicate that within 10 years, 50 per cent or more of the flock may be infected. Theoretically, the rate of infection from the introduction of one infected sheep into an uninfected flock will be initially slow, perhaps taking a number of years before 2 per cent of the flock became infected. As more and more sheep became infected, the amount of shedding would increase, with the number of sheep infected rising exponentially till most sheep in the flock were infected. The Committee understands, however, that it is very difficult to obtain such data from the field and that modelling would be required.104Factors Affecting Pasture Contamination and Survival of the Organism
7.55 More-intensive farming systems that involve high stock densities increase the potential for heavy bacterial pollution of pastures by M. paratubercuosis. Where animals are lot-fed or confined to sheds for lengthy periods this potential is greatly increased. Australian farming systems generally lead to low environmental contamination compared with the situation in other countries.105 This is particularly the case in the dry inland areas and is one of the reasons why it is commonly believed that OJD is unlikely to be a significant problem in these areas. The other reason is the extreme weather conditions experienced there.
7.56 The length of time that M. paratuberculosis can survive in the environment is critical to any decontamination program.106 The bacterial cells are more resistant to environmental factors such as heat, cold, sunlight, desiccation and ultraviolet radiation than are most other bacteria. 107 M. paratuberculosis has a low metabolic activity that contributes to its survival in adverse environments. It has been recovered from water after 270 days and from faeces after 11 months.108 During hot, dry summers the survival period is likely to be shorter.109 Consequently disinfection of paddocks is considered to have been achieved within two summers. The bacterium is vulnerable to high temperatures. It can be killed by boiling for two minutes and by exposure to ultraviolet light.110Dr Prowse found tentative evidence that rainfall may be an important fact in the survival of M. paratuberculosis in the environment.111 He compared distributions of rainfall and OJD. Most infected flocks fall in areas with rainfall greater than 1,600 mm per year - that is, the eastern, south-central and south-western regions. The Committee does not considered this association as conclusive evidence of the importance of high rainfall, as these areas also correspond to those parts of Victoria where sheep are often run at higher stocking rates and to areas where OJD may have been first introduced.
7.57 However, the Department of Natural Resources and Environment has concluded that permanently wet or shaded areas may allow prolonged survival of M. paratuberculosis.112Influence of Soils on Survival and Distribution
7.58 A tenuous association between the occurrence of OJD and acid soils has been reported.113 The strength of the association and reasons for it remain to be determined.
7.59 Correlations between OJD and acid soils have been demonstrated in several countries - for example, South Africa, the United Kingdom and the Netherlands.114
7.60 In England it was observed that cases of clinical Johne's disease do not develop along the south-west coast where the soils are formed from sands with high lime content, but they are found on nearby soils which are deficient in lime.115 In the Netherlands Johne's disease (bovine) was also found to be most common on acid soils, which also (inevitably) lack lime.116 Accepted epidemiological criteria were used to examine association between soil acidity and symptoms of Johne's disease. Some, but not all, criteria were met. The researchers who undertook the analysis concluded that available information is inadequate to infer a causal relation between soil pH (acidity) and Johne's disease.
7.61 The suggestion has been made that availability of iron may be low in strongly alkaline soils and that this could influence survival of the bacterium in the environment. However, Dr Sargeant explained that iron at the soil surface is present in its insoluble oxidised (ferric) form.117 Low soil pH would not render this form of iron soluble. Dr Sargeant also explained that M. paratuberculosis, which is particularly poor at taking up iron, might obtain iron in a suitable form for uptake from decaying organic matter, should it require iron for survival outside a host. The availability of iron from this source is independent of pH.
7.62 The possibility that other factors, for example soil drainage, might be involved was not examined in the English studies. Sandy soils are characterised by good drainage, as are many soils that have a high lime content.118 There does appear to be a need for more information on soil factors, particularly physical ones, which might influence survival of OJD contamination. Some research that is currently being done in Australia is aimed at providing such information (see Table 7.3 at the end of this chapter).
7.63 There is reasonably good information available about the distribution of sheep flocks that are severely affected by OJD.119 This information has been largely derived from observing clinical disease in sheep. Given that there may be a number of years between sheep becoming infected and their exhibiting clinical symptoms, this is not a good proxy for determining the distribution of infection. However, as sheep with advanced infection are also those most likely to spread the disease (that is, by shedding bacteria), flocks with clinical disease are good indicators of the centres and sources of infection.
7.64 Use of trace-back and trace-forward testing techniques from such known infected flocks can, as discussed in the next chapter, then be used to identify other infected flocks and in turn trace-back and trace-forward testing from these flocks may identify additional infected flocks. Currently blood tests are being used to detect infected flocks, particularly in Victoria, New South Wales, South Australia and Western Australia, with a newly developed pooled-faecal culture technique also being used. The methods are described in Chapter 4 and have been used comprehensively, particularly in Western Australia, New South Wales and Victoria. There are two disadvantages of the approach. It relies on possibly imperfect knowledge of the original infected flocks and movement of breeding animals to and from these flocks and the sampling is neither random nor systematic. The extensive testing undertaken to date does, however, provide a good indication of the distribution of infected flocks that appear to be at highest risk.
7.65 Two other testing activities, also described in the next chapter, are helping to build up a picture of the distribution of OJD, albeit to a limited extent. These are testing associated with the Market Assurance Program, and abattoir surveillance. Testing under the Market Assurance Program generally indicates absence of infection, but a few infected flocks have been identified through the Program.120 Abattoir surveillance has been used on a trial basis in Victoria (mostly since 1998) and more extensively in NSW. While it only identifies the prevalence of sheep already showing signs of the disease, it has the potential to sample all flocks in the State. There is a high correspondence between its findings of infected sheep so far and previously known locations of infection in both Victoria and NSW.121 Equally importantly it is not detecting infection in areas previously considered free or of low prevalence.
7.66 All the current methods of determining the distribution of OJD depend on tests or observations that are effective only after infection has been present in an animal for perhaps a year. Consequently it will take time, as well as systematic surveillance, to establish the full distribution and prevalence of OJD. It is always possible that there will be some flocks that are too recently infected to be identified.
7.67 The National OJD Program aims to establish the distribution of OJD across Australia and to this end it has established research programs into techniques such as the pooled faecal testing and abattoir surveillance. It has also provided resources for States to undertake surveillance and co-ordinate results. Results are published in regular surveillance and Program reports. It is not expected that there will be conclusive results until the end of the six-year National OJD Program - that is, until 2003-04.
Victoria
7.68 As at December 1999, there had been 2535 investigations and 173,737 samples tested. Since 1997 there has been a steady increase in the total number of flocks detected; however, the number being detected as infected remains low, as is shown in Figure 7.2. The rate of infected flock detection has not increased. This is what might be expected, as most high-risk flocks from known clusters of infection have now been tested.
Source: Department of
Natural Resources and Environment (2000), unpublished data supplied 20 October
2000.
7.69 In total, by mid-2000, 188 infected flocks had been detected in Victoria. Under the Victorian OJD Control Program most of the affected properties (169) had been totally or partially destocked, or were in the process of destocking.122 There remained, at March 2000, sixteen known infected properties (and 66 suspect flocks and 394 flocks under investigation).
7.70 From such figures, Dr Prowse suggests that, if no further foci or clusters of infection are found, the greater proportion of infected properties may already have been identified. Most of these have already been destocked. According to information provided by the Department of Natural Resources and Environment , the parts of the State that have the largest proportion of Victoria's flock still show no evidence of the infection.123 These areas include most of the land west of Geelong to the South Australian border.
7.71 Prowse estimated that a further 60-70 infected flocks are likely to be detected in Victoria if no new node of infection is discovered.124 Others believe that the figure could be higher, and this would be the case if a new cluster of infection like that found in 1999 around Yea were to be detected.125 Several people who made submissions to the Inquiry or provided evidence at Hearings expressed the belief that OJD is widespread in Victoria.126 The Committee was provided with no evidence to support this belief. The early abattoir surveillance results that have been provided to the Committee support the hope that the distribution of OJD is well indicated by the present identified distribution.127
While the full distribution of OJD will not be known until 2003, all available evidence indicates that it is restricted in occurrence and endemic only in a few parts of Australia and in no parts of Victoria. Available evidence indicates that there are unlikely to be major new clusters of infection in Victoria.
7.72 Many of the submissions to the Inquiry raised doubts about the feasibility of eradicating OJD when there is evidence that species other than sheep can be infected by M. paratuberculosis, including the specific strain of the bacterium that causes OJD.128Between Domestic Animals
7.73 Evidence was provided to the Committee that M. paratuberculosis can infect many animals, particularly ruminants, including cattle, goats, alpacas and deer.129 There have been a few reports of the bacterium infecting non-ruminants, including pigs, rabbits and horses. While M. paratuberculosis is involved in each case, the strains involved generally appear to differ with species.130 Host preference for M. paratuberculosis is relative, however, rather than absolute.131 Cross-species infection has been shown to occur where there is a very large intake of the bacterium, especially by young animals. There also appear to be strains found in other countries that have host ranges that differ from those of the two Australian forms - the ovine and bovine strains.
7.74 Strains found in Iceland and Eastern Europe appear capable of being passed reasonably readily from sheep to cattle and back to sheep.132 A strain found in Scotland passed from sheep to rabbits.133
7.75 In New Zealand, both the ovine and bovine strains of M. paratuberculosis have been found infecting deer. In Australia, two deer herds have been detected with the bovine strain (in 2000) and none with the ovine strain.134OJD has been diagnosed in goats and cattle in Australia, with a few instances of calves being infected with OJD when they have been grazing heavily infected pastures. It has not been identified in deer or camelids (alpaca and llama).135 Bovine Johne's disease has also been recorded in three sheep - one of which was recorded on a cattle farm that testing indicated was not infected with the disease. It was only identified after DNA testing.136 Goats can become infected with both the ovine and bovine strains of Johne's disease.137 There is strong evidence, however, that spread of infection between sheep and cattle with the strains of M. paratuberculosis that are present in Australia is rare.138
7.76 With one exception, there has been no observation of M. paratuberculosis in wildlife in Australia, although considerable investigations have been done.139 Specifically, rabbits have been sampled in the Southern Tablelands area of New South Wales and parts of Victoria.140In NSW approximately 600 have been sampled in the highest risk areas with no confirmation of Johne's disease. A similar number of kangaroos have been surveyed. At the Victorian Institute of Animal Science more than 300 rabbits and 100 kangaroos on affected farms have been examined, with no evidence of Johne's disease in any of them.141
7.77 One wallaby on Kangaroo Island had M. paratuberculosis isolated from a tissue culture, but it had no lesions. The presence of M. paratuberculosis organisms in the animal's gut may have been the result of passive ingestion without infection.142 This is being investigated further.
7.78 Dr W. Sykes, research veterinarian, in giving evidence to the Committee, concluded that:
At this stage the probability of wild animals being involved in Australia in the maintenance of OJD is low. There is probably a different degree of risk with goats and cattle.143He also emphasised that the primary risk of infection comes from other sheep, but added that goats present a significant risk, while cross-species infection from other species, though not negligible, is much lower.144Possible Risk to Humans
7.79 M. paratuberculosis, particularly the bovine strain, has been proposed by some as a possible cause of Crohne's disease in humans.145 Crohne's disease is a slow-developing, recurring inflammatory condition of the intestines, usually the ileum.146 It can affect any part of the human gastrointestinal tract and it also may lead to other symptoms involving arthritis, skin problems and inflammation of the eyes and mouth. The causes of Crohne's disease have not been identified, although a genetic predisposition is recognised. There is also involvement of the immune system.147
7.80 Successful treatment of a minor sub-set of Crohne's patients with drugs that are active against mycobacteria can result in long-lasting reduction in symptoms, which has led to suggestions that there may be a sub-set of Crohne's disease cases which involves M. paratuberculosis.148
7.81 Two other lines of evidence are presented to support a link. The first is similarity between symptoms of Johne's and Crohne's diseases.149 While a recent study confirmed the close similarity between the symptoms of the two diseases, these similarities are not perfect.150 The other evidence suggesting a link comes from reported presence of M. paratuberculosis in tissue of some Crohne's disease sufferers.151 Other researchers were not able to reproduce these results and there is also an untested possibility that M. paratuberculosis may be present in healthy people.152There is, however, evidence against a link between the two diseases - in particular the lack of a higher incidence of Crohne's disease among farming families, particularly dairy farmers, who could be expected to have considerably higher exposure to M. paratuberculosis than the rest of the community. Johne's disease is common in dairy herds and M. paratuberculosis is found in the milk of infected cows - milk normally consumed untreated by farmers.153 Further, there is no consistent evidence of an immune response to M. paratuberculosis in Crohne's disease patients.154 The likelihood of a link between M. paratuberculosis in sheep and human health would appear to be very low - first because there is no evidence that the bacterium can multiply in muscle tissue and second, because sheep meat is usually eaten cooked and so any bacteria in it would be killed.155A recent report by the Scientific Committee on Animal Health and Animal Welfare of the European Union concluded, after examining a substantial body of research:
The currently available evidence is insufficient to confirm or disprove that Mycobacterium paratuberculosis is a causative agent of at least some cases of Crohne's disease in man.156According to Tony Higgs, Senior Veterinary Officer, Albany, WA:
On the balance, it seems prudent to insure against the potential risk that M. paratuberculosis poses to human health and, as the Dutch have done, work towards reducing that risk as a major objective in a Johne's disease control program. Having the objective of reducing the risk of complications associated with a perceived or real link to Crohne's disease would significantly influence the strategies chosen to deal with the disease compared to a program that is designed solely for eradication.157Finding 7.5
The Committee was unable to find any evidence that indicated a causal relationship between OJD and human disease.
7.82 Many submissions received by the Committee assert that little is known about OJD. Evidence gathered by the Committee indicates that this is not in fact the case. The Committee found, in fact, that a considerable amount is known about the disease. However, detailed information upon which to base management is still much less than ideal. Its long incubation period and the covert nature of OJD make it a difficult disease to study. Lengthy research is needed.158
7.83 As noted in the introduction to this chapter, effective control need not await perfect knowledge, but the available knowledge does need to be sufficient for the task. Schnurrenberger suggested that a number of questions need to be considered when the adequacy of technical knowledge is being assessed. These questions are concerned with:
a) diagnostic procedures;
b) disease occurrence - distribution and prevalence of OJD;
c) epidemiological studies applicable to the region concerned, including the species capable of acting as reservoirs of infection;
d) routes of transmission; and
e) on-site disinfection.
7.84 As has been outlined in this chapter, there is a substantial amount of knowledge about all of these matters (although, note that the first of these questions deals with matters discussed in the next chapter). Much of this knowledge has only been obtained in recent years and was not in fact known when OJD control programs commenced in Australia and other countries around the world.
7.85 Various organisations and agencies have identified areas where they consider more information is needed.159 These relate to both the biology of the disease and methods of control. Technical aspects of the latter are discussed in the next chapter, but remaining information needs, and thus priority research areas have been described as relating to:160options for better diagnostic tests and sensitivity of abattoir monitoring;
a) distribution of infection;
b) the epidemiology of the disease under Victorian conditions, including all factors that influence the spread of OJD;
c) routes of transmission, including the risk of cross-infection between sheep and other species,161risks associated with artificial insemination and embryo transplant, ways to minimise these risks and better information on different strains of M. paratuberculosis, including ones that have not yet been found in Australia;
d) factors that influence elimination of infection from properties, particularly the length of time the bacterium can live in the Victorian environment, factors affecting its survival and techniques for detecting the level of infection in paddocks;162and
e) a range of issues that influence minimisation of OJD at the farm level - such as factors that hasten expression of disease symptoms, production losses, prior to mortality, mortality rates that can be expected under a range of management and environmental conditions and effects of vaccination on infection, disease expression and the value of the animal. 163The Committee also considers that research data on the rate of infection spreading through a flock is also required.
7.86 Research throughout Australia on OJD is being co-ordinated by the National Ovine Johne's Disease Control and Eradication Program.164 There is also other research on OJD being undertaken by several organisations. Meat and Livestock Australia regularly prepares summaries of research and the National Program provides quarterly updates.165
7.87 Though the Committee found that knowledge in many areas is less than ideal, there is a considerable amount of additional research and monitoring currently being undertaken. Table 7.3 summarises key research and surveillance work that is currently being undertaken, progress, expected outcomes and time lines for these outcomes.
7.88 The Committee has related this work to research needs listed above, that is, research concerned with:
a) diagnostic procedures;
b) disease occurrence - distribution and prevalence of OJD;
c) epidemiological studies applicable to the region concerned;
d) routes of transmission;
e) on-site disinfection; and
f) minimising OJD.
7.89 It appears that much of the current research and surveillance is likely to meet many of the information needs as listed. Dr R. Whittington and Dr W. Sykes, leading OJD research scientists, told the Committee that current research will provide a substantial increase in knowledge of OJD within the next three to four years.166
Table 7.3: Current research on OJD and anticipated outcomes
|
Research area |
Progress |
Expected outcomes |
Expected years to complete |
|
Diagnostic procedures |
|||
|
Blood test |
Improved sensitivity |
Ongoing |
|
|
Pooled faecal culture.167 |
Routine test available |
Test refined, reduction in cost |
1 |
|
Gamma interferon test 168 |
Being developed for bovine Johne's disease, investigations for OJD started |
Moderately sensitive test that can detect infection before shedding |
Uncertain |
|
`Gene probes' test169 |
Preliminary results only |
Quick test that differentiates between strains of OJD |
Uncertain |
|
Disease occurrence - distribution and prevalence of OJD |
|||
|
Abattoir surveillance |
Routine surveillance adopted in some abattoirs |
With flock identification, assessment of distribution and prevalence of OJD |
1 |
|
Epidemiological studies applicable to the region concerned |
|||
|
Possible relationship between Johne's and Crohne's diseases170Studies initiated |
Risk to human health |
Ongoing |
|
|
Potential to eradicate infection from sheep in the presence of wildlife and other farm species, including cattle and goats171Risk of reinfection from wildlife or cattle assessed as very low |
Options for alternative enterprises during destocking established; risk of reinfection from other species determined |
2 |
|
|
Routes of transmission |
|||
|
Factors that influence transmission of infection within flocks. 172Study initiated |
Better management of OJD at property level |
3+ |
|
|
Vulnerability of sheep to infection at different ages173Preliminary results available |
Information on ways that sheep can be managed to minimise the risk of infection and contamination of pastures |
2 |
|
|
Risk of infection through artificial insemination and embryo transfer. Research on the potential risk of embryo transfer needed174Semen study and preparation of protocol under way; risk appears low |
Safe method to preserve genetic resource |
4 |
|
|
On-site disinfection |
|||
|
Factors that determine survival of M. papatuberculosis in the Australian environment 175Preliminary results available |
Destocking time needed to achieve decontamination under various conditions of climate, soil type and management; methods of farm management to minimise OJD |
1 |
|
|
Different lengths of destocking under different conditions for decontamination of pastures176 |
Preliminary results indicating where four months, rather than fifteen months, may be adequate |
Locations where short destocking can achieve decontamination; more efficient decontamination |
5 |
|
Minimising OJD |
|||
|
Strains of OJD - mapping of genome - European work |
In progress |
Improved vaccines and testing methods |
Probably 10+ |
|
Quantification of all losses from OJD at the farm level177Initiated |
Better on-farm management and cost/benefit analysis |
3+ |
|
|
Use of a killed vaccine178Preliminary results indicate low cost and limited damage to animal |
Control of disease symptoms, reduced pasture contamination, potential for eradication from some flocks |
2+ |
|
|
Development of improved vaccines179Preliminary development and testing |
A vaccine that does not interfere with diagnosis of OJD and produces improved protection from infection and disease |
2+ for first results; also ongoing |
|
|
Property-based management of OJD180Preliminary |
Potential for paddock-by-paddock eradication |
5 |
|
Sources: Dr Paul Wood, Research and Development Manager, CSL Ltd, Minutes of Evidence, 24 July 2000, Sykes (1999), Meat and Livestock Australia (1999) and Australian Animal Health Council Ltd. (2000b).
1 Gee (1999b), p. 3.
2 Associate Professor Andrew Vizard and Dr John Larsden of the Mackkinnon Project - University of Melbourne: Minutes of Evidence, 24 July 2000 and Written Submissions, OJD 101.
3 Notably, Rendell, D. Minutes of Evidence, 21 June 2000 and Written Submissions, OJD 112.
4 For example, Blennerhassett, S. (2000), Written Submissions, OJD 008.
5 A review paper by Whittington, R., NSW Agriculture, was particularly mentioned as one paper that should have been used by Prowse. However, at the time of writing his report, Whittington's paper had not been published. Prowse, however (as has the Committee), made use of the paper's contents as a personal communication with the author's permission.
6 Scientists concerned included Dr D. Whittington and others with NSW Agriculture as well as Sydney University.
7 Kefford, B. (2000), Executive Director Agriculture, Written Submissions, OJD 087.
8 For example, Blennerhassett, B. (2000), Written Submissions, OJD 001, Irving, F. M. and R. F. (2000), Written Submissions, OJD018.
9 Schnurrenberger, Sharman and Wise (1987), p. 51.
10 Johne's Information Centre (1997a).
11 Prowse (2000), p. 7.
12 Denholm, Ottaway, Cornish and Merton (1997).
13 Denholmn, L. (2000), NSW Agriculture, personal communication, 8 June 2000.
14 Reid (1981), p. 507.
15 Johne's Information Centre (1997a).
16 Meat and Livestock Australia (1999), p. 23.
17 CSIRO (2000).
18 Meat and Livestock Australia (1999), p. 45; and also Cousins, Williams, Hope and Eamens (1999).
19 Denholmn, L., (2000), NSW Agriculture, personal communication, 8 June 2000.
20 Meat and Livestock Australia (1999), p. 44.
21 Whittington (1999).
22 Johne's Information Centre (1997d).
23 Johne's Information Centre (1997a); and also Johne's Information Centre (1997c).
24 In the case of M. paratuberculosis, this defence fails as this particular bacterium is capable of surviving and multiplying within the macrophage cells; Johne's Information Centre (1997c).
25 Meat and Livestock Australia (1999), p. 10.
26 Johne's Information Centre (1997c).
27 NSW Agriculture (1999b); and also Meat and Livestock Australia (1999), p. 13; and Condron, R. J. (2000), Principal Scientist, Animal Health, Victorian Institute of Animal Science, Department of Natural Resources and Environment, Minutes of Evidence, 7 August 2000.
28 Johne's Information Centre (1997d).
29 Johne's Information Centre (1997d).
30 NSW Agriculture (1997b).
31 CSIRO (2000).
32 NSW Agriculture (1997b).
33 NSW Agriculture (1997b).
34 With acute intestinal infections such as those that cause scouring of young animals, it may sometimes be necessary to avoid foods that encourage growth of the infective agent or irritate sensitive bowels.
35 Used to treat tetanus in humans and could be used for livestock.
36 For example, for some forms of mastitis - Reid (1981), p. 507.
37 Britton (2000).
38 Hermon-Taylor (1999).
39 Hermon-Taylor (1999), p 520.
40 Esson, C. (2000) Written Submissions, OJD 025.
41 Ellis, B. (2000) Written Submissions, OJD 037.
42 Prowse (2000), p. 5.
43 Denholm, Ottaway, Cornish and Merton (1997); and also Eppleston and Simpson (1999).
44 West (1997). The disease was also found, on post mortem, to be present in up to 30 per cent of mature ewes that died on infected properties.
45 Cummins, S. (2000), Minutes of Evidence, 17 May 2000, p. 58.
46 Newcomen, E. (2000), Minutes of Evidence, 17 May 2000, p. 58.
47 Eppleston and Simpson (1999).
48 Eppleston and Simpson (1999).
49 Eppleston, Simpson, O'Neill, Thornberry, Lugton, Taylor and Hall (2000).
50 Ellis, B. (2000) Written Submissions, OJD037.
51 Denholm, L.(2000), personal communication, 8 June 2000; and also Wittington, R. (2000) personal communication, 8 June 2000.
52 NSW Agriculture (1997a); and also Hirst, R. (2000), James Cook University, Townsville, Written Submissions, OJD 068.
53 Meat and Livestock Australia (1999), p. 13.
54 NSW Agriculture (1997a).
55 NSW Agriculture (1997a).
56 Bryce, E (2000), Minutes of Evidence, 17 May 2000, p. 58.
57 Prowse (2000), p. 5.
58 Johne's Information Centre (1997a); and also Tuck, L. (2000), The Science, the Economics, the Politics of Ovine SJohne's Disease, attachment to Blennerhassett, B. (2000), Written Submissions, OJD 008.
59 Johne's Information Centre (1997c).
60 Prowse (2000), p. 5.
61 NSW Agriculture (1997a).
62 Whittington (1999); and also Chaitaweesub, Abbott, Wittington and Marshall (1999).
63 Johne's Information Centre (1997a).
64 Johne's Information Centre (1997a); and also Prowse (2000), p. 5.
65 Johne's Information Centre (1997c).
66 NSW Agriculture (1997a).
67 Oliver, G. (2000), National President Pole Dorset Association, Minutes of Evidence, 10 July 2000.
68 Savage, J. M. (2000), Vice-President, Australian Corriedale Association, Minutes of Evidence, 10 July 2000.
69 Hall, J. (2000), Minutes of Evidence, 10 July 2000.
70 NSW Agriculture (1999a).
71 Condron, R. J. (2000), (2000), Principal Scientist, Animal Health, Victorian Institute of Animal Science, Department of Natural Resources and Environment, Minutes of Evidence, 7 August 2000.
72 Kefford, B. (2000), Executive Director, Agriculture, Department of Natural Resources and Environment, Minutes of Evidence, 7 August 2000.
73 Kefford, B. (2000), Executive Director, Agriculture, Department of Natural Resources and Environment, Minutes of Evidence, 7 August 2000.
74 Kefford, B. (2000), Executive Director Agriculture, Department of Natural Resources and Environment, Written Submissions, OJD 087.
75 Kefford, B. (2000), Executive Director Agriculture, Department of Natural Resources and Environment, Written Submissions, OJD 087.
77 Condron, R. J. (2000), (2000), Principal Scientist, Animal Health, Victorian Institute of Animal Science, Department of Natural Resources and Environment, Minutes of Evidence, 7 August 2000.
78 For example, Harris, S., (2000) Written Submissions, OJD 013, and Minutes of Evidence, 18 May 2000.
79 NSW Agriculture (1997a), and also Prowse (2000), p 5.
80 Blennerhassett, S. (2000), Written Submissions, OJD 008.
81 Colbey, P. (2000), Written Submissions, OJD 031; and also Kent, R. B. and P. J. (2000), Written Submissions, OJD 060 and Attachment to submission - Blennerhassett, S. (2000), Written Submissions, OJD 008.
82 Prowse (2000), p. 33.
83 Hoskins, Caple, Halpin, Brown, Paynter, Conley and North-Coombes (1986), pp. 9-16.
84 Kent, R. B. and P. J. (2000), Written Submissions, OJD 060.
85 Blennerhassett, S. (2000), Written Submissions, OJD 008.
86 Juste (1997), and also Fridriksdottir, Gunnarsson, Sigurdarson and Gudmundsdottir (1999).
87 Johne's Information Centre (1997a).
88 Scientific Committee on Animal Health and Animal Welfare (2000), p. 52.
89 Johne's Information Centre (1997c).
90 Johne's Information Centre (1997a).
91 Egan and Malcolm (2000), p. 16.
92 Although as this report goes to press, the Committee received reports that a small number of OJD infected flocks have been identified in the Riverina region of New South Wales.
93 Kefford, B. (2000), Executive Director Agriculture, Department of Natural Resources and Environment, Written Submissions, OJD 087.
94 Kefford, B. (2000), Executive Director Agriculture, Department of Natural Resources and Environment, Written Submissions, OJD 087, p. 1.
95 NSW Agriculture (1997c).
96 CSIRO (2000).
97 Kefford, B. (2000), Executive Director Agriculture, Department of Natural Resources and Environment, Written Submissions, OJD 087; and also Johne's Information Centre (1997c).
98 NSW Agriculture (1999a).
99 NSW Agriculture (1999a); and also confidential information provided to the Committee during Hearings.
100 Johne's Information Centre (1997a).
101 Kefford, B. (2000), Executive Director Agriculture, Department of Natural Resources and Environment, Written Submissions, OJD 087.
102 Many of the farmers who presented evidence to the Committee were at a loss to know the source of infection in their flocks - for example, Ahsam, B., Written Submissions, OJD 004.
103 Prowse, S. (2000), Program Manager, Infectious Diseases and Food Safety, Animal Health Laboratories, CSIRO, Minutes of Evidence, 24 July 2000.
104 Prowse, S. (2000), Program Manager, Infectious Diseases and Food Safety, Animal Health Laboratories, CSIRO, personal communication, 13 October 2000.
105 Meat and Livestock Australia (1999), p. 37.
106 Telford, A. B. (2000), Written Submissions, OJD 070.
107 Prowse (2000), p. 31.
108 Meat and Livestock Australia (1999), p. 37.
109 NSW Agriculture (1997a).
110 Prowse (2000), p. 31.
111 Prowse (2000), p. 31.
112 As is evidenced by such areas being required to be excluded from grazing in some `Property Disease Eradication Plans'; Department of Natural Resources and Environment (2000), Written Submissions, OJD 087.
113 Johne's Information Centre (1997a).
114 Michel and Bastianello (1999); and also Bastianello (1999) and Prowse (2000), p. 32.
115 Johnson-Ifearulundu and Kaneene (1997).
116 Lime is not found in soils that are not strongly alkaline and is characteristic of strongly alkaline soils.
117 Sargeant (2000).
118 Johnson-Ifearulundu and Kaneene (1997).
119 It is hard not to notice mortality rates of greater than 10 per cent as are often found in heavily infected flocks.
120 Examples were given to the Committee in submissions; for example, Ahsam, B., Written Submissions, OJD 004.
121 Kefford, K. (2000), Executive Director, Agriculture, Department of Natural Resources and Environment, correspondence VT/001/0001, received 22 September 2000; and also Roth, I. (2000), Program Manager Wool and Sheep Meat Services, NSW Agriculture, personal communication, 3 July 2000.
122 Dr B Kefford, (2000), Executive Director, Agriculture, Department of Natural Resources and Environment, Minutes of Evidence, 7 August, 2000.
123 Dr B Kefford, (2000), Executive Director, Agriculture, Department of Natural Resources and Environment, Minutes of Evidence, 7 August, 2000.
124 Estimates made by staff of the Department of Natural Resources and Environment and quoted in Prowse (2000).
125 Denholmn, L. (2000), NSW Agriculture, personal communication, 25 May 2000.
126 For example, Ritchie, M. (2000), Written Submissions, OJD 054 and McDonald, J. W. (2000), Written Submissions, OJD 057.
127 For example, Australian Animal Health Council Ltd. (2000c).
128 For example, McQueen, C. (2000), Written Submissions, OJD 041, Blennerhassett, S. (2000), Written Submissions, OJD 008, Tehan, J. (2000), Strathbogie Branch, Victorian Farmers Federation, Written Submissions, OJD 043.
129 Johne's Information Centre (2000).
130 NSW Agriculture (1997a).
131 Meat and Livestock Australia (1999) p. 4.
132 Meat and Livestock Australia (1999) p. 4.
133 Meat and Livestock Australia (1999) p. 35.
134 Meat and Livestock Australia (1999) p. 23; and also Millar. H, (2000), personal communication, 22 October 2000.
135 Australian Animal Health Council Ltd. (2000b); and also Kennedy and Harkin (1998).
136 Sarritt, B. (2000), personal communication, October 2000.
137 Hall, J. (2000), Minutes of Evidence, 10 July 2000.
138 NSW Agriculture (1999a).
139 Prowse (2000), p. 29.
140 Sykes, W. (2000), Minutes of Evidence Melbourne, 24 July 2000.
141 Condron,R. J. (2000), Minutes of Evidence, 7 August 2000.
142 Prowse (2000), p. 29; and also Denholmn, L. (2000), NSW Agriculture, personal communication, 25 May 2000.
143 Sykes, W. (2000), Animal Health and Research Consultant, Minutes of Evidence, 24 July 2000.
144 Sykes, W. (2000), Animal Health and Research Consultant, Minutes of Evidence, 24 July 2000.
145 Johne's Information Centre (1997e).
146 Prowse (2000), p. 30.
147 Prowse (2000), p. 30; and also Selby (1999).
148 Meat and Livestock Australia (1999) p. 9.
149 Prowse (2000), p. 30.
150 Naser, Schwartz and Shafran (2000).
151 Selby (1999).
152 However, a recent small investigation suggests that there is a need for more research in this area. This involved a study of seven breast-feeding mothers, two with Crohne's disease and five without the disease. It found M. paratuberculosis in the milk of the mothers with Crohne's disease, but not in the milk of the mothers without the disease. The researchers involved drew no conclusions from this study but recommend further studies along similar lines; Naser, Schwartz and Shafran, (2000).
153 Prowse (2000), p. 31.
154 Prowse (2000), p. 31.
155 Prowse, S. (2000), Program Manager, Infectious Diseases and Food Safety, Animal Health Laboratories, CSIRO, personal communication, 4 October 2000; and also Slocombe (1982).
156 Scientific Committee on Animal Health and Animal Welfare (2000), p. 56.
157 Meat and Livestock Australia (1999) p. 19.
158 Kefford, B. (2000), Executive Director Agriculture, Department of Natural Resources and Environment, Written Submissions, OJD 087.
159 Kefford, B. (2000), Executive Director Agriculture, Department of Natural Resources and Environment, Written Submissions, OJD 087, Meat and Livestock Australia (1999), Sykes (1999).
160 Kefford, B. (2000), Executive Director Agriculture, Department of Natural Resources and Environment, Written Submissions, OJD 087, Meat and Livestock Australia (1999), Sykes (1999); Blennerhassett, S. (2000), Written Submissions, OJD 008, Hirst, R. (2000), James Cook University, Townsville, Written Submissions, OJD 068.
161 Tehan, J. (2000), Strathbogie Branch, Victorian Farmers Federation, Written Submissions, OJD 043.
162 Ellis, B. (2000), Written Submissions, OJD 037.
163 Ritchie, M. (2000), Written Submissions, OJD 054.
164 Australian Animal Health Council Ltd. (2000b).
165 Sykes (1999) and, for example, Australian Animal Health Council Ltd. (2000c).
166 Whittington, R. (2000), NSW Agriculture, personal communication, 8 June 2000 and Sykes, W. (2000), Veterinary Research Consultant, personal communication, 22 July 2000.
167 Sykes (1999).
168 Prowse, S. (2000), Program Manager, Infectious Diseases and Food Safety, Animal Health Laboratories, CSIRO, personal communication, 24 July 2000.
169 Johne's Information Centre (1997b).
170 Meat and Livestock Australia (1999) p. 9.
171 Sykes (1999).
172 Sykes (1999).
173 Sydney University study; Sykes (1999).
174 Sykes (1999).
175 Meat and Livestock Australia (1999) pp. 38-39.
176 Sykes (1999).
177 Sykes (1999).
178 Britton, A. (2000), Veterinary Services Manager, CSL Veterinary, Written Submissions, OJD 079.
179 Prowse, S., Minutes of Evidence, Senate Standing Committee on Regional and Rural Affairs and Transport, Melbourne, 24 July 2000.
180 Sykes (1999).
