|Wet Litter in Turkeys: Diseases and
Presented at ADAS/NFU Turkey Conference, Childford Barns, October 1998
Enteritis, inflammation of one or more parts of the intestinal tract, can occur in turkeys of any age, though it is more common in young birds. However, for various reasons, it tends to be associated with outbreaks of "wet litter" in older birds. There are, of course, other causes of wet litter as discussed by other contributors. Viruses, bacteria, parasites and fungi can all contribute to the occurrence of enteritis and wet litter, alone or in combination with other pathogens and other nutritional and environmental factors. Interactions are likely to be complex and are rarely fully understood for a particular case. Regardless of the "initiating cause" outbreaks will tend to rapidly deteriorate where conditions favour faecal-oral recycling of pathogens - a "vicious circle". A range of tools are available which may be adapted to the control of this problem at the level of a particular company or farm.
Outbreaks of disease characterised by wet droppings commonly occur in growing turkeys. One, but by on means the only, cause of wet droppings is enteritis or inflammation of the intestine. It must be remembered that abnormal kidney function can also contribute the level of moisture in the droppings. Physical conditions can also contribute to the degree to which wet droppings result in a practical problem of "wet litter". Wet litter is more likely to be perceived as age increases partly because the volume of faeces produced relative the absorption capacity of litter is increasing, but also because of progressively lower house temperatures reducing evaporation.
|..............||Causes of intestinal disease
A broad range of pathogens may cause disease of the intestinal tract and may contribute to droppings moisture.
|Table 1. UK Survey of Turkey Enteric Viruses - 178 samples|
|R.E.Gough and S.E.Drury, 1998|
A broad range of bacteria inhabit the intestinal tract of all animals. It has been estimated that 90% of the cells in and on the human body are bacterial (???) the same is probably true for other mammals and birds. Unlike the viruses bacteria grow readily in the absence of living cells and may be easily cultured and observed microscopically. Although E.coli has long been recognised as an important cause of serious systemic disease in poultry and of intestinal disease in many species of young mammals, its role in intestinal disease in poultry has only begun to be studied relatively recently. It is now recognised that a proportion E.coli isolates associated with enteritis of chickens (Joya, et al1990, Akashi et al.1991) and of turkeys (Edens 1997) are capable of causing intestinal damage. Because E.coli and related bacteria are relatively easily culture they are also often used as general indicators of contamination of faecal origin in water, feed, the environment etc. Another group of bacteria of particular importance with respect to intestinal disease are the anaerobes Clostridium sp, especially C. perfringens. Although, as with E.coli, this bacterium is commonly present in the intestine of healthy birds, it is capable of causing or contributing to serious disease, typically manifest as necrotic enteritis. This disease is more common in chickens but has been described in turkeys (Gazdzinski & Julian-RJ, 1992). Some species of bacteria such as Salmonella and Campylobacter tend to be discussed with respect to poultry as largely innocuous and of importance primarily with respect to food safety. However it seems likely that at least certain serotypes or strains of these bacteria may, perhaps only as contributing factors, influence intestinal disease in commercial poultry (Lam et al. 1991). A variety of other bacteria, such as megabacteria of cage birds, and ""long-segmented filamentous organisms"(Goodwin et al 1991) have been identified in stomachs and/or intestines of birds suffering intestinal disease. The extent to which such organisms are pathogenic for commercial poultry (and not simply indicators of an imbalance in the flora) is open to some doubt. It must be recognised that the "normal flora" is highly complex, and varies, with age, with location in the tract, among animals within a flock and between flocks. It is affected by the microbes present, the nutrients present (the raw materials on which the bacteria grow), enzymes (endogenous in the feed, added, supplied by the bird), inhibitory substances, (endogenous, microbial, added) and gut function.
Parasites range from small single-celled organisms such as coccidia and Histamonas meleagridis through hair worms (Capillaria) to the large and easily visible round worms (Ascaridia). All of these parasites are capable of initiating or potentiating intestinal disease but there seems to be little evidence that they are currently a major factor as a cause of enteritis in turkeys in the UK.
Although not usually primary causes of enteritis/wet litter they may contribute where other factors are involved. Fungi can act either as infections (Yeast\'92s such as Monilia/Candida, causing thickening of crop and intestine) are as producers of mycotoxin (such as aflatoxin, ochratoxin, T 2 toxin etc.). Moniliasis is commonly associated with birds which are immuno-suppressed or have had antibiotic medication or where hygiene is poor. Fungi which are capable of producing toxins are commonly associated with a range of feed raw materials. The extent of toxin production is usually dependent on factors such as the extent of grain damage, and temperature and humidity profiles.
|Effects of Intestinal Disease
Regardless of the specific pathogen involved there will be a tendency, at least on an individual bird basis, for an inflammatory reaction to occur in the affected tissue(s) and for this gradually to subside as immunity develops. The normal signs of inflammation are reddening, swelling, liquid secretion, loss of function. At a microscopic level there is damage or loss of the absorptive epithelial cells lining the villi, and shortening of villi. As healing begins it is common for the villi to be re-populated with relatively immature, and poorly absorptive epithelial cells. The combined effect of direct damage and the inflammatory response may cause wet litter by reducing resorption of fluid from intestine, increasing water consumption, reducing absorption of nutrients (osmotic) or increasing secretion of fluid into intestine. Surprisingly, work done with viral enteritis in turkeys using dye to establish mean gut transit times suggests that the movement of food through the track is actually slowed down (Goodwin et al. 1985) , probably as an adaptive response to the poor digestion and absorption. However, we must always remember that enteritis does not necessarily cause wet litter and wet litter can occur by various mechanisms without there being enteritis.
|..............||Post-mortem Diagnoses of Enteritis in
In our practice all post-mortem findings (and most other types of veterinary data) are recorded in a dedicated information system (McMullin, 1997). This allows us to rapidly produce summary tables and graphs of large numbers of post-mortem examinations. Table 2 on the next page shows such a summary based on routine post-mortem examination of 8161 turkey grower carcasses over a 30 month period. Enteritis was recorded in 10% of carcasses at an average age of 34 days. Typhlitis (inflamed caecae) was also a common finding especially in young birds (average age 22 days). Although typical Haemorrhagic enteritis was relatively rarely diagnosed, milder forms are likely to be diagnosed simply as enteritis.
|The distribution of the individual affected birds (in this case only those with enteritis and typhilitis are included) by weight and age may be better appreciated from Figure 1 below. Males are shown as hollow circles and females as solid squares. Note that although there is a particular concentration among young birds, there is a broad range of affected ages. These data under-represent the actual occurrence of enteritis in older birds because they seem to be less likely to die from the disease than those under 10 weeks of age.|
|Although Haemorrhagic enteritis is rarely diagnosed
in its typical form, there are a number of reasons to
believe that this my underestimate its significance as a
cause of disease in growing turkeys:
1. Infection with this virus is common as judged by serology - Figure 2 shows mean titre groups for groups of sera collected from commercial growers of different ages.
2. This virus is known to be immunosuppressive so it could well influence the response to other pathogens (Pierson, F.W. and Domermuth,1997).
3. Experience of the use of live HE vaccine in turkey growers suggest excellent protection against the disease but also generally improved liveability.
Since it has recently been shown that this virus commonly replicates in turkey kidney tissue (Trampel et al. 1992) there is the additional possibility that it may impact wet litter by a direct effect on the kidney.
|Figure 2. Mean Elisa titre groups (KPL kit) for commercial turkey growers by age.|
One of the objectives of this paper was to go beyond a simple description of the various diseases affecting the intestinal tract and consider how they might interact among one another and with other factors. The classical description of an infectious disease is based on a single pathogen which can be easily shown to reproduce the features of the disease simply by inoculating susceptible animals. This "simple" form of disease (Figure 3) is dealt with by diagnosis and specific prevention or treatment. As such classical diseases are effectively dealt with we are left with what are often described as "disease complexes". In the case of turkey enteritis and wet litter we can recognise microbial, nutritional and environmental factors.
|At least one very serious form of enteritis of complex aetiology has recently been described in the United States - "Poult Enteritis and Mortality Syndrome" or PEMS. This is a highly acute enteritis which has caused serious losses, mainly the south-eastern states, over the past few years, especially during the summer months. It affects poults mainly in their 3rd and 4th week of life. It can be readily reproduced by inoculating poults with intestinal contents of affected poults, but no single microbe has been found which fully reproduces this syndrome. It has recently been demonstrated that brooding temperature and litter moisture can strongly influence the outcome (Edens et al 1998). A large research effort has been mounted by the US industry in an attempt to find a solution for this problem. This may well provide useful information for the control of other intestinal diseases of turkeys.|
|Why do Turkeys Scour ?
We have seen that there are a multitude of potential causes. Before considering measures available for prevention and control we should ask ourselves "why are at least some outbreaks so explosive?". The most likely explanation, in my opinion, is that so well documented for enteric disease in a number of species (including man) faecal/oral transmission associated with deteriorating hygiene in a "positive feedback loop". What we mean by this is that, regardless of the initial cause of enteritis and diarrhoea, even if only in a small proportion of the flock, if the diarrhoea results in physically contaminated birds and, hence feeders and drinkers, a "vicious circle" can ensue. Infection or re-infection of a progressively increasing number of birds can lead to a "chain reaction" and a dramatic deterioration.
|...............||Prevention and Control
Given that we are likely to have limited success in getting our turkeys to "wash their hands after going to the toilet" we need to consider a range of control measures.
A. Hygiene : Dirty/Clean Barriers The application of basic biosecurity measures is basic to the control of a broad range of diseases, including those causing these problems. However it is not realistic to expect commercial poultry to be germ free. Potentially pathogenic bacteria will always be present, but the use of sound clean-out and isolation procedures can reduce the likelihood that they will result in clinical disease. Particular attention needs to be paid to feed and water syste.
B. Vaccination against Haemorrhagic Enteritis. Live vaccine for this disease is available in some other EU countries and was readily available in the UK under the "personal import" rules in 1996 and 1997. It will certainly not prevent all wet letter but it may be useful adjunct in the control programme. The British Veterinary Poultry Association has made strong representations to the Veterinary Medicines Directorate to facilitate the restoration of this product to the UK market as soon as possible.
C. Digestive Enhancement A range of compounds are currently licensed under EU feed additive regulations (Directive 70-524) which can have a significant impact on intestinal disease by the control of specific parasites (histamonas and coccidia) and by modulating the intestinal flora. In turkeys one of the anti-histamonas products and some of the anticoccidials have significant beneficial "side effects" in modulating intestinal flora. These compounds are not fed for the whole life of the bird and their removal my result in a transient change in the balance of the flora. The use of antimicrobials specifically approved for digestive enhancement aims to:
While the exact mechanism whereby this is achieved probably varies in detail among the various products, there is an extensive literature which demonstrates the benefits of these products for the general environment and the specific environment of the animals, through reduced faecal volume, litter moisture, gases.
D. Drinking water sanitation Given that nearly all turkeys will drink from bell-type drinkers which are relatively easily contaminated by house dust, the birds themselves and potentially litter and faeces, a programme of drinking water sanitation which achieves effective levels of approved sanitiser at the level of the drinker is likely to be beneficial. It should be kept in mind that inadequate sanitising may sometimes be as bad as or worse than not sanitising as it may encourage overgrowth of some particularly hardy bacteria such as Pseudomonas sp. If sanitising is introduced during the crop it is wise to gradually build up the level of active over a couple of days to reduce the risk of affecting water intake. Cleanliness and height management of the drinker is obviously equally important.
E. Nutrition: Ingredients/Programme Nutritionist's and feed manufacturers spend much time and effort in evaluating the formulation, and ingredient quality. No specific tests are available with which to predict an association between a specific ingredient of formulation and a wet litter problem.
F. pH - the "natural" defence? In the normal animal and bird the production of acid in the stomach, in addition to activating the digestive enzyme trypsin, exerts a sanitising effect on the ingesta. As shown in Table 3 below, not all bacteria will have the same sensitivity to low pH. Activity is likely to be dependent on the time during which the food resides in the crop (where pH is lowest).
|Reduced pH is a potential way of controlling microbial challenge. There is a limited amount of information available on the use of sodium bisulphite to acidify litter, for both broilers and turkeys. Little has been published on the subject of litter treatments in scientific journals. Reassurance would need to be sought on safety for farm staff, the poultry and the consumer. Acidification of feed, on the other hand, is widely practised, primarily to control contamination with Salmonella sp. The data presented in Figure 4 below was generated as part of a trial of a specific feed acidifier based on phosphoric acid in broiler chickens (Izat et al. 1990). These data nicely show that numbers of E.coli increase by a factor of 100 as we move from duodenum to ileum. The experiment demonstrated that counts throughout the small intestine could be reduced by a factor of 10 (1 log) by 0.4% or higher of the product. This was achieved in spite of no reduction in intestinal pH. This suggests that the decreased challenge was achieved by its effect in the feeder system or, perhaps in the upper GI tract (crop, proventriculus, gizzard). It should be kept in mind that it is possible to overdo the reduction in pH, - very low pH in inputs such as feed and water may reduce normal production of acid by the proventriculus.|
|...............||G. Competitive Exclusion The
administration of "normal adult caecal flora"
to young birds is commonly carried out as part of Salmonella
control programmes. Such products do not cause disease
and may well be beneficial in replacing pathogenic
strains of intestinal bacteria when used in combination
with effective programmes of cleaning and disinfections.
No programme is guaranteed to prevent all outbreaks of enteritis. If an acute scour occurs in turkeys over 6 weeks of age there is a definite risk that it will lead to a serious wet-litter problem with substantial welfare and economic effects. Prompt action to cut the cycle of contamination is urgently required. Typically this will involve correcting any management fault, re-littering, supplying heat and ventilation and sanitising drinkers and water. Some non-prescription treatments may be tried at the same time such as water acidification and perhaps the amino acid betaine. Some flocks may require medication with a suitable antibacterial product active within the intestine so early communication with your veterinary surgeon is vital.
A variety of pathogens can cause enteritis and wet litter in turkeys. Regardless of the initiating factors many cases end up as an acute bacterial enteritis/typhlitis, probably as a result of progressive deterioration of water and feed hygiene. Early diagnosis and concerted action can minimise the need for medication.
Thanks are to my colleague Keith Gooderham and our clients, and to ADAS and NFU for the kind invitation.
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