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This article was published in 1978
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Enteropathies in the Post Weaned Pig
R.I. Walker, B.V.Sc., Veterinary Inspector, Young
INTRODUCTION
While my topic indicated in the programme is 'Enteritis in Pigs' I do not wish to, certainly would not have the scope to cover that entire subject.
Instead I will restrict my talk to various enteropathies in the post weaned pigs which are known, in the literature at least, as Necrotic Enteritis (NE), Regional Ileitis (RI) Porcine Intestinal Adenomatosis (PIA) and Proliferative Haemorrhagic Enteropathy (PHE) the last one being only recently documented in Australia (Love et al.). For the purposes of discussion I will mention also Swine Dysentery by way of comparison.
The subject is confusing and although inexpert in this field I hope to clarify certain features of these diseases.
As field veterinarians, we have an opportunity of seeing quite a range of diseases, for which our clients hope we can give them a name and a cure. In most cases we can do just that but when it is obvious from the stunned look on his face that he has no comprehension of the name, you realise very quickly it is more important to tell him what do to about it. What hope of success would we have with those names above. What I hope we can do is clarify what you are likely to see in the field when confronted with an enteropathy and what you can offer the owner as a treatment.
Enteritis in the pig is a common ailment whether it be in a back yard, shanty town or an elaborate intensive housing estate.
Enteropathies in the post weaned pig are certainly common in many establishments and even though the names are new, even when coded in symbols, the diseases they describe are not and I presume many of you have seen them albeit by other names. Researchers now inform us that, with the exception of Swine Dysentery the others are related by common aetiology. The confusion is enhanced however when we try to translate these facts to the field situation. We will ultimately be dependent on pathologists in many cases to give a diagnosis or failing that a meaningful histopathology report which doesn't read like a page from Black's Veterinary Dictionary. I hope you will bear with me as I describe these diseases, in a way that will hopefully give you a head start when a report is received from the laboratory. Once those are explained, an understanding of the relationships and the epidemiology should give you an idea what to recommend as a treatment.
Lets mention Swine Dysentery first by way of comparison with this other group.
1. Swine Dysentery
This was formerly known by various names, including Vibrionic Dysentery, and associated with various aetiological agents. The causal agents are now known to be Campylobacter coli (formerly Vibrio coli) and a spirochaeta Treponoma hyodysenteriae. It is typically a disease of the large bowel with the small intestine only very rarely involved. The disease affects pigs between 8-14 weeks and severity can be measured by a mortality rate as high as 50%.
Clinically - the disease is recognised by a sudden onset of diarrhoea or by the finding of a dead pig, without presenting any clinical signs. Diarrhoea of 1-2 days standing will contain a variable amount of blood. Such pigs become dejected, dehydrated, with sunken eyes and tucked up abdomen. Cases which become chronic show a persistent mild diarrhoea for up to a month. Relapses in recovered pigs are common.
Port mortem - Early lesions are found in the coiled colon and the contents are grey to yellow. As the dysentery progresses the contents become reddish brown to black with deep congestion and thickening of the mucosa. There is only superficial loss of epithelium of the mucosa. Some inflammation of the stomach has been recorded by Jubb and Kennedy. Quite ofter one can see nodules in the wall of the caecum and colon which are Spirochaetal bowel nodules, and resemble 'pimply gut' lesions in sheep.
Treatment - While there are many treatments, it is probable that no one treatment is completely efficient.
Organic arsenicals have been used for some years now, viz Arsanilic Acid at 250 ppm for a short period, which can be reduced to some 150-180 ppm for a longer time depending upon the appearance of the 'drunken sailor' type syndrome noting the onset of toxicity to Arsanilic Acid (Progen - Abbott).
Other chemicals in use are Streptomycin (0.5 - 2.0 g/pig) daily for 2-5 days in the drinking water; Bacitracin 100,000 units per os daily for 6 days; Chlortetracycline at 45 mg/kg daily for 3-5 days per os; Tylosin at 200 mg per pig by injection or 1.0 grams/gallon of water for 3 days.
Nitrofurazone - 15 grams in 40 gals water given over 5-7 days and Furazolidone at 2.0 - 2.5 Kg/tonne have been used also.
Carbadox - 50 gm/Ton for a prolonged period have also eliminated the condition.
Ronidazole (MS&D).
Swine Dysentery must however be regarded as an enzootic disease.
2. Porcine Intestinal Adenomatosis (PIA)
In 1972 Rowland and Rowntree working with the Haemorrhagic Bowel Syndrome found that survivors from this disease, affecting only the ileum and not the caecum and colon, had a very poor growth rate which was indicated only by a poor appetite. Pathology studies of such pigs revealed the wall of the ileum to be thickened and there was subserosal oedema. The mucosa was thrown into folds not unlike Johne's Disease. There was some involvement of the upper third of the coiled colon and included the caecum. These lesions were called Intestinal Adenomatosis which can best be summarised as a transient proliferation of the intestinal mucosa of the weaned pig and resembling a transient neoplasm.
In 1974 Lawson and Rowland observed and isolated from such lesions an organism which they called Campylobacter sputorum, subspecies mucosalis. This organism has not been isolated from normal intestinal mucosa.
It is inferred that these organisms may be intracytoplasmic, or at least, that part of their action is in this site.
In PIA the epithelial cells are immature and deprived of their protective mucous coat and in this state are more susceptible to bacterial or protozoal challenge. The researchers explain that the logical sequence of events is in most cases that Necrotic Enteritis and Regional Ileitis develop from PIA, The organism (Campylobacter sputorum sp. mucosalis) does not occur in Swine Dysentery and does not occur in normal pigs, but it is found in NE, RI and now recently in PHE which we will mention later. (Rowland and Lawson 1975).
3. Necrotic Enteritis
Using the description of Jubb and Kennedy we find that necrotic enteritis (diphtheritic enteritis) is a bacterial disease a form of necro-bacillosis (Fusiformis necrophorus) which is predisposed by other bacterial inflammations, (viz Salmonellosis and Swine Dysentery) of the intestine and that these in turn may be predisposed to by dietary and sanitary inadequacies.
By this definition we are restricting the lesions to the small intestine only and while I don't have any pictures or slides to accompany the paper, I would refer you to good photographs in articles by Rowland and Rowntree (1972) and Rowland and Lawson (1975).
The distribution of necrotic enteritis closely corresponds to the stress of PIA. The affected mucosa is replaced by grey / yellow necrotic zone (ileum) which is commonly deeply fissured. The surface often shows attached food particles.
Histologically the lesion consists of coagulative necrosis with an inflammatory response in the underlying tissue which varies from acute exudation to substantial granulation tissue proliferation.
More recently, workers (Roberts, Rowland and Lawson 1977) have experimentally reproduced PIA and NE by dosing 18 hour old pigs with C. sputorum and homogenised adenomatous mucosa. Pigs killed at around 53-59 days showed PIA and NE and had gained weight poorly.
4. Regional Ileitis
In this disease the lower ileum becomes thickened, firm and almost rigid and the term 'hosepipe gut' is descriptive. The submucosa showed granulation tissue extending to the muscle coats which were substantially hypertrophied. Being connected to PIA by aetiology it is possible to get a range of this type of extensive adenomatous change. It is in effect a functional obstruction.
5. Proliferative Haemorrhagic Enteropathy (PHE)
In 1972 Rowland and Rowntree described the Haemorrhagic Bowel Syndrome, known now as PHE, in a group of 54 pigs of all ages of which 7 died, followed by a fall in growth rate in survivors and unaffected pigs in the 6-16 week old age group. It was (an) episode that lasted 4 months and did not recur.
Clinically a haemorrhagic diarrhoea was seen even in adult pigs. Pathology on the affected pigs showed deep congestion in the ileum with massive frank haemorrhage into the lumen and subsequent clotting. Haemorrhage did not develop from the wall of the large intestine, which was largely normal.
It is not until a recent report by Robert Love, a former V.I. at Condobolin and his wife associated with Marsh Edwards, of PHE in an intensive piggery that the magnitude and seriousness of this disease and probably the whole group is realised.
An outbreak occurred in two episodes which affected 372 adult pigs in the breeding units of a minimal disease piggery. 186 pigs died. The second episode was restricted only to pigs which entered the breeding units.
More importantly, these workers isolated Campylobacter sputorum subsp mucosalis from the affected mucosa and confirmed the & association with PIA, that Rowland and Rowntree had proposed.
Morbidity rates of about 22 per cent of the breeding herd were recorded, and of these affected animals, 45-50% mortality; irrespective of age, was seen.
Epidemiology is detailed in this paper (Love et al. 1977) and I refer you to that for precise details.
What was seen clinically was that the pigs were frequently found dead, without having shown any premonitory signs. Affected pigs were usually inappetent.
Degree of dysentery was varied, but was usually profuse, watery, black and foul-smelling. Death occurred in 8-24 hours after the onset of dysentery.
Gross Pathology once again involved only the small intestine (terminal ileum for 3-4 metres). The ileum contained blood stained fluid or large blood clots contoured to the mucosal folds. Bacteria were found in the cytoplasm of glandular epithelial cells, resembling C. sputorum.
Epidemiology and Treatment
As far as we are concerned it is interesting to look at this latter example for the epidemiology and the treatment instituted, as far as PHE is concerned and possibly in relation also to NC, RI and PIA.
The first regime of treatment was given to all breeding units of Tylosin and Sulphadimidine (100 grams/ton of feed of each drug) was successful within three days when new cases ceased appearing. This combination was used for 2-3 weeks.
Another treatment regime was ASP 250 Cyanamid (Chlortetracycline sulphadimidine - penicillin) and used in the same manner with the same results.
Treatment, using antibiotics in the feed for adult pigs, was instituted when it was realised that the grower pigs, in which PHE did not occur, were fed on a ration using an antibiotic mixture as a growth promotant. It was only when pigs on this ration were transferred to the breeding units which weren't on medicated feed that the condition developed.
As this situation is now the accepted procedure in all intensive piggeries, i.e. medication of grower feed at least to the level of growth promotants, it is worthwhile keeping this observation in mind when considering an outbreak of diseases in this group, i.e. young pigs may be protected until such time as they are placed onto unmedicated feed.
Another angle on the control of PHE comes from epidemiological studies. Selected gilts and boars from the grower shed were placed onto medicated feed. This allowed for a controlled infection but medication introduced during the incubation period would prevent the progression of the disease. From the above study extension of the exposure period past 21 days greatly increased the risk of pigs developing PHE. Controlled infection will however only substantially reduce the incidence of the disease and not completely eliminate it.
With these brief discussions on Swine Dysentery and the PIA group and the positive treatments through antibiotics and through epidemiology it should be possible to differentiate the cause on gross pathology and clinical signs and institute control measures. These are more likely to succeed however in the intensively housed piggeries, but the same measures may be adopted in less organised piggeries to reduce losses where economically feasible.
What these enteropathies emphasise is the need for good data from the piggeries and the closeness we need to foster to the total pig production enterprise.
REFERENCES
O'Neil, P.A. (1970) Vet. Rec. 87:742-747
Rowland, A. & Rowntree, P.G.M., (1972) Vet. Rec. 91:235-241
Rowntree, P.G.M., (1972) Vet. Rec. 91:347
O'Hara, P.J., (1972) Vet. Rec. 91:517
Redman Chu, R.M. & Hong, C.B., (1973) Vet. Rec. 93:563
Rowland, A.C. & Lawson, G.H.K. (1975) Vet. Rec. 97:178-180
Roberts, L., Rowland A.C. & Lawson, G.H.K. (1977) Vet. Rec. 100:12
Love, R.J., Love, D.N. & Edwards, M.J. (1977) Vet. Rec. 100:65-68
Love, R.J. & Love, D.N. (1977) Vet. Rec. 100:473
Love, D.N., Love R.J. & Bailey M., (1977) Vet. Rec. 101:407
Jubb, K.V.F. & Kennedy P.C. (1970) Pathology of Domestic Animals. Vol. 2
Lawson, G.H.K. & Rowland, A.C. (1974) Res. Vet. Sci. 17:331
Rowland, A.C., & Lawson G.H.K., (1974) Res. Vet. Sci. 17:323
Edwards M.J. (1973) Proceedings No. 20 - Post Grad. Foundation - Pig Diseases
Taylor, D.J. (1976) Vet. Rec. 99:453-456 - Ronidazole for Swine Dysentery.