Flock and Herd logo

ARCHIVE FILE


This article was published in 1962
See the original document

INSTITUTE OF INSPECTORS OF STOCK OF N.S.W. YEAR BOOK.

Ovine Coccidiosis

J. H. IRVINE, B.V.Sc, Veterinary Inspector, Bathurst

INTRODUCTION

In the past it has been maintained by many Australian authorities that in this country Ovine Coccidiosis is a disease of no practical importance; due, it is claimed, to the conditions under which sheep are grazed here as compared with those existing in Europe and U.S.A.

In overseas countries sheep frequently are crowded into small enclosures, often for long periods. It iso has been suggested that outbreaks are likely to occur only under conditions of poor hygiene and where paddocks are overstocked for long periods, and during wet weather. Seddon (1952), however, has expressed the opinion that the incidence of this disease is probably higher than generally realised, since it is confused not infrequently with Trichostrongylosis.

This statement is not surprising, as on clinical grounds alone it is difficult to differentiate Coccidiosis from either Trichostrongylosis or Nematodiriasis. Further, the conditions under which serious out breaks of Coccidiosis in sheep have been encountered are similar to those under which outbreaks of the latter two diseases might be expected. Often, too, worm infestation and Coccidiosis may go hand in hand and the effects of the latter be overlooked.

INCIDENCE

Walker (1958) appears to have been the first to record the condition as occurring in any proportion in N.S.W.

Over recent years a total of more than 20 outbreaks of Ovine Coccidiosis has been investigated in the Bathurst P.P. District. In 1960 this disease was particularly prevalent, being diagnosed in most areas of the District. Although Seddon (1952) states that pathogenic effects have been observed only in lambs and weaners, several outbreaks of Coccidiosis have been seen in adult sheep. The latter were sheep only recently introduced from the Western Division.

AETIOLOGY

It is well known that most sheep harbour Coccidia and that they may be present in fairly large numbers in apparently healthy lambs. It appears, however, that the clinical disease develops only when conditions favouring a massive invasion of susceptible sheep prevail.

There are at least nine species of Coccidia capable of infecting sheep and mixed infections, with two or more species are the rule, rather than the exception.

There appears to be a general consensus of opinion that E. arloingi is one of the most pathogenic species. Unfortunately, there has been little work done with artificial infections with pure strains. Lotze (1952 and 1953) reported on the pathogenicity of pure strains of E . arloingi and E. ninae-kohl-yakimovi in experimentally induced infections in lambs. The pathological picture in the two infections was quite different.

PATHOGENESIS

The life history of E. arloingi is probably typical of that of the remaining species of Coccidia found in sheep. Infection arises from ingestion of sporulated oocysts from which the sporozoites are liberated within the small intestine. The sporozoites invade the endothelial cells lining the central lacteals of the villi and it is within these cells that the schizonts are formed. There is only one generation of schizonts; producing enormous numbers of merozoites which invade the epithelial cells and in turn differentiate into microgametocytes and macrogametocytes. The fusion of these gametocytes produces the oocyst, which is discharged in the faeces in not less than twenty (20) days following infection.

E. arloingi destroys many cells besides these parasitised by it. During the course of development of the schizonts within the central lacteals of the villi, the latter become enormously distended, lose their epithelial covering and eventually disintegrate. As a consequence of maturation of schizonts and the release of merozoites, severe reactions follow. The wall of the small intestine becomes oedematous and thickened. Associated with this oedema is the development of diarrhoea. Invasion of the epithelial cells by the merozoites leads to their eventual rupture, with consequent exfoliation of the epithelial lining of the mucosa.

Experimental work by Lotze (1952) suggests that less damage is done by the sexual stages than the asexual, as he found the condition of an infected animal tends to improve before oocysts are excreted.

CLINICAL

The first symptom is the sudden onset of severe diarrhoea, which is fluid and foul-smelling. The faeces are usually a dark brown, or chocolate colour. They may contain mucus, but rarely blood. In only isolated instances has blood been seen in the faces in outbreaks investigated. The condition at first may be seen in only an odd animal, but within a few days a large number of the flock is affected. Severe straining is characteristic of the diarrhoea, often unaccompanied by the passage of faeces. The latter are much more fluid in character than is usually the case in outbreaks of Nematodiriasis or Trichostrongylosis and the straining is so severe that often they are evacuated in projectile fashion, shooting out 12 inches or more. Pressure on the abdomen, as when catching an animal will, in acute cases, produce this effect. There is abdominal pain, inappetence and dullness. The flanks hollow within a few days and the animal soon tucks up. There is rapid loss of condition and wasting, which may proceed to extreme weakness and death.

In young lambs, death may eventuate within four to five days of the onset of diarrhoea. Anaemia is seen only in the more severely affected cases, and in chronic cases of long standing. In most outbreaks it is quite common to find scours abating in some animals and just starting in others. The mortality rate usually is not high, but there are exceptions - in one outbreak involving two hundred and fifty (250) Merino lambs, aged 3-10 weeks, 75 lambs died over a period of one month. The mortality was checked by treatment, but the remainder of the flock never recovered properly and subsequent worm infestation accounted for a further fifty (50) deaths over the ensuing months in spite of drenching and good feed. When seen as weaners they were still a miserable lot, stunted and unthrifty.

In another outbreak involving three hundred and fifty crossbred lambs, 2-8 weeks old, thirty seven (37) were lost within seven days. This flock was more fortunate in that treatment checked the mortality almost immediately and infected lambs made an uneventful recovery. Climatic conditions may have exercised an influence here.

In a flock the course of the disease appears to be governed by a number of factors:—

(a) Age of sheep: Heavy mortality which can be attributed directly to Coccidiosis has been seen only in lambs under three (3) months.

(b) Plane of nutrition: Where the plane of nutrition is high, the condition mostly clears up spontaneously within 1-3 weeks.

(c) Climatic conditions: Naturally, when weather conditions are severe the mortality rate in badly affected lambs is increased.

(d) A concurrent helminthosis.

AUTOPSY

Examination of the small intestine will reveal usually a catarrhal enteritis, which is often patchy. The mucous membrane is mostly covered by a dirty white or greyish exudate, especially over the first 5-10 feet; the mucous membrane in this region having a furry or velvety appearance. The wall of the small intestine is thickened throughout its length, sometimes markedly so, and the mucous may show corrugations, or more often longitudinal ridging.

The predominant lesions are seen in the mucosal surface of the small intestine as large numbers of well defined, slightly raised, dirty white spots, or patches; varying in size from pinpoint lesions, just visible to the naked eye, up to quite large lesions, approximately 7 mm. in diameter. The larger patches have a rather irregular outline, whilst the smaller lesions are roughly circular. All but the smallest lesions can be seen from the serosal surface prior to opening the intestine. These spots or patches are comprised of groups of enlarged villi containing enormous numbers of macrogametocytes and oocysts, which can be seen readily in simple smears. Some of the pinpoint spots undoubtedly are enlarged villi containing schizonts.

Together with the above, in all of the more serious outbreaks papilliform-like growths have been observed in the small intestine. These are quite firm and fleshy and can be felt readily through the wall of the intact gut. In some cases, these lesions are numerous. They have not been seen in the first few feet of the small intestine, but become more numerous as the terminal part of the gut is approached. Usually their size varies from 3-5 mm. in diameter, but in one lamb lesions of this type were so large and numerous as almost to obliterate (in places) the lumen of the bowel. Although most writers refer to these tumour-like masses as being pedunculated, it has been only in the case just mentioned that this characteristic has been seen. Generally, these lesions are of a pale pink colour and have been observed to have a well attached base. They result from hyperplasia of the mucous membrane, including both the villi and the glandular stratum.

The epithelial cells in these tumours contain coccidial parasites at various stages of development.

Frequently, tiny erosions can be seen in the mucosa of the small intestine and it seems probable that these result from disintegration of villi following maturation of schizonts.

In a few cases examined, the wall of the colon has shown marked thickening and sometimes erosions. It is noted that in respect of this Lotze (1953) and Becklund (1957) both reported involvement of the large intestine in infections with E. ninae-kohl-yakimovi.

The mesenteric lymph nodes are always grossly enlarged and juicy.

TREATMENT AND CONTROL

In some of the more severe outbreaks investigated, treatment with sulphamezathine at the dose rate of 1 gm. per 15 lb. body weight daily for 3 days has checked losses sharply and resulted in the improvement of infected sheep. However, in less serious outbreaks, which usually run a short course, it was found generally that by the time treatment was instigated, untreated sheep in the same flock already were showing signs of recovery.

Unfortunately, at present very little is known of the epidemiology of Coccidiosis in grazing lambs and it is impossible to predict outbreaks. Seddon (1952) claims that the disease is most common during the winter months and that it is associated often with poor feed and cold, wet weather conditions. Outbreaks have been recorded here at most periods of the year, but generally have been far more severe during the winter months. It has been noted that where the disease has been experienced on a property, a recurrence may be anticipated in some future year.

It is doubtful if rotational grazing will have any effect in controlling or preventing Coccidiosis. In wet, cool situations, oocysts may accumulate and remain viable for many months, Moist, temperate or cold conditions favour sporulation, whereas dryness impedes it. Under dry conditions and at high temperatures, oocysts are destroyed within a few weeks. At an optimum temperature of 20-25 deg. C. and under moist conditions oocysts sporulate in 2-3 days.

DISCUSSION

Experience in this area would suggest that Ovine Coccidiosis is becoming of increasing economic importance. It is primarily a disease of lambs, but adult sheep may be affected; particularly susceptible sheep introduced from the Western Division. Although, as indicated by the losses incurred in some outbreaks involving young lambs, it can be directly responsible for heavy mortality, this is not usually the case and its economic importance lies mainly in its high morbidity rate. The growth and rate of weight gain in young sheep may be checked temporarily and their resistance to helminth parasites greatly reduced. To the fat lamb producer any check of this nature to his lambs is of paramount importance, and it well may result in inability to market them as prime fats.

To date, with one exception, all outbreaks seen have occurred on well improved pastures only, where of course the rate of stocking is high. The exception occurred on a property where to protect his lambs from predators, the owner regularly yarded ewes and lambs overnight in sheep yards. Wet weather conditions prevailed at the time.

Infection, and also rapid multiplication of Coccidia, is promoted by conditions likely to lower the resistance of sheep; such as poor milk supply, helminthosis and insufficient feed. It has been observed in outbreaks in fat lambs that if the quality of the pastures is good and the lambs are maintained free from worms, the check resulting from Coccidiosis is not serious. However, if the feed is going off, or worms are allowed to gain a hold, the consequences may be disastrous. The presence of oocysts, even in moderately large numbers, in the absence of symptoms does not justify a clinical diagnosis of Coccidiosis. Individuals may show a high oocyst output due to non-pathogenic species of Coccidia, On the other hand, a consideration of the life cycle of E. arloingi makes it clear that symptoms of acute Coccidiosis may develop before oocyst production has commenced.

Diagnosis should be based largely on symptoms and the finding at autopay of large numbers of the white coccidial spots, or patches The finding of a few scattered spots cannot be regarded as grounds for a positive diagnosis, as odd lesions of this type are seen frequently in the gut of healthy sheep.

In the absence of suitable post-mortem specimens it is considered that diagnosis on a flock basis may be made on the presence of a fluid, foetid diarrhoea affecting a high percentage of the flock; and the finding in the faeces, of a reasonable sample of the mob, of a very large number of oocysts.

References

  1. Becker, E. R., (1948) — "Diseases of Poultry": The Iowa State College Press. Ames, Iowa, U.S.A.
  2. Becklund, W. W., (1957) — N. Amer. Vet., 38: 262
  3. Belschner, H. G., (1953) — "Sheep Management and Diseases": Angus & Robertson, Sydney
  4. Blood, D. C. and Henderson. J. A., (1960) — "Veterinary Medicine" Bailliere, Tindall and Cox, London
  5. Christensen, J. F. (1938) — Journ. Parasit., 24: 5: 453
  6. Dunlop, J. S., Hawkins, P. A. and Nelson, R. H., (1949) — Annals of the N.Y. Academy of Sciences, 52: 505
  7. Foster, A. O., (1949) — Annals of N.Y. Academy of Sciences, 52: 410
  8. Gaiger and Davies (1955) — "Veterinary Pathology and Bacteriology"; Bailliere, Tindall and Cox, London
  9. Hagan and Bruner (1951) — "The Infectious Diseases of Domestic Animals"; Comstock Publishing Associates, Ithaca, New York
  10. Hart, L. (1939) — Aust. vet. J., 15: 30
  11. Lotze, J. C., (1952) — Cornell Vet., 42: 510
  12. Lotze, J. C., (1953) — Am. J. vet. Res., 14: 86
  13. Robertson, J. G., (1953) — Vet. Rec., 65: 183
  14. Salisbury, R. M., and Whitten, L. K., (1953) — N.Z. vet. J., 1: 69
  15. Seddon. H. R. (1952) — "Diseases of Domestic Animals in Australia, Part 4": Service Publication (Division of Veterinary Hygiene) Number 8. Department of Health, Canberra
  16. Thomson, J. G., and Hall, G. N. (1931) — Journ. Trop. Med. and Hyg., 34: 22; 369
  17. Walker, D. J., (1958) — Vet. Insp., pp. 27
  18. Whitten. L. R. (1956) — N.Z. vet. J., 4: 25

Site contents Copyright 2006-2026©