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This article was published in 1983
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Ovine Coccidiosis and Sulpha - Responsive Scours
P.J. Ahrens, B.V.Sc., Veterinary Inspector, MOLONG
OVINE COCCIDIOSIS - A CASE REPORT HISTORY
In September 1978 a group of 219 merino ewes 2-3 years of age was brought from Wilcannia in Western N.S.w. to a Molong property and depastured in a 37 hectare paddock of phalaris, sub-clover and ryegrass. Until 5 days previously the paddock had been stocked with local wethers at a stocking rate of 16 sheep per hectare.
Upon arrival (Day 1) the ewes were drenched with thiabendazole and vaccinated with 5-in-1 vaccine. On day 14 the owner increased the mob size to 291 by the addition of 72 homebred ewes.
Deaths commenced in the Wilcannia ewes on or before day 18 when 8 carcases were found in various states of decomposition. By day 20, when veterinary help was called, about 80 per cent of the Wilcannia awes, but none of the homebred ewes, were scouring and the mob was noticeably 'less frisky'. Quite a number of ewes showed evidence of fresh blood around the breech. The sheep were moved to a fresh paddock and by day 25, without any treatment, the owner said that the condition of the mob had improved substantially. The final mortality figure was 20. None of the homebred ewes were affected.
AUTOPSIES
On days 20 and 21, autopsies were carried out by I. Gardner, Veterinary Officer, Orange, and myself.
Specimens were submitted to the Veterinary Research Station, Glenfield.
1. One four-tooth ewe was unwilling to follow the mob, was depressed and showed cyanotic mucous membranes and fresh blood around the anus. It was destroyed by exsanguination. The major lesion was in the lower colon where pitting of the mucosa was associated with profuse free blood in the lumen mixed with mucus. Elsewhere, there was diffuse pallor of the liver, and congestion of the subcutaneous blood vessels and kidney cortex. The mesenteric lymph nodes showed no inflammatory response to the haemorrhagic colitis. No small intestine lesions were observed.
2. A ewe which died overnight and therefore showed slight decomposition, had haemorrhagic typhlitis as well as colitis. The colon wall was more friable than normal and there was marked congestion of the serosal blood vessels. In the caecum there were two areas of ulceration about 1.5 cm diameter with a haemorrhagic surface. The colonic mucosa generally exhibited the same pitting and erosion as in sheep 1 with petechial haemorrhages and blood effusion into the lumen. This lesion extended to the rectum. Again there was diffuse pallor of the liver, congestion of kidneys, heart and subcutaneous tissues and nil reaction in lymph nodes.
LABORATORY FINDING
The report from Glenfield indicated a diagnosis of coccidiosis. There were large numbers of coccidial forms, both schizonts and gametogonous stages in the thickened, oedematous mucosae of caecum, colon and rectum. In necrotic areas large numbers of filamentous bacteria had gathered presumably as secondary invaders of damaged mucous membrane - possibly Fusiformis necrophorum.
The kidneys of both sheep showed some tubule degeneration and deposition of a little calcified material in the collecting ducts along with focal dilation of proximal tubules. The medulla too was congested. There was diffuse cloudy degeneration of the liver. Haematology of two severely affected ewes showed haemoconcentration and in one case a leucocytosis.
Following receipt of the laboratory report, 17 faecal samples were sent to R.V.L. Armidale for identification of coccidial oocysts by A.R. Jackson. He reported low oocyst counts. Five out of 17 were negative and the highest count was 5,600 e.p.g. Six species were identified - Eimeria arloinga, E. ahsata, E. faurei, E. crandalis, E. parva and E. intricata, in quite mixed proportions. Jackson commented that the counts of oocysts were very much lower than might have been expected but the time interval of 4 weeks since the outbreak to the taking of the samples was probably the explanation.
DISCUSSION
One species which is missing from the above list, and which has a record of severe pathogenicity for the large bowel, is Eimeria - ninakohlyakimovae. Either this species was not present or an effective immunological response had eliminated it entirely from all 17 ewes sampled. The only other species known to cause colitis is Eimeria parva. (Pout D.D. and Catchpole J. 1974). According to histopathology finding gametogony was occurring in the colon.
Although coccidiosis presents many problems in diagnosis it seems likely in this case that coccidiosis was the cause of the outbreak and that one species, presumably E. parva, was not present in the Wilcannia environment where these awes had been bred. A substantial amount of E. parva contamination must have been left in the Molong paddock by the wethers which were there until 5 days previously and all ewes must have picked up a heavy infection in the first few days of grazing in their new environment.
Some predisposing causes such as the stress of transport and the dietary change may have influenced the situation in the first few days but would hardly have contributed to the severity of the outbreak at the time of first symptoms. Immune mechanisms rapidly came into play and the surviving sheep quickly threw off the attack.
Outbreaks of coccidiosis are rare in adult sheep but are not unknown. In lambs at pasture it is probable that most outbreaks occur before 10 weeks of age. In North America outbreaks have been reported in older lambs coming from range country into a feedlot system, symptoms occurring 12-16 days after arrival (Pout, 1969). Mortalities of 1-6% and morbidities of 10-40% have been ascribed by various authors to coccidiosis in lambs entering a feedlot, and mass medication with drugs such as sulphadimidine, nitrofurazone, amprolium or monensin, is frequently employed in feedlots to prevent such outbreaks. However there are very few studies indicating economic advantage in coccidiostats for sheep (Fitzgerald, 1980).
SULPHA RESPONSIVE SCOURS - A CASE REPORT HISTORY
In the severe drought conditions of November, 1982, a group of 120 merino weaners aged 7-8 months were being kept in good growing condition by hand feeding. A daily ration of oat grain and lucerne hay was being given in feed troughs placed in a 25 hectare paddock where the sheep could graze the remains of a failed wheat crop. 120 twelve month old hoggets had grazed the crop until 1 month previously when the merino lambs were weaned onto it. This was obviously not a good practice for parasite control but the season was such that parasitism was most unlikely.
Water was available in a dam which appeared to be reasonably clean. There had been no rain for some time.
SYMPTOMS
At 1 month after weaning the lambs began to scour. The owner observes his lambs very closely and normally expects this situation to respond to anthelmintic treatment. At 4-5 days after drenching, no response was evident. A week after drenching about 30 per cent of the weaners showed evidence of scour and over 50 percent had lost condition. The scour material was mid to dark brown in colour and varied in consistency from soft formed to thin fluid. Lambs with fluid scour may tend to strain or show exaggerated movements of the flanks. The quantity of faeces becomes less and less and tenesmus may be unproductive. These animals lose condition rapidly and become very hollow. There was often a high percentage of mucus in the scour material, and sometimes blood.
AUTOPSIES
One of the latter lambs was destroyed by exsanguination. A total worm count was carried out with essentially negative results. The mucosa of the caecum and colon was thickened and was covered in a copious mucoid secretion into which extensive capillary haemorrhage had occurred. Bowel contents otherwise were scanty. Faeces were fluid and bloodstained.
Grossly, no coccidial colonies were visible in the walls of the small or large intestine. Intestinal lymph nodes were not significantly enlarged. At parasitology no coccidial oocysts were seen in smears of mucosa or in faecal flotation. No strongyle eggs were found.
On my recommendation the owner drenched 60 lambs on two consecutive days with sulphadimidine at 120-140 mg/kg per day. However further cases developed in the untreated sheep and before these were treated another animal was autopsied, this time at the Regional Veterinary Laboratory, Orange.
The only lesion in this second animal was a moderate degree of 'tiger stripe' haemorrhage formation throughout the large bowel. The report notes that the gastrointestinal tract below the level of the abomasum was practically devoid of contents.
Faecal examination showed no strongyle eggs but there were occasional coccidial oocysts, but in such low numbers as to make a count not worthwhile.
Bacteriology showed no significant bacteria. Cultures were negative for Salmonella, and the intestinal contents at 3 sites showed only coliforms and diphtheroid (coryneform) bacteria. Haematology showed a minor leucocytosis (18.3 x 103 WBC). Histopathology demonstrated 'moderate' numbers of coccidial forms in various stages of development in ileum, caecum and colon.
TREATMENT
Response to oral sulphadimidine in these cases is invariably good. Because of the excellent response observed in the affected lambs, the owner in this case felt that all the lambs should have been treated to prevent an ongoing problem. (It has been traditionally my advice to treat only the affected animals, for 2 or 3 consecutive days.)
DISCUSSION
The criteria for diagnosis of ovine coccidiosis, are rather imprecise. Pout (1969) in a critical review of the disease explains the great difficulty in distinguishing between the state of parasitism and that of parasitic disease. He suggests that an imbalance of the host-parasite relationship is more often assumed than proven in scouring lambs, and even quotes some authors as suggesting that the response to sulphadimidine treatment in their cases was so striking that coccidiosis must have been responsible.
It is my view that the disease described in this report is not coccidiosis. Firstly the lambs were not introduced from another property and should long since have been exposed and become immune to all coccidial species on their home property. In lambs at pasture oocysts first appear in the faeces at two weeks of age and Jackson. (1983) believes the chances of coccidiosis disease occurring in lambs over 10 weeks of age is extremely remote.
Secondly, the oocyst count was very low. It is possible to have a negative oocyst count with acute coccidiosis such as that described in the first part of this paper but at 4-5 weeks after exposure to a contaminated environment there should be at least 100,000 oocysts per gram in some of the lambs. (Even then a diagnosis of coccidiosis is not confirmed. Glastonbury (1980) states that in sheep it is impossible to confirm a clinical diagnosis of coccidiosis by faecal oocyst counts because of the continual parasitism lambs normally undergo. Counts as high as 3,000,000 e.p.g. can sometimes be found in healthy lambs during normal oocyst 'showers').
A good description of the clinical and post-mortem findings in ovine coccidiosis is given by Irvine (1962).
'Sulpha-responsive scours' as an entity has not as yet been defined, although the condition has been recognised in the field for many years. Jackson (1983) considers there could be two forms, one of which tends to relapse after treatment. At this stage diagnosis is largely a matter of ruling out other possible causes of diarrhoea, if possible. It is therefore a negative rather than positive diagnosis, but the field veterinarian and the owner are satisfied if there is a good response to sulphonamide therapy. By definition, or rather by title at this stage, this response is essential, however, this factor had undoubtedly hampered attempts to understand the disease.
Numerous outbreaks of diarrhoea for which oral sulphadimidine was recommended occurred in the Molong district in the last 6 months. Most of them were just telephone consultations, but generally due to extreme drought conditions, drenching history and occasional faecal sampling, causes other than 'sulpha-responsive scours' seemed unlikely. Coccidiosis may have been possible in a few cases. Several owners reported later that the sulphadimidine treatment had worked well, while none reported failure of the treatment.
REFERENCES
Blood, Henderson and Radostits (1979). 'Veterinary Medicine' 5th Edit. Baillier Tindall p 738-744
Davies, Joyner and Kendall (1963) 'Coccidiosis'. Oliver & Boyd, p 69-79
Fitzgerald, P.R. (1980) Economic Impact of Coccidiosis'. Adv. Vet. Sci. Comp. Med. 24:121-143
Glastonbury, J.R.W. (1980) in Gastroenteric Conditions Seminar, Post-Graduate Vet.Sc. Refresher Course Proceedings No. 51, The University of Sydney p. 125
Irvine, H.J. (1962) 'Ovine Coccidiosis', Vet. Inspector N.S.W. 26: 61-65 See www.flockandherd.net.au
Jackson, A.R. (1983), Officer-in-Charge, Colin Blumer, Veterinary Laboratory, Dept. Agriculture, Armidale N.S.W. - personal communication
Munday, B.L. (1981) in 'Refresher Course on Sheep', Post-Graduate Vet. Sc. Proceedings No. 58. The University of Sydney, p.77
Pout, D.D. (1976) 'Coccidiosis of Sheep. A review.' Vet. Rec. 24:340
Pout, D.D. and Janet Catchpole (1974). 'Coccidiosis of Lambs. The Clinical Response to Long Term Infection with a Mixture of Different Species of Coccidia,' British Veterinary Journal 130:388-399
Pout, D.D. (1969) 'Coccidiosis of Sheep'. Vet. Bull. 39:609-617