Reports the major specific causes of sheep mortality in the Debre Berhan area between July 1986 and June 1987. Includes data on seasonal crude death rates, causes of mortality, frequency and age at death

Degefa, M.

Kasali, O.B.

Njau, B.C.

Scholtens, R.G.

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Field and laboratory studies of causes of sheep mortality in the Ethiopian highlands, 1986/87 B.C. NJAU, O. B. KASALI, R. G. SCHOLTENS and MESFIN DEGEFA  International Livestock Centre for Africa P.O.Box 5689, Addis Ababa, Ethiopia SUMMARY THE SPECIFIC causes of 99 deaths in sheep in Debre Berhan, Ethiopia, during 1986/87 were investigated. The highest mortality (43.4%) occurred in lambs younger than 1 month, and particularly within 3 days of birth. Neonatal losses were highest in the wet and late dry seasons, and were associated with the starvation-mismothering-exposure (SME) complex, dystocia and abomasal impaction. Coenuriasis was a prominent cause of mortality in adult sheep, occurring throughout the year. Both neonatal mortality and coenuriasis were major constraints to overall sheep productivity in the area. INTRODUCTION One thousand and twenty-five sheep died around ILCA's research station in Debre Berhan during 1982–86, representing an average annual loss of 256 animals, or 21.3 monthly (pp. 19–22 of thisBulletin issue). Fascioliasis, neonatal mortality and cerebral coenuriasis caused most of these losses. There was direct evidence that sheep died of fascioliasis and coenuriasis, but no conclusive evidence was found for the causes of the other deaths. Intensive surveillance of sheep flocks in Australia showed that neonatal lamb losses are the major constraint to the country's sheep industry. These losses were associated with genetic factors, severe deficiency of specific nutrients during pregnancy and after birth, predators, infections (both congenital and acquired after birth), aberrant maternal and neonatal behaviour, and injury to the central nervous system of the foetus at birth (Haughey, 1983). The survival of young lambs is essential to the success of sheep farming (Upton, 1985). Lack of data on the specific causes of many neonatal losses in Africa (Trail and Sacker, 1966; Wilson et al, 1985) impedes the prevention of neonatal mortality. Clinical, postmortem and laboratory examinations were used to identify the causes of sheep mortality in the Debre Berhan area between July 1986 and June 1987; this paper reports on the major specific causes found. METHODS The causes of sheep mortality in Debre Berhan during 1986/87 were investigated in six flocks with an average population of 726 sheep. The sheep were counted on the first day of each month and categorised according to age into three groups: <3 months old, 3–6 months old, and >6 months old. Deaths in the population and the ages of the dead sheep were also recorded. Dead sheep were examined within 24 hours post mortem. Sections of the lung, heart and liver were preserved in ice and submitted to the Veterinary Diagnostic Laboratory in Addis Ababa, Ethiopia, for bacterial isolation. Abortions and stillbirths were examined using the placenta and a sample of the contents of the foetal stomach. Routine histopathological investigation of such losses was carried out on tissues and portions of the afterbirth fixed in 10% buffered formalin. Aborting ewes were bled, and the plasma and/or serum were separated and screened for brucellosis at ILCA's laboratory. The deaths of neonates were distinguished as described by Eales et al (1983) and Haughey (1983): deaths within 3 days of birth were defined as perinatal while those after 3 days were defined as postnatal. Anteparturient death was indicated by the autolysis of organs and by blood-stained fluid in the serous cavities. Liver haemorrhages (including rupture), haemorrhagic meninges and partial lung expansion were used as criteria for parturient death. Postnatal death was indicated by full lung expansion, swellings on the foetal head (particularly the eyelids and mouth parts) or swollen limbs, shrivelled umbilical cord, and food in the stomach. The annual and seasonal crude death rates for the period July 1986/June 1987 were calculated as described on p.19 of this Bulletin issue. RESULTS The 99 sheep mortalities recorded between July 1986 and June 1987 represented an annual crude death rate of 13.6%. The seasonal crude death rates were highest in the wet (5.4%) and late dry seasons (3.8%) (Figure 1). Figure 1. Seasonal crude death rates for sheep around Debre Berhan, Ethiopia, July 1986–June 1987.  One third (33.3%) of the total deaths occurred in newborn lambs within 3 days of life (Table 1). Eight of these lambs had a low birth weight (<1 kg) and failed to suckle, seven had coarse plant and/or animal material in the abomasum, and five had ruptured and haemorrhagic livers. The remaining losses included three abortions, four stillbirths, three deaths resulting from profuse diarrhoea, one starvation due to mastitis, one mortality indicated by meningeal haemorrhages and one by swollen eyelids and mouth parts.     Table 1. Causes of sheep mortality, their frequency and age of animals at death, Debre Berhan, Ethiopia, July1986–June 1987. Cause  Frequency A ge (months) at death Number of deaths attributed to the cause Percent of total Average Range Perinatal losses 33 33.3 0.06 0.03–0.1 Coenuriasis 16 16.2 13.4 8.0–19.7 Abomasal impaction 9 9.1 1.0 0.3– 2.4 Pneumonia 7 7.1 15.8 0.3–45.2 Accidents 6 6.1 5.2 4.4– 7.2 Bloat 6 6.1 16.9 5.0–41.0 Gastro-intestinal parasites 6 6 1 5.2 0.8–14.6 Pulpy kidney disease 4 4.0 4.4 1.8-–1.3 Fascioliasis 3 3.0 17.2 6.0–32.5 Unknown 2 2.0 21.5 7.0–36.0 Swayback 2 2.0 5.9 0.6–11.3 Lactic acidosis 2 2.0 4.9 4.7–5.1 Congenital defect 1 1.0 0.5a n.a.b Diarrhoea (salmonellosis) 1 1.0 >50a n. a. Starvation 1 1.0 0.8a n. a. Total 99 100.0 n.a. n. a. a Individual ages. b n.a. = not applicable. Nine lambs (average age 0.98 months) died shortly after developing anorexia. The postmortem examination revealed that they had indigestible plant tissues and/ or hair impacted in the abomasum. These foreign materials were either free or mixed with putrefying milk curds which were sometimes firm and rubber-like and had black spots. Coenuriasis was diagnosed in 16 (16.2%) of the 99 dead sheep; the disease was a problem in all seasons. Pneumonia accounted for 7.1% of the deaths, while bloat, gastro-intestinal parasites and accidents were each associated with 6.1 % . Accidental death occurred in three lambs dosed with valbazine tablets and in two fed molasses; the sixth lamb was strangulated in a fence. Pulpy kidney disease (enterotoxemia) and fascioliasis caused 4.0 and 3.0% of the deaths respectively. Swayback, lactic acidosis, a congenital defect, diarrhoea, starvation and unknown causes were each associated with < 2% of the total deaths. One lamb had been born with a cleft palate (congenital defect) and died of milk-inhalation pneumonia 2 weeks after birth. Swayback was noticed in two lambs which died 3 months after birth. One of the lambs afflicted with swayback had large sections of the spinal cord abnormally soft (malacia), and its meninges were infiltrated with lymphocytes. The meninges contained sequestrated pinkish material enclosed by reactive astrocytes and giant cells, and the surrounding nervous tissues were atrophic. The lateral ventricles of the cerebrum were similarly infiltrated with lymphocytes and reactive astrocytes. These lesions were found also in the other lamb that succumbed to swayback, but were less severe. The copper concentration in the lambs' liver was 66.5 and 64.9 µg g 1respectively. Pasteurella multocida was isolated from the lungs of four of the six sheep whose infected lungs were examined bacteriologically. A histological examination of the lungs showed that their alveoli were filled with neutrophils and a few oat-streaming macrophages, while the interalveolar spaces were dilated with abundant fibrinous exudate. The lung of the seventh sheep suspected of succumbing to pneumonia had an adenomatous proliferation on the alveoli linings, which is suggestive of chronic progressive pneumonia. The lambs that died either peri- or post-natally had histologically normal lungs, spleen, livers and abomasal and intestinal walls. However, some had a few lymphocytes and neutrophils in the abomasal submucosa and the bronchi. Gram-negative coccobacilli were cultured from the abomasal contents of two aborted foeti, but no bacteria were isolated from a third foetus lost through abortion. Some lambs had gram-positive bacteria (rods) in the intestinal contents, and their kidneys underwent rapid autolysis. Both symptoms are suggestive of enterotoxemia type D. The most common gastro-intestinal parasites found were Ostertagia spp, Trichostrongy1us colubriformis, Haemonchus contortus, Trichuris ovis and tapeworm (Moniezta spp). One lamb which developed diarrhoea, alopecia and a potbelly, and finally died, had Moniezia expansa blocking the intestine. DISCUSSION During the 1986/87 study period, the average monthly sheep mortality around Debre Berhan was 8.3. Mortality was highest during the wet (July–September) and late dry (January–March) seasons, particularly in lambs up to 1 month of age (Figure 1). Perinatal mortality was the primary problem at the station; its relative frequency (33%) was comparable to that (22%) reported for sheep in Australia by Dalton (1979) and Haughey (1983). Trail and Sacker (1966) reported lower perinatal losses: 0.0–2.9% for indigenous sheep and 4.0–11.8% for crossbred East African Blackhead ewes. The highest rate, 11.8%, was observed in single lambs from crossbred gimmers. Both peri- and post-natal lamb losses occurred year round, with a peak during the late dry season. The primary causes of neonatal mortality were dystocia, anorexia caused by abomasal impaction with phytobezoar and/or trichobezoar, and diarrhoea. These causes collectively constitute the starvation-mismothering-exposure (SME) complex which is responsible for about 65% of perinatal lamb losses in Australia (Haughey, 1983). Other factors included in the SME complex are cold-induced starvation, abnormal behaviour of newborn lambs, inadequate milk supply and udder and teat abnormalities, all of which caused variable lamb losses in this study. The offspring of gimmers that suffered from dystocia at lambing had ruptured or patechiated livers (indicated by abdominal haemorrhages), and haemorrhagic lesions in the meninges, ureter(s) and the urinary bladder. According to Dalton (1979), dystocia is the main cause of perinatal mortality in lambs born as singles. Haughey (1983) reported that foetopelvic disproportion resulting from small maternal pelvis or foetal oversize, or both, is the main cause of injury at birth and subsequent death. This is indirectly supported by Trail and Sacker (1966) who found highest mortality (11.8%) among singles from crossbred East African Blackhead gimmers. Osuagwuh et al (1980) reported that 5.7% of the dystocia-associated lamb losses observed in their study occurred in outbred West African Dwarf sheep. The losses were attributed to the effects of the breeding sire and poor ewe nutrition during pregnancy. The first may have been a significant factor in our study, as mature rams were used for breeding while the age of gimmers at mating was not controlled. It is possible that the direct relationship that exists between birthweight (the key factor for lamb survival) and dystocia might favour increased lamb survival if the age at mating were controlled (Dalton, 1979). The frequent association between anorexia and abomasal impaction with phytobezoar or trichobezoar would indicate early exposure of the neonates to pathogenic agents; good hygiene in lambing pens is necessary to avoid this peril. In very young lambs, the foreign indigestible materials were either mixed among decomposing (black) milk curd, or they were present alone. Similar impactions were found in the stomach of older lambs (aged 1 month on average, Table 1). In these lambs, the indigestible materials were impacted in round, rubber-like coagulated milk curd of 2–5 cm in diameter. Coagulated milk has been found to block the pylorus, thereby causing abomasal impaction and sudden high mortality in neonatal and young buffaloes in Vietnam (Hall, 1962; Sharma et al, 1983). Sharma et al (1983) reported that high calf losses occurred especially in the hot–dry (26.3%) and hot-humid (78.7%) seasons. The black spots in the milk curd containing indigestible matter are indicative of bacterial rather than host-enzyme fermentation. In neonatal lambs, milk is delivered to the abomasum via the oesophageal groove which bypasses the rumen, thus avoiding bacterial fermentation (Church, 1984). However, since the abomasum of neonates is more developed than their forestomach, it is more accessible to dirty foreign bodies. Neonatal losses could be significantly reduced by maintaining neonates on good-quality pasture, thereby minimising the danger of such bodies being ingested. The failure to isolate microbial agents in lambs that died suddenly ruled out parasitic causes, as did histopathological examinations. It would thus appear that neonatal mortality in the study flocks was mainly due to complications caused by factors of the SME complex. The absence of inflammatory changes in tissues eliminated infections as a major cause of neonatal mortality, but it may also reflect certain unresponsiveness of the immature immune system to foreign antigens. Fascioliasis was a minor cause of sheep mortality during 1986/87, accounting for 3% of all deaths. Immature liver flukes (1.8–7 mm long) were recovered from three sheep that died in January 1987; some of the flukes protruded from ruptures in the liver capsule, while a few others were in the peritoneal cavity, the lung, the kidney and the pancreas. Their number in the hosts varied from 9 to 17. Schillhorn Van Veen (1979), Schillhorn Van Veen et al (1980) and Jacinta (1983) found more than 100 flukes in similarly ruptured livers, and Reinecke (1983) reported that as few as 60 flukes can seriously damage the liver capsule and cause acute death. According to Hanna (1976), the presence of flukes of the size found in this study indicates a 4–6 week-old infection. Reinecke (1983) reported that acute fascioliasis occurs in sheep within 4–6 weeks of ingesting infective flukes. The decreased significance of fascioliasis as a cause of sheep mortality in Debre Berhan in 1986/87 is probably due to the rigorous fluke control measures introduced in March 1986. These involved preventive treatment every 3 months, adjusting the stocking rate, and confining animals during the rainy season when fluke incidence is high. Hosie (1985) reported that during the rainy season, sheep rarely frequent potential snail habitats in the bottomlands, because sufficient feed and water are available elsewhere. Confining animals in this season may not therefore be necessary to control fascioliasis. CONCLUSION This study proved that neonatal lamb losses and coenuriasis are serious problems in the sheep flocks around Debre Berhan. While enough is known to control coenuriasis (Karim, 1979; Skerritt and Stallbaumer, 1984), this is not true for neonatal mortality (Trail and Sacker, 1966; Eales et al, 1983). Hence neonatal lamb losses will continue to pose problems for sheep husbandry. Accidents, gastro-intestinal parasitism, dystocia, predation, congenital defects, swayback, pneumonia, bloat, enterotoxemia and lactic acidosis occurred rarely and caused minor losses. Trail and Sacker (1966), Eales et al (1983) and Haughey (1983) reported that 21.0-38.5% of neonatal losses occur between birth and weaning at 6 months of age. Losses of this magnitude negate efforts to increase ovulation rate and conception (Dalton, 1979), as well as gains obtainable through selection. Veterinary care of neonates is therefore indispensable for profitable sheep farming (Eales et al, 1983; Haughey, 1983). To reduce lamb losses, special attention must also be given to the nutrition of ewes before the onset of heat, the management of lambing ewes, the diagnosis and treatment of hypothermia, and the management of 2–7 day-old lambs. In addition, prompt diagnosis and treatment of perinatal conditions are imperative. REFERENCES Church D C. 1984. The gastro-intestinal tract and nutrient utilisation. In: D C Church (ed.), Livestock feeds and feeding. 2nd edition. O & B Books, Oregon, USA. Dalton D C. 1979. Sources of perinatal mortality. In: Proceedings of the 29th Lincoln College Farmers' Conference, 19–21 May 1979. Lincoln College of Agriculture, Canterbury, New Zealand. Eales F A, Small J and Gilmour J J. 1983. Neonatal mortality of lambs and its causes. In: W Haresign (ed.), Sheep production. Butterworths, London. pp. 289–298. Hall S A. 1962. Gastric dyspepsia in calves. Veterinary Record 74:814–816. Hanna R E B. 1976. Ovine fascioliasis. Research in Veterinary Science 21:244–246. Haughey K C. 1983. New insights into rearing failure and perinatal lamb mortality. Sheep production and preventive medicine. Proceedings No. 67, University of Sydney, Australia. pp. 135–147. Hosie B D. 1985. Use of anthelmintics to control fascioliasis. Tropical Animal Health Production 17:248–251. Jacinta E. 1983. Investigations on fascioliasis in the Ethiopian highlands around Debre Berhan. M.Sc. thesis, Institute of Tropical Medicine and Parasitology, Leiden University, The Netherlands. Karim M A. 1979. A survey of coenuriasis in sheep in northern Iraq. Tropical Animal Health and Production 11:157–158. Osuagwuh A I A, Taiwo B B A and Ngere L O. 1980. Incidence of dystocia and parturition losses. Tropical Animal Health and Production 12:85–89. Reinecke R K. 1983. Fasciolidae. In: R K Reinecke (ed.), Veterinary Helminthology. Butterworths, Durban, South Africa. pp. 256–257. Schillhorn Van Veen T W. 1979. Ovine fascioliasis (Fasciola gigantica) on the Ahmadu Bello University farm. Tropical Animal Health and Production 12:97–104. Schillhorn Van Veen T W, Folaranmi D O B, Usman S and Isheya T. 1980. Tropical Animal Health and Production 12:97–104. Sharma M C, Pathak N N, Hung N N, Vuc N V. 1983. Abomasal milk impaction: An emerging disease of buffalo calves. Indian Journal of Veterinary Medicine 3:117–119. Skerritt G C and Stallbaumer M F. 1984. Diagnosis and treatment of coenuriasis (gid) in sheep. Veterinary Record 115:399–403. Trail J M C and Sacker G D. 1966. Production records of lambs from East African Blackhead ewes and Dorset Horn rams. East African Agricultural and Forestry Journal 332(2):133–136. Upton M. 1985. Models of improved production systems for small ruminants. In: J E Sumberg and K Cassaday (eds), Sheep and goats in humid West Africa. Proceedings of the workshop on small ruminant production systems in the humid zone of West Africa, held in Ibadan, Nigeria, 23–26 January 1984. ILCA, Addis Ababa. Wilson R T, Traore A, Peacock C P, Mack S and Agyemang K. 1985. Early mortality of lambs in African traditional livestock production systems. Veterinary Research Communications 9:295–301.  

Field and laboratory studies of causes of sheep mortality in the Ethiopian highlands, 1986/87

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Field and laboratory studies of causes of sheep mortality in the Ethiopian highlands, 1986/87

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