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Challenging cases in small ruminant medicine (Proceedings)


Small ruminants constitute a rewarding component of a mixed or rural veterinary practice. In such practice scenarios, certain common medical disorders of small ruminants may be encountered on a fairly regular basis. The following cases are valuable teaching cases because they involve differential diagnoses that are commonly encountered in small ruminant practice.

Small ruminants constitute a rewarding component of a mixed or rural veterinary practice. In such practice scenarios, certain common medical disorders of small ruminants may be encountered on a fairly regular basis. The following cases are valuable teaching cases because they involve differential diagnoses that are commonly encountered in small ruminant practice.

Case 1. Weight loss in adult sheep

In March of 1998, two adult, crossbred ewes were presented for evaluation of thin body condition that was unresponsive to dietary changes and anthelmintic treatment. The clinical course for these ewes reflected a 5-6 month trend in declining body condition scores in adult sheep in the owner's 200-head commercial flock, located in northeastern Kansas. Most of the affected animals were ewes and rams of 3-4 years of age; a few 2 year-olds and yearling ewes and rams were affected. Thin body condition was estimated by the owner to affect 30% of the flock. Death losses in the adults were estimated to be 2-3%, with most adults leaving the flock as culls for infertility (which often occurred in the thin animals) or lameness. The ration consisted of native grass pasture, brome grass hay, a mineral supplement for sheep, and well water. No data on pregnancy rates were available. The affected ewes were afebrile, bright, and alert and were assessed to have body condition scores of 1 and 2/5. Soft, clumped stool was apparent in one ewe. Physical examinations, including dental examinations, were otherwise unremarkable.

The diagnosis in these ewes was confirmed at necropsy to be Johne's disease (JD). The most consistent clinical sign of JD in small ruminants is weight loss.1 As compared to cattle with JD, sheep tend to develop clinical signs of disease at an earlier age. In infected flocks with heavily contaminated environments, clinical signs may appear in yearlings. Diarrhea is a far less common clinical sign in small ruminants than in cattle, occurring in only 10 - 20% of affected small ruminants.1 When present, diarrhea tends to develop late in the disease course. In those rare instances, the feces may be watery or may merely be clumped and softer than normal. Affected animals usually maintain a good appetite and are afebrile, although poor appetite, weakness, dehydration, and lethargy may be evident in the terminal stages of the disease.

Johne's Disease should be suspected in small ruminants suffering from weight loss in the face of good nutrition, parasite control, and dental health. Differential diagnoses for JD in small ruminants include malnutrition (macro- or micronutrients), limited access to feed because of flock or herd hierarchy, dental disease, gastrointestinal parasitism, the internal form of caseous lymphadenitis, ovine progressive pneumonia, scrapie, chronic bacterial pneumonia, and chronic renal or hepatic disease. Impaired access to feed caused by inadequate feeder space or social hierarchy should also be ruled out. In Suffolk sheep, abomasal emptying defect should be also be considered as a differential diagnosis for individual animals showing weight loss and anorexia.

Gross lesions of the intestinal tract may be subtle or nonexistent in small ruminants with JD, although concurrent gastrointestinal parasitism is often found.1 When present, gross lesions of JD are most commonly found in the ileum and ileocecal junction. Thickening of the bowel wall, cording of the serosal and mesenteric lymphatics, and enlargement of the mesenteric and ileocecal lymph nodes may be apparent. Corrugation of the intestinal mucosa, a relatively common finding in clinically affected cattle, is present in roughly one half of affected sheep.1 Edema, ascites, and hydropericardium may be evident if the sheep is severely hypoproteinemic. Concurrent gastrointestinal parasitism is a frequent finding, and upon finding this, the veterinarian must remember not to stop the search for a diagnosis.2 Sheep with advanced JD are hypothesized to have compromised mucosal immunity, making them more susceptible to parasitism. In light of the frequently subtle and variable nature of gross lesions with JD in small ruminants and the possible presence of coexistent lesions of gastrointestinal parasitism, the veterinarian performing necropsy examination of an adult small ruminant with wasting disease should strongly consider histological examination for JD. Sections of the ileum, ileocecal junction, and the associated mesenteric lymph nodes should be submitted for histological examination and acid-fast staining.1,2

Hypoproteinemia, characterized by hypoalbuminemia and normal serum concentrations of globulin, may be evident on serum biochemistry analysis of affected small ruminants.2 The serum total calcium concentration may be low as a result of hypoalbuminemia. Mild anemia may also be present.

Case 2. Weakness and lethargy in a recently-docked lamb

In late March of 2004, a 3 week-old male Suffolk cross, singleton lamb was presented for recumbency and weakness that was first noticed the morning of admission to the hospital. The ram lamb had been tail banded 2 weeks previously, and was apparently healthy until being found recumbent and unable to rise that morning. The owner administered Clostridiumperfringens type C and D antitoxin and procaine penicillin G to the lamb, with no apparent effect. The 120-head flock of Suffolk and Suffolk-cross sheep was maintained near Fort Collins, CO. The sheep were allowed to graze on native grass pasture. Late-pregnant and lactating ewes were also fed alfalfa hay and cracked corn. Trace mineral-supplemented salt for sheep was available ad libitum. The flock was vaccinated annually with a multivalent toxoid derived from C. perfringens types C and D and C. tetani.

At admission, the lamb was quiet and alert, with normal hydration status and mucous membrane color. Tachycardia (230 beats/min) was present. Edema, swelling, and serosanguinous fluid were present at the tail dock site, which was painful to palpation. Symmetrical tetraparesis with normal limb tone and reflexes was evident. The ram could stand if assisted, and walked briefly before resuming recumbency. The gait was short-strided, and fasciculations of the triceps were evident when the lamb stood still. Palpation of the joints, muscles, spinal column, and umbilicus revealed no abnormalities.

The differential diagnosis included disseminated sepsis from the tail dock site (with potential skeletal or joint involvement), polyarthritis caused by Chlamydophila pecorum, myopathy, traumatic injury, botulism, and enterotoxemia. Botulism was considered unlikely because cranial nerve function was normal, and enterotoxemia was discounted because the clinical signs of disease had failed to progress. Myopathy was substantiated by the presence of significantly increased serum activity of the enzymes creatine phosphokinase and aspartate aminotransferase (86,949 IU/l and 24,014 IU/l, respectively; normal ranges, 100-300 IU/l and 80-120 IU/l, respectively). Subsequent analysis of blood samples obtained at admission revealed normal whole blood selenium concentration but a profoundly low serum concentration of Vitamin E. Treatment with parenteral vitamin E (1,200 IU SC) was performed, and the lamb slowly recovered normal strength over the following 2 weeks.

Nutritional muscular dystrophy (NMD), also termed white muscle disease, can occur in livestock deficient in selenium or vitamin E, or both. Mild deficiencies in one of these nutrients may be compensated for by adequate levels of the other; however, the two nutrients are not mutually replaceable. Severe deficiencies in either nutrient will result in deficiency syndromes even if animal is replete in the other.3 Possible causes for vitamin E deficiency in this lamb included inadequate colostrum ingestion, poor maternal vitamin E status, or insufficient milk intake. Colostrum is the primary source of vitamin E for the neonate, as little passes across the placenta to the fetus.4 Maternal vitamin E stores in body fat can be reduced during grazing on drought-stressed pastures, as the vitamin E content of dormant forages is lower than that of green forage. Prolonged storage and exposure to sunlight can also deplete the vitamin E content of hay.5 In an Ontario study, 90% of liver samples taken from market lambs were found to be deficient in vitamin E.6

The owner refused further investigation of the flock's vitamin E status; instead, he believed that the impending spring's grass growth would correct the problem without other intervention. No other cases were reported until March, 2008, when a lamb with nearly identical clinical signs and laboratory data was presented for evaluation. This lamb also responded to treatment with vitamin E.

The author has found that many causes of neonatal illness can be included in the mnemonic "SHADES." This mnemonic includes sepsis (bacterial infection), hypoglycemia, acidosis (metabolic or respiratory), diarrhea, (vitamin) E and selenium, and suffocation (perinatal hypoxia).

Case 3. Wool loss in a ewe

A 2 ½ year-old Finnsheep cross ewe was presented in April, 1998 for evaluation of the sudden onset of wool loss. The affected ewe was one of four ewes kept as a hobby flock on a suburban property outside of Manhattan, KS. The other ewes and their lambs were unaffected. The affected ewe was normal until roughly 4 days prior to admission, when wool loss was noticed over one of her hips. The owner had not witnessed any signs suggestive of pruritis. The affected ewe had given birth to a live singleton lamb approximately 10 weeks previously. The lamb was healthy and unaffected. The diet consisted of native grass hay, improved pasture, and trace mineral-supplemented salt for sheep.

The affected ewe was bright and alert, with a body condition score of 3/5. Almost all of the wool was missing over the dorsal half of the thorax and abdomen. The skin of the bare areas was slightly reddened but supple, with no evidence of excoriation. The scant, remaining wool in these areas could be easily epilated by hand, revealing healthy-appearing skin beneath. Fleece in the other areas of the body could be easily removed. No ectoparasites could be found.

At first glance of the animal from a distance, scrapie was considered as an important consideration. Upon closer examination, the ewe's body condition and neurologic status were inconsistent with that diagnosis; further, no excoriation was apparent. The diagnosis of "wool break" (wool slip, telogen effluvium, telogen defluxion, anagen defluxion) was made on the basis of the physical examination. In this disease, a stressful event (parturition, febrile disease, surgery, parturition) causes the immediate cessation of growth in anagen follicles. The fleece is then composed of hair follicles in roughly the same stage of the catagen phase and subsequent telogen phases of hair growth. A large number of telogen hairs are subsequently shed in synchrony, resulting in widespread loss of the fleece. Wool break often follows severe stress, disease, or high fever by a few days.7 Diseases that cause severe pyrexia, such as bluetongue virus infection or foot and mouth disease, have been incriminated as causes of subsequent wool break. In many cases, the causative event cannot be identified.

Wool break is usually a disease of the individual animal, although the author was recently consulted on an apparent flock-wide occurrence of nearly simultaneous wool break in nearly 100 head of crossbreed sheep in southern Wyoming. Adults are most often affected; this condition appears to be less common in juveniles and neonates.

Differential diagnoses for wool break include non-pruritic or inconsistently pruritic skin disorders such as secondary (hepatic) photosensitization, ringworm / club lamb fungus, and rain scald (Dermatophilus congolensis infection). Diseased skin is apparent in these disorders. Common pruritic diseases of sheep include infestation with ectoparasites (lice and keds) and scrapie. In fatal cases with severe excoriation evident, pseudorabies should be considered.

Summary Points

     • Johne's Disease is an important differential diagnosis for small ruminants with weight loss; diarrhea is often not evident.

     • Differential diagnoses for weight loss in adult small ruminants includes malnutrition, limited access to feed because of flock or herd hierarchy, dental disease, gastrointestinal parasitism, the internal form of caseous lymphadenitis, ovine progressive pneumonia, scrapie, and chronic pneumonia.

     • Adult sheep with advanced Johne's Disease may also show heavy burdens of internal parasites.

     • Hypovitaminosis E is a potential cause of generalized weakness in lambs; affected animals can be selenium replete.

     • Wool loss in the absence of underlying skin disease is characteristic of telogen defluxion or wool break.


Carrigan MJ, Seaman JT. The pathology of Johne's disease in sheep. Aust Vet J 67:47-150, 1990.

Van Metre DC, Tyler JW, Stehman SM. Diagnosis of enteric disease in small ruminants. Vet Clin North Amer: Food An Pract, 16: 87-115, 2000.

Maas J, Bulgin MS, Anderson BC, et al. Nutritional myodegeneration associated with vitamin E deficiency and normal selenium status in lambs. J Am Vet Med Assoc 184:201-206, 1984.

Pehrson B, Hakkarainen J, Blomgren L. Vitamin E status in newborn lambs with special reference to the effect of dl-a-tocopherol acetate supplementation in late gestation. Acta Vet Scand 31:359-367, 1990.

Weiss WP. Requirements of fat-soluble vitamins for dairy cows: A review. J Dairy Sci 81:2493-2501, 1998.

Menzies PI, Boermans H, Hoff B, et al. Survey of the status of copper, interacting minerals, and vitamin E levels in the livers of sheep in Ontario. Can Vet J 44:898-906, 2003.

Scott DW. Color Atlas of Farm Animal Dermatology. Ames, IA: Blackwell Publishing, 2007, p. 189.

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