In July 2019, six 2-year old elk (Cervus elaphus) hinds were noted to be dull and depressed. The six animals were part of a herd of 17 animals (16 hinds and 1 bull), located on the National Animal Disease Center (NADC) campus in Ames, Iowa. Collectively, the herd was also noted to be anorexic for a few days prior to the identification of clinical signs. Closer examination revealed the six depressed hinds to be in poor body condition and had failed to completely shed their winter coats.
A second herd, consisting of 17 animals (16 hinds and 1 bull), housed in an adjacent pasture was also evaluated. Only one hind (#84) in this group was found to be in poor body condition. Blood samples from clinical animals were obtained for complete blood counts, serum chemistries, and infectious diagnostic testing. Fecal samples were also collected.
Complete blood counts (CBC) were unremarkable for all animals tested. However, serum chemistries (Table 1) showed a marked hypoalbuminemia. In two of the animals (#100 and #113), serum albumin levels were below the instrument's level of detection (i.e., < 1 mg/ml). Fecal floatation examinations were performed on individual animals, as well as from pooled fecal samples. Findings revealed occasional strongyle-type eggs (1-10 per slide) and occasional operculated eggs consistent with a trematode spp.
Blood and serum samples from all affected animals were submitted to the National Veterinary Service Laboratories (Ames, IA) for bluetongue virus (BTV), epizootic hemorrhagic disease virus (EHDV), malignant catarrhal fever (MCF), and bovine leukemia virus (BLV) testing. Three of the clinical animals were seropositive for EHDV, but no virus was recovered via PCR from any of the tissues submitted, suggesting exposure to EHDV, but no ongoing infection. All other test results were negative. Fecal samples were negative for Johne's (Mycobacterium avium subsp. paratuberculosis) via culture and polymerase chain reaction (PCR) for the IS900 genetic element.
At necropsy, all four elk were thin, with rough hair coats (Figure 1A) and decreased subcutaneous and renal fat stores. One of three hinds had fecal staining of the perineum consistent with diarrhea, while the remaining hinds had normal formed feces.
Abomasa from three of the four hinds were characterized by variable degrees of irregular abomasal mucosal thickening, which was most prominent in the fundus, but also extended well into the body. In one animal, the abomasal mucosa was cobblestone in appearance, with numerous raised, pale, nodular foci, 5-10 mm in diameter (Figure 1B), that coalesced in severely affected areas. In all four animals, the mucosal surface was covered with moderate to large amounts of mucus, while scattered throughout the thickened abomasal mucosa were small 1-3 mm red foci. At all levels of the small intestine, the mucosa was diffusely hyperemic. The cecum was less affected, with small multiple hyperemic foci. More distal regions of the large intestine were normal in appearance.
Sections of abomasum from all four hinds were characterized by variable degrees of hyperplasia and metaplasia. Elongated gastric pits were lined by tightly packed mucous cells with increased mitotic figures (mucous cell hyperplasia) resulting in moderate thickening of the abomasal mucosal layer (Figure 2A). Multifocally, mucous cells replace gastric parietal cells (mucous cell metaplasia). Within the lamina propria were moderately increased numbers of lymphocytes, plasma cells, and eosinophils (Figure 2B). Occasional dense aggregates of lymphocytes (lymphoid nodules) were seen in the abomasal lamina propria. Within the abomasal lumen multiple cross sections of a nematode, roughly 100 mum in diameter, were present (Figure 2C). Morphologic features were typical of Trichostrongyles, including a thin cuticle with prominent longitudinal ridges, pseudocoelom, and a platymyarian-meromyarian musculature (Figure 2C). The digestive tract was typical oligocytous strongylin with few visible cells and multiple nuclei.
Based on our initial clinical findings of poor body condition, diarrhea, and severe hypoalbuminemia, with no clinical pathologic evidence of hepatic or renal involvement, we proposed a tentative diagnosis of protein-losing enteropathy. Gross and histological findings of proliferative abomasitis and identification of nematodes consistent with Ostertagia spp. provided a definitive diagnosis of protein-losing enteropathy due to ostertagiasis. Furthermore, identification of increased number of lymphocytes, eosinophils, and plasma cells in the abomasum, confirmed type II ostertagiasis.
Anti-helminthic treatment was started immediately and consisted of a combination of transdermal Cydectin  (5 mg moxidectin/ml, 5 ml/kg; Bayer Healthcare, Shawnee Mission, KS) and injectable Noromectin  Plus (1% ivermectin and 10% clorsulon; 2 ml/45 kg; Norbrook Inc, Overland Park, KS). Clinical animals also received vitamin B complex (1 ml/45 kg; Huvepharma, Inc., St. Joseph, MO), administered subcutaneously. Five weeks after presentation of clinical signs, all elk were reevaluated. Previously-clinical animals remained thin, but their body condition had started to improve. Blood samples were collected and serum chemistries reanalyzed 5 weeks following treatment. In three of the four animals, albumin levels had started to improve (Table 2). Ten weeks after initial treatment, all animals were re-treated with injectable Noromectin  Plus, and serum chemistries were again evaluated in previously-clinical animals (Table 2). At this sampling timepoint, serum albumin levels were within normal range for all animals analyzed.