A three-year-old male castrated huacaya alpaca weighing 81 kg presented in late November 2019 to UCD Veterinary Hospital along with a healthy companion alpaca. The alpaca had a two-day history of colic signs (rolling and vocalisation), tenesmus and reduced faecal output. He had been seen by the referring veterinary practitioner, who treated him with albendazole and dexamethasone and started him on a course of potentiated amoxycillin, but he failed to respond to this treatment. Prior to that, he had most recently received antiparasitic treatment in the form of albendazole in early September. He received annual vaccinations against clostridial disease. He was kept outdoors with a second alpaca and grazed alongside sheep. On initial clinical exam, the alpaca was quiet, alert and responsive. Body condition was moderate to good. His respiratory rate was increased at 36 breaths per minute (normal range: 10–30), likely due to the stress of travelling and restraint, but his heart rate (88 beats per minute, normal range: 60–90 beats per minute) and temperature (38.2 °C, normal range: 37.5–38.9 °C) were within normal limits []. Mucous membranes were a pale pink colour. First compartment (C1) contractions were reduced in frequency at one every 2 min. He resented abdominal palpation, particularly in the cranioventral region, signified by a loud grunting sound and attempts to escape restraint. Otherwise, there were no abnormalities identified. Over the following 24 h of hospitalisation however, the alpaca demonstrated prolonged recumbency, frequently lying in a semi-lateral position with the limbs partially extended rather than cushing with all four legs tucked underneath him. This was assumed to be indicative of abdominal pain. He also displayed intermittent episodes of tenesmus and passed minimal numbers of faecal pellets of a normal colour and consistency. He consumed only a very small amount of hay and was not observed eating the concentrate feed offered. Blood for haematology (Advia 2102, Siemens, Dublin, Ire) and plasma biochemistry (Atellica CH 930, Siemens, Dublin, Ire) was collected via jugular venipuncture on the day of admittance to the hospital and on the fifth and seventh days of hospitalisation. Reference intervals (RI) for alpacas specific to the UCD clinical pathology lab were not available, so RI described in Cockcroft et al. [] and Dawson et al. [] were used to interpret results. Haematologic analysis indicated moderate, macrocytic, hypochromic anaemia with moderate reticulocytosis. This regenerative anaemia could not be attributed to the accompanying, moderate hypophosphatemia found with biochemical analysis, which was insufficiently severe to cause haemolysis. Nor could it be attributed to mycoplasma infection, which could not be identified on blood smears. Marked inflammation was indicated by marked leucocytosis due to marked neutrophilia, moderate monocytosis, and mild eosinophilia, along with moderate, reactive thrombocytosis. This was confirmed on the biochemistry panel by marked hyperproteinaemia due to marked hyperglobulinaemia, and mild hypoalbuminaemia. Mild lymphopaenia and moderate hyperglycaemia may be attributable to stress. There was mild azotaemia with mildly increased urea and creatinine. This may have been pre-renal as eating and drinking were reduced. Marked hepatopathy was indicated by a marked (6-fold the upper limit of normal[ULN]) increase in gamma-glutamyl transferase (GGT), with a moderate (3-fold ULN) increase in hepatocellular glutamate dehydrogenase (GLDH) activity. Total calcium, beta-hydroxy-butyrate, calcium, magnesium, aspartate aminotransferase (AST), creatine kinase, and pancreatic lipase were within reference range. Clinical pathology changes substantially deteriorated from day 1 to day 5. There was a mild deterioration in the anaemia and hypoproteinemia. A poor prognosis was indicated by the development of a degenerative left shift by day 5, with mild neutropaenia, increase in bands to a higher count than segmented neutrophils (degenerative left shift) and mild toxic changes seen in neutrophils on blood smears. The eosinophilia had worsened to a moderate severity. A mild rubricytosis developed. Also, the severity of the azotaemia had doubled. However, due to the difficulty in collecting a urine sample, renal tubular concentrating ability could not be determined. Hepatobiliary pathology deteriorated with GGT activity having increased by a third, whereas hepatocellular GLDH activity decreased by 15%. Pancreatic lipase had doubled, a mild ketonemia developed, and there was a further, mild increase in blood glucose. Unfortunately, the clinical pathology lab was unable to re-analyse phosphate as it had run out of reagent. On the seventh day, there were a few further, noteworthy changes in clinical pathology parameters. The anaemia had mildly worsened. However, the leukogram had largely normalised, although there was persistent monocytosis and a mild lymphocytosis had developed. The ketonemia was mild, although ketones had doubled. Pancreatic lipase had normalized. Faecal flotation using McMaster’s technique was performed on the day of admittance, with no nematode eggs detected. The reduced sensitivity of this technique compared to the modified Stoll’s technique is acknowledged []. However, if high counts are expected, as with a burden of gastrointestinal nematodes causing clinical disease, McMaster’s technique can still be appropriate []. Faecal sedimentation was not requested on the first day of hospitalisation as, due to the history of recent treatment with albendazole, an adult fluke infestation was not suspected. Faecal flotation was repeated and sedimentation carried out as the combination of anaemia, increased hepatobiliary enzyme activity and rising eosinophilia made F. hepatica infestation a more likely differential diagnosis. Again, no nematode eggs were detected. However, F. hepatica eggs were present. Faeces were assessed for the presence of occult blood, consistent with third compartment ulceration (TCU), yielding a negative result. However, due to reduced faecal output, the required 50 g sample could not be provided, reducing the sensitivity of the test. It was also acknowledged that the negative predictive value of the faecal occult blood test for TCU in camelids is questionable []. Gastrointestinal obstruction or peritonitis secondary to perforation of a TCU or other source, consistent with the presenting signs of abdominal pain and reduced faecal output, were questioned. Standing, unsedated, lateral abdominal radiographs demonstrated a moderate enlargement of C1 and a normal soft tissue-gas opacity interface within the same compartment. Multiple foci of mineral opacity superimposed the ventral aspect of the third compartment. There were no extra-compartmental gas opacities or evidence of poor serosal detail suggestive of a peritoneal effusion. These findings were interpreted as mild dilation of C1, with no evidence of a mechanical obstruction or peritonitis. An abdominal ultrasound examination was performed. The fibre was not clipped, but rather parted at the skin, and surgical spirit was applied directly to the skin of the abdominal body wall. The caudal pleural interface and liver were first imaged through the ninth, tenth and eleventh intercostal windows, with no abnormalities identified. Within each of these spaces, the probe was moved ventrally until the third stomach compartment (C3) could be imaged. No disruption to the integrity of the wall of C3, indicative of TCU, nor any extracompartmental fluid or gas suggestive of perforation of the compartment, could be imaged. Small intestinal loops were imaged caudal to C3. Motility was subjectively reduced. An elongated, irregularly outlined mass was identified in the right ventral abdomen, adjacent to the abdominal wall. The appearance was similar to hepatic parenchyma but was mildly heterogeneous in echogenicity. When the probe was moved cranially along the mass, it appeared contiguous with the liver, but protruded caudal to the costal arch. In new world camelids, the liver is normally only visible intercostally []. The kidneys, intact bladder, spleen and wall of C1 were also imaged, with no abnormalities detected. No excessive free peritoneal fluid was detected during the ultrasound examination. An ultrasound-guided fine needle aspirate of the abdominal mass was performed. The alpaca was restrained unsedated while cushing and an area of fibre was clipped from the abdominal wall overlying the mass. The skin was prepared with chlorhexidine scrub, followed by surgical spirit. The mass was localised and a 1.5″ 18 g needle attached to a 2 ml syringe introduced alongside the probe, through the body wall and into the mass until it could be imaged within the mass. Negative pressure was applied using the syringe and the needle redirected within the mass. Negative pressure was released and the needle withdrawn. The contents of the needle were then expelled onto a glass slide and smeared with a second slide. The process of fine needle aspiration was repeated twice. The smeared, air-dried samples were submitted for cytological examination. The cytological findings were in fact consistent with cells of hepatic origin, with clusters or sheets of large, epithelioid, monomorphic, polygonal cells with basophilic cytoplasm occasionally containing small amounts of blue-green pigmented granules, consistent with bile. In the background were large numbers of granulocytes and mononuclear cells. There were no criteria of malignancy. It was concluded that there was mild hepatocellular cholestasis along with mild, mixed granulocytic and mononuclear inflammation. Photomicrographs of the cytological samples were taken using Motic BA410 microscope, Motic Moticam 10 (10.0 megapixels) camera and Motic Images Pluse 2.0 image processing software, all purchased from Motic Europe, Barcelona, Spain. Following eventual euthanasia, a post-mortem examination was carried out. Overall, the animal was in moderate body condition with moderate subcutaneous and visceral fat reserves. The main pathological findings centred on the liver which was enlarged (6% of body weight) and contained multiple yellow foci of necrosis ranging from 0.3 to 3 cm in diameter which were surrounded by a haemorrhagic rim. In addition, there were linear pale and red areas of possible fibrosis and haemorrhage scattered throughout the hepatic parenchyma consistent with parasitic migration tracks. Bile ducts were dilated with thickened walls and, on cut-surfaces, contained immature trematodes within their lumens. In addition to the hepatic changes the animal was also suffering from a fibrinous peritonitis and pericarditis, congestion and oedema of the mucosa of C3 and the duodenum, enlargement of the hepatic, mesenteric and tracheobronchial lymph nodes and multifocal petechial haemorrhages in the subcutaneous tissues of the thorax, the muscles of the neck and the pleura. Histologically over 80% of selected liver sections were markedly to severely disrupted by inflammatory changes. Multifocally there was complete loss of normal architecture which was replaced by massive numbers of inflammatory cells (mostly eosinophils, with fewer lymphocytes and neutrophils) and cellular debris, surrounded by a rim of haemorrhage. Focally there was extensive individualisation and loss of hepatocytes with associated marked disruption of normal cord architecture. Multifocally to coalescing there were markedly increased numbers of mixed inflammatory cells within sinusoids. Multifocally to coalescing there was a moderate to marked proliferation of fibroblasts (fibrosis). Photomicrographs of the histopathological slides were taken using an Olympus BX43 microscope, HD Chrome Exofocus camera and TCapture imaging software. As haematology and biochemistry demonstrated inflammatory processes (eg. leucocytosis, degenerative left shift and hyperglobulinaemia) which could have been due to infection, the alpaca was maintained on once daily potentiated amoxycillin (7 mg/kg amoxycillin, 1.7 mg/kg clavulanic acid, intramuscularly) throughout hospitalisation. An intravenous catheter was placed in the jugular vein and he was administered esomeprazole (0.4 mg/kg, intravenously) once daily to treat and prevent TCU. Initially, no non-steroidal anti-inflammatory drug was given due to concerns about TCU as the possible cause of the abdominal pain he presented with. Instead, buprenorphine (0.01 mg/kg) was administered intravenously. This resulted in severe dysphoria, with vocalisation and frenzied activity. Following this, meloxicam was given once daily to provide pain relief (0.25 mg/kg, intravenously). When concerns were raised about chronic or acute fasciolosis, the alpaca was treated with triclabendazole (15 mg/kg, per os). As his condition began to deteriorate on day eight, he was administered intravenous fluids (Hartmann’s solution, 6 ml/kg/hour) and a blood transfusion was performed. This was collected from the healthy companion alpaca into a 450 ml pre-citrated blood collection bag. Due to lack of cooperation on the part of the donor alpaca, only 300 ml of whole blood could be collected and delivered. Initially, the alpaca’s condition improved. He was observed standing easily or cushing rather than lying in a semi-lateral position and eating a small amount of hay and concentrate feed. Unfortunately, on day six of hospitalisation he began to deteriorate. He returned to spending long periods lying in a lateral or semi-lateral position with the limbs partially or fully extended. He became completely anorexic. On day eight, he assumed complete lateral recumbency and was unable to rise, with a heart rate of 128 beats per minute. In comparison to day one, there was an approximate decrease in both haematocrit and total protein by 15%, suggestive of mild haemorrhage. His condition did not improve, in spite of supportive care, and he was euthanised with an overdose of intravenous barbiturate (100 mg/kg). On post-mortem examination it was determined that acute fasciolosis was the likely cause of death. The companion alpaca was also treated with triclabendazole (15 mg/kg, per os) and faeces were collected from him for flotation and sedimentation. 50 strongyloid eggs per gram were present, as well as one fluke egg. Fluke control measures were subsequently discussed with the owner, including chemical prophylaxis, regular faecal egg counts and, if possible, the identification and fencing off of fluke habitats to reduce reliance on fasciolicides.