1. 1 HISTORICAL FINDINGS AND PRESENTING SIGNS 4 year-old Warmblood gelding used for pleasure riding (455 kg) No history of previous illness Regular deworming and vaccination program. Teeth checked once every a year by a local equine dentist ------------------------------------------------------------------------------------------------ Vaccinated against influenza and EHV-4 12 days prior to presentation and developed a fever (40.6 ˚C), mild colic and anorexia two days later The horse was treated with NSAIDs by the referring veterinarian and the colic resolved; however the horse remained inappetent, intermittently pyrexic and began to develop oedema in all four legs ------------------------------------------------------------------------------------------------ Slide 1/6 CASE A

2. 2 CLINICAL FINDINGS (on day of presentation) On presentation, the horse was depressed and in moderate body condition (CS 5/9) HR 52 bpm, RR 18 bpm, T 39.6 ˚C On cardiac auscultation, heart rhythm was normal and no murmurs could be heard On respiratory auscultation, normal tracheobronchial sounds were heard over the large airways and there was no evidence of wheezes or crackles On abdominal auscultation, gut sounds were decreased in all four quadrants Pitting oedema was evident in all four legs, the muzzle and the ventral aspect of the thorax Digital pulses were palpable but not bounding. The feet were cool on palpation and the horse was able to walk comfortably No abnormalities were identified on transrectal palpation Slide 2/5

3. 3 CLINICAL FINDINGS (on day of presentation) The mucous membranes were pale pink with petechial and ecchymotic haemorrhages evident on the gingiva, nasal mucosa and third eyelid Slide 3/5

4. 4 CLINICAL FINDINGS (on day of presentation) It was also noted that the horse was bleeding excessively from the jugular venipuncture site Slide 4/5

5. 5 When you enter the examination room, you will be asked to 1.Identify and interpret the clinical problems using information obtained from the history and physical examination 2.Formulate a list of differential diagnoses using your problem list and be able to justify your choices 3.Comment on how you would further differentiate between the main differential diagnoses From this stage onwards, further information (clinical and laboratory data) will be provided either on your request or automatically. You will be asked to comment on this data. Slide 5/5

6. 6 PERITONEAL FLUID ANALYSIS

7. 7

8. 8 RESULTS OF OTHER ANCILLIARY DIAGNOSTICS PERITONEAL FLUID CULTURE: pure growth of Streptococcus equi sub species Zooepidemicus SKIN BIOPSY: no evidence of leukocytoclastic vasculitis PLATELET COUNT: thrombocytopenia (31.1 x 10 9 /l) COAGULATION PROFILE: PT; PTT; and activated clotting time normal. Plasma AT III concentration normal. No FDPs ANTIPLATELET ANTIBODY TEST: normal SEROLOGY: Coggins negative for EIA PCR: negative for Anaplasma phagocytophilum and EVA

9. 9 LABORATORY DATA (on day of presentation)

10. 10 CASE PROGRESSION (on day 2) The horse was treated with intravenous ringer’s acetate; flunixin meglumine (1.1 mg/kg IV SID); penicillin (22000 iu/kg QID IV) and gentamicin (6.6.mg/kg IV SID) Administration of platelet rich plasma was considered at this point but it was decided to wait for 24 hours and see if the horse had responded to the initial treatments, as the horse was not in immediate danger of fatal haemorrhage. On day 2, the horse was very depressed and remained inappetant HR 52 bpm, RR 24 bpm, Temp 39.4 deg C A repeat CBC was obtained

11. 11 LABORATORY DATA (on day 2)

12. 12 BONE MARROW ASPIRATE Bone marrow aspirates from the sternum were haemodilute and did not contain spicules, megakaryocytes, polychromasia or appreciable iron reserves. The differential cell count was composed of 42% lymphoid cells, 5% differentiated myeloid cells, 24% erythroid cells (predominantly rubricytes and metarubricytes) and 29% blast cells with occasional plasma cells. The low cellularity of the specimen meant that an accurate M:E ratio could not be calculated

13. 13 DIAGNOSIS T or B cell markers (CD3, CD79a) were not detected on immunohistochemical analysis of the surface of the blast cells, ruling out lymphoid leukaemia There was no positive result to lysozyme (muramidase) which identifies monocytes and neutrophils, ruling out granulocytic leukaemia or monocytic leukaemia. The tumour cells were therefore most likely undifferentiated round cells (probably precursor cells from the monocytic or myelocyte lines) The clinicopathological diagnosis was MALIGNANT MYELOMONOCYTIC LEUKAEMIA (initially aleukaemic)