Case summary A female neutered domestic longhair cat, aged 1 year and 5 months, presented with lymphadenomegaly and anaemia following therapy with phenobarbital for idiopathic epilepsy. Physical examination revealed pale pink mucous membranes and peripheral lymphadenomegaly. Haematology showed a regenerative anaemia (haematocrit 19.3%, reticulocyte count 118.08 ×109/l), and saline agglutination was positive. Infectious disease screening was negative and lymph node cytology was consistent with reactive lymphoid hyperplasia. A diagnosis of phenobarbital-induced reactive lymphoid hyperplasia and immune-mediated anaemia was suspected. Complete resolution of the lymphadenomegaly and anaemia was documented within 4 weeks of phenobarbital discontinuation. Relevance and novel information There are limited case reports of phenobarbital-induced haematological changes and lymphadenomegaly; however, the combination has not previously been reported in cats and is similar to the rare but significant syndrome in humans known as ‘anticonvulsant hypersensitivity syndrome’. Anticonvulsant hypersensitivities should be considered as a potentially serious, yet reversible, sequela to phenobarbital treatment that may be mistaken for more severe illness such as neoplasia.
A 1-year 4-month-old, male, neutered domestic longhair was presented for investigation of lameness and lethargy. Pyrexia and swelling of the left antebrachium was noticed on clinical examination. Despite treatment with various antibiotics (cefovecin, then amoxicillin and marbofloxacin), the pyrexia and lameness persisted. A computed tomography scan revealed a cavitary lesion and diffuse soft tissue swelling in the left axilla/thoracic wall, with associated moderate to marked lymphadenomegaly of multiple lymph nodes. Aspirates from the cavitary lesions revealed neutrophilic inflammation, and the lymph nodes were consistent with reactive lymphoid hyperplasia and neutrophilic lymphadenitis. Routine aerobic and anaerobic bacterial cultures were negative. A Mycoplasma culture was positive, and the Mycoplasma felis polymerase chain reaction was positive at a high level (Ct 16.6). The patient was subsequently treated with doxycyline and the clinical signs resolved. The difficulty of culturing Mycoplasma spp. should raise the awareness of veterinarians to perform specific culture or polymerase chain reaction for Mycoplasma spp. K E Y WO R D S abscess, feline, lymphadenomegaly, Mycoplasma BACKGROUNDIt is not uncommon for cats to be presented for veterinary attention due to abscesses, especially following cat fights. 1 The most common bacteria involved in the development of infection following a bite are Pasteurella multocida, Peptostreptococcus spp., Actinomyces spp., Bacteroides spp. and Fusobacterium spp. 1-4 However, infection with Mycoplasma spp. should be suspected in cats presented with an abscess that are not responding to first-line antibiotics, as Mycoplasma spp. have been found in 15.4% of cat bite abscesses. 5 Abscesses are often treated with local cleaning ± surgical debridement and antibiotic therapy, where beta-lactam antibiotics are often empirically prescribed in veterinary medicine. 6,7 Mycoplasma spp. have been reported to be generally commensal and part of the normal flora of the mouth of cats (as they reside on the surface of mucus membranes). However, they have been associated with disorders of the conjunctiva, 8 respiratory 9-11 or urinary systems. Mycoplasma has been sporadically reported in bite abscesses in cats, 5,[12][13][14] presumably due to the fact that Mycoplasma spp. are part of the normal flora of the mouth.Mycoplasma spp. are cell wall-deficient organisms, and for this reason are resistant to beta-lactam antibiotics. 15 However, a pilot study showed that routine cleaning and use of beta-This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
ObjectivesTo update canine immune-mediated polyarthritis (IMPA) through retrospective analysis of the data of 85 dogs, with special interest in percentage of relapse and outcome.
A 3‐year‐old entire female Springer Spaniel, with a previous diagnosis of meningoencephalitis of unknown origin diagnosed 2 years before presentation and treated with long term administration of prednisolone, developed proteinuria. Laboratory findings revealed hypoalbuminemia, hypercholesterolemia, and proteinuria. Further investigations excluded underlying causes. Renal biopsies were performed. The glomeruli and the tubulointerstitial compartment did not show any anomalies on light microscopy and immunofluorescence staining did not reveal abnormalities. Transmission electron microscopy revealed moderate podocyte injury consisting of foot process effacement and microvillus transformation of the cytoplasm. The dog was diagnosed with primary minimal change disease of the podocytes and treated with telmisartan and mycophenolate mofetil. Abnormalities of serum albumin, cholesterol, and proteinuria resolved within 4 weeks. Minimal change disease has been reported in dogs, but this is a case report of proteinuria secondary to minimal change disease successfully treated with mycophenolate mofetil and telmisartan.
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