Clinical history and questions
H&E stained section of liver of a 12 year-old castrated male cat.
Euthanasia followed several weeks of inappetance, moderately severe non-regenerative anaemia, and the presence of large non-healing ulcers on the pharyngeal pillars, which almost met over the posterior part of the soft palate.
The cat had been treated with parenteral antibiotics and multivitamins, with no real response.
At necropsy, the carcass was lean but not wasted. The only significant gross finding recorded (beside the oral lesions) was enlargement of the submandibular lymph nodes. The liver was of normal size, shape, overall colour and texture, but the capsular and cut surfaces bore a faint, regular acinar pattern.
- Describe the histological abnormalities
- Discuss them in relation to the clinical history and necropsy findings.
An interpretation of Diagnostic Exercise No. 3 – Roger Kelly
While no stromal components (portal triads or hepatic venules) were visible in this photomicrograph of a mature cat’s liver, the periacinar parenchyma was distinguished from the periportal by markers in the document as circulated.
The most obvious features of this specimen are:
- The granular, somewhat refractile golden-brown pigment that is so obvious in cytoplasm of periacinar hepatocytes, yet hardly evident in the periportal zone, and
- The frequent distension of sinusoids by empty circular profiles, presumably left by fat droplets. Associated with some of these globules are small, dark, distorted nuclei, presumably of cells located in sinusoids, rather than of hepatocytes.
Granular cytoplasmic pigment in hepatocytes of any species is most likely located in lysosomes. Brownish pigments include lipofuscins, haemosiderin, melanins, bile and porphyrins. Porphyric animals (very rare in cats) can be expected to have some photodynamic dermatitis; bile usually has a more greenish hue and might reasonably be seen as canalicular plugs and Kupffer cell deposits; melanins are rarely if ever seen in cat livers (see in gray horses with melanoma and ruminants with environmental melanosis). Haemosiderin can be indistinguishable from lipofuscin in H&E sections, and I would ask for a Perls to be sure, since this animal’s anaemia (although given as non-regenerative), might have had a haemolytic component (eg haemobartonellosis in a chronically ill animal). Lipofuscin pigmentation of periacinar hepatocytes is almost universal in mature cats; it steadily increases with age and seems to be unrelated to diet or to other conditions that might be present.
Droplets of triglyceride can usually be found in sinusoidal fat-storing (Ito) cells in most species. Usually these droplets are only demonstrable by EM, but in mature cats the Ito cells seem to steadily stash away the fat until many look like this. Again, there seems to be no relationship with anything other than age, so this change, like the lipofuscinosis, is diagnostically useless. These conditions only help you realise that you are dealing with an older cat, if you didn’t already know that.
The oral ulcers in this cat might have been an example of chronic lymphoplasmacytic stomatitis, a poorly-understood condition possibly related to FIV infection. They probably provided enough antigenic stimulation to cause local lymphadenopathy.
I hope that people who want to discuss about this case will feel free to respond to it, either by communicating with me individually at Roger-Kelly@aapt.net.au or by opening wider discussion by posting their responses on the mailing list.