Our study highlights that in cats with acute FPV, the gastrointestinal tract shows several ultrasonographic changes. The most frequent findings were diffuse small intestine mucosal layer thinning, muscular layer thickening and mucosal hyperechogenicity. Hyperechoic mucosal band paralleling the submucosa and irregular luminal surface were frequent in the jejunum.
Although described mostly in chronic enteropathies [12, 13, 14, 15, 16], our study identified diffuse small intestine muscular layer thickening, and hyperechoic mucosal band paralleling the submucosa, along with increased mucosal echogenicity in cats with acute gastroenteritis induced by FPV.
Thickening of the muscular layer was observed in the duodenum and jejunum in approximately 50% and 60% of cats, respectively, which has previously been associated with chronic enteropathies (e.g., eosinophilic enteritis), intestinal foreign body and lymphoma; potential causes are infiltrative diseases and smooth muscle hypertrophy or hyperplasia [12, 13, 15, 16]. No histopathological analysis was performed in our cats, and occult chronic enteropathy (e.g., food intolerance) or lymphoma cannot be rule out in our cases.
However, it seems unlikely that 60% of these young cats had an underlying disease. We assume that muscular layer thickening in cats with acute panleukopenia may be due to the inflammatory condition. Enteritis has been shown to cause diffuse intestinal wall thickening associated with edema, hemorrhage, fibrosis and/or necrosis in dogs [25]; these changes are expected to cause intestinal wall thickening also in cats, including the muscular layer.
In our study, the hyperechoic mucosal band paralleling the submucosa was present in the jejunum in one-third of the cats, while not in the duodenum. Using ultrasound, one study [14] described the presence of a mucosal hyperechoic band paralleling the submucosa in all cats with full-thickness intestinal biopsy presenting with gastrointestinal signs. Based on histology, the hyperechoic mucosal band likely represented an ultrasonographic interface due to the presence of mucosal fibrosis. In the same investigation [14], the authors prospectively evaluated clinical signs of cats showing a visible hyperechoic mucosal band on ultrasound but without performing histopathology. Most cats had vomiting or diarrhea, but one-third had no clinical signs or other ultrasonographic intestinal abnormalities. It was concluded that this band can also be observed in apparently healthy cats [14].
We observed increased mucosal echogenicity in approximately 40% of cats in the duodenum, and 30% in the jejunum. In addition, irregularity of the luminal surface was found in 10% of cats in the duodenum, and in 30% of cats in the jejunum. Mucosal changes, such as increased mucosal echogenicity, hyperechoic speckles, and striations have been reported in several conditions in chronic enteropathies in dogs and cats. Increased mucosal echogenicity has been described in lymphoplasmacytic enteritis and eosinophilic enteritis and in cats with mucosal fibrosis [14,15]. Hyperechoic speckles and hyperechoic striations have been reported in dogs with chronic enteropathies [18]. A thick hyperechoic mucosal border on the luminal margin of several jejunal segments was observed in dogs with acute enteritis [19].
In our cats with FPV, it is possible that these findings were due to mucus, cellular debris, gas entrapped in the mucosal crypts, and protein accumulation caused by necrosis and inflammation associated with the acute form of the disease, as reported in puppies with CPV [20].
In our study, mucosal thinning of the duodenum and jejunum was observed in two-thirds of cases, along with an irregular luminal surface in two cats (11.8%) in the duodenum, and in seven (33.3%) cats in the jejunum. Villous atrophy secondary to viral-induced crypt cell destruction, necrosis, and sloughing of epithelial cells associated with FPV are reasonable explanations for the reduced thickness. This finding is similar to previous observations in 40 puppies with CPV where the duodenal and jejunal mucosa thickness was significantly decreased and the luminal surface of the duodenal and jejunal mucosa was irregular [20]. The thinning of the mucosal layer due to the aforementioned causes, could explain the severe reduction in the jejunal wall that we observed in one cat in which the thickness was 0.6 mm.
In cats with ultrasonographic information on the jejunal lymph nodes, echogenicity, echotexture, and size were normal. This finding is similar to previous observations in puppies with CPV [20], in which parvovirus infection was not associated with jejunal lymphadenopathy by abdominal ultrasound. In the above mentioned study the authors assumed that cortical atrophy was the result of the tendency of CPV to rapidly divide cells of the lymphoid tissue [20]. It is also possible that the same explanation accounts for the sonographically normal lymph nodes in our study, although histology would have been required for confirmation.
In almost half of the cats with available images of the spleen, a “moth-eaten” parenchyma was observed, and in only one was this finding associated with splenomegaly. A “moth-eaten” parenchyma is characterized by numerous small hypoechoic nodules spread throughout the organ causing a spotted echotexture. However, this finding is non-specific, and in a previous study was observed in cats with lymphoid hyperplasia, extramedullary hematopoiesis, passive congestion, lymphoma, carcinoma, and histiocytosis, as well as in healthy animals [21]. The use of very high-frequency transducers (11-18 MHz), which improve the quality of images, may also be partly responsible for the high rate of this particular pattern in our cats.
Regarding the associations between ultrasonographic features and clinical findings, vomiting was positively associated with free peritoneal fluid. Due to lack of gastrointestinal biopsies and fluid analysis, the cause for this association remains unclear. Mild abdominal effusion has been described in puppies with CPV, although associations with clinical signs were not investigated [10]. Age was also positively associated with jejunal wall thickening. However, the reason for this finding is not clear, hence a casual association rather than a cause-and-effect relationship cannot be excluded.
Interestingly, based on ultrasonography, the abdominal effusion of the present cats was anechoic. Feline infectious peritonitis seemed unlikely because in this disease the effusion is usually echogenic and with mobile particles [30]; it is still nevertheless possible. The fluid was not collected to clarify its pathogenesis.
With regard to survival and abdominal ultrasonography, a favorable outcome was positively associated with higher jejunal mucosal echogenicity and hyperechoic mucosal band in FPV cats. The hyperechoic mucosal band may represent an ultrasonographic interface due to the presence of mucosal fibrosis [14]. Unfortunately, histopathology was not performed in our cats with FPV to verify whether fibrous tissue was present in the jejunum. Given that FPV has an acute onset in most cats [3], the presence of fibrous tissue would be unexpected. However, in some cats FPV may be more subclinical, longer lasting and with a better outcome [1]. It is also possible that intestinal fibrosis develops in some of these cases.
Although to the author’s knowledge there is no study describing acute enteritis in FPV cats, thinning and hyperechogenicity of the mucosa, thickening of the muscular layer, reduction of the intestinal motility and gastric and intestinal distention with fluid and/or echogenic material yield information about the severity of the enteropathy in these patients; prospective studies are needed to test this hypothesis.
The main limitations of the present study are the relatively small number of cats included and the retrospective nature of the investigation. Some medical records were incomplete, in particular those pertaining to images and videos of the ultrasound. Hence, it was not possible to measure all segments of the gastrointestinal tract, although the attending radiologist reported them as normal.
Moreover, follow-up abdominal ultrasound and histological examinations were not performed, which would have characterized the underlying causes of some of the ultrasonographic features. Finally, no control group of shelter cats with other gastrointestinal diseases was available for comparison. However, shelter cats with vomiting or diarrhea but otherwise in good conditions are treated symptomatically by the shelter veterinarian without performing further diagnostics, such as abdominal ultrasound, thus precluding the possibility of a control group.
Collectively, the present ultrasonographic findings in FPV cats may be useful to characterize the enteritis and assess its severity, and to set the basis for further prospective studies.