The present study shows that in cats with FPV the acute form of the disease is associated with ultrasonographic changes compatible with gastroenteritis, including loops distended by fluid/echogenic material, irregular luminal surface, decreased motility, and duodenal and jejunal mucosal thinning. Of note, although described mostly in chronic enteropathies [11, 12, 13, 14, 15], based on this study diffuse small intestine muscular layer thickening, hyperechoic mucosal band paralleling the submucosa, and increased mucosal echogenicity can be observed in cats with acute gastroenteritis induced by FPV.
In particular, thickening of the muscular layer was observed in the duodenum and jejunum in approximately 50% and 60% of cats, respectively, which has been associated with chronic enteropathies; potential causes are infiltrative diseases and smooth muscle hypertrophy or hyperplasia [11, 12, 14, 15]. The reason for this finding is uncertain in the present series of cats since histology was not performed. However, it cannot be excluded that edema of the muscular layer due to severe intestinal inflammation or transient infiltration with inflammatory cells played a role.
In our study, the hyperechoic mucosal band paralleling the submucosa was present in the jejunum in one-third of cats, while in none in the duodenum. With ultrasound, Penninck and coworkers (2010) retrospectively described the presence of a mucosal hyperechoic band paralleling the submucosa in a group of 11 cats with full-thickness intestinal biopsies corresponding to histopathologic diagnosis of segmental mucosal fibrosis. All cats had gastrointestinal signs, including vomiting, diarrhea, weight loss, anorexia, or constipation. Differently from our study, this band was present in all cats in the jejunum and in one-third of cats in the duodenum, along with wall thickening and altered layering. The authors suggested that this band represents an area of mucosal fibrosis. However, in the same study, they prospectively examined 35 cats with visible hyperechoic mucosal band by ultrasound, without performing histopathology. Eleven had no clinical signs or other sonographic intestinal abnormalities. It was concluded that this band can be observed even in apparently healthy cats [13]. Undoubtedly, in cats with acute gastroenteritis caused by FPV this finding cannot be explained by fibrosis, which typically develops in chronic processes; whether the band represents visible lymphatic vessels similar to dogs [16] requires further investigation.
In the present study, increased mucosal echogenicity was observed in approximately 40% of cats in the duodenum and 30% in the jejunum; additionally, irregularity of the luminal surface was noted in 10% in the duodenum and in 30% 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 [13, 14]. Hyperechoic speckles and hyperechoic striations have been reported in dogs with chronic enteropathies [17]. Anecdotally, a hyperechoic mucosal border on the luminal margin has been noted in dogs with acute enteritis [18]. In our cats with FPV, it is possible that these findings are 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 [19].
In the present series, mucosal thinning of the duodenum and jejunum were observed in two-thirds of cases. 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 made in 40 puppies with CPV gastroenteritis wherein the duodenal and jejunal mucosa thickness was significantly decreased [19]. In cats with ultrasonographic information pertaining to the jejunal lymph nodes, echogenicity, echotexture, and size were normal. This finding is similar to previous observations in puppies with CPV [19], in which parvoviral infection was not associated with jejunal lymphadenopathy by abdominal ultrasound. Stander and coworkers (2010) assumed that cortical atrophy caused by the predilection of CPV for rapidly dividing cells of the lymphoid tissue was responsible. It is also possible that the same explanation accounts for the sonographically normal lymph nodes of the present series, 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 normal animals [20]. The use of very high-frequency transducers, improving the quality of images, may also be partly responsible for the elevated frequency of this particular pattern in our cats.
Considering associations between ultrasonographic features and clinical and laboratory findings, among gastrointestinal signs approximately one-fourth of cats had vomiting, which was positively associated with free peritoneal fluid. This may be justified by the fact that cats with abdominal effusion are expected to have more severe enteritis, worsening their clinical status. Additionally, age was positively associated with jejunal wall thickening, suggesting that the chances of identifying ultrasonographic abnormalities of the intestine are increased in older cats (> 12 months). This result might be explained by a more severe form of FPV enteritis in older cats which causes more edema and swelling of the intestine or by the concurrent presence of an underlying enteropathy that, in turn, modified jejunal wall thickening. Both hypotheses need to be confirmed by further studies.
Herein, short-term survival was positively associated with increased jejunal mucosal echogenicity and hyperechoic mucosal band; moreover, these latter findings were positively associated. It is possible that they represent the ultrasonographic appearance of defense mechanisms occurring in the intestine, eventually leading to a more favorable outcome in cats with FPV. Nonetheless, the association between shot-term survival and increased mucosal echogenicity and hyperechoic mucosal band remains elusive and histology would have been required for definitive diagnosis. Lastly, the negative association between thrombocytopenia and peritoneal fluid may suggest that inflammation is particularly pronounced in cats with more severe enteritis, in turn causing platelet consumption. However, a causative link between abdominal effusion and thrombocytopenia needs to be confirmed.
The main limitations of the present study are represented by the relatively small number of cats included and by the retrospective nature of the investigation; some medical records were incomplete, in particular those pertaining to ultrasound. However, it is worth mentioning that cats with FPV are often in critical conditions and abdominal ultrasonography may therefore be incomplete. In addition, follow-up abdominal ultrasound and histological examinations were not performed, which would have allowed characterization of the progression and causes of some ultrasonographic features.