5-Year-Old FS Labrador Retriever

Signalment & History

A 5 year old FS Labrador Retriever presents for the presenting complaint of persistent inappetence and vomiting. The owner reports a one month history of occasional vomiting and left hindlimb lameness. In the last 4 days she started vomiting at least 2 times a day, spontaneously. On physical examination, she is quiet, alert and responsive. Marked sialorrhea is noted. No regurgitation or vomit is elicited on palpation. However, on abdominal palpation she appears uncomfortable and reluctant to stand. Palpation reveals slightly thickened intestinal loops. The remainder of the examination is unremarkable.

Left lateral thorax Right lateral thorax VD thorax


A smoothly marginated, round to oval soft tissue opacity, measuring approximately 8 cm in diameter, is noted at the level of the cranial abdomen, on both lateral views. This represents severe circumferential thickening of the pylorus and it’s best seen on the left lateral view. In addition a thin pleural fissure line is seen between the right middle and the right caudal lung lobes.mMild multifocal spondylosis deformans is present at T8-T11, T13-L2. Minimal osteophyte formation is noted along the caudal aspect of the left humeral head.


You have found a severe (approximately 2 cm thick) circumferential thickening of the pyloric region of the stomach. In addition, you have seen a thin pleural fissure line between the right middle and right caudal lung lobes. Mild multifocal thoracolumbar degenerative changes and minimal left shoulder osteoarthrosis have been noted. These radiographic abnormalities are consistent with a suspect pyloric mass. Differential include neoplasia (adenocarcinoma, leiomioma/leiomiosarcoma, lymphoma), focal infiltrative gastritis (eosinophilic, granulomatous disease –Pytium insidiosum, aberrant Spirocerca lupi), pyloric muscular or mucosal hypertrophy, localized hyperplastic gastropathy. A gastroduodenal and a separated jejunal mass, associated with moderate mesenteric and pancreaticoduodenal lymphadenomegaly and scant peritoneal effusion were revealed during ultrasonographic examination of the abdomen. FNAs of the masses were performed and confirmed the presence of gastrointestinal Phytium infection.


Phytiosis is a chronic pyogranulomatous infection which has been reported from many subtropical regions including southeast Asia, Australia, New Zealand, South America, the Carribean and United States. The etiologic agent is Pythium insidiosum, an aquatic oomycete in the kingdom Stramenopila, and as such is more closely related to algae than to true fungi. Mainly the disease may occurs in gastrointestinal (GI) or cutaneous forms.

In dogs, in contrast to horses, the gastrointestinal form of phytiosis occurs more often than the cutaneous form. Infection by P. insidiosum is more frequent in young immunocompetent adults. Infection by this acquatic pathogen is most common in young large breed dogs which have had exposure to standing water during warm months.

The gastrointestinal form is characterized by nonspecific signs referable to the gastrointestinal tract. Frequently pyogranulomatous lesions are quite extensive by the time of clinical presentation. Lymphatic and vascular invasion is common and successful surgical resection is rare for this reason. Most patients die within three months of diagnosis. Vascular invasion or involvement of the root of the mesentery may also result in segmental infarction of part of the GI tract resulting in acute onset of the clinical signs. In chronic infections the disease may involve adjacent organs (pancreas, mesentery, liver or uterus).

Routinely imaging modalities such as abdominal radiographs or ultrasound may reveal the severe segmental thickening of the canine GI tract caused by the oomycete. Ultrasound is frequently used to evaluate the GI system in such patients. Findings may include thickening of the stomach and intestinal wall and enlargement of regional lymph nodes. Although these represent nonspecific ultrasonographic features, GI phytiosis should be considered in the list of differential diagnosis when the patient comes from endemic areas and shows these US findings. Nevertheless, pathological examination of tissue is required for definitive diagnosis.

Phytium insidiosum is a oomycete and it’s the only etiologic agent of phytiosis in mammals. The infection occurs mainly in tropical and subtropical areas, particularly in horses, dogs and humans but it has also been reported in calves, cats, sheep, a bird and several captive exotic species. Infection is acquired through small wounds via contact with water that contains motile zoospores or hyphae. Depending on the site of entry infection can lead to different form of phytiosis (cutaneous, vascular, ocular, gastrointestinal or a systemic form-which is rarely seen). The infection is a rarely occurring, non-transmissible disease.

In the canine patient the oomycete causes severe segmental thickening of the canine GI tract. Clinical symptoms of GI phytiosis include vomiting, weight loss, intermittent diarrhea, and palpable abdominal masses. The infection can extend to pancreas, mesenteric lymph nodes and bile ducts.

A positive diagnosis for P. insidiosum infection can be obtained by culturing and wet mount examination, histopathology, and serological or molecular diagnosis from samples of the infected tissues.

The prognosis of canine gastrointestinal pythiosis is poor. Often most affected dogs are presented in an advanced stage of the disease, by which time tissue damage is too extensive. This damage is most severe when infarctions occurs or when vital structures such as bile duct or pancreas are invaded. Also no currently used therapies seem to be effective against this pathogen in the dog. Most antifungal are ineffective against the pathogen, and immunotherapy has been successfully used in humans and horses to manage this disease. Current reported therapies in veterinary medicine include radical surgery, antimicrobial agents, immunotherapy or a combination of these.


Phytium insidiosum: An overview. Gaastra W et al. Vet Microbiol 2010 (20); 146 (1-2): 1-16.