Intestinal Obstruction Caused by Taenia taeniaeformis Infection in a Cat

Introduction

Taenia (T.) taeniaeformis is a common endoparasite of cats. Infection occurs via ingestion of the intermediate rodent host containing the cestode’s infectious strobilocercus. When the cat (the definitive host of this parasite) eats the infected rodent, the cestode attaches to the small intestinal mucosa with its protoscolex. The prepatent period for T. taeniaeformis ranges from 32 to 80 days. The cestodes can live for up to 3 years in the feline small intestine, and they can measure up to 60 cm in length.¹ Routine diagnosis of adult tapeworm infections is via recovery of proglottids or the microscopic visualization of taeniid eggs upon fecal examination.

No cases have been published describing disease or deleterious signs of infection associated with adult taeniid tapeworms in the intestinal tract of the feline host.² Generally in cats (as in humans), cases of intestinal taeniasis are well tolerated. Two human cases have been documented where intestinal obstruction and pancreatitis have been associated with the adult beef tapeworm, T. saginata.³ Reported in this paper is what the authors believe to be the first described case of intestinal obstruction caused by T. taeniaeformis infection in a cat.

Case Report

A 5-year-old, 6.3-kg, neutered male domestic shorthair (DSH) cat was presented with a history of acute vomiting, anorexia, lethargy, and dyspnea. The patient was a “barn cat,” with an indeterminate history of vaccination and anthelmintic administration. He was described by the owner as an excellent “mouser.”

On initial examination, the cat was overweight, severely dyspneic, pyrexic (40.5°C), and tachypneic (70 breaths per minute [bpm]). The dyspnea resolved with administration of analgesia and was thus reattributed to tachypnea, a manifestation of acute abdominal pain. Tachycardia (200 bpm) was noted, with a grade II/VI murmur and gallop arrhythmia heard loudest over the right cardiac apex. The cat displayed tenderness on cranial abdominal palpation. No foreign bodies, intussusception, or organ enlargements were palpable. Fecal flotation was not performed because of the acute presentation of clinical signs and rapid deterioration of the cat’s status.

Survey radiographs revealed mild cardiomegaly with right-sided ventricular enlargement. No pulmonary or pleural changes were detected [Figure 1]. Abdominal radiographs showed a generalized, ground glass appearance of the peritoneum and abdominal organs. No radiographic indicators of intussusception or abdominal organ abnormalities were seen. Despite poor serosal detail, cranial intestinal loops resembled a “string of pearls”—a radiographic sign frequently associated with linear foreign bodies. Ill-defined, radiopaque, linear foreign bodies were observed within cranial intestinal loops. Caudal intestinal loops were distended and evinced despite poor radiographic contrast [Figure 2].

Blood was collected via jugular venipuncture. An intravenous (IV) catheter was introduced to the left cephalic vein, and lactated Ringer’s solution (LRS) was administered at 2.5 mL/kg per hour. Buprenorphine^a analgesia was administered at 0.01 mg/kg subcutaneously (SC) q 6 hours. Amoxicillin/clavulanic acid^b was administered at 62.5mg SC.

A complete blood count revealed a mild left shift neutrophilia (16.1 × 10⁹/L, reference range 2.5 to 12.5 × 10⁹/L) with band forms (0.9 × 10⁹/L, reference range <0.4 × 10⁹/L) and moderate lymphopenia (0.7 × 10⁹/L, reference range 1.5 to 7.0 × 10⁹/L). Biochemical analyses revealed hypochloremia (112 mmol/L, reference range 115 to 123 mmol/L); reduced bicarbonate levels (15 mmol/L, reference range 16 to 24 mmol/L); hypercalcemia (2.62 mmol/L, reference range 1.75 to 2.50 mmol/L); hypophosphatemia (1.15 mmol/L, reference range 1.29 to 2.26 mmol/L); hyperalbuminemia (41 g/L, reference range 22 to 35 g/L); and elevated lactate dehydrogenase (307 U/L, reference range 50 to 300 U/L).

The clinical pathology interpretation was dehydration with an inflammatory leukogram suggesting infection and tissue necrosis. Serum calcium levels were increased, putatively in concert with increased albumin levels, due to vascular fluid loss. Hypercalcemia, an increase in the total serumcalcium(as assayed in this case), is frequently associated with dehydration and vascular space contraction.⁴ Hypophosphatemia was attributed to anorexia or decreased gastrointestinal absorption. Hypochloremia was putatively caused by gastric acid loss from vomiting. In the absence of hypokalemia, an alternative explanation for the hypochloremia is the presence of an anion gap secondary to metabolic acidosis. This would account for unquantified anions produced from the lactic acidosis accompanying dehydration. The cat was euthyroid and suffering acute metabolic acidosis—probably as a result of vomiting and dehydration. Blood gas analysis was not available.

The following day, the cat was afebrile (rectal temperature 37.7°C); however, abdominal tenderness had increased markedly, and the cat’s mentation and general condition were deteriorating rapidly. Clinical signs were consistent with a proximal small intestinal obstruction, and abdominal ultrasonography was unavailable; therefore, a decision was made to perform an exploratory celiotomy.

Anesthesia was induced with 1 mg IV diazepam.^c A 3.5-mm endotracheal tube was placed, and anesthesia was maintained with 2% isoflurane in 1 L oxygen per minute, using a nonrebreathing T-piece circuit. Lactated Ringer’s solution was administered at 10 mL/kg per hour throughout the surgery in addition to a slow, intraoperative IV infusion of amoxicillin sodium^d at 22 mg/kg.

A ventral midline incision was made. On survey celiotomy, abdominal organs appeared grossly normal. A copious, translucent abdominal effusion was present. Upon manually tracing the intestinal tract from the lesser curvature of the stomach and pylorus to the descending colon, plication of the duodenum and jejunum occurred. Four enterotomies were created along the antimesenteric border of the duodenum, jejunum, and ileum. Numerous cestodes were removed manually with thumb forceps and placed in formalin.

In total, >30 adult cestodes were removed. The portion of worms that were recovered and retained for identification weighed 6 grams or 0.1% of the cat’s body weight. Cestodes were later identified as T. taeniaeformis [Figure 3].

A sample of abdominal effusion was collected. Microscopic examination showed red blood cells and lymphocytes, but no polymorphonucleocytes or bacteria. A presumptive diagnosis of sterile, reactive peritonitis was made.

The entire intestinal serosa was vital; no adhesions, strangulation, torsion, or intussusceptions were visualized. Using absorbable polydioxanone suture, enterotomy incisions were closed with simple interrupted, crushing sutures. Prior to closure, the abdominal cavity was lavaged twice with sterile, prewarmed LRS.

Recovery from anesthesia was without incident. The cat was maintained on analgesia, antibiotics, and nil per os (PO) for 24 hours. For 48 hours following surgery, the cat was monitored for clinical signs of peritonitis secondary to enterotomy site leakage.

Bland food was introduced 24 hours following surgery. The cat remained afebrile and had a good appetite. Postoperative buprenorphine^a (0.01 mg/kg IV q 6 hours) and amoxicillin sodium^d (22 mg/kg IV q 8 hours) were administered. After making an uneventful recovery, the cat was discharged 48 hours following surgery.

Upon reexamination 3, 7, and 10 days postsurgery, the cat showed no remarkable clinical signs. A broad-spectrum anthelmintic tablet (Drontal)^e was administered PO 10 days after surgery, when skin sutures were removed.

Discussion

The authors believe this is the first description of intestinal obstruction caused by T. taeniaeformis. Although it is expected that similar cases of obstruction have been observed previously by veterinarians, apparently no reports have been published regarding either impactions or clinical signs associated with adult cestodiasis in cats. In this case, the cat responded successfully to surgical intervention with multiple enterotomies and removal of entire cestodes and their segments from the small intestine. With quarterly administration of praziquantel at 5 mg/kg PO, no further recurrence of clinical signs was observed.

Linear foreign bodies are regular causes of gastrointestinal disease in animals. Clinical signs are generally those of partial or complete gastric or small intestinal obstruction. They include vomiting with or without anorexia, depression, or diarrhea. Blood assays can be variable and often are not diagnostic. The presence of abdominal pain is variable. If the intestine becomes devitalized, promulgating septic peritonitis, the animal may be presented as moribund or in septic shock.⁵ The clinical course and signs are more severe in animals with complete and more orad obstructions.⁶

Linear foreign bodies in cats are commonly anchored under the tongue or located at the gastric pylorus. Frequently, because of gastrointestinal arboreal motion, linear foreign bodies can cause intestinal plication, which may be visualized with barium radiography. Peristalsis can cause these foreign bodies to perforate the mesenteric border of the small intestine, causing fatal peritonitis and septic shock.^6–8 In this case, the intestinal obstruction failed to be diagnosed via radiography or abdominal palpation. Abdominal ultrasonography, which often allows identification of not only the presence of the obstruction but also the cause(s), was not available.

Cats are commonly infected with T. taeniaeformis. In Australia, infections have been frequently reported in surveys. Infection prevalence rates include 63% of feral cats from Kangaroo Island, 3% of cats from Tasmania, 48% of cats from the Northern Territory, and 9% of urban and 35% of rural cats from Perth and Swan River, respectively.^9–12 In Taipei, Taiwan, 18% of cats were infected; in the Korea Republic, 12% of 215 stray cats were infected.^13,14 A fecal survey of cats in the United States demonstrated that 2.4% of 452 feline fecal samples were positive for cestode proglottids.¹⁵ A similar study demonstrated that 4% of 2000 feline fecal samples were positive for proglottids of Dipylidium caninum, Mesocestoides spp., or T. taeniaeformis.¹⁶ Ahigher prevalence of cestode infections has been reported in European cats, with 33% of cats infected with T. taeniaeformis in Austria, and 20% to 28% of sampled Belgian cats being infected.^17,18

Intestinal obstruction from cestodiasis, specifically T. saginata, has been described in one human case in which a bolus of cestodes caused acute mechanical intestinal obstruction at the level of the ileocecal valve.¹⁹ Another human case report described acute edematous pancreatitis resulting from obstruction of Wirsung’s canal by T. saginata. ²⁰ Both cases were resolved surgically.

Cestode infections are not currently treated by some of the products that provide cats with protection against heart-worm and various ectoparasites and endoparasites. Thus, when these products are used, the cats are not protected against nor treated for cestode infections. It is important, therefore, that cats receive annual physical examinations, including a fecal examination. Where possible, hunting by cats should be discouraged; but for those cats that do hunt, some form of routine tapeworm prevention may be considered.

Conclusion

This is the first reported account of cestodes causing small intestinal obstruction in a cat. Although T. taeniaeformis rarely causes clinical disease in cats, this report indicates it should be included as a differential diagnosis in feline cases of acute intestinal obstruction. In particular, vigilance ought to be employed with at-risk feline patients having histories of access to rodents and no regular treatment for cestodiasis.

Acknowledgments

The authors thank Professor Ian Beveridge, BVSc (Hons), PhD, from the Department of Parasitology, University of Melbourne,Werribee, Victoria, Australia, for identifying the cestodes. They also thank Dr. Helen Vanderbom, BVSc (Hons), of South Cranbourne Veterinary Surgery, South Cranbourne, Victoria, Australia, for providing the radiographs.