Toxocara cati (Schrank, 1788) Brumpt, 1927
(Figures 4-27 through 4-32)
ETYMOLOGY:Toxo - arrow + cara = head, and cati for the domestic cat.
SYNONYMS:Ascaris cati Schrank, 1788; Fusaria mystax Zeder, 1800; Ascaris felis, Gmelin, 1790; Belascaris mystax (Zeder, 1800; Leiper, 1907; Belascaris cati (Schrank, 1788), Brumpt, 1922; Toxocara mystax (Zeder, 1800) Stiles & Brown, 1924.
HISTORY: A detailed history of the name Toxocara cati is presented by Sprent (1956). Goeze (1782) illustrated a worm from the cat that had large cervical alae. Schrank (1788) gave this worm the name Ascaris cati. Zeder (1800) introduced the specific name mystax for this parasite. The name of “cati” of Schrank, who referred to the figure of Goeze, therefore has priority. The genus Toxocara was established by Stiles and Hassal (1905) and Lumbricus canis, the dog ascarid, of Werner (1782), was considered th type species. Leiper (1907) created the genus Belascaris with Ascaris mystax of Zeder (1800) as the type species, and Leiper differentiated the genus Belascaris from other ascarids by the ventriculus located at the base of the esophagus. Stiles and Brown (1924) confirmed that the genus Toxocara had priority over Belascaris, and they created the name Toxocara mystax for the Toxocara species of the cat. However, the name of Schrank has priority over that of Zeder, and, therefore, the common Toxocara of the cat is Toxocara cati (Schrank, 1788) Brumpt, 1922.
GEOGRAPHIC LOCATION:Toxocara cati is a cosmopolitan parasite of the domestic cat and probably one of the most commonly encountered parasites. Some prevalences that have been recorded in different countries include: Germany, 45% of 155 cats (Schuster et al., 1997); France, 31% of 129 cats (Petithory et al., 1996); Tasmania, 89% of 39 cats (Milstein and Goldsmid, 1997); Taipei, 42% of 95 cats (Fei and Mo, 1997); Japan, 18.2% (Oikawa et al., 1991); Somalia, 28 % of 50 cats (Gadale et al., 1989): South Africa, 11% of 1,502 cats (Baker et al., 1989). Interestingly a survey of 188 feral cats from the Northern Territory of Australia revealed that only 1% of the cats were infected with Toxocara cati (O’Callaghan and Beveridge, 1996). In a careful study of the parasites occurring in litters of kittens in Germany, Toxocara cati infections were found in 54 litters of the 70 litters of free-ranging farm cats that were examined (Beelitz et al., 1992). On the other hand, of 30 litters of house cats where both the mothers and kittens had received anthelmintic treatment between weeks 2 through 12 after delivery, only one litter had an infection with Toxocara cati. As with many other helminth infections, juvenile cats are more likely to maintain patent infections, as shown in the survey performed in South Africa where the overall prevalence of infection with Toxocara cati was 11%, but the prevalence in juvenile cats was 41%.
LOCATION IN HOST: Adults are found in the small intestine.
PARASITE IDENTIFICATION: The adult worms are cream-colored to pinkish and have a length of up to 10 cm (Fig 4-27 and 4-28). Warren (1971) reports males as 3 to 7 cm long and females as 4 to 10 cm long. The adults have distinct cervical alae that are short and wide giving the anterior end the distinct appearance of an arrow. The esophagus is about 2% to 6% of the total body length and terminates in a glandular ventriculus that is about 0.3 to 0.5 mm long. The vulva of the female occurs about 25% to 40% of the body length behind the anterior end. The spicules of the males range from 1.7 to 1.9 mm in length. The egg measures 65 μm by 77 μm and has the pitted eggshell typical of the eggs of this genus of ascaridoids (Fig 4-29). The pits on the eggs of Toxocara cati are smaller than the pits observed on the eggs of Toxocara canis.
LIFE CYCLE: The adult worms live in the small intestine and the female produces eggs that are passed in the feces of the cat. The egg is typically passed containing a single cell, and after a period of time in the environment, two molts occur within the eggshell to produce the infective third-stage larva. There has been considerable debate about the number of molts occurring within the eggshell of the ascaridoid parasites, but the majority of evidence seems to be that for certain genera, anyway, that the infective stage is the third-stage larva.
Sprent (1956) described the details of the development of Toxocara cati in the feline host following oral infection with eggs and with mice that had been orally infected with eggs. After having infected kittens with 10,000 embryonated eggs, Sprent found that the larvae were found to migrate away form the alimentary tract before commencing development. By three days after infection, larvae were found in the live and lungs, and there were also larvae present in the stomach wall. Five days after infection, there were larvae in the lungs, tracheal washings, and stomach wall (Fig 4-30 to 4-31). After the tenth day of infection, many larvae were in the lungs and stomach wall, and a number of larvae began to be recovered from the muscle tissues of the cat. The larvae that make the liver-lung migration and return to the stomach wall via the trachea then undergo considerable growth. When kittens were fed mice that had been infected with 10,000 infective eggs of Toxocara cati, almost all larvae were found to complete their development without undergoing a liver-lung migration, and larvae were only rarely recovered form the muscle tissues of the infected cats. The larva that escapes from the eggshell measures 0.31 mm to 0.42 mm in length. Within the stomach wall of the cat, the larvae grow from 0.4 mm to about 1.3 mm in total length. The molt from third-stage to fourth-stage larvae occurred when the larvae measured 0.999 to 1.235 mm in length, and during this molt there was a marked reorganization of the mouth with the development of the lips characteristic of ascaridoid nematode. The fourth stage larvae were found in the stomach contents, intestinal wall, and intestinal contents. In egg-infected cats, fourth-stage larvae were first observed at 19 days after infection; whereas, in mouse-infected cats, fourth-stage larvae were first observed at 10 days after infection. When the fourth-stage larvae reach a length of about 1.5 mm, it is possible to readily distinguish males from females on the morphology of the genital rudiment, and as growth progressed the spicules of the males become evident and the tails of the males were broader than the tails of the female larvae. The molt from the fourth to the fifth larval or young adult stage occurred within the intestinal lumen when the larvae were 4.3 to 6.5 mm in length. The fourth-stage larvae could be distinguished from the young adults of similar length by the much thinner cuticular annulations on the adults. The smallest female observed by Sprent to have eggs in its uterus was 55 mm long. Eggs were first observed in the feces beginning 56 days after the infection of the cats. Dr. Stoye (personal correspondence with Dr. J.C. Parsons) has reported that in four older cats which were each experimentally infected with 500 embryonated eggs, the observed prepatent peiod was 38, 39, 39, and 40 days.
Sprent (1956) looked for the possibility of transplacental transmission from the queen to the developing kittens. During the last 4 weeks of gestation, a pregnant queen was given three inocula of 10,000 embryonated eggs. Larvae were not recovered from the tissues of the kittens examined 3 or 4 days after birth.
Swerczek et al. (1971) showed that transmammary transmission commonly occurs with Toxocara cati. The examination at birth of 78 kittens from 20 queens that were naturally infected with Toxocara cati and 14 kittens from 7 queens that were experimentally infected with 300 to 2,000 eggs of Toxocara cati per day from day 2 to 56 prepartum revealed no larvae in the organs of the kittens when they were examined. When 12 kittens were examined 15 to 22 days after natural delivery from 5 queens that had been orally infected with 2,000 eggs of Toxocara cati for 1 to 10 days prepartum, a total of 7,959 larvae were recovered, with most of the larvae being recovered from the gastrointestinal tract. Larvae were not found in the 5 littermates (one from each litter) that has not been allowed to nurse. These authors also found larvae in the mammary glands and milk of these 5 queens. The authors went on to show that 19 kittens that were derived by caesarean section from 6 queens and raised colostrum-free to maturity remained free of infections with Toxocara cati.
Paratenic hosts are probably routinely involved in the life cycle of Toxocara cati. The larvae are capable of persisting in the tissues of cockroaches (Sprent, 1956), earthworms (Okoshi and Usui, 1968); mice (Schön and Stoye, 1986), chickens (Okoshi and Usui, 1968, Sprent, 1956), dogs (Sprent, 1956), and lambs (Sprent, 1956). Beaver et al. (1952) showed that both Toxocara cati and Toxocara canis produced lesions in white mice that were similar to those observed in human cases of visceral larva migrans (Fig 4-32). Fülleborn (1921), Hoeppli et al., 1949, and Sprent (1952) showed that the larvae undergo a liver-lung migration in the mouse before they settled down in the musculature or brain. Sprent (1956) found that the larvae of Toxocara cati mainly are found in the somatic musculature. Nichols (1956) described the morphology of the larva of Toxocara cati and differentiated it from the larva of Toxocara canis, the major difference in the two worms was the diameter of the body which is narrower in Toxocara cati (Toxocara cati larvae have a width that is never greater than 18 m, while the larvae of Toxocara canis are typically 18 m wide or wider.)
CLINICAL PRESENTATION AND PATHOGENESIS: Kittens infected with Toxocara cati often show no clinical signs due to the infection. However, it is generally considered that kittens are capable of displaying signs similar to puppies with moderate worm burdens, i.e., a pot-bellied appearance and a general failure to thrive. On occasion it may be possible to palpate thickened intestines.
Aoki et al. (1990) reported on a 7-year-old domestic male cat that had anorexia, vomiting, and an enlarged abdomen. A laparotomy revealed an adult Toxocara cati in the abdominal cavity and a gastric ulcer that had perforated the stomach wall. The next day, acute perforations of the stomach again occurred, and during a second surgery, the two new gastric perforations were repaired and four adult Toxocara cati were removed from the abdominal cavity. Unfortunately, the cat died during recovery from the second emergency surgery. It is difficult to determine whether the ascaridoids were the cause of the gastric perforation or were simply migrating into lesions caused by some other underlying cause.
Swerczek (1969) and Swerczek et al. (1970) in studies on the comparative development of medial hypertrophy of the pulmonary arteries in cats with various helminth infections, described the hematological changes in experimentally infected cats. He reported that eosinophils may increase to up to 35% of the total leukocytes. Also, he found that anemia was typically not associated with the infection. Swerczek concluded that “T. cati migration produces severe lesions and is probably the most common cause of MHPA [medial hypertrophy of the pulmonary vessels] in cats.” This was observed in cats that had received doses of eggs of a period of several weeks; cats that received a single inoculum had less severe lesions that were similar to those of cats receiving weekly inocula. After a single inoculum, the lungs of cats would appear to have slight lesions 10 weeks after infection and would appear normal 14 weeks after infection. The histopathological lesions of MHPA can be quite remarkable with media of the arteries becoming very enlarged. Potential causes of the observed hypertrophy of the media of the vessels are allergy with histamine release (Weatherly and Hamilton, 1984) or pulmonary hypertension (Mecham et al. 1987).
TREATMENT: Treatment of gastrointestinal infections with Toxocara cati is relatively straightforward. Approved compounds include piperazine, pyrantal, dichlorvos, febantel formulated with praziquantel, selamectin, milbemycin oxime, moxidectin, emodepside formulated with praziquantel and pyrantel formulated with praziquantel. Ridley et al. (1991) reported on the use of pyrantel pamoate for the treatment of Toxocara cati in kittens experimentally infected by the feeding of infected mice; at 20 mg of base per kg body weight, this compound was 100% effective in removing the worms from these cats. The febantel formulated with praziquantel has been shown to be 100% effective in removing Toxocara cati from cats (Corwin et al., 1984). Ivermectin (200 g per kilogram body weight) has been found to remove adult Toxocara cati from infected cats (Kirkpatrick and Megella, 1987). Milbemycin oxime (500 g per kilogram body weight) is also effective against the adults of Toxocara cati.
Pharmacological prevention of the transmammary transmission of larvae has been shown using a topical formulation containing emodepside and praziquantel (Böhm, et al., 2015). When this formulation was placed on the pregnant queen at day 60 of pregnancy, vertical transmission of Toxocara cati was reduced 98.7% compared to controls.
EPIZOOTIOLOGY: Cats can be infected by one of three routes, by the ingestion of infective eggs, by the ingestion of a mouse containing larvae, or by the transmammary infection of kittens. Dubinsky et al. (1995) showed that small mammals were probably a major means by which the infection is maintained in cats that are allowed to hunt in Slovakia. Webster and Macdonald (1995) examined a total of 510 brown rats from 11 rural farms in the United Kingdom, and they found that 15% of the rats were infected with the larvae of Toxocara cati. Sprent (1956) infected chickens and recovered 10 larvae from only one of the four chicks that were given 5,000 eggs. Okoshi and Usui (1968) successfully infected a number of chickens by feeding them the eggs of Toxocara cati and verified that the larvae were present in the tissues of the chickens for at least three months after infection. However, there has been very little effort to determine the role of birds in the transmission of Toxocara cati to cats. Sprent did recover larvae from earthworms that were fed embryonated eggs. Takahashi et al. (1990) showed that cockroaches that ingest the eggs of Toxocara canis were capable of excreting the eggs in their feces over a two day period and that these eggs were still infectious; they went on to postulate that such insects can serve as vectors as they carry the eggs from fecal contaminated areas to food stuffs. It is unclear how often cats are infected by the ingestion of infective eggs. Uga et al (1996) examined the defecation habits of cats around three sand lots in public parks in Nishinomiya City, Japan, through the use of video-recordings. Around 4 to 24 cats visited each of the sand lots. Cats were observed to defecate in the three sand lots a total of 961 times in about 4 ½ months while dogs were only observed to defecate in these areas 11 times. One of the three sand lots was highly contaminated with the eggs of Toxocara, and 8 of the 12 cats that visited this site were observed to be infected with Toxocara cati. However, although cats are routinely visiting these sites there is no information on whether they are becoming infected from this type of source. In a survey of 181 cats for Toxocara in Dublin (O’Lorcain, 1994), no cats less than 4 weeks old were found to be infected, the highest prevalence of infection was found in cats between 12 to 24 weeks of age, and there was no apparent difference in the prevalence of infection between male and female cats. The work of Beelitz et al. (1992) would suggest that, as expected, the levels of transmission are greatest between free-ranging cats and lowest when cats receive adequate veterinary care.
HAZARDS TO OTHER ANIMALS:Toxocara cati will infect small mammals but their is little information on the effects on these hosts. The experimental infection of mice with the eggs of Toxocaracati, unlike those of Toxocaracanis, seldom result in ocular lesions in the infected mice (Olson and Petteway, 1971). Prociv (1986) showed that in guinea pigs the larvae of Toxocara cati tend to remain in the musculature rather than moving into the nervous system as do the larvae of Toxocara canis.
Roneus (1963 and 1966) presented rather convincing evidence that the larvae of Toxocara cati were capable of being a cause of “white-spot” disease in the liver of pigs. He showed that following infections with Toxocara cati, Toxocara canis, Parascaris equorum, or Ascaris suum that white spots appears on the surface and deep in the livers of infected pigs between a few days and up to two months after infection. Thus, although the disease induced in swine may not be great, there is the potential for economic loss due to this parasite if pigs are infected.
HAZARD TO HUMANS: There have been reports of humans who have passed the adult stage of Toxocara cati. To quote from Dr. Paul C. Beaver (Beaver et al., 1984) "Intestinal infections with adult-stage T. canis and T. cati have been reported in humans, but such records are generally unreliable. In the few cases in which an adult worm was unquestionably passed from the anus or mouth of a child, circumstances have suggested that the worm had been ingested as a mature or, more likely, an immature adult, having been taken form the feces or vomitus of an infected dog or cat (von Reyn et al., 1978)."
It is believed that most cases of human larval toxocariasis (visceral larva migrans) are due to the larvae of Toxocara canis. In histological sections, the larvae of Toxocara cati are slightly smaller, have a diameter of 15 to 16 μm, than the larvae of Toxocara canis which have a diameter or 18 m or greater. Thus, when biopsies are performed it is often possible to identify the larvae that are observed as the larvae of Toxocara canis. There have been two cases where the larvae of Toxocara cati have been identified in the tissues of humans. Karpinski et al (1956) report on two cases of human larval toxocariasis, and in a two-year-old boy from Philadelphia, they found small larvae in a liver biopsy that they thought were Toxocara cati due to their small size and the boy being in contact with an infected kitten and without any known canine contact. In a second case, Schoenfeld et al., 1964 found numerous larvae that were identified as Toxocara cati in the brain tissue of a five-year-old girl who died after entering a hospital in Israel, comatose with fever and convulsions. Nogakura et al. (1990) reported on a serological procedure for differentiating Toxocara canis and Toxocara cati in a gel diffusion method and examined sera from 17 cases of suspected toxocariasis. Virginia et al. (1991) examined the sera of 54 children from Recife City, Brazil who had signs of, tropical eosinophilia syndrome. They found 21 sera that were positive for antibodies to Toxocara, and after further analysis of sera from six of these children, they identified one that was felt to be due to Toxocara cati.
CONTROL/PREVENTION: The control of Toxocara cati in the cat still depends on the diagnosis of infection and treatment of cats shedding eggs. The monthly preventative approved for cats, ivermectin at 24 μg/kg, does not significantly reduce the number of adult Toxocara cati; Blagburn et al. (1987) showed that a dose of 300 μg/kg of ivermectin administered subcutaneously was required for the removal of adult Toxocara cati. However, monthly preventatives containing milbemycin, selamectin or moxidectin are effective at killing Toxocara cati. However, it is still prudent to prevent cats from obtaining infections by the ingestion of infective eggs or mammalian paratenic hosts.
Transmammary transmission should be presumed to occur, and kittens should be considered as infected and treated every 3 weeks, beginning at 3 weeks of age, until they are old enough to be given one of the approved preventatives on a monthly basis for the rest of their lives.
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Figure 4-27. Toxocara cati. Adult worms on the mucosa of the small intestine of a naturally infected cat.
Figure 4-28. Toxocara cati. Adult male and female worms, formalin fixed. Notice that the female tail is straight while both the head and the tail of the male are curled.
Figure 4-29. Toxocara cati. Egg passed in the feces of an infected cat with the thick shell that has a dimpled surface.
Figure 4-30. Toxocara cati. This histologic section is through a larva that was discovered as an incidental finding in a cat at necropsy.
Figure 4-31. Toxocara cati. Larva teased by Dr. M. Georgi from the heart tissue of the cat described above.
Figure 4-32. Toxocara cati. Section through the liver of a mouse that has been experimentally infected with Toxocara cati by the feeding of eggs containing infective larvae. Note the large lateral cords characteristic of these larvae in tissue sections.