Ascarids of Dogs and Cats Toxocara canis Toxocara canis (common dog ascarid) is the most important of the two canine ascarids from the standpoint of prevalence, virulence and public health importance.
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Toxocara canis (common dog ascarid) is the most important of the two canine ascarids from the standpoint of prevalence, virulence and public health importance.
T. canis occurs in about 15-20% of dogs of all ages, except in sparsely populated, dry areas where infection rates are less (arrow refers to incidence in Hawaii). Puppies have much higher incidence rates however, because of maternally acquired prenatal and perinatal infections. Without evidence to the contrary, it is often presumed that virtually all puppies
are infected with larvae of T. canis.
Toxocara canis is a typical ascarid in that it is large and fairly robust. The females commonly are 12-15 cm. long by about 2 mm. wide. Males are somewhat shorter and thinner. When found in the ingesta of a freshly dead dog, they usually are coiled tightly, but after the carcass has cooled, the parasites relax and straighten. The anterior end of both sexes is bowed ventrally. The name, Toxocara, means "bowed head”.
This slide shows two major features of Toxocara canis. One is the 3 large, fleshy lips typical of all ascarids. These lips are used for "browsing" on internal epithelial surfaces - they are not suited for attachment. The other feature is the 2 wing-like cervical alae typical of T. canis. These alae are cuticular inflations which arise from the lateral body wall and may be seen grossly. They occur in both sexes at the bowed portion of the anterior end.
Ascarids do not attach to the mucosa but rely on
maintaining their position in the gut by a powerful swimming ability .
Clinical effects of T. canis are greatest in puppies. A thorough knowledge of the life cycle is necessary for a complete understanding of the pathogenicity of Toxocara canis. Effects are primarily due to adult worms, although migrating larvae are sometimes directly responsible for virulence.
Toxocara canis, like most ascarids, are prolific egg producers and may produce > 100,000 eggs/day/female worm. Eggs become infective after 10-15 days on the ground at normal temperatures and contain an infective second stage larvae protected by a thick highly resistant egg wall (for other nematode groups, third stage larvae are infective). Infective eggs may remain viable for years. They survive cold well but are killed at temperatures above 37°C. After ingestion of infective eggs by dogs, the infection may take one or two courses depending on age, sex and previous exposure of the host.
After ingestion by pups less than 6 months of age, and especially in pups less than 5 weeks of age, the L2 is released in the gut, migrates via the hepatic-tracheal route, and returns to the digestive tract. Second stage larvae reach the liver via the hepatic portal system in 1-3 days, the lungs as third stage larvae at 3-5 days, the stomach as L4 by 10 days, and are in the duodenum as young adults (L5) by 3-4 weeks. The prepatent period for infection via the hepatic-tracheal route is 4-5 weeks.
Both an age resistance and an acquired resistance due to a previous exposure occurs against T. canis infections. Suckling or weanling pups are fully susceptible, but become progressively more resistant thereafter until age resistance reaches maximal levels at about 6 months of age. True acquired immunity would constitute an additive resistance factor. As resistance builds, more and more larvae migrating through the lungs cross over into the somatic circulation and are disseminated into various tissues where they are trapped in small granulomas as dormant second stage larvae. These “arrested” larvae remain viable for years.
When a bitch becomes pregnant, latent somatic larvae are activated at 30-40 days of gestation and larvae migrate across the placenta into the liver and lungs of the fetus during the last trimester. This is thought to be the major life cycle survival strategy and is the main way to insure infection levels in dog populations .
In the fetus, juvenile larvae accumulate in the liver and lungs until whelping. At birth they resume migration by the hepatic-tracheal route and most larvae (L5) are in the small intestine by the 6th day of life. Infection by the prenatal route results in a more abbreviated prepatent period than that resulting from direct ingestion of eggs by pups, and eggs are passed as early as 2-3 weeks of age. Although most larvae migrate to the fetus in one pregnancy, three pregnancies are required to completely clear the tissues of a bitch, assuming there is no further exposure to Toxocara canis eggs.
“Activated" larvae have also been shown to accumulate in the mammary glands to be later acquired by suckling pups . Larvae have been found in milk taken at birth and up to 22 days after parturition. Larvae in the milk assume a typical hepatic-tracheal migration.The importance of this mode of infection is thought to be minor (2% ) and the transplacental route is most important for Toxocara canis in dogs, accounting for
98% of infections in pups. It is commonly observed that an increase in Toxocara infections occurs in nursing bitches. There are two possible explanations for this: 1) infection of a bitch may occur by passage of partially mature larvae in the feces of pups, and subsequent ingestion during cleaning of pups; larvae pass to the small intestine and mature directly without further migration, or 2) some " activated " larvae may find their way to the gut of the bitch and mature there. The effect in either case is that the bitch and her pups may harbor ascarids of exactly the same stage of maturation.
Although it is a minor source of infection it is possible for dogs to become infected by ingestion of a variety of paratenic hosts (including rats, mice, swine, sheep, birds, and others) which contain arrested L2 stages in somatic tissues. After ingestion, direct development occurs without hepatic-tracheal migration
Damage due to Toxocara canis consists primarily of digestive disturbances due to worms in the intestinal tract, but there may be lesser signs due to migrating forms, especially in the liver and lungs.
Hemorrhagic tracts and foci occur in the liver due to migrating larvae a few days after infection. eosinophilic, granulomatous cellular infiltrates result histologically and rapid healing occurs with little or no contribution to clinical signs of ascariasis .
In the lungs, usual infections result in small petechiae or ecchymoses when larvae break out of capillaries into alveoli.
In very heavy infections, large numbers of larvae simultaneously passing through the lungs may lead to lobular pneumonia with the alveoli filled with edema, RBC's, eosinophilic exudate and larvae.
Lesions progress to granulomatous interstitial change. Lung signs, if they occur,are seen 3-7 days post-infection in association with massive infections which on very rare occasions may be lethal. Very heavy maternal infections of pups can result in acute death of entire litters at 2-3 weeks of age due to pulmonary sequelae of massive Toxocara migration +/- dehydration associated with diarrhea and vomiting.
Presence of adult worms in the intestine result in irritation and mild catarrhal enteris manifested as diarrhea and sometimes vomiting. Direct effects ascribed include competition with the host for nutrients, damage from ascarid "browsing" on villi and an obscure interference with normal mechanisms of the host absorptive process. Intestinal obstruction is very unusual even with very large numbers of worms. Blockage due to migration up bile ducts may occur on rare occasions. Adult worms live an average of 4 months in the proximal small intestine.
Microscopically, lesions consist of relatively mild catarrhal inflammation with an increase in the number of goblet cells and mild mucosal infiltration with plasma cells, lymphocytes and eosinophils.
A variable eosinophilia in peripheral blood is seen with heavy chronic infections. Eosinophilia is classically seen clinically as a result of infection by helminths, some ectoparasites, and in allergic conditions.
Toxocara canis infections may result in the unthriftiness, dull hair coat and the "poor-doer" pups that are typical of chronic parasitism. Pups are stunted and have a "pot-bellied” appearance. Digestive disturbances include vomiting, diarrhea and constipation. Worms are
often presented to veterinarians for identification after being found in vomitus by owners. Young pups may die of weakness and dehydration if heavy infections are not treated. Some clinicians can detect a "sweetish odor" to the breath.
Older dogs are more resistant to T. canis and clinical signs, when they occur, are generally manifested only as unthriftiness, or diarrhea. The resistance of older dogs may be explained on the basis of both age resistance and acquired resistance due to prior exposure.
Age resistance. A true age resistance of obscure mechanisms begins at weaning and becomes progressively stronger until it reaches a maximum at about six months of age. The percentage of animals shedding T. canis eggs in the feces of mature (over 1 year) and immature dogs (0-6 months) over a five year period at Iowa State University is presented in this chart. The percentage of infected immature dogs was 40-50% (white bars) versus an infection rate of 5-10% in mature dogs (red bars).
The acquisition of resistance results in an incompletely understood phenomenon called" self -cure”, which occurs with other nematodes in addition to Toxocara canis. A local anaphylactic reaction in the digestive tract is postulated as the mechanism of self cure and results in the clinical observation of diarrhea, high fever (pyrexia) and passage of ascarids in feces.
On the basis of experimental evidence, it is theorized that ascarid antigens combine with local mast cells at surface IgE receptors. At a critical Ag-Ab level, the mast cells are "triggered" to lyse, producing histamine-like substances which in turn cause release of locally produced secretary IgA antibody and increased mucosal permeability. Mucosal infiltration with inflammatory cells occurs concurrently. The net effect of this "local anaphylaxis" reaction is the damage of worms by products of inflammation, antibody and/or cells from the mucosa and expulsion of the worms. The old practitioner's adage that "a fever causes the passage of ascarids" may be due to this phenomenon.
In vitro studies on the immune response to ascarids provide support for the self-cure theory . This Toxocara juvenile has been incubated in the serum of an ascarid-infected dog. Casts and plugs have formed from antigen-antibody reactions around the juvenile's mouth. Such reactions may weaken the worm and impede its activity, but will not kill the juvenile outright.
A second manifestation of immunity against ascarid juveniles is the in vitro attraction and adhesion of leukocytes to the juveniles cuticular integument (as seen here). The counterpart of this reaction in tissues would act on larvae migrating through tissues and explain their
Large numbers of larvae are "arrested" in dormancy or are killed in tissues of resistant hosts (as seen grossly in this kidney). Granulomatous encapsulation of larvae is typical in resistant hosts and is believed to be a cell-mediated or delayed hypersensitivity type response.
Diagnosis of Toxocara canis infection may be done by demonstrating typical large, dark, thick-shelled eggs at fecal examination.
Identification of worms in vomitus or diarrhea is also diagnostic.
Toxascaris leonina has a wide distribution in the U.S. but has a much lower incidence as compared to Toxocara in the south. (Some call it the "northern roundworm").
Toxascaris leonina occurs in dogs, cats and various wild canidae and felidae.
Toxascaris is morphologically similar to Toxocara. Females measure 10 cm. and males are up to 7 cm long.
Cervical alae and other major morphological characters are similar in appearance to Toxocara canis and these two species are difficult to differentiate on this basis.
The eggs of Toxascaris leonina are easily differentiated from either Toxocara species, and can be found by fecal examination or by dissecting mature eggs from adult female specimens .
The life cycle of Toxascaris leonina is much simpler than Toxocara.Toxascaris leonina does not normally utilize the hepatic-tracheal or somatic migration patterns and prenatal infections do not occur. Infections occur by direct ingestion of eggs or via transport (paratenic) hosts. After ingestion of infective
eggs (eggs are infective after about 1-2 weeks on the ground) larval development occurs in the wall of the small intestine. Second stage larvae enter into the intestinal wall for 9-10 days and return directly to the lumen where they molt twice to produce fourth stage larvae (L4) by 35 days, molt to L5 (sexually immature adult stage) by 6 weeks and produce eggs at about 75 days post-infection. Toxascaris is therefore not found by fecal examination until 2 1/2-3 months of age at the earliest (vs. 2-3 weeks for T. canis).
Paratenic hosts. When mice and other small abnormal hosts ingest infective eggs, larvae hatch out and migrate to various body tissues and become encapsulated. Dogs, and especially cats, may become infected by ingestion of these paratenic hosts .
Clinical effects of Toxascaris leonina are similar to Toxocara in the digestive tract (mild catarrhal enteritis) but since larvae do not migrate, there is no liver and lung involvement. The potential for infection is not as high as for Toxocara since prenatal or transmammary does not occur, and infections in puppies under
2 1/2-3 months of age are not seen.
Demonstration of typical eggs in feces is diagnostic or adults may be identified in vomitus, feces or at necropsy. Toxascaris leonina (right side) eggs are more oval, slightly smaller and lighter in color than Toxocara (left side) and the shell is "rough on the inside" with some space observed between the embryo and shell as opposed to Toxocara eggs which are "roughened on the outside" with a very dark, complete filling of the shell.
T. cati is morphologically similar to Toxascaris leonina, which also occurs in cats, but may be differentiated by the broader "arrowhead" cephalic alae and the "bowed" head.
Adult worms live in the small intestine of cats and produce eggs (similar in morphology to T. canis) that become infective 3-4 weeks after passed. When eggs are ingested, larvae undergo hepatic-tracheal migration as L2's which return to the GI tract, enter the stomach wall for a time, return to the lumen and after 3 molts are found in the small intestine as L5's. The prepatent period is longer than T. canis, about 8 weeks .
A number of animals can serve as paratenic hosts of T cati, especially mice and rats. Since migration occurs in paratenic hosts, no migration is seen in the cat and direct development to adults occurs in the gut.
Transmammary passage of larvae occurs in colostrum and throughout the first three weeks of lactation. This mode of transmission is the most important source of infection in kittens. Transplacental (prenatal) infections are not thought to occur.
Gut lesions are similar, but other damage due to T. cati is less severe than T. canis for several possible reasons. Infections obtained by transmammary or transport hosts undergo direct development in the gut and do not migrate by the hepatic-tracheal route like T .canis. Although a migratory phase occurs after ingestion of infective T. cati eggs, the effect of larvae on lungs is less than T. canis, possibly because no molts occur in the liver and lungs .
Clinical signs occur mostly in young animals and consist of stunting, pot-belly, diarrhea, poor coat and occasional deaths related to dehydration and weakness in heavy infections. Diagnosis is made by finding typical eggs or identifying adults. Heavily infected kittens are common and often show dramatic improvement in general health and condition following treatment. Remember: weanling cats may not yet be shedding eggs.
A wide assortment of drugs are available for use against ascarids. Older drugs are often cheap but have narrower spectrum against other parasites and include: Piperazine (ascarids only), methylbenzene (®Methycide) and dichlorvos (®TASK, ®TASK-tabs). Newer drugs include the broad spectrum
benzimidazoles (Mebendazole, Fenbendazole, Febantel, Oxybendazole) and the avermectin's (®Ivomec, milbemycin) but are generally more expensive.
Parantel pamoate (®Nemex) has gained wide routine usage in puppies and kittens because of its safety and easy acceptability of the malt flavored liquid vehicle. Parantel has only moderate effectiveness (80-90%) against mature ascarids and hookworms, however, and 2 or more follow-up treatments 1-2 weeks apart are often required to completely clear infections. Fenbendazole (SID for 3 days) has the advantage of high efficacy against both adult and immature L4 stages.
Diethylcarbamazine (®DEC) is reasonably effective (80%) in preventing new ascarid infections in concentrations used for prophylaxis of heartworms. The addition of oxybendazole to DEC (®filarabits-plus) produces a highly effective preventive against ascarids, hookworms and whipworms. Milbemycin (®Interceptor) is effective against roundworms, hookworms, and whipworms at the heartworm preventive dose. The addition of pyrantel to ivermectin (®Heartgard-Plus) adds efficacy against both roundworms and hookworms. Preventive heartworm medications that have efficacy against roundworms are effective and can be used in lieu of this regimen if they are begun at the recommended time at weaning .
If used with preventative sanitation measures listed below, drugs are currently available to allow near eradication of ascarids in both kennel and household environments. A good rule is to treat pups at 2,4, and 6 weeks after parturition and at vaccinations thereafter. Kittens (and queens) should be treated at 4 and 6 weeks of age (prior to egg shedding by worms) and at vaccinations .
This will prevent the passage of eggs by the pup or kitten. Repeat treatment
at 2-4 week intervals is needed to get adults produced from new infections
or larvae which may have been in tissues at time ofthe first treatment. Ascarid
burdens are known to increase in nursing bitches for unclear reasons.
Bitches should be treated before parturition toreduce egg exposure of pups and again on the same schedule used for the litter (at 2 weeks and each 2-4 weeks thereafter).
Since eggs require an incubation period of 2 weeks or more outside the host before they become infective, cleaning of cages at frequent intervals and disposing of feces containing eggs help lower the contamination by eggs. Use of 10% chlorox makes eggs less "sticky", allowing hoses to be effective. Construct kennel so that all of the floor is exposed to direct sunlight sometime during the day (at least 2 hours). While the eggs of T. canis are resistant to desiccation and chemicals, they are killed by sunlight, UV light, and high temperature. Feed and water resources should be high enough to avoid fecal contamination.
Toxocara canis and T. cati have important public health significance as a cause of larval migrans. Reports in both the popular press and the scientific literature reflect an inreasing awareness of the association between pet ownership and "visceral larva migrans “VLM) and "ocular larva migrans" (OLM) of children.
VLM was first recognized in 1952, as a case of extreme eosinophilia and
hepatomegaly in children due to accidental infection with the dog roundworm,
Toxocara canis. The feline ascarid, T. cati, has since also been implicated. Although adults may become infected, children between the ages of 1 to 4 are the most likely victims as a result of ingesting
contaminated soil or by sucking on fingers or toys contaminated with infective eggs. Children of low socio-economic status and children who habitually eat dirt (pica) are most prone to infection. Up to 30% of children under 6 years old have been observed to have pica. Larvae hatch out of infective eggs in the intestine and pass via the portal system to the liver and then lungs, through which they migrate extensively.
Humans are not a suitable host for development of Toxocara larvae so they continue to migrate as immature (L2) forms for months. Eosinophilic granulomatous lesions develop in the wake of the worms and some are immobilized or killed within eosinophilic granulomas. Clinical effects of severe infections eventually subside slowly over a period of 2-3 years. In a review of 20 cases in children 1-4 years old, signs included fever (55%), anemia (80%), eosinophilis of over 30% (100%), cough (20%), hepatomegaly (85%), and splenomegaly (45%).
Sometimes larvae are disseminated to other tissues, such as the brain or eye. Invasion of the eye (ocular larva migrans) has proven to be especially common and serious because of visual disturbance, possible blindness and because the lesion can be confused with malignant retinoblastoma wbich requires enucleation. Interestingly, OLM occurs most often in "light" infection exposure. Exposure to large numbers of infective eggs (over 200 are enough) leads to the more general sequelae of VLM . Larvae may remain alive in the eye with intermittent reactivation and migration for 4 years or more.
As one of the most common parasites of dogs and cats, an extensive reservoir for Toxocara exists in the pet population. Female worms are prolific egg producers, at 100,000 eggs/day/worm. Eggs become infective when they contain a fully developed second stage larvae, a process that ordinarily requires 10 days to several weeks on the ground. Like many ascarids, Toxocara eggs are remarkable for their longevity and resistance and may survive months or years. Contaminated soil, not fresh feces, is therefore be a source of infection whether ingested directly, on objects, or on the hair coat of a puppy. Most authorities agree that the possibility of acquiring VLM/OLM by simply petting a well cared for pet is remote.
As it appears that the transmission potential of Toxocara is high, that control is difficult, and that puppies and kittens are the primary source of infection, how great is the actual public health danger of toxocariasis? Serologic evidence indicates that the human exposure rate to Toxocara may be considerable. Serum samples from children in the Amite, Louisiana area in the 1970's revealed approximately 5% positive reactors by indirect hemagglutination. The question then becomes how this relates to actual incidence of clinical disease. Available information indicates that exposure may be widespread, but that most cases are silent, and incidence of serious disease is quite low. A 1984 survey of public parks in Baton Rouge revealed that only 0.4 % of over 1500 solid samples contained Toxocara eggs although other surveys have revealed up to 20-30%. Nationally, CDC reports a 1/3 seropositive rate of 2000-3500 suspect sera submitted each year; 70% had OLM, 20% had VLM and 10% were asymptomatic. Records at Tulane University revealed 14 cases of ocular toxocariasis from Louisiana during a one year period in 1975. Most had a history of pica or close contact with pets.
As a public health problem, veterinarians should make pet owners aware of the significant, albeit not alarming, dangers of Toxocara in dogs and cats, especially in families with small children. Routine fecal examination and regular deworming are standard procedure in veterinary hospitals and can substantially reduce the danger of visceral larva migrans. However, a recent survey indicates there is much room for improvement by better compliance and use of new preventive treatment regimens (Harvey et al, 1991).
Good pet hygiene will prevent soil contamination. Feces in yards can be disposed of regularly and litter boxes should be kept clean so that parasite eggs are not allowed enough time to become infective.
Kennel owners and breeders should treat breeding animals regularly. Litters are ideally treated at 2 weeks of age when Toxocara is in the intestinal tract but not yet shedding eggs which will contaminate the environment. Pups should be retreated at 4 and 6 weeks and at vaccinations thereafter. This regimen will obviate egg shedding in pups, a major source of new infection in other hosts. Older dogs and cats should be routinely checked and wormed at 6 month to yearly intervals. Broad-spectrum heartworm preventive drugs are highly effective against ascarids (e.g. Milbemycin, Diethylcarbamazine-Oxybendazole , Ivermectin-pyrantel).
A number of drugs may be used by veterinarians against Toxocara and other parasites of dogs and cats. If veterinary care is not sought, owners may use many of a number of old commercial pet wormers sold over the counter in pet shops and most grocery stores. Although many of these preparations do not effectively control certain parasites such as the blood sucking hookworms, most are effective against Toxocara. EXPERIMENTAL evidence indicates that it is possible to prevent transplacental and transmammary transmission to pups by treating pregnant bitches with FBZ repeatedly (50 mg/kg/day from gestation day 40 to 201days post partum) or with ivermectin (1 mg/kg at 20 and 40 days of gestation).
A final control measure is to not allow children to eat soil, sandbox sand or other material that may be contaminated with eggs, especially by young kittens and puppies that are poorly cared for. Public places where pets are allowed to roam such as public parks have sometimes been shown to be contaminated with Toxocara eggs. These sources of infection will be eliminated only by responsible pet ownership and widespread awareness of existing public health danger from dogs and cats.
Ascarids of wild animals have also been incriminated in VLM/OLM, especially for species that tend to occur near human habitation. The raccoon ascarid, Baylisascaris procyonis,
has been shown to be a highly pathogenic, neurotropic cause of VLM in man and other animals that ingest infective eggs in areas contaminated by raccoon feces. Fatalities have been documented in children due to Baylisascaris VLM. Experimental infection of a variety of laboratory animals commonly results in neurologic disease and death.
VLM caused by Baylisascaris, Toxocara canis, and Toxocara cati can be differentiated serologically through the Division of Parasite Diseases, Centers for Disease Control by Tests, Atlanta, GA.
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