Most parasitologists would agree that feline internal parasites, particularly helminths, have received less attention as disease agents or as potential causes of zoonotic human diseases than their canine counterparts. This is due in part to the perception that many feline internal parasites, particularly Toxocara cati and Ancylostoma spp. are uncommon. However, the few fecal and/or necropsy surveys that have been conducted in cats in the United States do not support this presumption. In fact, results of these surveys indicate that feline roundworms and hookworms represent the more common internal helminth parasites of cats, regardless of the geographic region in which the studies were conducted. It is also interesting that although effective anthelmintics have been available for many years, worldwide prevalences of feline internal parasites do not appear to have changed significantly. In this article, I will discuss several potentially pathogenic internal protozoal and helminth parasites of cats. Some of these parasites also are capable of causing disease in humans. This latter point will be emphasized given the recent initiatives by governmental agencies and professional associations to prevent transmission of certain helminth parasites from pets to people. I will also review available anthelmintics, antiprotozoals and recommended strategies for controlling common feline internal parasitic diseases (see Suggested Reading, end of article).

Giardiasis Giardia infections in cats are caused by Giardia intestinalis (also called G. lamblia). The parasite usually resides in the small intestine, although exceptional infections in the lower bowel cannot be ruled out. Giardia is a dimorphic parasite in that it exists as a fragile flagellated binucleate trophozoite and a quadrinucleate cyst. The trophozoite attaches to the surface of epithelial cells in the small intestine; encystment (formation of cysts) occurs in the ileum, cecum or colon. Although the mechanism(s) of Giardia-induced disease remain unknown, evidence suggests that the disease is likely multifactorial involving inhibition of brush border enzymes or other factors such as altered immune responses, nutritional status of the hosts, presence of intercurrent disease agents, and the strain of Giardia involved in the infection. Although many infected animals remain asymptomatic, the most common presenting sign is small bowel diarrhea. Feces are usually semi-formed, but may be liquid. Blood usually is not present. Feces have been described as pale (often gray or light brown), fetid and containing large amounts of fat. Cats with giardiasis may present with poor body condition, and weight loss. Vomiting or fever are not common presenting signs.

Photo 1: Iodine-stained cysts of Giardia from fecal flotation.

As mentioned previously, it is not unusual to find Giardia present with other gastrointestinal diseases such as inflammatory bowel disease. Giardiasis is best diagnosed by fecal flotation using zinc sulfate (specific gravity = 1.18) as the flotation solution. Centrifugation of the preparation increases the likelihood of recovering cysts. Also, the addition of a small amount of Lugol's iodine to the slide prior to placement of the coverslip containing the concentrated cysts will aid in visualizing the small (10-12 um) cysts (Photo 1).

Table 1: Treatment of feline giardiasis

Use of barium sulfate, anti-diarrheals or enemas prior to sampling feces may interfere with detection of cysts and should be avoided if possible. Other diagnostic techniques that can be used to recover trophozoites, cysts, or proteins produced by the parasite include direct examination of feces (wet-mount), immunofluorescent procedures, and ELISA techniques. These techniques are either too insensitive (direct examination) or impractical for the practicing veterinarian because of cost, required equipment or because of the effort required to conduct the test. Some controversy exists surrounding the potential of some animal strains of Giardia to infect humans. Although it is known that some host specificity among animal strains of Giardia does exist, I believe that it is best to be conservative about the potential for human infections with animal strains of Giardia. Consequently, it is my view that all animals that are positive by fecal examination or suspected of having giardiasis should be treated. Several options are available for treatment of Giardia infections in cats (see Table 1). Cats are best treated with metronidazole as indicated. Use of metronidazole in cats is generally safe if the total daily dose remains below 50 mg/kg. Additional attributes of metronidazole are its antibacterial effects, its activity against other protozoans, and its possible immune modulating effects. Studies documenting the efficacy of the benzimidazole anthelmintics such as fenbedazole against Giardia in cats have not been conducted. However, fenbendazole administered at 50 mg/kg daily for three to five days, as recommended for giardiasis in dogs, is also likely to be safe and effective in cats. Veterinarians now have an available vaccine to assist in the control of feline giardiasis. Based on available data, vaccinated cats are less likely to get infected with Giardia than nonvaccinated cats. Also, vaccinated cats that do get infected generally experience less severe diarrhea and shed fewer organisms for a shorter period of time. Veterinarians should assess each situation to determine whether a particular animal or group of animals are potential vaccine candidates.

Coccidial Coccidial infections in cats are caused by Isospora spp., also called Cystoisospora (see Table 2). The principal agents in the cat are I. felis and I. rivolta. These parasites reside in the posterior small intestine or in the large intestine depending on the species. Their life cycles are generally self-limiting, after which the infection is terminated. The parasites replicate first asexually by schizogony resulting in destruction of many host enterocytes in which they develop. Asexual development is followed by production of gametes that fuse to produce non-infective oocysts that are passed in feces. The developmental cycles in the feline host require four to 11 days depending upon the species.

Table 2: Developmental information on common feline coccidia

Development to the infective stage (sporulation) usually requires one to several days in the animal's environment. Only sporulated oocysts are infective to susceptible hosts. Clinical signs of coccidiosis include hemorrhagic or mucoid diarrhea, abdominal pain, dehydration, anemia, weight loss, emesis, as well as respiratory and neurologic signs.

Photo 2: Isospora felis (right) and I. rivolta (above) oocysts from fecal flotation.

Death can result from extreme cases, particularly in young kittens. Nursing animals, recently weaned animals, or those that are immunocompromised are more likely to develop clinically apparent infections. Diagnosis of coccidiosis is based on signalment (usually kittens), clinical signs and recovery of oocysts in feces (Table 2 and Photo 2). Fecal flotation remains the most practical means of recovering oocysts. A point to remember is that recovery of oocysts alone in feces is not sufficient proof to implicate coccidia as the cause of clinical signs. I have observed coccidial oocysts in the feces of many animals without evidence of intestinal disease.

Table 3: Treatment of feline coccidiosis

Although sulfadimethoxine is the anticoccidial medication most commonly used in cats, several other agents have been used with success (see Table 3). Little can be done to disinfect environments because of the ability of the oocysts to withstand chemicals and adverse environmental conditions. Good sanitation, including prompt removal of feces to prevent development of oocysts to the infective stage and treatment of queens with anticoccidial agents prior to parturition, have been shown to reduce the occurrence of coccidiosis in young animals.

Toxocara cati (Roundworm) Toxocara cati is the most common of the intestinal nematodes of cats, and in the opinion of many, the most important. These are the largest of the feline intestinal nematodes (3-10 cm) and are similar in appearance to the canine roundworm, T. canis. The few prevalence studies that have been conducted in cats in the United States indicate that T. cati is the generally the most common. For example, T. cati was present in 43 percent of 60 cats surveyed in Kentucky and Illinois, and in 92 percent of the 13 control cats acquired for the anthelmintic study conducted in Arkansas. Researchers at Cornell University have conducted fecal examinations on both shelter cats and cats that were privately owned. The combined prevalence of T. cati in the two cat populations was 33 percent (n=263 cats). The prevalence of T. cati in shelter cats was 37 percent. Surprisingly, the prevalence in privately owned cats was 27 percent. Although some of the surveys indicated that juvenile cats are more likely than adult cats to maintain patent infections, other sources indicate that cats retain their susceptibility to T. cati infections throughout their lives.

Toxocara cati can be contracted in several ways: ingestion of embryonated eggs, consumption of transport hosts such as mice, birds, cockroaches, and earthworms, and by transmammary transmission from the queen to her kittens. The transmammary route is apparently quite common. Toxocara cati undergoes a liver-lung migration, typical of other ascaridoid nematodes, before establishing in the small intestine. The developmental period for T. cati in the cat varies depending on the route of infection and host factors such as age. Adult worms are prolific egg producers and are estimated to produce as many as 24,000 egg per day. Eggs require three to four weeks in the environment to become infective, and can remain viable in the soil for months or years.

Kittens infected with T. cati can display signs of infection similar to those observed in puppies infected with T. canis, i.e. enlarged abdomen and failure to thrive. Vomiting and diarrhea also have been observed. Infections also can result in pulmonary lesions, as well as signs such as coughing and sneezing as a result of migration of the parasite through the lungs or upper respiratory tract. Migration through the liver apparently occurs without adverse effects.

Photo 3: Egg of Toxocara cati from fecal flotation.

Diagnosis of T. cati infections are confirmed by recovering the typical nonembryonated eggs in feces (see Photo 3). Eggs are smaller than those of T. canis, but are structurallysimilar to them. Occasionally feces and vomitus will contain expelled worms.

Table 4: Selected feline internal parasiticides

Ancylostoma tubaeforme/A.braziliense (Hookworms) These are small (5-12 mm) worms, that live in the small intestine of cats (See photo 4). Ancylostoma tubaeforme is similar in life cycle and pathogenicity to the common hookworm of dogs, Ancylostoma caninum. Ancylostoma tubaeforme appears widely distributed geographically, while A. braziliense is limited to tropical and subtropical regions of the world. Many veterinarians believe that hookworms are neither common nor of any significance as causes of disease in cats. Unfortunately, neither of these presumptions is always true. In the study mentioned above, Ancylostoma. tubaeforme was recovered from 75 percent of the 60 cats of cats from Illinois and Kentucky. In the other study cited above, Ancylostoma tubaeforme was present in 77 percent of cats examined in Arkansas. In the Arkansas study, A. tubaeformae was exceeded in prevalence only by Toxocara cati. In my laboratory, we are in the process of determining the prevalence of internal parasites in cats from east central Alabama. We have examined 52 cats to date. Thus far, we have recovered A. tubaeforme from 27 percent of the cats and T. cati (see previous) from 23 percent. Interestingly, seven cats harbored both parasites. Also, these parasites were found in cats ranging in age from 1 to 6 years and not just in kittens as one might suspect. We have also recovered both of these parasites from similar numbers of male and female cats.

Photo 4: Intestine from a cat experimentally infected with Ancylostoma tubaeforme. Note the presence of blood on the mucosal surface and attached hookworms. Top: Enlargement of an attached hookworm.

Studies have shown that A. tubaeforme can cause hookworm disease in cats. Experimental infections can cause weight loss and anemia in infected cats. Depending upon the rate of exposure to infective larvae, the outcome can be reduced hemoglobin levels, reduced packed cell volume or death. The number of worms recovered from infected cats is usually not high. In one study, a mean of 100 worms per cat was all that was necessary to cause death in 16 cats.

Apparently A. braziliense is less pathogenic than A. tubaeforme. Experimental infections with A. braziliense have failed to induce clinical disease similar that described for A. tubaeforme. However, A. braziliense is the hookworm species responsible for most cases of creeping eruption, a condition characterized by serpiginous dermal lesions in humans following penetration and migration of hookworm larvae.

Photo 5: Egg of Ancylostoma tubaeforme from fecal flotation.

Several products are highly effective against A. tubaeforme or A. braziliense in cats (Table 4). Prevention of predatory behavior in outdoor cats can reduce levels of infection for hookworms and roundworms, but this is difficult given the strong instinctive nature of this behavior. Although maintaining cats as entirely indoor pets could reduce the exposure to worm parasites, this is difficult to achieve in many situations. Periodic or monthly treatment remains the most effective means of controlling internal parasites. As mentioned above, the latter is more easily justified now that some available products show claims for prevention or control of heartworm and/or fleas and veterinarians are more likely to use the products to prevent or control these parasites.

Suggested Reading

• Centers for Disease Control, National Center for Infectious Diseases, American Association of Veterinary Parasitologists: How to prevent transmission of intestinal roundworms from pets to people. Publication No. MS F22, Division of Parasitic Diseases, Centers for Diseases Control, Atlanta, GA, 1996.
• Kazacos KR: Visceral and ocular larva migrans. Seminars Vet Med Surg (Small Anim) 6: 227-235, 1991.n Spain CV, Scarlett JM, Wade SE et al: Prevalence of enteric zoonotic agents in cats less than 1 year old in central New York State. J Vet Int Med 15: 33-38, 2001.
• Hill S, Lappin MR, Cheney J, et al: Prevalence of enteric zoonotic agents in cats. J Am Vet Med Assoc 216: 687-692, 2000.
• Olson ME, Ceri H, Morch DW: Giardia vaccination. Parasitol Today 16: 213-217, 2000.
• Feline Clinical Parasitology. DD Bowman (Ed.). Iowa State University Press, Ames, 2002, 469 pp.
• Akao N, Takayanagi TH, Suzuki R et al: Ocular larva migrans caused by Toxocara cati in mongolian gerbils and a comparison of ophthalmic findings with those produced by T. canis . J. Parasitol. 86: 1133-1135, 2000.