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Parasitology, Practical Parasitology

Parasite Protocols: Canine Intestinal Helminths


Dwight D. Bowman, MS, PhD, Diplomate ACVM (Parasitology, Hon), Cornell University & Tom Nelson, DVM Animal Medical Center, Anniston, Alabama

Many dogs are affected by helminths despite prescribed broad-spectrum parasite control. This article focuses on helminths that affect the gastrointestinal system and highlights the importance of an annual fecal examination.

The mission of the Companion Animal Parasite Council (CAPC) is to foster animal and human health, while preserving the human–animal bond, through recommendations for the diagnosis, treatment, prevention, and control of parasitic infections. For more information, including detailed parasite control recommendations, please visit capcvet.org.

Helminth parasites are regularly diagnosed in dogs in the U.S (Table 1). Despite approximately 2 decades of excellent anthelmintic therapeutics, large numbers of dogs are still infected with common hookworms, roundworms, whipworms, and tapeworms.1 Many dogs are also affected by helminths that occur locally or sporadically in the U.S. These helminths may not be controlled by the different products available for prescribed broad-spectrum parasite control, which highlights the importance of an annual fecal examination.

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While helminths can affect many different systems and organs, such as the heart and lungs, this article will focus on those that affect the gastrointestinal (GI) system.


Ancylostoma caninum, Ancylostoma braziliense, & Uncinaria stenocephala

Distribution. Hookworms are found in dogs throughout the U.S. (Figure 1). Prevalence in the southeast is about twice the national prevalence; numbers are lower than the national average in the southwest and upper Midwest.

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  • A caninum is the most significant agent of hookworm-induced anemia,2 and its eggs account for the preponderance of positive samples represented in Figure 1.
  • U stenocephala is thought to occur more commonly in northern climates.
  • A braziliense is found in the Caribbean and southeastern U.S., and along the Gulf and Atlantic coasts.

Clinical Signs. In puppies infected via transmammary transmission, sometimes fatal anemia may develop as early as 2 to 3 weeks of age, usually occurring before eggs appear in the feces. Affected puppies may present with pale mucous membranes, anemia, ill thrift, failure to gain weight, poor haircoat, dehydration, and melena. Puppies harboring many worms develop an acute normocytic, normochromic anemia, followed by hypochromic, microcytic anemia due to iron deficiency.

Without immediate intervention, these animals may die. Those that survive usually continue as “poor doers,” with chronic anemia. Respiratory disease and pneumonia may occur in puppies when large numbers of larvae migrate through the lungs.

Diagnosis. Eggs are found in the feces of dogs, and are best identified by centrifugal fecal flotation. The eggs of U stenocephala are larger than those of Ancylostoma species; most laboratories can now distinguish the eggs on fecal examination.

Treatment & Prevention. See Table 2.

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Toxocara canis, Toxascaris leonina, & Baylisascaris procyonis

Distribution. As shown in Figure 2, T canis is found in dogs throughout the U.S., with areas in the northeastern and western U.S. above the national average. T leonina is less common, but considered to be more common in the colder areas of the U.S. B procyonis is commonly found in raccoons throughout much of the U.S., but, fortunately, infections in dogs are rare.3

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Transmission. Puppies are often infected with T canis in utero via transplacental transmission.2 After birth, dogs primarily become infected with ascarids via ingestion of:

  • Larvated eggs from a contaminated environment (all ascarid species)
  • Other vertebrate hosts that have consumed larvated eggs and, thus, have larvae in their tissue.

Clinical Signs. Disease caused by infection with T canis is most severe in young puppies, and can occur before eggs are present in the feces. Puppies infected in utero may present with ill thrift, failure to gain weight, and a poor haircoat; a pot-bellied appearance is also common. Those with heavy infections may expel a large mass of worms in vomitus at 4 to 6 months of age, causing the owner distress as the worms are large and usually alive.

Severe infections in neonatal pups can result in acute death at a few days of age because the large numbers of larvae acquired in utero cross the alveoli en route to the small intestine. Adult dogs—even those infected in utero—can be repeatedly infected with adult T canis if the dog is orally exposed to even a few (25–100) infective eggs.

Diagnosis. Eggs are identified in the feces of dogs by centrifugal fecal flotation. The eggs of all 3 species can be readily observed in a fecal sample; the eggs of B procyonis are smaller and darker than eggs from other roundworm species (Figure 3).

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Treatment & Prevention. See Table 2


Trichuris vulpis

Distribution. T vulpis eggs are found throughout the U.S. (Table 1). Prevalence rates are lower in the north central and mountain states, but T vulpis is present in more than 1% of canine fecal samples from Washington and Michigan (Figure 4).

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Clinical Signs. Some T vulpis infections result in hemorrhagic typhilitis or colitis, characterized by diarrhea streaked with mucus and fresh blood.2 Severe infections due to the presence of thousands of worms may occur when a dog lives in a highly contaminated area, resulting in bloody diarrhea, weight loss, dehydration, anemia and, in the most extreme cases, death.

Diagnosis. Eggs are identified in the feces of dogs by centrifugal fecal flotation, and require a flotation solution of higher specific gravity than hookworms and roundworms to insure maximal recovery.

Treatment & Prevention. See Table 2.



  • Dipylidium caninum
  • Taenia species
  • Echinococcus species


  • Diphyllobothrium latum
  • Spirometra species

Distribution & Transmission. CAPC does not collect data on tapeworm prevalence because the common species found in dogs are unlikely to be diagnosed by simple fecal examination, and fecal flotation alone almost certainly underestimates the frequency of infection. This difficulty is due to the focal distribution of proglottids (and, thus, eggs) in fecal material and the eggs’ weight, which keeps them from readily floating. Even in the presence of infection, a fecal sample may be negative for tapeworm segments—called proglottids—or eggs. Based on various published studies, prevalence of canine tapeworms varies from 4% to 60%.4

D caninum & Taenia species. The 2 most common tapeworms in U.S. dogs and cats are D caninum (associated with fleas) and T pisiformis (acquired from rabbits). Other Taenia species are found throughout North America and may infect dogs that ingest sheep or wild ungulates.4 All Taenia species in North America utilize mammals as intermediate hosts, and dogs as final hosts.

Intermediate hosts of tapeworms become infected from eggs in a dog’s feces.

  • D caninum: The egg is eaten by a flea larvae; the dog becomes infected when it eats an adult flea containing the fully mature larval stage. After a dog ingests an infected flea, it begins shedding proglottids in its feces approximately 3 weeks later.
  • Taenia species: The rabbit or ungulate intermediate host becomes infected by ingesting eggs while grazing; then the dog becomes infected when it ingests the viscera (or muscles) that contains larval stages of the tapeworm. Taenia species need 6 to 8 weeks to mature before they begin shedding segments in the dog’s feces.

E multilocularis & E granulosus. These parasites are found in the northern U.S. and Canada. E multilocularis cycles through small rodents and foxes; E granulosus cycles through large, wild ruminants, such as moose and wolves. The ranges of both are expanding, and concern exists that these dangerous zoonotic agents may begin affecting domestic dog populations.

D latum & Spirometra species. Infections with D latum are acquired from ingestion of freshwater fish and tend to sporadically occur in the northern U.S. and Canada. S mansonoides occur in the eastern U.S. and are acquired from ingestion of larvae in tissues of a variety of vertebrate intermediate hosts.

Clinical Signs. Disease resulting from adult tapeworms is probably underappreciated.

Humans with adult Taenia infections may report vague abdominal discomfort, hunger pains, loss of appetite, chronic indigestion, persistent diarrhea, or alternating diarrhea and constipation.5 However, dogs are infected with different Taenia species than humans.

Tapeworms cause marked thickening of the intestinal mucosa in dogs, and cases of fatal impaction have been reported in young puppies with fleas and massive tapeworm infections. When examined at necropsy, the intestines of a dog with 50 T pisiformis are usually packed to the intestinal lumen’s full capacity.

Infections with S mansonoides have been associated with GI disease in dogs and cats.4 Reported clinical signs include diarrhea, weight loss, and vomiting, which usually resolve following appropriate anthelmintic therapy.

Diagnosis. A D caninum egg packet or taeniid egg in a fecal sample is diagnostic of tapeworm infection, and proglottids can be readily identified as either Dipylidium or Taenia (Figure 5). However, the chances of finding an egg in the feces are minimized because eggs are intermittently shed in segments and are usually too dense to float in common flotation solutions.

Because Echinococcus and Taenia are morphologically similar, and Echinococcus is a significant and dangerous zoonotic agent, there is cause for concern if a taeniid egg, but no proglottids, is identified in the feces of a dog located where Echinococcus is also found. Tests are available in Europe that distinguish Echinococcus eggs from Taenia eggs, but these tests are not yet available in the U.S.

The eggs of D latum and Spirometra species are also found in the feces, and resemble a trematode egg (Figure 6). These eggs are shed from the tapeworm strobila within the dog’s intestine rather than being passed in terminal segments.

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Treatment. See Table 2.


Alaria canis, Alaria marcianae, & Nanophyetus salmincola

Distribution. Alaria species are found throughout the U.S,6 while N salmincola is found in the coastal northwest.7

Clinical Signs. Alaria alone does not cause signs in dogs. However, dogs that contract N salmincola, especially those new to or visiting endemic areas of Oregon and Washington, may present with fever, diarrhea, and thrombocytopenia, which results from the rickettsial agent, Neorickettsia helminthoeca.

Diagnosis. Dogs become infected with N salmincola by ingesting metacercariae in salmonid fish; these flukes often begin shedding eggs within a short time after infection, and a fecal examination with a direct smear revealing eggs in a dog with clinical signs of neorickettsiosis will help verify the clinical diagnosis.

N salmincola (Figure 7) eggs are small and heavy (they float best in a saturated sugar solution and centrifugal flotation), while Alaria eggs are larger.

Treatment. See Table 2. Tetracyclines are considered the treatment of choice for neorickettsial disease associated with N helminthoeca. Short-acting corticosteroids may be used supportively.

Prevention. See Table 2.


Few things are as disruptive to the human–animal bond as a puppy or adult dog passing a worm in its stool, vomiting a wad of worms, or depositing a tapeworm proglottid on the owner’s lap. Since some intestinal helminths also have zoonotic potential, control and prevention of these parasites are imperative to preserve this bond.

Prevalence. Intestinal helminths are common in all dogs, especially stray dogs and dogs found in shelters. Surveys of shelter dogs in the U.S. demonstrate higher numbers of helminths than the numbers seen in the general canine population.8

  • In the Northeast, 1 or more of every 10 dogs has roundworms, hookworms, and whipworms.
  • These numbers are higher in the Midwest, approaching 1 in every 5 dogs, and highest in the South, ranging from 1 in 5 to 1 in every 2 dogs.
  • Even in western states, 1 in 10 to 1 in 20 dogs sampled are positive for these parasites.

Because roundworm and whipworm eggs can persist in the environment for several years, clients need to understand that their pets are at risk for infection when outside. In addition, stray dogs defecating in the yard or park are not receiving treatment and likely infected.

Diagnosis. Dogs should have fecal examinations performed 2 to 4 times during their first year of life and 1 to 2 times per year as adults, depending on patient health and lifestyle factors.

Treatment & Prevention.

  • Routinely deworm puppies beginning at 2 weeks of age, with deworming repeated every 2 weeks.
  • Begin administering a monthly control product with efficacy against intestinal helminths when puppies reach 4 to 8 weeks of age (Table 2).
  • Broad spectrum parasite control products should be administered monthly year round.

Inform clients that routine parasite control typically results in negative fecal examinations, confirming the efficacy of routine parasite prevention. Other preventive measures they can implement include:

  • Keeping dogs on a leash or in a fenced yard to prevent predation and scavenging activities; this limits the opportunity for dogs to acquire infection via ingestion of vertebrate hosts (ascarids) or from a feces-contaminated environment.
  • Promptly removing feces from the yard to prevent eggs from being released from fecal material or dispersing into the environment.
  • Preventing contamination with eggs of B procyonis by not keeping raccoons as pets and avoiding areas frequented by dogs and wildlife.

GI = gastrointestinal

Dwight D. BowmanDwight Bowman, MS, PhD, is professor of parasitology at Cornell University College of Veterinary Medicine. He received his MS and PhD in parasitology from Tulane University.


Charles Thomas NelsonTom Nelson, DVM, is co-owner of the Animal Medical Center, Anniston, Alabama. He received his DVM from the College of Veterinary Medicine at Texas A&M University.


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  2. Epe C. Intestinal nematodes: Biology and control. Vet Clin N Am Sm Anim Pract 2009; 39(6):1091-1107.
  3. Kazacos KR. Unusual faecal parasite in a dog. NAVC Clin Brief 2006; 4(6):37-39.
  4. Conboy G. Cestodes of dogs and cats in North America. Vet Clin N Am Sm Anim Pract 2009; 39(6):1075-1090.
  5. Beaver PC, Jung RC, Cupp EW. Cyclophyllidean tapeworms. Clinical Parasitology. Philadelphia: Lea & Febiger, 1984, pp 505-543.
  6. Gaunt MC, Carr AP. A survey of intestinal parasites in dogs from Saskatoon, Saskatchewan. Can Vet J 2011; 52(5):497-500.
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