Parasite Protocols: Canine Protozoa

Recommendations from the Companion Animal Parasite Council

Susan E. Little, DVM, PhD, Diplomate ACVM, and Emilio DeBess, DVM, MPVM

This new column explores the diagnosis, treatment, prevention, and control of parasitic infections based on CAPC’s detailed recommendations. First up for discussion are canine protozoan parasites.

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.

Protozoan parasites, including vector-borne infections and intestinal protozoa, are responsible for a number of different diseases in dogs (Table). Although many infections are acquired by direct ingestion of infective stages, others may be transmitted by arthropods. These parasites are distributed worldwide or regionally. Accurate, prompt diagnosis and appropriate, specific treatment are critical to managing and preventing protozoan parasitic diseases in dogs.

VECTOR-BORNE INFECTIONS

Babesia Species

Distribution. Worldwide, dogs may become infected with Babesia canis, B vogeli, B rossi, B gibsoni, B conradae, and other small and large Babesia species, some that have yet to be named.^1,2

Vectors & Transmission. Many different tick species transmit Babesia species when feeding on dogs; the most common U.S. species include:

• B vogeli (formerly, B canis vogeli), transmitted by Rhipicephalus sanguineus ticks
• B gibsoni; transmission with this species has been associated with dog fighting.

Transmission of any Babesia species can occur following blood transfusion.¹
Diagnosis. Dogs with babesiosis present with fever, anorexia, depression, and often, hemolytic anemia.¹ Diagnosis is achieved by examining stained blood smears for characteristic piroplasms in erythrocytes (Figure 1).

Figure 1. Piroplasms of a large Babesia species in canine erythrocytes.

Treatment. Preferred treatment options include:³

• Imidocarb diproprionate for large Babesia species (B canis, B vogeli, B rossi)
• Atovaquone/azithromycin for small Babesia species (B gibsoni, B conradae).

Prevention. Infection prevention requires careful attention to tick control and avoidance of fighting among dogs.

Hepatozoon Species

Distribution. Hepatozoon americanum has only been described in the U.S., while H canis is found worldwide.⁴

Vectors & Transmission. H canis and H americanum are transmitted to dogs by ingestion of the vector—ticks—rather than their bite. H americanum can also be transmitted by ingestion of paratenic vertebrate hosts.

Diagnosis. H americanum infection presents as severe, febrile disease, with lethargy, myalgia, and muscle wasting commonly reported. It also infects skeletal and cardiac muscle, and induces pyogranulomatous myositis. Chronically infected dogs often develop periosteal proliferative lesions on their long bones and bloodwork reveals profound neutrophilia. Clinical disease with H canis is relatively mild by comparison.⁵
Diagnosis of both Hepatozoon species can be made by:⁵

• Identifying gamonts in leukocytes on stained blood smears; gamonts are rare in H americanum infection but much more common in H canis infection (Figure 2).
• Polymerase chain reaction (PCR) of whole blood
• Histologic examination of muscle biopsy (more sensitive in detecting H americanum infection than PCR).

Figure 2. Gamont of Hepatozoon americanum in canine leukocyte

Treatment. H canis infection is treated with imidocarb diproprionate. H americanum requires more aggressive and long-term therapy consisting of ponazuril or trimethoprim/sulfamethoxazole combined with clindamycin and azithromycin, followed by long-term decoquinate therapy and pain management with nonsteroidal anti-inflammatory drugs.⁵

Prevention. Tick control helps prevent infection by limiting the number of ticks ingested. Prevention of H americanum also requires limiting consumption of paratenic hosts, especially rabbits and rodents.⁶

Leishmania Species

Distribution. Althought fairly uncommon in North America, dogs are infected with Leishmania species throughout much of the world. Infection has been diagnosed in dogs imported from endemic areas, such as the Mediterranean basin and Central and South America.

Vectors & Transmission. In many areas of the world, phlebotomine sandflies that have fed on an infected vertebrate transmit Leishmania species to dogs. In the U.S., transmission by sandflies has not been epidemiologically demonstrated, but canine infections are recognized, particularly in foxhound kennels, and are presumably acquired by direct transmission between dogs.⁷

Diagnosis. Infected dogs may remain asymptomatic or can develop severe, chronic disease, involving muscle wasting, ocular signs, renal disease, and alopecia and other skin lesions.⁸ Diagnosis is made by serology or identification of amastigotes in impression smears from affected tissues (Figure 3); PCR assays are also available.

Figure 3. Amastigotes of Leishmania species from ruptured macrophages on impression smear.

Treatment. Canine leishmaniasis is difficult to treat, although pentavalent antimonials and allopurinol can be used.

Prevention. In endemic areas, protecting dogs from sandflies by routine application of repellent insecticides decreases transmission of Leishmania species⁹; isolation of infected dogs is recommended to prevent direct transmission.

Zoonosis. Dogs are a major reservoir host for leishmaniosis—a zoonotic disease. Euthanasia of infected dogs has been recommended to limit transmission to humans and other dogs, particularly in regions where vector-borne Leishmania transmission is not yet endemic.

Trypanosoma cruzi

Distribution. Trypanosoma cruzi is the agent of American trypanosomiasis or Chagas disease. Autochthonous cases are occasionally reported from dogs in the southern U.S., where natural maintenance cycles exist, and are common in parts of South and Central America and Mexico.^10,11

Vectors & Transmission. Infection is transmitted from kissing bugs (triatominae) to dogs and humans. Canine infections occur when infected kissing bugs are ingested or the bugs’ feces, which contain the organism, are deposited on or around the skin wound created by their feeding activity; infection is also transmitted transplacentally.¹²

Diagnosis. Dogs with acute disease develop generalized lymphadenopathy, lethargy, enlarged liver and spleen, and myocarditis. Chronic infection often results in dilative myocarditis.¹²

Trypomastigotes may be identified on stained blood smears from acutely infected dogs (Figure 4); serology and PCR are also available.

Figure 4. Trypomastigotes of Trypanosoma cruzi on blood smear of dog

Treatment. Benznidazole, the drug of choice for treating T cruzi in dogs, is not available in the U.S., and infected dogs are often euthanized.

Prevention. Preventing infection requires limiting access to kissing bugs by sealing kennels and keeping dogs inside. Limiting predation is also recommended because, although unproven, ingestion of infected reservoir hosts is a suspected route of transmission.¹²

Zoonosis. T cruzi is zoonotic and, in endemic areas, people are readily infected from a feeding bug vector’s feces. In the U.S., most human infections are associated with blood transfusion or travel to endemic areas.¹¹

INTESTINAL PROTOZOA

Cystoisospora Species

Distribution. Coccidia is a common finding in dogs, with some studies suggesting approximately 1% to 5% of dogs may be infected worldwide.

Vectors & Transmission. Canine infection with Cystoisospora species (Isospora species) commonly occurs upon ingestion of:^13,14

• Sporulated oocysts from an environment contaminated with feces
• Transport hosts.

Diagnosis. Many infected dogs remain asymptomatic, developing immunity to limit infection and protect them from future infections; however, diarrhea, weight loss, dehydration, and even death can occur in severe infections, particularly those in young animals.¹⁵ Infections are diagnosed by fecal flotation, which reveals the characteristic oocysts (Figure 5).

Figure 5. Oocytes of Cystoisospora canis on fecal float

Treatment. Treatment with sulfadimethoxine, which is labeled as effective against the enteritis associated with coccidiosis, or ponazuril is recommended.

Prevention. Oocysts are resistant to environmental degradation; careful attention to sanitation, particularly in kennels and shelters where large numbers of young dogs are cohoused, is necessary to prevent infection.¹⁵

Cryptosporidium Species

Distribution. Cryptosporidium species infect a variety of vertebrate hosts, including dogs and humans. Active infections are present in a very small percentage of dogs; most of these are due to C canis, which rarely infects people.¹⁶ The more common zoonotic agent, C parvum, is not known to occur in dogs.

Vectors & Transmission. Oocysts of Cryptosporidium species are immediately infective when shed in the feces, which usually occurs 3 to 6 days after infection.¹³

Diagnosis. Infections can cause secretory diarrhea, which can be particularly severe in immunocompromised individuals. Diagnosis is by sucrose flotation of feces, but recognizing minute oocysts can be difficult and use of a referral parasitology laboratory is recommended.

Treatment. Treatment is difficult—few drugs are consistently effective against Cryptosporidium species in dogs.

Prevention. Canine infections are considered a low-risk zoonosis; C canis has only been reported in immunocompromised humans in the U.S.¹⁶

Giardia Species

Distribution. Infection with Giardia duodenalis is common in U.S. dogs.¹⁷
Vectors & Transmission. Infection occurs following ingestion of cysts from fecal-contaminated water, food, or fomites, or through self-grooming. The different assemblages of G duodenalis are considered to be fairly host specific.

Figure 6. Cysts of Giardia duodenalis on canine fecal float

Diagnosis. Following infection, trophozoites attach to intestinal villi, resulting in maldigestion, malabsorption, and diarrhea. Diagnosis is achieved by detection of:

• Trophozoites in direct smear of feces
• Cysts on fecal flotation with zinc sulfate (Figure 6)
• Antigen in feces of symptomatic dogs.

Intermittent shedding of cysts and trophozoites can make direct microscopic identification of infection challenging.

Treatment & Prevention. No drugs are approved for treatment of canine giardiasis in the U.S., but fendbendazole and febantel have shown effectiveness.¹⁸ Bathing dogs removes cysts adhered to the hair and helps prevent re-infection.¹⁹

Zoonosis. Giardia is a common infection in humans, although the most common assemblages found in humans are distinct from those most often found in dogs.²⁰ Human giardiasis contracted from a dog has not been conclusively demonstrated in North America.

APPLICATION TO CLINICAL PRACTICE

Protozoal parasites of dogs can critically affect canine and human health, with overt clinical disease from canine protozoa most often seen in debilitated or young animals. Infected dogs often present with signs of disease; however, asymptomatic infections also occur, and some protozoa may live undetected within the host for years.⁸

Identification

Identifying protozoal infections largely depends on awareness so that appropriate diagnostic tests are pursued, particularly with vector-borne infections. Careful history taking and physical examination, along with a judicious use of diagnostic tools, can lead to better management and improved outcomes.

Prevention

INTESTINAL PROTOZOA. Prevention of infection with intestinal protozoa requires careful attention to environmental sanitation. Re-infection following treatment often occurs, particularly in canine giardiasis.¹⁹

VECTOR-BORNE INFECTIONS. Canine vector-borne diseases are highly prevalent, increasing in distribution, and often difficult to treat; preventing infection by consistent use of insecticides and acaricides and limiting exposure to ticks and other arthropod vectors are the most effective ways to protect dogs from these diseases.

Protection

Protecting dogs from protozoal parasites is critical to human health. Some of these infections, such as Leishmania species and T cruzi, are well recognized zoonoses, while others, such as canine Cryptosporidium or Giardia infections, are considered to carry a very low zoonotic risk.^8,12,16,20 Veterinarians should pay close attention to:

• Limiting protozoal parasite infections in dogs
• Staying up-to-date on emerging zoonotic diseases.

ELISA = enzyme-linked immunosorbent assay; IFA = indirect fluorescent assay; PCR = polymerase chain reaction

References

1. Irwin PJ. Canine babesiosis. Vet Clin North Am Small Anim Pract 2010; 40(6):1141-1156.
2. Sikorski LE, Birkenheuer AJ, Holowaychuk MK, et al. Babesiosis caused by a large Babesia species in 7 immunocompromised dogs. J Vet Intern Med 2010; 24(1):127-131.
3. Di Cicco MF, Downey ME, Beeler E, et al. Re-emergence of Babesia conradae and effective treatment of infected dogs with atovaquone and azithromycin. Vet Parasitol 2012; 187(1-2):23-27.
4. Little SE, Allen KE, Johnson EM, et al. New developments in canine hepatozoonosis in North America: A review. Parasit Vectors 2009; 2(Supp 1):S5.
5. Allen KE, Johnson EM, Little SE. Hepatozoon spp. infection in the United States. Vet Clin North Am Small Anim Pract 2011; 41:1221-1238.
6. Johnson EM, Panciera RJ, Allen KE, et al. Alternate pathway of infection with Hepatozoon americanum and the epidemiologic importance of predation. J Vet Intern Med 2010; 23:1315-1318.
7. Petersen CA, Barr SC. Canine leishmaniosis in North America: Emerging or newly recognized? Vet Clin North Am Small Anim Pract 2009; 39(6):1065-1074.
8. Solano-Gallego L, Miro G, Koutinas A, et al. LeishVet guidelines for the practical management of canine leishmaniosis. Parasit Vectors 2011; 4:86.
9. Otranto D, de Caprariis D, Lia RP, et al. Prevention of endemic canine vector-borne diseases using imidacloprid 10% and permethrin 50% in young dogs: A longitudinal field study. Vet Parasitol 2010; 172:323-332.
10. Kjos SA, Snowden KF, Craig TM, et al. Distribution and characterization of canine Chagas’ disease in Texas. Vet Parasitol 2008; 152:249-256.
11. Esch KJ, Petersen CA. Transmission and epidemiology of zoonotic protozoal diseases of companion animals. Clin Microbiol Rev 2013; 26:58-85.
12. Barr SC. Canine Chagas’ Disease (American Trypanosomiasis) in North America. Vet Clin North Am Small Anim Pract 2009; 39:1055-1064.
13. Dubey JP, Lindsay DS, Lappin MR. Toxoplasmosis and other intestinal coccidial infections in cats and dogs. Vet Clin North Am Small Anim Pract 2009; 39:1009-1034.
14. Gates MC, Nolan TJ. Endoparasite prevalence and recurrence across different age groups of dogs and cats. Vet Parasitol 2009; 166:153-158.
15. Lappin MR. Enteric protozoal diseases. Vet Clin North Am Small Anim Pract 2005; 35:81-88.
16. Lucio-Forster A, Griffiths JK, Cama VA, et al. Minimal zoonotic risk of cryptosporidiosis from pet dogs and cats. Trends Parasitol 2010; 6(4):174.
17. Carlin EP, Bowman DD, Scarlett JM, et al. Prevalence of Giardia in symptomatic dogs and cats throughout the United States as determined by the IDEXX SNAP Giardia test. Vet Ther 2006; 7(3):199-206.
18. Barr SC, Bowman DD, Heller RL. Efficacy of fenbendazole against giardiasis in dogs. Am J Vet Res 1994; 55:988-990.
19. Payne PA, Ridley RK, Dryden MW, et al. Efficacy of a combination febantel–praziquantel–pyrantel product, with or without vaccination with a commercial Giardia vaccine, for treatment of dogs with naturally occurring giardiasis. JAVMA 2002; 220:330-333.
20. Covacin C, Aucoin DP, Elliott A, Thompson RC. Genotypic characterisation of Giardia from domestic dogs in the USA. Vet Parasitol 2011; 177:28-32.

Susan E. Little, DVM, PhD, Diplomate ACVM, is the Director of the National Center for Veterinary Parasitology at Oklahoma State University’s Center for Veterinary Health Sciences, where she serves as Regents Professor and the Krull-Ewing Chair in Veterinary Parasitology. Her research focuses on zoonotic parasites and tick-borne diseases. She has been recognized for teaching excellence, receiving the Pfizer (Norden) Distinguished Teaching Award (1999, 2010) and national Student AVMA Excellence in Teaching Award (1998, 2005), and for her outstanding research with the Pfizer Award for Research Excellence (2012). Dr. Little received her DVM from Virginia Tech and completed her PhD at University of Georgia.

Emilio DeBess, DVM, MPVM, is the state public health veterinarian with the Oregon Health Authority. His primary job is to track zoonotic diseases in both humans and animals in Oregon. He has received 2 Director Excellence Awards from the Department of Human Services in Oregon. Dr. DeBess conducts surveillance projects related to zoonotic diseases, including leptospirosis, toxoplasmosis, cryptococcosis, West Nile virus, and tick-borne illnesses. He received his DVM from University of California–Davis.