Animal Trypanosomiasis Types, Transmission, and Control

Caused by protozoa of the genus Trypanosoma

Affects all domesticated animals

Tsetse-transmitted Trypanosomiasis

• Major Veterinary Species: T. congolense, T. vivax, T. brucei brucei, T. simiae

• Zoonotic Species (People are predominant host): T. brucei rhodesiense, T. brucei gambiense

  • Domestic animals act as reservoirs for human infections

• Transmission:

  • Primarily cyclic via tsetse flies (genus Glossina)

  • Can be mechanical by biting flies (including tsetse)

    • T. vivax is found outside tsetse-infested areas, carried mechanically by biting flies like Tabanus spp

• Geographic Distribution: Africa (South, eastern, West, central, including Uganda), Central and South America, West Indies

  • Tsetse flies restricted to Africa (~15°N to 29°S)

• Animals Mainly Affected:

  • Cattle, sheep, goats: T. congolense, T. vivax, T. brucei brucei (in order of importance)

  • Pigs: T. simiae (most important)

  • Dogs and cats: T. brucei (probably most important)

  • Horses and camels: Order of importance difficult to assign; T. vivax and T. simiae listed

  • Wild animals: Various species susceptible

• Pathogenesis:

  • Infected tsetse inoculate metacyclic trypanosomes into skin

  • Reside in skin for days, cause localized inflammation (chancres)

  • Enter lymph and lymph nodes, then bloodstream

  • Divide rapidly by binary fission

  • T. congolense attach to endothelial cells, localize in capillaries/small blood vessels

  • T. brucei species and T. vivax invade tissues and cause damage

  • Immune response is vigorous; immune complexes cause inflammation (contributes to fever/signs)

  • Antibodies kill trypanosomes via surface coat glycoproteins

  • Antigenic variation: Trypanosomes switch variable surface-coat glycoproteins to evade immunity

    • Results in persistence of organism

    • Prevents protective vaccine development

    • Permits reinfections

• Clinical Findings and Lesions:

  • Severity varies with animal species/age and trypanosome species

  • Incubation: 1–4 weeks

  • Primary signs: intermittent fever, anemia, weight loss

  • Cattle: Usually chronic course with high mortality, especially with poor nutrition/stress

    • May recover if low tsetse challenge, but stress causes relapse

  • Necropsy (nonspecific):

    • Acute cases: Extensive petechiation (serosal membranes), swollen lymph nodes/spleen

    • Chronic cases: Swollen lymph nodes, serous atrophy of fat, anemia

• Diagnosis:

  • Presumptive: Anemic animal in poor condition in endemic area

  • Confirmation: Demonstrating trypanosomes

    • Stained blood smears

    • Wet mounts (especially buffy coat of centrifuged PCV tube - most sensitive rapid method, look for motile parasites)

  • Serologic testing: Measures antibody

    • More suitable for herd/area screening than individual diagnosis

  • Rapid agglutination tests: Detect circulating species-specific antigens

    • Available for individual and herd diagnosis, reliability varies

  • Molecular techniques (PCR): Detection and differentiation

    • Developed but not generally available for routine field use

  • Exclude other causes of anemia/weight loss (babesiosis, anaplasmosis, theileriosis, haemonchosis) by examining stained blood smear

• Treatment:

  • Use of chemotherapeutics

  • Examples: Diminazene aceturate, Homidium bromide/chloride, Isometamidium chloride, Quinapyramine sulfate/dimethylsulfate, Suramin

  • Most have a narrow therapeutic index; correct dose is essential

  • Drug resistance occurs and should be considered

• Control:

  • Reduction of tsetse fly populations

    • Frequent spraying/dipping of animals

    • Aerial/ground spraying of insecticides on breeding areas

    • Insecticide-impregnated screens/targets

    • Bush clearing and habitat removal

    • Sterile Insect Technique (SIT) used successfully in Zanzibar

    • Pan African Tsetse and Trypanosomiasis Eradication Campaign (PATTEC)

  • Use of prophylactic drugs

    • Animals given drugs prophylactically in high-challenge areas

    • Drug resistance must be monitored

  • Enhancing host resistance

    • Some breeds of cattle/water buffalo have innate resistance

    • Resistance may be lost due to poor nutrition/heavy challenge

  • Ideally achieved by combining methods (reduce challenge + enhance resistance + prophylactic drugs)

Surra

• Caused by T. evansi

• Transmission: Primarily by other biting flies (e.g., Tabanus spp), probably from interrupted feedings

• Geographic Distribution: Within and outside tsetse areas; North Africa, Middle East, Asia, Far East, Central and South America

• Affected Animals: Essentially camels and horses, but all domestic animals susceptible

• Severity: Can be fatal, particularly in camels, horses, and dogs

• Reservoirs: Other animals where T. evansi appears nonpathogenic, a few wild animals

• Pathogenesis, clinical findings, lesions, diagnosis: Similar to tsetse-transmitted trypanosomes

• Treatment: Similar to tsetse-transmitted trypanosomes; Melarsomine dichlorhydrate listed specifically for T. evansi in camels

Dourine

• Caused by T. equiperdum

• Transmission: Chronic venereal disease, transmitted during coitus

• Geographic Distribution: Mediterranean coast of Africa, Middle East, southern Africa, South America, probably wider

• Affected Animals: Horses

• Clinical Findings: Develop over weeks/months

  • Early: Mucopurulent discharge (urethra in stallions, vagina in mares), gross edema of genitalia

  • Later: Characteristic skin plaques (2–10 cm), progressive emaciation

  • Mortality: 50%–70% in untreated cases

• Diagnosis:

  • Demonstration of trypanosomes: Difficult (urethral/vaginal discharges, skin plaques, peripheral blood), may require centrifugation

  • Complement fixation test: Can detect infected horses

    • Only reliable where T. evansi or T. brucei are absent due to common antigens

  • ELISA test: May become available

• Treatment: Horses may be treated in endemic areas (drugs listed in table)

• Control (when eradication required):

  • Strict control of breeding

  • Elimination of stray horses

  • Euthanasia mandatory for infected horses identified by complement fixation test

Chagas Disease (American Trypanosomiasis)

• Caused by T. cruzi

• Type: Zoonotic, vector-borne disease

• Transmission:

  • Mainly by triatomine bugs (genera Triatoma, Rhodnius, Panstrongylus) - "kissing bug," "assassin bug," etc.

    • Infective metacyclic trypomastigotes shed in insect feces

  • Consumption of infected bugs or materials contaminated with insect feces (major mode in insectivorous animals like dogs)

  • Opossums: Can complete entire life cycle without vector; shed infective trypomastigotes in feces or urine

  • Transplacental

  • Blood transfusions and organ transplant

• Geographic Distribution:

  • Endemic in 21 countries of South/Central America and Mexico

  • Increasingly reported in southern USA

  • Emerging disease in Europe (Spain, Switzerland, France, Italy, Germany, England) due to migration

• Affected Animals: All mammals susceptible (>100 species)

  • Best recognized in dogs and people

  • Dogs serve as a major domestic reservoir

  • Domestic pigs and cats can be infected, but limited reservoir role

  • Wildlife reservoirs: Opossums, armadillos, raccoons, woodrats, nonhuman primates

  • Avian species are not susceptible

• Pathogenesis:

  • Metacyclic trypomastigotes enter bloodstream, actively invade many cell types

  • Exit parasitophorous vacuole, become nonflagellated amastigotes

  • Intracellular amastigotes divide

  • Transform back into trypomastigotes, lyse the cell

  • Released trypomastigotes invade new cells

  • Tropism for cardiac and smooth muscle, but found in numerous other tissues

• Clinical Findings and Lesions: Divided into acute and chronic phases

  • Incubation: 5–42 days before acute disease

  • Acute phase:

    • Asymptomatic or nonspecific febrile illness

    • Chancre at parasite entry site

    • Dogs may have regional/generalized lymphadenopathy, anorexia, lethargy, vomiting, diarrhea, hepatomegaly or splenomegaly

    • Rarely, acute clinical myocarditis

    • Parasitemia peaks 2-3 weeks post-infection, dissipates as organism moves to tissues

  • Chronic phase:

    • Latent phase: Months to years

    • Symptomatic chronic disease: Generalized weakness or sudden death

    • Common presentation in dogs: Right-side congestive heart failure

    • Can progress to myocarditis, arrhythmias, bilateral cardiac dilation

    • Histologic findings in cardiac muscle: unruptured pseudocysts (no inflammation) or ruptured pseudocysts (inflammation)

    • Death secondary to heart failure is common

• Diagnosis:

  • Visualization of organism: Direct examination of blood smear (acute phase)

    • T. cruzi is C-shaped, extracellular, single flagellum on Giemsa stain

  • Detection of DNA: PCR or culture (uncommon in field)

  • Antibody detection: Primary importance during chronic phase

    • Tests: Immunochromographic "dipstick," immunofluorescent antibody (IFAT), ELISA

    • Cross-reaction with Leishmania antibodies can occur

    • Recommend testing with at least two different methodologies or antigens

  • Tissue analysis (chronic phase): PCR for DNA, immunohistochemical analysis for amastigotes

• Treatment:

  • Benznidazole: Drug of choice (5–10 mg/kg/day, PO, for 2 months in dogs)

  • Nifurtimox can also be used

  • Note: In the USA, these drugs lack FDA approval and require CDC permission as investigational protocols

  • Symptomatic treatment for heart failure and arrhythmias recommended

• Control:

  • No vaccine available

  • Focuses on preventing disease transmission

  • Vector control: Applying pesticides, decreasing vector attraction to dwellings (turning off outdoor lighting)

  • Discourage breeding of positive bitches

  • Screening of blood donors recommended

  • Disinfection of contaminated surfaces (10% bleach or 70% ethanol)

  • Infected dead insects remain a source for varying times depending on temperature

• Reservoirs: Dogs, people, wildlife

Nonpathogenic Trypanosomes

• Species: Trypanosoma theileri or similar (Theileri group)

  • T. melophagium (sheep)

  • T. theodori (goats) - may be a synonym for T. melophagium

• Transmission:

  • T. theileri: Contamination after cycle in tabanid flies

  • T. melophagium: Transmitted by the sheep ked

• Affected Animals: Cattle, domestic and wild buffalo, wild ungulates (T. theileri); sheep (T. melophagium), goats (T. theodori)

• Distribution: Worldwide (T. theileri, T. melophagium)

• Parasitemia: Usually subpatent

• Diagnosis: May be seen in blood smear or hemocytometer chamber examined for pathogenic protozoa

• Pathogenicity: Never proven experimentally