Tritrichomonas foetus is a common feline protozoan parasite that causes diarrhoea and inflammatory bowel disease in high-density populations of young, purebred cats worldwide[2][3].

This parasite should be included in any differential of feline gastroenteritis[4], where other common gut protozoa such as Giardia spp and more rarely, Pentatrichomonas hominis[5][6] have also been reported[7].

Beginning in 1996, several reports have documented the presence of large numbers of trichomonads in faecal specimens from young, densely housed cats with chronic large-bowel diarrhea[8]. On the basis of sequence identity of 18S rRNA, the feline organisms have been identified as T. foetus. Following experimentally induced infection, T. foetus colonizes the feline ileum, caecum, and colon, resulting in diarrhoea characteristic of the natural infection[9].

Trichomonads are flagellated protozoans that reproduce by binary fission and undergo direct transmission from host to host. Both commensal and pathogenic species of trichomonads exist. In domestic cats, T. foetus colonizes the colon, resulting in chronic large-bowel diarrhea. The infection is prevalent among young, densely housed cats. Trophozoites of T. foetus can be difficult to distinguish from those of Giardia spp, except that the former has a distinct undulating membrane, does not form cysts, and is refractory to treatment with antiprotozoal drugs such as metronidazole and fenbendazole.


Infection with T foetus is common in cats. Random surveys in NZ show that up to 75% of cats may have this gut parasite[10], although incidences in Australia[11], USA and Europe[12] appear to be much lower. Although reported commonly in young purebred cats, T. foetus has been reported as a cause of diarrhoea in adult non-pedigree cats as well[13].

Concurrent infections with Giardia spp and Isospora felisToxocara spp and Eucoleus spp are frequent. The prevalence of T. foetus infection can vary from pet cats where it is generally low to cats housed in catteries where incidences are much higher[14]. There appears to be no breed predisposition, age, or sex differences between infected and uninfected cats. High density housing such as that of catteries and shelters appears to be a predisposing factor. However, a higher incidence in purebred cats has been reported, with Maine coon cats over-represented in Germany[15].

T. foetus has a relatively high resilience at ambient temperatures[16]. Therefore, T. foetus may be transmitted from the queen to kittens or between cats using common litter trays. Research has also shown that T. foetus can be introduced into catteries from food contaminated with faeces from garden slug(s) infected with T. foetus[17]. Garden slugs may also facilitate passive transfer between cats. A change in intestinal environment due to T. foetus infection may allow proliferation of Isospora felis in the intestinal tract[18].

One of the distinctive features of feline trichomonad-induced colitis is that affected cats are typically young. While it has not been found in the faeces of feral cats or healthy indoor cats living in colonies that do not suffer from diarrhoea it is frequently seen in households containing young pedigree cats, especially those where diarrhoea is common, in young cats from rescue centres, and in cats from other multicat households. While cats of all ages can become infected, and may develop diarrhoea, clinical disease is seen most commonly in young cats and kittens, and the majority of cats with T foetus-associated diarrhoea are under 12 months of age. The parasite has been shown to be resilient to environmental degradation and may survive for days in feces outside the host (Hale et al, 2009).

T.foetus appears to be species species regarding the host, and experimental infections of cats with bovine T. foetus was unsuccessful[19].

Clinical signs

Studies have shown that this parasite mainly causes colitis (large bowel diarrhoea) with increased frequency of defecation, bubbly semi-formed to liquid faeces, and sometimes fresh blood or mucus in the faeces. Peri-anal dermatitis is also common[20]. With severe diarrhoea, some cats may develop faecal incontinence. Although cats of all ages can be affected with diarrhoea, it is most commonly seen in young cats and kittens, the majority being under 12 months of age. Most of the affected cats have come from rescue shelters and pedigree breeding colonies. Abdominal ultrasound examination may show corrugation of the large bowel and local lymphadenopathy. Colonic biopsies from affected cats typically show mild to severe inflammatory changes with predominantly infiltration of lymphocytes and plasma cells – a pattern commonly seen with other infectious agents and with inflammatory bowel disease. However, the parasites may be seen in close association with the mucosa. Although the diarrhoea may be persistent and severe, most affected cats are otherwise well, and do not show significant weight loss.

Infection is most commonly seen in colonies of cats and multicat households, where presumably the organism is spread between cats by close and direct contact. There has been no evidence of spread from other species, or spread via food or water. In one study, 31% of cats at a cat show were identified as being infected with this organism, suggesting that this may be an important, common, and previously unrecognised cause of diarrhoea in cats.

Although most information on T foetus infection has come from studies of cats in the USA, several cases of infection in cats has been seen in England (mostly in young pedigree cats, and all from multicat households generally with more than one cat being affected ), and it has also been identified in several cats in Scotland (and also in cats from Germany)[21]. The evidence therefore suggests that infection is probably quite widespread in cat populations, and infection is most likely where there is a high density of cats sharing the same environment[22].

Reproductive disease due to T. foetus, as is observed in other species of animals, appears to be rare in cats[23]. Accordingly, it is unlikely that reproductive tract infection with T. foetus plays an important role in overall disease transmission.


Feline T. foetus infection is diagnosed by direct faecal smear examination for motile trophozoites with saline dilution cultivation of faeces using a commercially available system (In PouchTM TF), or extraction of DNA from faeces and amplification of T. foetus rDNA by use of PCR analysis with species-specific primers[24]. The ZR Fecal DNA kit appears to afford the greatest analytical sensitivity and reproducibility and was able to detect ≥ 10 T. foetus organisms per 100 mg feces in 100% of PCR reactions[25].

The presence of colonic trichomonads is consistently associated with a mild-to-moderate lymphoplasmacytic and neutrophilic colitis, with crypt epithelial cell hypertrophy, hyperplasia and increased mitotic activity, loss of goblet cells, crypt microabscesses, and attenuation of the superficial colonic mucosa. Eosinophils are not a prominent feature of the inflammatory infiltrate. Macrophages are identified in cats in which trichomonads have infiltrated into the lamina propria and beyond.

Trichomonads are detected in approximately 50% of samples examined. This figure may not accurately reflect the true prevalence of the organism in colonic sections from infected cats as trichomonads are identified less often in sections with little adherent mucus. As such, tissue collection and processing could impact the ability to detect the organism. When tissue is collected by biopsy or at necropsy, our findings suggest that examination of multiple sections of colon will increase the likelihood of detecting trichomonads in infected cats. To have 95% confidence that trichomonads will be present in at least one section, six sections of colon should be examined[26].

Experimental studies have fulfilled Koch’s postulates regarding the ability of T. foetus to act as a primary enteric pathogen in cats. However, the current understanding of factors mediating pathogenicity of trichomonads is limited. Identified mechanisms include alterations in host endogenous bacterial flora, adherence to the epithelium, and the elaboration of cytotoxins and enzymes[27].


In young cats with large-bowel diarrhoea that is unresponsive to antimicrobial therapy, underlying infection with T. foetus should be given strong consideration. Current information suggests that the long term prognosis for infected cats is good, as most will eventually overcome the infection. However, this can be a slow process, taking from 2 months to 3 years, with a median of 9 months. Most infected cats continue to shed low levels of organism in their faeces for many months after the resolution of the diarrhoea. These cats, and clinically-affected cats, appear to be the major reservoir of infection to other cats. This is believed to occur via faecal-oral spread as there is no evidence of spread from other species, or spread via food or water[28].

Currently, therapeutic interventions to reduce clinical signs and stop protozoal shedding are limited; many medications (including tinidazole[29], metronidazole and fenbendazole) are poorly effective[30], and although recent work has indicated that treatment with ronidazole may be successful there is currently no licensed form of this product, and its administration to cats can result in adverse reactions (typically lethargy, ataxia, tremors and occasionally, seizures)[31][32]. Resistance to ronidazole has also been reported[33]. A new drug, secnidazole, is effective against Giardia spp in cats but no reports of its use against feline tritrichomoniasis has been reported.

  • Fenbendazole – 50 mg/kg oid for 2 weeks; resistance reported
  • Metronidazole – 50 mg/cat oid for 2 weeks; resistance reported
  • Ronidazole – 30 – 50 mg/kg oid for 2 weeks
  • Secnidazole – 30 mg/kg given as a single dose treatment
  • low residue diet (e.g. Hills Z/D)
  • probiotics

A small number of cats have developed neurological signs. Initial studies suggest a dose of 30-50mg/kg once to twice daily for two weeks is capable of both resolving clinical signs and potentially eradicating infection with T foetus. Ronidazole is commonly used to treat trichomoniasis in birds (e.g. pigeons). However, care should be exercised in the use of ronidazole , as there are very few studies of its use in cats, and long-term studies in other species have suggested some potential toxicity concerns[34].


  1. ↑ Lim S et al (2010) First report of feline intestinal trichomoniasis caused by Tritrichomonas foetus in Korea. Korean J Parasitol 48(3):247-251
  2. ↑ Tolbert MK & Gookin J (2009) Tritrichomonas foetus: A New Agent of Feline Diarrhea. Compend Contin Educ Vet 31(8):374-381
  3. ↑ Miró G et al (2011) First description of naturally acquired Tritrichomonas foetus infection in a Persian cattery in Spain. Parasitol Res Apr 21
  4. ↑ Xenoulis, PG et al (2010) Detection of Tritrichomonas foetus in cats in Greece. JFMS 12:831-833
  5. ↑ Romatowski J (2000) Pentatrichomonas hominis infection in four kittens. J Am Vet Med Assoc 216:1270–1272
  6. ↑ Romatowski J (1996). An uncommon protozoan parasite (Pentatrichomonas hominis) associated with colitis in three cats. Feline Pract 24:10
  7. ↑ Scorza, AV & Lappin, MR (2010) Gastrointestinal protozoal infections. In August, JR (Ed): COnsultations in feline internal medicine. Vol 6. Elsevier Saunders, Philadelphia. pp:200
  8. ↑ Payne PA & Artzer M (2009) The biology and control of Giardia spp and Tritrichomonas foetus. Vet Clin North Am Small Anim Pract 39(6):993-1007
  9. ↑ Gookin JL et al (1999) Diarrhea associated with trichomonosis in cats. J Am Vet Med Assoc 215:1450–1454
  10. ↑ Kingsbury DD et al (2010) Identification of Tritrichomonas foetus and Giardia spp. infection in pedigree show cats in New Zealand. N Z Vet J 58(1):6-10
  11. ↑ Bissett SA et al (2009) Observed occurrence of Tritrichomonas foetus and other enteric parasites in Australian cattery and shelter cats. J Feline Med Surg 11(10):803-807
  12. ↑ Frey CF et al (2009) Intestinal Tritrichomonas foetus infection in cats in Switzerland detected by in vitro cultivation and PCR. Parasitol Res 104(4):783-788
  13. ↑ Holliday M et al (2009) Tritrichomonas foetus infection in cats with diarrhoea in a rescue colony in Italy. J Feline Med Surg 11(2):131-134
  14. ↑ van Doorn DC et al (2009) Prevalence of Tritrichomonas foetus among Dutch cats. Tijdschr Diergeneeskd 134(17):698-700
  15. ↑ Kuehner KA et al (2011) Tritrichomonas foetus infection in purebred cats in Germany: prevalence of clinical signs and the role of co-infection with other enteroparasites. J Feline Med Surg 13(4):251-258
  16. ↑ Hale S et al (2009) Prolonged resilience of Tritrichomonas foetus in cat faeces at ambient temperature. Vet Parasitol 166(1-2):60-65
  17. ↑ Van der Saag M et al (2011) Cat genotype Tritrichomonas foetus survives passage through the alimentary tract of two common slug species. Vet Parasitol 177(3-4):262-266
  18. ↑ Burgess DE et al (1990) Cytotoxic and hemolytic effects of Tritrichomonas foetus on mammalian cells. Infect Immun 58:3627–3632
  19. ↑ Stockdale HD et al (2008) Experimental infection of cats (Felis catus) with Tritrichomonas foetus isolated from cattle. Vet Parasitol 154(1-2):156-161
  20. ↑ Burgener I et al (2009) Tritrichomonas fetus: a new intestinal parasite in Swiss cats. Schweiz Arch Tierheilkd 151(8):383-389
  21. ↑ Gunn-Moore, DA, et al (2007) Prevalence of Tritrichomonas foetus infection in cats with diarrhoea in the UK. Journal of feline medicine and surgery 9:214-218
  22. ↑ Gookin JL et al (2003) Use of a commercially available culture system for diagnosis of Tritrichomonas foetus infection in cats. J Am Vet Med Assoc 222:1376–1379
  23. ↑ Gray SG et al (2010) Assessment of reproductive tract disease in cats at risk for Tritrichomonas foetus infection. Am J Vet Res 71(1):76-81
  24. ↑ Gookin JL et al (2002) Single-tube nested PCR for detection of Tritrichomonas foetus in feline feces. J Clin Microbiol 40:4126–4130
  25. ↑ Stauffer SH et al (2008) Evaluation of four DNA extraction methods for the detection of Tritrichomonas foetus in feline stool specimens by polymerase chain reaction. J Vet Diagn Invest 20(5):639-641
  26. ↑ Foster DM, Gookin JL, Poore MF, Stebbins ME, Levy MG (2004). Outcome of cats with diarrhea and Tritrichomonas foetus infection. J Am Vet Med Assoc 225:888–892
  27. ↑ Hale S et al (2009) Prolonged resilience of Tritrichomonas foetus in cat faeces at ambient temperature, Vet Parasitol 166:60
  28. ↑ Gookin JL et al (2001) Experimental infection of cats with Tritrichomonas foetus. Am J Vet Res 62:1690–1697
  29. ↑ Gookin JL et al (2007) Efficacy of tinidazole for treatment of cats experimentally infected with Tritrichomonas foetus. Am J Vet Res 68(10):1085-1088
  30. ↑ Kather EJ et al (2007) Determination of the in vitro susceptibility of feline tritrichomonas foetus to 5 antimicrobial agents. J Vet Intern Med 21(5):966-970
  31. ↑ Levy MG et al (2003) Tritrichomonas foetus and not Pentatrichomonas hominis is the etiologic agent of feline trichomonal diarrhea. J Parasitol 89:99–104
  32. ↑ LeVine DN et al (2011) Ronidazole pharmacokinetics after intravenous and oral immediate-release capsule administration in healthy cats. J Feline Med Surg 13(4):244-250
  33. ↑ Gookin JL et al (2010) Documentation of in vivo and in vitro aerobic resistance of feline Tritrichomonas foetus isolates to ronidazole. J Vet Intern Med 24(4):1003-1007
  34. ↑ Gookin JL et al (2004) Prevalence of and risk factors for feline Tritrichomonas foetus and giardia infection. J Clin Microbiol 42:2707–2710

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