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bovine venereal trichomonosis

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Datasheet

bovine venereal trichomonosis

Summary

  • Last modified
  • 03 January 2018
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • bovine venereal trichomonosis
  • Overview
  • Bovine trichomonosis (trichomoniasis)is a venereal disease caused by the flagellated protozoan, Tritrichomonas foetus. The disease is characterized by relatively early and typically occult loss of pregnanc...

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    Compendia
    CAB International
    Wallingford
    Oxfordshire
    OX10 8DE
    UK
    compend@cabi.org
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PictureTitleCaptionCopyright
Tritrichomonas foetus; note three anterior flagellae and recurrent flagellum attached along one side as the 'undulating membrane'. The large nucleus is visible in the anterior portion of the protozoan, and the axostyle can be seen extending from the posterior end. Diff-Quik and iodine staining procedure (Lun and Gajadhar, 1999); original image approx. 1000 X.
TitleTritrichomonas foetus
CaptionTritrichomonas foetus; note three anterior flagellae and recurrent flagellum attached along one side as the 'undulating membrane'. The large nucleus is visible in the anterior portion of the protozoan, and the axostyle can be seen extending from the posterior end. Diff-Quik and iodine staining procedure (Lun and Gajadhar, 1999); original image approx. 1000 X.
CopyrightRobert H. BonDurant
Tritrichomonas foetus; note three anterior flagellae and recurrent flagellum attached along one side as the 'undulating membrane'. The large nucleus is visible in the anterior portion of the protozoan, and the axostyle can be seen extending from the posterior end. Diff-Quik and iodine staining procedure (Lun and Gajadhar, 1999); original image approx. 1000 X.
Tritrichomonas foetusTritrichomonas foetus; note three anterior flagellae and recurrent flagellum attached along one side as the 'undulating membrane'. The large nucleus is visible in the anterior portion of the protozoan, and the axostyle can be seen extending from the posterior end. Diff-Quik and iodine staining procedure (Lun and Gajadhar, 1999); original image approx. 1000 X.Robert H. BonDurant
Junction of placentomal and interplacentomal region of the uterus of an experimentally infected pregnant heifer.  Lymphocytes are infiltrating the superficial endometrium (E) and migrating through the mucosa on the left, and the epithelium is eroded. On the right, at the margin of the placentome (P), fetal chorionic epithelium is multifocally necrotic (arrow) and neutrophils are infiltrating these areas (see inset for higher magnification of the chorion). Bar =  1 mm.  H&E stain.
TitleHistopathology
CaptionJunction of placentomal and interplacentomal region of the uterus of an experimentally infected pregnant heifer. Lymphocytes are infiltrating the superficial endometrium (E) and migrating through the mucosa on the left, and the epithelium is eroded. On the right, at the margin of the placentome (P), fetal chorionic epithelium is multifocally necrotic (arrow) and neutrophils are infiltrating these areas (see inset for higher magnification of the chorion). Bar = 1 mm. H&E stain.
CopyrightRobert H. BonDurant
Junction of placentomal and interplacentomal region of the uterus of an experimentally infected pregnant heifer.  Lymphocytes are infiltrating the superficial endometrium (E) and migrating through the mucosa on the left, and the epithelium is eroded. On the right, at the margin of the placentome (P), fetal chorionic epithelium is multifocally necrotic (arrow) and neutrophils are infiltrating these areas (see inset for higher magnification of the chorion). Bar =  1 mm.  H&E stain.
HistopathologyJunction of placentomal and interplacentomal region of the uterus of an experimentally infected pregnant heifer. Lymphocytes are infiltrating the superficial endometrium (E) and migrating through the mucosa on the left, and the epithelium is eroded. On the right, at the margin of the placentome (P), fetal chorionic epithelium is multifocally necrotic (arrow) and neutrophils are infiltrating these areas (see inset for higher magnification of the chorion). Bar = 1 mm. H&E stain.Robert H. BonDurant
Endometrium from a heifer experimentally infected with Tritrichomonas foetus and inseminated. A neutrophilic superficial endometrial response accompanied by purulent luminal exudate is characteristic of the earlier stages of infection. Arrows indicate eosinophils, which are commonly seen in trichomonad infections below the endometrial mucosa.  Luna stain (see inset) demonstrates the prominent red granules of eosinophils.  Bar = 0.2 mm. Haematoxylin and eosin (H&E) stain.
TitleHistopathology
CaptionEndometrium from a heifer experimentally infected with Tritrichomonas foetus and inseminated. A neutrophilic superficial endometrial response accompanied by purulent luminal exudate is characteristic of the earlier stages of infection. Arrows indicate eosinophils, which are commonly seen in trichomonad infections below the endometrial mucosa. Luna stain (see inset) demonstrates the prominent red granules of eosinophils. Bar = 0.2 mm. Haematoxylin and eosin (H&E) stain.
CopyrightRobert H. BonDurant
Endometrium from a heifer experimentally infected with Tritrichomonas foetus and inseminated. A neutrophilic superficial endometrial response accompanied by purulent luminal exudate is characteristic of the earlier stages of infection. Arrows indicate eosinophils, which are commonly seen in trichomonad infections below the endometrial mucosa.  Luna stain (see inset) demonstrates the prominent red granules of eosinophils.  Bar = 0.2 mm. Haematoxylin and eosin (H&E) stain.
HistopathologyEndometrium from a heifer experimentally infected with Tritrichomonas foetus and inseminated. A neutrophilic superficial endometrial response accompanied by purulent luminal exudate is characteristic of the earlier stages of infection. Arrows indicate eosinophils, which are commonly seen in trichomonad infections below the endometrial mucosa. Luna stain (see inset) demonstrates the prominent red granules of eosinophils. Bar = 0.2 mm. Haematoxylin and eosin (H&E) stain.Robert H. BonDurant
Endometrium from an experimentally Tritrichomonas foetus infected heifer. Lymphocytes and plasma cells infiltrate the endometrium typically after 6-8 weeks post-infection and often form lymphoid aggregates surrounding glands. Mast cells (shown here by arrowheads in a Toluidene blue stained inset) show a precipitous decline in number between six and nine weeks post-infection, presumably due to degranulation. Bar = 0.5 mm.  H&E stain.
TitleHistopathology
CaptionEndometrium from an experimentally Tritrichomonas foetus infected heifer. Lymphocytes and plasma cells infiltrate the endometrium typically after 6-8 weeks post-infection and often form lymphoid aggregates surrounding glands. Mast cells (shown here by arrowheads in a Toluidene blue stained inset) show a precipitous decline in number between six and nine weeks post-infection, presumably due to degranulation. Bar = 0.5 mm. H&E stain.
CopyrightRobert H. BonDurant
Endometrium from an experimentally Tritrichomonas foetus infected heifer. Lymphocytes and plasma cells infiltrate the endometrium typically after 6-8 weeks post-infection and often form lymphoid aggregates surrounding glands. Mast cells (shown here by arrowheads in a Toluidene blue stained inset) show a precipitous decline in number between six and nine weeks post-infection, presumably due to degranulation. Bar = 0.5 mm.  H&E stain.
HistopathologyEndometrium from an experimentally Tritrichomonas foetus infected heifer. Lymphocytes and plasma cells infiltrate the endometrium typically after 6-8 weeks post-infection and often form lymphoid aggregates surrounding glands. Mast cells (shown here by arrowheads in a Toluidene blue stained inset) show a precipitous decline in number between six and nine weeks post-infection, presumably due to degranulation. Bar = 0.5 mm. H&E stain.Robert H. BonDurant
Tetratrichomonas sp. isolated from the prepuce of young bulls, and often from faeces as well. [Diff-Quik/iodine stain] (Lum and Gajadhar, 1999); original image approx.  100X.
TitleTetratichomonas sp.
CaptionTetratrichomonas sp. isolated from the prepuce of young bulls, and often from faeces as well. [Diff-Quik/iodine stain] (Lum and Gajadhar, 1999); original image approx. 100X.
CopyrightRobert H. BonDurant
Tetratrichomonas sp. isolated from the prepuce of young bulls, and often from faeces as well. [Diff-Quik/iodine stain] (Lum and Gajadhar, 1999); original image approx.  100X.
Tetratichomonas sp.Tetratrichomonas sp. isolated from the prepuce of young bulls, and often from faeces as well. [Diff-Quik/iodine stain] (Lum and Gajadhar, 1999); original image approx. 100X.Robert H. BonDurant
Pentatrichomonas hominis isolated from the prepuce of young bulls, and often from faeces as well. [Diff-Quik/iodine stain] (Lum and Gajadhar, 1999); original image approx.  100X.
TitlePentatrichomonas hominis
CaptionPentatrichomonas hominis isolated from the prepuce of young bulls, and often from faeces as well. [Diff-Quik/iodine stain] (Lum and Gajadhar, 1999); original image approx. 100X.
CopyrightRobert H. BonDurant
Pentatrichomonas hominis isolated from the prepuce of young bulls, and often from faeces as well. [Diff-Quik/iodine stain] (Lum and Gajadhar, 1999); original image approx.  100X.
Pentatrichomonas hominisPentatrichomonas hominis isolated from the prepuce of young bulls, and often from faeces as well. [Diff-Quik/iodine stain] (Lum and Gajadhar, 1999); original image approx. 100X.Robert H. BonDurant
Endometrium from a heifer experimentally infected with Tritrichomonas foetus. Chronic infection can lead to scarring of the uterus, characterized by multifocal glandular atrophy and dilation with annular periglandular fibrosis (arrows). For comparison, arrowheads point to relatively normal glands. A prominent lymphoplasmacytic infiltrate is still present between the areas of fibrosis. Bar = 0.5 mm.  H&E stain.
TitleHistopathology
CaptionEndometrium from a heifer experimentally infected with Tritrichomonas foetus. Chronic infection can lead to scarring of the uterus, characterized by multifocal glandular atrophy and dilation with annular periglandular fibrosis (arrows). For comparison, arrowheads point to relatively normal glands. A prominent lymphoplasmacytic infiltrate is still present between the areas of fibrosis. Bar = 0.5 mm. H&E stain.
CopyrightRobert H. BonDurant
Endometrium from a heifer experimentally infected with Tritrichomonas foetus. Chronic infection can lead to scarring of the uterus, characterized by multifocal glandular atrophy and dilation with annular periglandular fibrosis (arrows). For comparison, arrowheads point to relatively normal glands. A prominent lymphoplasmacytic infiltrate is still present between the areas of fibrosis. Bar = 0.5 mm.  H&E stain.
HistopathologyEndometrium from a heifer experimentally infected with Tritrichomonas foetus. Chronic infection can lead to scarring of the uterus, characterized by multifocal glandular atrophy and dilation with annular periglandular fibrosis (arrows). For comparison, arrowheads point to relatively normal glands. A prominent lymphoplasmacytic infiltrate is still present between the areas of fibrosis. Bar = 0.5 mm. H&E stain.Robert H. BonDurant

Identity

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Preferred Scientific Name

  • bovine venereal trichomonosis

International Common Names

  • English: bovine genital trichomoniasis; bovine genital trichomonosis; bovine trichomonad abortion; bovine trichomonad abortion; trichomoniasis, Tritrichomonas foetus in cattle; trichomonosis, bovine; trichomonosis, Tritrichomonas foetus in cattle; Tritrichomonas foetus infections in cattle

Overview

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Bovine trichomonosis (trichomoniasis)is a venereal disease caused by the flagellated protozoan, Tritrichomonas foetus. The disease is characterized by relatively early and typically occult loss of pregnancy, occasional post-coital pyometra, and temporary infertility of females. Males harbour the organism on the surface of the prepuce and penis, and show no detectable signs. Trichomoniasis is present wherever natural service of cattle is widely practiced, and is virtually unknown in herds where artificial insemination is exclusively used. The association of T. foetus with early bovine abortion was first described by Riedmüller in Europe (Riedmüller, 1928) and soon after in North America by Wenrich and Emmerson in 1933. Later investigations have strongly suggested that the organism causing early bovine abortion is identical to Tritrichomonas suis, a trichomonad first obtained from the gastrointestinal and naso-pharyngeal tracts of pigs, and described by Gruby and Delafond in 1843 (Tachezy et al., 2002). Moreover, there are now several reports of a gastroenteritis syndrome in domestic cats, closely associated with the presence of T. foetus in the diarrhoeic fluid (Gookin et al., 1999; Levy et al., 2003). Whether these indistinguishable trichomonads are different species or simply different strains within a species is not entirely agreed. Until this question can be resolved, retention of the name Tritrichomonas foetus is recommended for the cattle pathogen.

In cattle, trichomonosis causes significant, sometimes devastating economic losses, in part because of its occult nature. Females abort or reabsorb the conceptus, usually between 21 and 100 days of gestation, without overt signs (Parsonson et al., 1976). By the time a problem is recognized, usually at the time of herd pregnancy examination, the economic damage is done. Individual estimates of economic impact of trichomonosis are calculated differently by different authors, and are somewhat difficult to compare, but all produce estimates of very large monetary loss.

This disease is on the list of diseases notifiable to the World Organisation for Animal Health (OIE). The distribution section contains data from OIE's WAHID database on disease occurrence. Please see the AHPC library for further information on this disease from OIE, including the International Animal Health Code and the Manual of Standards for Diagnostic Tests and Vaccines. Also see the website: www.oie.int.

Hosts/Species Affected

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Transmission of trichomonosis is direct, through coital contact. No intermediate hosts or vectors are involved. Domestic cattle (Bos taurus and B. indicus and their hybrids) are considered the only natural hosts for Tritrichomonas foetus, although a few reports exist of a diagnosis of trichomonosis in water buffalo and camels (Abdel-Gawad, 1981; Wernery, 1991). Rigorous diagnostic standards have not been applied to organisms detected in non-Bos species. However, the phenotypic and apparent genotypic identity of T. foetus and Tritrichomonas suis, (Carili and Guerrero, 1977; Tachezy et al., 2002), and the presence in the domestic feline gastrointestinal tract of an organism that cannot be distinguished from T. foetus (Levy et al., 2003; Gookin et al., 1999) indicates that T. foetus and T. suis may represent a single species that has evolved to survive in several different environments in several different species. So far as is known, cattle are the only species to suffer significant reproductive disease due to T. foetus/T. suis.

Host factors that predispose naturally-serviced cattle to trichomonosis include age of the bull, use of borrowed or leased bulls, use of shared grazing, failure to test and eliminate infected bulls before they are turned in with cows, and failure to vaccinate females (BonDurant and Honigberg, 1994; Gay et al., 1996). Some studies have suggested a genetic predisposition, with Bos taurus bulls more likely to be infected than B. indicus in the same environment. Others did not find such an association (BonDurant et al., 1990). Such studies are difficult to conduct, because equal, within-herd access of both types of bulls to the same set of cows is required, but seldom practiced.

Of the listed risk factors, bull age is the most important. Most prevalence studies show a clear correlation of age with infection status. In one typical study, bulls older than 3 years were approximately three times more likely to be infected as bulls younger than three years. As bulls mature, the growth of the non-keratinized stratified squamous epithelium of the penis and prepuce produces folds, forming crypts, which provide a microenvironment suitable for T. foetus. Immuno-histochemical techniques reveal the protozoans in the deeper aspects of the crypts (Rhyan et al., 1999). These crypts are considerably more evident in bulls >3 years old than in bulls <3 years of age (BonDurant, 1985). Transmission is efficient from bull to cow, and very efficient from cow to mature bull (Clark et al., 1974b). Once infected, older bulls become chronic carriers, often for life (Christensen et al., 1977). Any seasonality associated with bovine trichomonosis is likely to be a consequence of seasonal breeding practices, and not due to climatic influences to which the parasite responds.

Distribution

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As cattle are grazed on every continent under extensive management practices, including the use of natural service, trichomonosis is presumed to exist worldwide. Statistics from OIE would appear to confirm this, although many nations do not report incidence or prevalence figures for Tritrichomonas foetus. In the western hemisphere, trichomonosis is reported from most major cattle-producing countries, from Argentina to Canada. Older prevalence reports from randomly sampled populations in California (USA) and Costa Rica, which found bull and herd infection rates of 5.0 to 7.2%, and 16.0 to 18.4%, respectively, have not been repeated (BonDurant et al., 1990; Perez et al., 1992). The lack of studies from randomly selected sample populations makes the assessment of the true prevalence of trichomonosis more difficult. A carefully designed study of Florida (USA) beef herds reported average within-unit prevalence amongst bulls of 11.9% in 1999, while the same author found 6% of all bulls and 30.4% of all herds infected in 2004 (Rae et al., 1999; Rae et al., 2004). Another prevalence study in randomly selected Brazilian herds showed a 1.67% and 0.71% herd and bull prevalence, respectively, in the state of Goias (Campos-Junior, 2002), while another comprehensive study in the state of Rio de Janeiro found 28% of dairy herds and 13.4% of bulls infected (Jesus, 2003). Several reports, based on convenience samples taken from herds in which there was suspicion of trichomonosis, probably overestimated the actual regional prevalence, but serve to inform that the disease is present in other areas of the USA, Brazil and Argentina (Kvasnicka et al., 1989; Pellegrin et al., 1998; Russo et al., 2000).

In general, very little bovine trichomonosis is documented from Europe, although France, Hungary, Malta, Moldavia, Romania, Russia and Spain reporting cases as recently as 2003 (see OIE Handistatus http://www.oie.int; Martin-Gomez et al., 1998). Because many studies use only the less accurate direct observation of genital secretions (wet mounts) to obtain a diagnosis, it is difficult to know their validity, given the occurrence of other, nonpathogenic trichomonads in and around the genitalia of cattle. Undoubtedly, the widespread use of artificial insemination has played an important role in the control of trichomonosis in Europe.

For current information on disease incidence, see OIE's WAHID Interface.

Distribution Table

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The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes

Asia

AzerbaijanNo information availableOIE Handistatus, 2005
BahrainDisease never reportedOIE Handistatus, 2005
BhutanNo information availableOIE Handistatus, 2005
Brunei DarussalamNo information availableOIE Handistatus, 2005
China
-Hong KongNo information availableOIE Handistatus, 2005
Georgia (Republic of)Last reported1997OIE Handistatus, 2005
IndiaPresentPresent based on regional distribution.
-RajasthanPresentPareek et al., 1994
IndonesiaReported present or known to be presentOIE Handistatus, 2005
IranNo information availableOIE Handistatus, 2005
IraqNo information availableOIE Handistatus, 2005
IsraelNo information availableOIE Handistatus, 2005
JapanLast reported1963OIE Handistatus, 2005
JordanOIE Handistatus, 2005
KazakhstanDisease not reportedOIE Handistatus, 2005
Korea, DPRDisease not reportedOIE Handistatus, 2005
Korea, Republic ofLast reported1989OIE Handistatus, 2005
KuwaitLast reported1995OIE Handistatus, 2005
LebanonLast reported1992OIE Handistatus, 2005
Malaysia
-Peninsular MalaysiaDisease not reportedOIE Handistatus, 2005
-SabahDisease never reportedOIE Handistatus, 2005
-SarawakNo information availableOIE Handistatus, 2005
MongoliaNo information availableOIE Handistatus, 2005
MyanmarDisease not reportedOIE Handistatus, 2005
NepalNo information availableOIE Handistatus, 2005
OmanDisease not reportedOIE Handistatus, 2005
PhilippinesDisease not reportedOIE Handistatus, 2005
QatarNo information availableOIE Handistatus, 2005
Saudi ArabiaDisease not reportedOIE Handistatus, 2005
SingaporeDisease never reportedOIE Handistatus, 2005
Sri LankaDisease never reportedOIE Handistatus, 2005
SyriaDisease not reportedOIE Handistatus, 2005
TaiwanDisease not reportedOIE Handistatus, 2005
TajikistanNo information availableOIE Handistatus, 2005
ThailandDisease not reportedOIE Handistatus, 2005
TurkeyNo information availableOIE Handistatus, 2005
TurkmenistanDisease not reportedOIE Handistatus, 2005
United Arab EmiratesDisease not reportedOIE Handistatus, 2005
UzbekistanDisease not reportedOIE Handistatus, 2005
VietnamNo information availableOIE Handistatus, 2005
YemenNo information availableOIE Handistatus, 2005

Africa

AlgeriaDisease not reportedOIE Handistatus, 2005
AngolaNo information availableOIE Handistatus, 2005
BeninNo information availableOIE Handistatus, 2005
BotswanaLast reported1995OIE Handistatus, 2005
Burkina FasoNo information availableOIE Handistatus, 2005
BurundiDisease never reportedOIE Handistatus, 2005
CameroonNo information availableOIE Handistatus, 2005
Cape VerdeDisease never reportedOIE Handistatus, 2005
Central African RepublicNo information availableOIE Handistatus, 2005
ChadNo information availableOIE Handistatus, 2005
Congo Democratic RepublicNo information availableOIE Handistatus, 2005
Côte d'IvoireDisease not reportedOIE Handistatus, 2005
DjiboutiDisease not reportedOIE Handistatus, 2005
EgyptNo information availableOIE Handistatus, 2005
EritreaCAB Abstracts data miningOIE Handistatus, 2005
GhanaDisease not reportedOIE Handistatus, 2005
GuineaDisease never reportedOIE Handistatus, 2005
Guinea-BissauNo information availableOIE Handistatus, 2005
KenyaCAB Abstracts data miningOIE Handistatus, 2005
LibyaDisease never reportedOIE Handistatus, 2005
MadagascarDisease not reportedOIE Handistatus, 2005
MalawiNo information availableOIE Handistatus, 2005
MaliNo information availableOIE Handistatus, 2005
MauritiusDisease not reportedOIE Handistatus, 2005
MoroccoNo information availableOIE Handistatus, 2005
MozambiqueNo information availableOIE Handistatus, 2005
NamibiaReported present or known to be presentOIE Handistatus, 2005
NigeriaNo information availableOIE Handistatus, 2005
RéunionNo information availableOIE Handistatus, 2005
RwandaNo information availableOIE Handistatus, 2005
Sao Tome and PrincipeNo information availableOIE Handistatus, 2005
SenegalNo information availableOIE Handistatus, 2005
SeychellesNo information availableOIE Handistatus, 2005
SomaliaNo information availableOIE Handistatus, 2005
South AfricaReported present or known to be presentOIE Handistatus, 2005
SudanLast reported1993OIE Handistatus, 2005
SwazilandNo information availableOIE Handistatus, 2005
TanzaniaNo information availableOIE Handistatus, 2005
TogoDisease not reportedOIE Handistatus, 2005
TunisiaNo information availableOIE Handistatus, 2005
UgandaNo information availableOIE Handistatus, 2005
ZambiaNo information availableOIE Handistatus, 2005
ZimbabweLast reported1996OIE Handistatus, 2005

North America

BermudaDisease not reportedOIE Handistatus, 2005
CanadaReported present or known to be presentOIE Handistatus, 2005
MexicoOIE Handistatus, 2005
USAReported present or known to be presentOIE Handistatus, 2005

Central America and Caribbean

BarbadosDisease never reportedOIE Handistatus, 2005
BelizeDisease never reportedOIE Handistatus, 2005
British Virgin IslandsDisease never reportedOIE Handistatus, 2005
Cayman IslandsDisease not reportedOIE Handistatus, 2005
Costa RicaNo information availableOIE Handistatus, 2005
CubaReported present or known to be presentOIE Handistatus, 2005
CuraçaoDisease not reportedOIE Handistatus, 2005
DominicaDisease not reportedOIE Handistatus, 2005
Dominican RepublicNo information availableOIE Handistatus, 2005
El SalvadorNo information availableOIE Handistatus, 2005
GuadeloupeNo information availableOIE Handistatus, 2005
GuatemalaNo information availableOIE Handistatus, 2005
HaitiDisease never reportedOIE Handistatus, 2005
JamaicaDisease never reportedOIE Handistatus, 2005
MartiniqueReported present or known to be presentOIE Handistatus, 2005
NicaraguaNo information availableOIE Handistatus, 2005
PanamaNo information availableOIE Handistatus, 2005
Saint Kitts and NevisDisease never reportedOIE Handistatus, 2005
Saint Vincent and the GrenadinesDisease never reportedOIE Handistatus, 2005
Trinidad and TobagoDisease never reportedOIE Handistatus, 2005

South America

ArgentinaReported present or known to be presentOIE Handistatus, 2005
BoliviaOIE Handistatus, 2005
BrazilReported present or known to be presentOIE Handistatus, 2005
ChileOIE Handistatus, 2005
ColombiaLast reported2001OIE Handistatus, 2005
EcuadorLast reported1994OIE Handistatus, 2005
Falkland IslandsDisease never reportedOIE Handistatus, 2005
French GuianaNo information availableOIE Handistatus, 2005
GuyanaDisease not reportedOIE Handistatus, 2005
ParaguayLast reported2002OIE Handistatus, 2005
PeruOIE Handistatus, 2005
UruguayOIE Handistatus, 2005
VenezuelaReported present or known to be presentOIE Handistatus, 2005

Europe

AndorraCAB Abstracts data miningOIE Handistatus, 2005
AustriaNo information availableOIE Handistatus, 2005
BelarusLast reported1960OIE Handistatus, 2005
BelgiumNo information availableOIE Handistatus, 2005
Bosnia-HercegovinaDisease not reportedOIE Handistatus, 2005
BulgariaNo information availableOIE Handistatus, 2005
CroatiaLast reported1992OIE Handistatus, 2005
CyprusLast reported1971OIE Handistatus, 2005
Czech RepublicDisease not reportedOIE Handistatus, 2005
DenmarkLast reported1990OIE Handistatus, 2005
EstoniaDisease not reportedOIE Handistatus, 2005
FinlandLast reported1952OIE Handistatus, 2005
FranceReported present or known to be presentOIE Handistatus, 2005
GermanyReported present or known to be presentOIE Handistatus, 2005
GreeceLast reported1999OIE Handistatus, 2005
HungaryOIE Handistatus, 2005
IcelandDisease never reportedOIE Handistatus, 2005
IrelandDisease not reportedOIE Handistatus, 2005
Isle of Man (UK)Disease not reportedOIE Handistatus, 2005
ItalyReported present or known to be presentOIE Handistatus, 2005
JerseyDisease never reportedOIE Handistatus, 2005
LatviaDisease never reportedOIE Handistatus, 2005
LiechtensteinDisease not reportedOIE Handistatus, 2005
LithuaniaDisease not reportedOIE Handistatus, 2005
LuxembourgNo information availableOIE Handistatus, 2005
MacedoniaNo information availableOIE Handistatus, 2005
MaltaLast reported2001OIE Handistatus, 2005
MoldovaLast reported2001OIE Handistatus, 2005
NetherlandsDisease not reportedOIE Handistatus, 2005
NorwayDisease never reportedOIE Handistatus, 2005
PolandLast reported1997OIE Handistatus, 2005
PortugalDisease not reportedOIE Handistatus, 2005
RomaniaOIE Handistatus, 2005
Russian FederationOIE Handistatus, 2005
SlovakiaDisease not reportedOIE Handistatus, 2005
SloveniaDisease never reportedOIE Handistatus, 2005
SpainNo information availableOIE Handistatus, 2005
SwedenDisease never reportedOIE Handistatus, 2005
SwitzerlandLast reported1997OIE Handistatus, 2005
UKLast reported1991OIE Handistatus, 2005
-Northern IrelandLast reported1966OIE Handistatus, 2005
UkraineDisease never reportedOIE Handistatus, 2005
Yugoslavia (former)No information availableOIE Handistatus, 2005
Yugoslavia (Serbia and Montenegro)Disease not reportedOIE Handistatus, 2005

Oceania

AustraliaReported present or known to be presentOIE Handistatus, 2005
French PolynesiaDisease not reportedOIE Handistatus, 2005
New CaledoniaCAB Abstracts data miningOIE Handistatus, 2005
New ZealandReported present or known to be presentOIE Handistatus, 2005
SamoaDisease never reportedOIE Handistatus, 2005
VanuatuDisease never reportedOIE Handistatus, 2005
Wallis and Futuna IslandsNo information availableOIE Handistatus, 2005

Pathology

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Infection of females occurs at coitus, but typically does not interfere with fertilization or early development of the ovulated oocyte to the blastocyst stage and later (Bielanski et al., 2004). Similarly, Parsonson et al. (1976) showed that virgin heifers exposed to infected bulls developed inflammatory lesions slowly, with significant endometritis and salpingitis not evident until about the sixth to ninth week of pregnancy. Fetal deaths peaked during this time as well. Specific immunoglobulin, especially IgA and IgG1, appear in secretions of the vagina and uterus, rising significantly from basal levels by the fourth or fifth week after infection (Skirrow and BonDurant, 1990a). In addition, specific IgE is measurable in secretions and serum at or before this time. The IgA is presumably secreted locally, but the route by which IgG1 arrives in the uterine or vaginal lumen is unknown. Clearance of the organism is associated with peak or near peak levels of luminal IgG1 (Corbeil et al., 1998).

There are no specific diagnostic lesions in either the male or female. The male shows no significant lesions, except for a mild catarrhal reaction on the surface of the penile and preputial epithelium, shortly after infection. Later, histological changes include the formation of lymphoid aggregates, some of which resemble lymphoid follicles, in the subepithelial stroma. Immunohistochemical methods suggest that the soluble (SGA) antigen shed from the surface of T. foetus is taken up by penile epithelial cells, an observation that, it is suggested, may explain the origin of specific immunoglobulin in the preputial cavity (Campero et al., 1990; Campero and Palladino, 1985).

Like the bull, the female’s initial response to T. foetus infection is neutrophilic, and usually rather mild. By week six after exposure, a mixed leukocyte response is evident, including lymphocytes, plasma cells, and eosinophils (Anderson et al., 1996). Infiltrates are seen below the surface epithelium and surrounding the glands in the stratum spongiosum. Numbers of submucosal mast cells, as detected by toluidine blue staining, show a precipitous decline between weeks six and nine, presumably due to degranulation. By week 12, mast cell numbers have returned to their week three levels, eosinophil numbers have diminished, and the inflammation is generally subsiding (Anderson et al., 1996). High levels of parasite-specific vaginal IgG1 and IgA continue for a few (IgG1) to several (IgA) months. An elevation in circulating complement-fixing antibody is also evident, rising three weeks after infection and peaking at about week seven (BonDurant et al., 1996). Clearance of the organism from the uterus and vagina begins about the seventh to ninth week in non-vaccinated females, and about week four to six in vaccinates. Fertility usually returns some time after weeks 12-18. Rarely, a cow will become a chronic carrier, harbouring the organism into the next breeding season where it can put the herd at risk again. As mentioned, the immunity gained during natural infection is short-lived, and many cows are susceptible again in the next breeding season.

Virulence factors have been little studied, but at least three mechanisms of cell damage have been proposed:

  • A contact-dependent cytotoxic action, mediated by a 190-kD adhesin, was described for HeLa cells co-cultured with T. foetus (Shaia et al., 1998)
  • A potentially non-contact-dependent cytotoxic activity in cysteine proteases present in trichomonad-conditioned medium has been demonstrated (Talbot et al., 1991; Thomford et al., 1996)

A delayed hypersensitivity response to shed trichomonad antigen that may cause degranulation of endometrial mast cells, triggering a cascade of cell- and antibody-mediated damage to the endometrium or trophoblast of the early pregnancy.

Diagnosis

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Clinical diagnosis


A presumptive, clinical diagnosis is made based on the presence of one or more risk factors, a history of infertility as manifest by low pregnancy rates and wide distribution of gestational ages for those cows that are pregnant, and knowledge of the prevalence of trichomonosis in the geographical area.


Lesions and clinical signs


The only clinical sign likely to be noticed is the late return to oestrus; typically about 50 to 60 days after coitus with an infected bull. There are no visible signs to indicate which animals might be infected.


Differential diagnosis


Another classical venereal disease of cattle, genital campylobacteriosis, exhibits a nearly identical epidemiological and clinical picture, and must be considered and ruled out whenever trichomonosis is considered. A few lesser known infectious agents can also be transmitted venereally, including Haemophilus somnus, Chlamydophylla spp., and Ureaplasma diversum (BonDurant, USA [address available from CABI]). Other differentials include poor body condition of females entering the breeding period and subfertility of males from any cause.


Laboratory diagnosis


In endemic areas diagnosis requires demonstration of the organism or its DNA. Serological tests are not currently specific enough to recommend their routine use in individual animal diagnostic efforts, and cannot distinguish between exposure and active infection. Some serological tests (complement-activated haemolytic test, and to a lesser extent, the mucus agglutination test) are relatively specific, and therefore somewhat useful as a herd screening tool, but definitive diagnosis requires direct evidence of active infection.


Diagnostic strategy


If they are available, it is best to begin with the bulls, since the transient nature of infection in cows makes it less likely that a positive result can be obtained from them. Currently, the best diagnostic test is the culture of preputial secretions/epithelial cells obtained by scraping or lavage of the prepuce. Although early reports favoured lavage, more recent studies report no difference in results obtained by scraping or lavage (Irons et al., 2002; Schönmann et al., 1994; Tedesco et al., 1979); scraping is generally considered faster and easier, and does not require a centrifugation step. Suitable media for culture include Diamond’s TYM, modified Plastridge (BGPS [Beef extract-glucose-peptone-serum]) medium, CPLM (cysteine-peptone-liver infusion-maltose) medium, and various modifications of these. All of these media contain serum, typically cattle, horse, or sheep. Diamond’s TYM is a trypticase peptone-yeast extract-maltose based medium with a reducing environment assured by the addition of L-cysteine, hydrochloric acid and L-ascorbic acid. A useful modification of the original formula is the addition of agar (0.5% w/v), which tends to trap contaminating microbes in the upper layers of the culture tube, allowing the motile trichomonads to flourish in the microaerophilic environment at the bottom of the tube. Under optimum conditions, in vitro growth through the logarithmic phase (typically one to two days) proceeds with a doubling time of approximately 2 to 4 h (Lun et al., 2000). Cultures are examined daily for up to 7 days by aspirating about 50 µL from the bottom of the culture tube, placing the sample on a warm glass slide, placing a cover-slip over the specimen and scanning the slide at 100x magnification for motile T. foetus. Suspect organisms can be confirmed at 400x to 1000x. In the InPouch system, the medium is examined directly through the clear plastic packet, paying particular attention to the bottom and side margins of the packet (BonDurant, 1997; Borchardt et al., 1992; Parker et al., 2003).

In either cows or bulls, culture is superior to direct observation of secretions in wet-mounts. In bulls, most comparisons of diagnostic sensitivity of the culture method using modified Diamond’s medium or InPouches find the two media to be nearly equivalent, with most discrepancies favouring InPouch. Diamond’s medium has demonstrated a diagnostic sensitivity of 82%-90% under field conditions; it will yield a positive culture in 82% of known infected bulls (Skirrow et al., 1985). InPouches has shown sensitivities of 88 to 92% (Parker et al., 1999; Thomas et al., 1990). Thus, false negative results can occur in 8 to 18% of infected bulls tested. For this reason, repeated sampling and culture is often recommended: Three consecutive negative cultures at weekly intervals lower the probability of a negative test being falsely negative to between 0.3 and 0.6%. Many commercial semen processing centres go even further, demanding six negative cultures at weekly intervals, a practice that theoretically reduces the probability of detection failure to approximately 0.003%. Complete sexual rest is considered essential during the testing period, to prevent a reduction in trophozoite numbers that apparently occurs at coitus.


Factors influencing diagnostic sensitivity and specificity


The transport medium has an important influence on the success of culture. Transporting samples in lactated Ringers solution for 24 hours before inoculating the mixture onto Diamond’s TYM medium resulted in a 14% loss in sensitivity relative to an aliquot of the same smegma inoculated onto culture medium immediately. Where InPouches are either unavailable or not affordable, reasonably suitable transport media include saline or lactated Ringer’s solution, each with 5% heat-treated steer serum, or boiled skimmed cow’s milk (Kimsey et al., 1980; Reece et al., 1983). Some have reported significantly lower sensitivity when smegma samples are transported in thioglycolate and cultured in Diamond’s, as opposed to immediate inoculation of smegma in InPouches. Regardless of the medium used, diagnostic sensitivity in females is lower than in males, probably because the female’s immune response reduces the number of trophozoites in the reproductive tract to sometimes-undetectable levels.

False positive results are possible, due to the presence of non-T. foetus trichomonads of faecal origin in the prepuce of some bulls. To date, members of the genera Tetratrichomonas and Pentatrichomonas have been isolated (BonDurant et al., 1999; Cobo et al., 2003; Grahn et al., 2005; Parker et al., 2003a). Attempts to establish chronic infection in either males or females with any of these trichomonads have been unsuccessful (Cobo et al., 2004; Agnew et al., 2004). They are therefore not considered pathogens. While the motility and general silhouette of all these organisms is somewhat similar to that of T. foetus, they can be differentiated by careful staining, and observing the number of flagellae.

Recently, polymerase chain reaction (PCR) techniques have been applied to the diagnosis of T. foetus infection. Most reports use PCR to confirm culture results; to show that the trichomonad grown in culture is or is not T. foetus. The specificity of such molecular diagnostics is theoretically very high. Most authors use primers from the area of the 5.8S ribosomal RNA gene known as the inter-transcribed spacer region (specifically the ITS1-5.8 S rRNA-ITS2 segment), an area that tends to be phylogenetically conserved (Felleisen,1997; Felleisen,1998; Felleisen et al., 1998; Parker et al.,2001). The biological sensitivity of PCR is potentially very high, with as few as 3 trichomonads (in culture medium) yielding a positive PCR assay (Parker et al., 2001). Most studies also show a decline in biological sensitivity when organisms are assayed in smegma, rather than culture medium (Ho et al., 1994).

List of Symptoms/Signs

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SignLife StagesType
Reproductive Signs / Abnormal length estrus cycle, long, short, irregular interestrus period Sign
Reproductive Signs / Abnormal length of estrus period, heat Sign
Reproductive Signs / Abortion or weak newborns, stillbirth Sign
Reproductive Signs / Anestrus, absence of reproductive cycle, no visible estrus Sign
Reproductive Signs / Enlarged uterus Sign
Reproductive Signs / Female infertility, repeat breeder Sign
Reproductive Signs / Fluid in uterus Sign
Reproductive Signs / Mucous discharge, vulvar, vaginal Sign
Reproductive Signs / Mummy, mummified fetus Sign
Reproductive Signs / Purulent discharge, vulvar, vaginal Sign
Reproductive Signs / Purulent or mucoid discharge, cervix or uterus Sign

Disease Course

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Trichomonosis is characteristically a transient infection in females and a chronic infection of males older than 3 years. Naïve cows, exposed at coitus to infected bulls, typically will conceive and lose the conceptus some time after maternal recognition of pregnancy, which occurs after between 17 and 24 days (Thatcher et al., 2003). Most fetal deaths occurred after 50-70 days. This is also the time of peak luminal IgG1 and IgA antibody responses in the female reproductive tract. Uterine clearance of trichomonads begins before vaginal clearance, but in any case, by 12-18 weeks after infection, most cows are free of the organism, and regain their fertility. Immunity is short-lived, however, and convalescent cows may be reinfected in the following breeding season. A small proportion of exposed cows, perhaps 5%, develop a post-coital pyometra.

Some bulls under 3 years of age may clear the infection once all breeding activity has ceased. Before this time, they can be mechanical vectors, although survival time of trophozoites in the prepuce of young bulls is thought to be brief, a matter of hours. Bulls older than 3 years of age are much less likely to spontaneously clear an infection.

Immunity

If no intervention is taken, increasing female herd immunity will allow a gradual increase in the proportion of cows calving, although those rates will probably never return to their pre-infection levels (Clark et al., 1983; Clark et al., 1986).

Epidemiology

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Transmission occurs at coitus, and is highly efficient. In experimental conditions, most cows exposed to mature infected bulls become infected. Infection is usually transient in the female, lasting approximately 8 to 18 weeks (BonDurant et al., 1993; Skirrow and BonDurant, 1990b). Rarely, probably in less than 0.1% of infected cows, a ‘carrier’ cow will remain infected throughout pregnancy and into the subsequent breeding season (Skirrow, 1987). Bulls are typically asymptomatic carriers, and in endemic herds are more likely to become permanent carriers as they age beyond 3 years (Clark et al., 1974a; Parsonson et al., 1974).

Exceptions to venereal transmission are rare, and include improper hygiene at the time of gynecological examination or artificial insemination (contaminated gloves, instruments, etc.) (Goodger and Skirrow, 1986), and the use of semen contaminated with T. foetus. The latter may occur when custom-frozen semen is processed without regard for hygienic procedures as exemplified by the Certified Semen Services (CSS) protocol (Monke and Mitchell, 1998). Because trichomonads are not affected by the antibiotics commonly added to semen extenders, and because they survive freezing to -196°C, they cannot be controlled after the semen has been collected. Therefore, artificial insemination centers take extraordinary measures to ensure that each bull whose semen is collected is in fact not harbouring T. foetus.

Impact: Economic

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Trichomonosis is included on the list of diseases notifiable to the World Organization for Animal Health (OIE). In the past, trichomonosis has been among the most economically devastating reproductive diseases. Losses have come mainly from abortions, although increased veterinary costs and culling costs also contribute. In some countries, including the USA, there is no approved efficacious treatment for cattle, so infected bulls, once identified, are culled. In 2004, crude estimates of the scale of economic losses for the state of California (USA) amounted to US $22 million for an industry with slightly less than 1 million beef cows exposed to bulls each year (Villarroel et al., 2004). A detailed epidemiology study of an outbreak of trichomonosis in a large commercial dairy in California estimated the loss at US $665 per infected cow. Summary figures for the USA are as high as US $650 million per annum (Speer and White, 1991). Such figures are bolstered by models developed in the USA that predict up to a 35% reduction in income per cow exposed to bulls when the prevalence of infection amongst bulls reaches 40% (Rae, 1989). Given the high transmission rates from bull to cow and cow to bull, 40% within-herd prevalence amongst bull batteries can be predicted within the first few weeks of the breeding season.

Zoonoses and Food Safety

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In spite of a report of an immuno-compromized human death due to T. foetus-associated meningoencephalitis (Okamoto et al., 1998), the bovine venereal pathogen is not considered zoonotic under most circumstances. There are no food safety concerns specific to Tritrichomonas foetus infection of cattle, unless they have been treated with a substance that requires a pre-slaughter withdrawal period.

Disease Treatment

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Because of the transient nature of infection in the female, if there is any treatment at all, only the bulls are treated. Tritrichomonas foetus has shown susceptibility to several antimicrobials in vitro, but to very few agents in vivo. Among the latter, only two types of treatment are in use. The first is acriflavine (also called trypaflavine, or bovoflavine) ointment (1%), which is applied topically to the skin of the glans penis, the shaft of the penis, and the prepuce in the area of the fornix (Jesus et al., 1996). As the active agent stains human skin yellow and can cause significant skin irritation, protective gloves should be worn when administering this treatment. Furthermore, in order to exteriorize the penis for the 10-15 min required for treatment, it is usually necessary to administer a pudendal nerve block to the bull. The treatment may be repeated in 2-14 days. Large, controlled efficacy trials have not been run for more than a half century, and among the smaller, more recent clinical reports available, none examine longevity of the trichomonad-free state following treatment beyond approximately 3 weeks. However, these studies indicate that most acriflavine-treated bulls were culture-negative for at least a fortnight after treatment. Older studies that used less sensitive diagnostic methods reported a ‘cure’ in 89% of 239 treated bulls (Bartlett, 1949; Bartlett, 1950).

[NOTE: In some countries, the use of substituted nitroimidazoles in food animal species is illegal. Check local regulations.]

The substituted nitroimidazole compounds dimetridazole and ipronidazole have been used to treat infected cattle, usually bulls. Dimetridazole has been given orally at a dose of 50-150 mg/kg per day for five consecutive days, with some authors repeating the treatment after 14 days. Others have also applied up to a 2% solution topically in addition to the systemic treatment (Suteu et al., 1979). Efficacy would appear to be rather high for all dimetridazole-based treatments, as 15/15 bulls treated with the 2 x 5 daily oral drench protocol were negative for T. foetus 15 days after the last treatment. In another investigation 5 bulls were successfully treated by intravenous injection of 50mg/kg of benzoylnitroimidazole in 20% dimethyl sulfoxide (DMSO) (Módolo et al., 1991). The latter is not recommended until further studies on possible negative effects of the treatment can be evaluated.

Several members of the nitroimidazole group of compounds are known to be mutagens, and mice fed high doses have developed lung tumors (Honigberg and Burgess, 1994). For this reason, the family of substituted nitroimidazoles is banned from use in food animals in the USA (Guest, 1988) and other countries.

Prevention and Control

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From a strictly biological perspective, the cessation of all natural service and the immediate implementation of artificial insemination (AI), using semen from reputable sources, makes the most sense. But AI is often not practical in extensively managed herds, due to low stocking density, difficulties with oestrus detection, and lack of trained personnel. The use of timed artificial insemination (TAI) programmes that attempt to synchronize ovulation, and thus reduce or eliminate oestrus detection, can increase client compliance with this protocol.

In dairies diagnosed with trichomonosis, a TAI plan is more readily implemented. Other methods of herd therapy include culling all bulls (to be sold for slaughter only), and culling any cows with post coital pyometra. For the remainder of the cows, fertility should return in 2-3 months.

In extensively managed cattle, prevention requires a disciplined, cooperative, regional application of testing and removal of infected bulls before the breeding season, maintenance of fencing, use of younger (ideally virgin) bulls whenever possible, and appropriate use of vaccine, where available. In the 1970’s, Clark and others showed that natural infection brought at least some immunity, as cows exposed season after season to infected bulls gradually regained much, but not all of their fertility (Clark et al., 1983; 1974c). This process can be accelerated if all infected bulls, or all bulls more than 3 years old regardless of infection status, are replaced with virgin bulls.

Some governments have imposed T. foetus testing requirements. In the USA, several western states have recently instituted programmes designed to reduce the threat of trichomonosis. A few states, such as Idaho, have mandatory annual testing of all non-virgin bulls, and a positive diagnosis mandates slaughter of the bull and quarantine of the herd. Other western states have varying degrees of stringency regarding, for example, penalties and populations to be tested.

Currently, a killed, whole-cell vaccine is available (Ft. Dodge Animal Health, Ft. Dodge, Iowa, USA) (Kvasnicka et al., 1992) and other, subunit-type vaccines are being investigated (Corbeil et al., 2001; Kvasnicka et al., 1992). As a ‘bacterin,’ the commercial vaccine requires two intramuscular injections 2 to 4 weeks apart, preferably with the second coming no more than a week before exposure to potentially infected bulls, so that immunological anamnestic response peaks near the time of service. One published report showed a clear benefit of vaccinating females twice (3- to 4-week interval) immediately before exposure to an infected bull. Challenge in this experiment was rigorous; immediately after mating all cows were further exposed by intravaginal instillation of nearly 10 million T. foetus trophozoites. The proportion of cows calving was nearly twice as high (61%) for vaccinates as for controls (31%) (Kvasnicka et al., 1992). No test for efficacy of this vaccine in bulls has been published. The vaccine is expensive (approximately US $2.50 per dose), so it is used strategically. If any of the major risk factors are evident, the vaccine will reduce the impact of herd exposure to T. foetus. In most cases it will not prevent infection, but it will reduce the time to clearance of T. foetus from the reproductive tract. Whereas non-vaccinates rid themselves of infection over 8-18 weeks, clearance will occur before the 7th week of infection in most vaccinates. This might be soon enough to salvage an existing pregnancy, since Parsonson et al. (1976) showed that fetal deaths peak at about 8-10 weeks after infection. A mathematical model predicts that vaccinating is cost effective in situations where trichomonosis has been diagnosed in an adjacent property, where bulls are not routinely checked for T. foetus infection before the breeding season, or where shared grazing is used.

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Tritrichomonas foetus - microscopy and diagnosis videoshttp://faculty.vetmed.ucdavis.edu/faculty/rhbondurant/T_Foetus_Videos.htmThree videos showing Tritichomonas foetus, similar non-T. foetus organisms and the testing and diagnosis of bulls for bovine trichomonosis. All videos are copyright of University of California, Davis, California, USA, and were kindly made available to users of the Animal Health and Production Compendium by Prof. Robert BonDurant.

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