Definition
Dourine is a chronic trypanosomal disease of Equidae. The disease
is transmitted almost exclusively by coitus and is characterized by edematous lesions of
the genitalia, nervous system involvement, and progressive emaciation.
Etiology
Dourine is caused by Trypanosoma equiperdum (Fig. 48) (Doflein, 1901), a protozoan parasite related
morphologically and serologically to T. brucei, T. rhodesiense, and T.
gambiense (of the subgenus Trypanozoon of the Salivarian section of
organisms of the pathogenic genus Trypanosoma). Different strains of the parasite
vary in pathogenicity (5).
Host Range
Dourine is typically a disease of horses and donkeys. Positive CF
tests have been obtained from zebras, although it has not been shown that zebras can be
infected with T. equiperdum or transmit the disease. The organism has been adapted
to a variety of laboratory animals (5,6,9).
Improved breeds of horses seem to be more susceptible to the
disease. The disease in these animals often progresses rapidly and involves the nervous
system. In contrast, native ponies and donkeys often exhibit only mild signs of the
disease. Infected male donkeys, which may be asymptomatic, are particularly dangerous in
the epidemiology of the disease, for they may escape detection as carriers.
Geographic Distribution
Once widespread, this disease has been eradicated from many
countries. It is currently present in most of Asia, southeastern Europe, South America,
and in northern and southern Africa (3)
Transmission
This venereal disease is spread almost exclusively by coitus.
Organisms are present in the urethra of infected stallions and in vaginal discharges of
infected mares. The organism may pass through intact mucous membranes to infect the new
host. Infected animals do not transmit the infection with every sexual encounter, however.
As the disease progresses, trypanosomes periodically disappear from the urethra or vagina;
during these periods, the animals are noninfective. Noninfective periods may last for
weeks or months and are more likely to occur in the later stages of the disease. Thus,
transmission is most likely early in the disease process.
It is possible for mares to become infected and pregnant after
mating with an infected stallion. Foals born to infected mares may be infected. It is
unclear if this occurs in utero or during birth. Because trypanosomes may occur in the
milk of infected mares, these foals may be infected per os during birth or by ingestion of
infected milk. Foals infected in this way may transmit the disease when mature and develop
a lifelong positive CF titer. This method of disease transmission is rare, however. Some
foals may acquire passive immunity from colostrum of infected mares without becoming
actively infected; in such foals, the CF titer declines, and the animal becomes
seronegative by 4 to 7 months of age. Although the possibility of noncoital transmission
remains uncertain, it is supported by sporadic infections in sexually immature equids
(1,3,5).
Incubation Period
The incubation period is highly variable. Clinical signs usually
appear within a few weeks of infection but may not be evident until after several years
(1,5,7).
Clinical Signs
Clinical signs vary considerably, depending on the virulence of
the infecting strain, the nutritional status of the infected animal, and the presence of
other stress factors. The strain prevalent in southern Africa (and formerly in the
Americas) is apparently less virulent than the European, Asian, or north African strains
and produces an insidious, chronic disease. In some animals, clinical signs may not be
apparent for up to several years (so-called latent infection). Clinical signs may be
precipitated by stress in these animals.
In mares, the first sign of infection is usually a small amount of
vaginal discharge, which may remain on the tail and hindquarters. Swelling and edema of
the vulva develop later and extend along the perineum to the udder and ventral abdomen.
There may be vulvitis and vaginitis with polyuria and other signs of discomfort such as an
elevated tail. Abortion is not a feature of infection with mild strains, but significant
abortion losses may accompany infection with a more virulent strain.
In stallions, the initial signs are variable edema of the prepuce
and glans penis (Fig. 49), spreading to
the scrotum and perineum and to the ventral abdomen and thorax. Paraphimosis may be
observed. The swelling may resolve and reappear periodically. Vesicles or ulcers on the
genitalia may heal and leave permanent white scars (leukodermic patches). Transient
cutaneous plaques are a feature of the disease in some locations and strains but not
others. When they occur, they are pathognomonic. Conjunctivitis and keratitis are often
observed in outbreaks of dourine and may be the first signs noted in some infected herds.
Nervous disorders may be seen soon after the genital edema or may
follow by weeks or months. Initially these signs consist of restlessness and the tendency
to shift weight from one leg to another followed by progressive weakness and
incoordination and ultimately by paralysis and recumbency. Anemia and emaciation sometimes
accompany development of clinical signs even though the appetite remains unaffected.
Dourine is characterized by stages of exacerbation, tolerance, or
relapse that may vary in duration and occur several times before death or recovery. The
course of the disease may last several years after infection with a mild strain.
Experimentally, horses have survived for up to 10 years after infection. The course is
apparently more acute in the European and Asian forms of the disease in which the
mortality rate is higher (1,5).
Gross Lesions
Anemia and cachexia are consistent findings in animals that have
succumbed to dourine. Edema of the genitalia and ventral abdomen become indurated later in
the course of the disease. Chronic lymphadenitis of most lymph nodes may be evident.
Perineural connective tissue becomes infiltrated with edematous fluid in animals with
nervous signs, and a serous infiltrate may surround the spinal cord, especially in the
lumbar or sacral regions (1,5,7).
Mortality
Although the course of the disease may be long, it is usually
fatal. Uncomplicated dourine does not appear to be fatal unless the nervous system is
involved. The progressive debilitation associated with the neurological manifestation of
the disease predisposes infected animals to a variety of other conditions. Because of the
long survival time in some experimental cases, reports of recovery from dourine should be
regarded with skepticism.
Diagnosis
Field Diagnosis
Diagnosis on physical signs is unreliable because many animals
develop no sign. When signs are present, however, they are suggestive of a diagnosis of
dourine. If "silver dollar plaques" occur, they are pathognomonic for dourine.
Specimens for Laboratory
Detection of trypanosomes is highly variable and is not a reliable
means for diagnosis of dourine. The following specimens should be submitted: serum, whole
blood in EDTA, and blood smears.
Laboratory Diagnosis
A reliable complement-fixation test (CFT) has been the basis for
the successful eradication of dourine from many parts of the world. The antigen used in
the CFT is group-specific, leading to cross-reactions with sera of horses infected with T.
brucei, T. rhodesiense, or T. gambiense. The test is therefore most
useful in areas where these parasites do not occur. Indirect fluorescent antibody, card
agglutination, and enzyme-linked immunosorbent assay test (ELISA) have also been developed
for dourine but have not replaced the CFT (1,3,4,5,6,10,11).
Differential Diagnosis
The perineal and ventral abdominal edema characteristic of dourine
may also be seen in horses with anthrax. These signs may also resemble infection with
equine infectious anemia or equine viral arteritis. Coital exanthema and purulent
endometritis (as occurs in contagious equine metritis) should also be considered.
Treatment
Although there are reports of successful treatment with
trypanocidal drugs (e.g., suramin at 10 mg/kg IV, quinapyramine dimethylsulfate at 3-5
mg/kg SC), treatment is more successful when the disease is caused by the more virulent
(European) strains of the parasite. In general, treatment is not recommended for fear of
continued dissemination of the disease by treated animals (1,6). Treatment may result in
inapparent disease carriers and is not recommended in a dourine-free territory.
Vaccination
Immunity to trypanosomiasis is complicated. T. equiperdum has the ability periodically to replace major surface glycoprotein antigens, which is a
strategy supporting chronic infections (2). No method of immunization against dourine
exists at present.
Control and Eradication
The most successful prevention and eradication programs have
focused on serologic identification of infected animals. Infected animals should be
humanely destroyed or castrated to prevent further transmission of the disease. Some
geldings may still show service behavior and constitute a risk. All equids in an area
where dourine is found should be quarantined and breeding should be stopped for 1 to 2
months while testing continues.
Sanitation and disinfection are ineffective means of controlling
the spread of dourine because the disease is normally spread by coitus.
Public Health
Humans are not susceptible to infection with T. equiperdum.
GUIDE TO THE LITERATURE
1. BARROWMAN, P.R. 1976. Observations on the transmission,
immunology, clinical signs and chemotherapy of dourine (Trypanosoma equiperdum infection)
in horses, with special reference to cerebro-spinal fluid. Onderstepoort J.Vet.Res.,
43:55-66.
2. BUCK, G.A., LONGACRE, S., RALBAUD, A., HIBNER, U., GIRAUD, C.,
BALTZ T., BALTZ, D. and EISEN, H. 1984. Stability of expression-linked surface antigen
gene in Trypanosoma equiperdum. Nature, 307:563566.
3. CAPORALE, V.P., BATTELLI, G., and SEMPRONI, G. 1980.
Epidemiology of dourine in the equine population of the Abruzzi Region. Zbl. Vet. Med.,
(B) 27:489-498.
4. HERR, S., HUCHZERMEYER, H.F., TE BRUGGE, L.A., WILLIAMSON,
C.C., ROOS, J.A., and SCHIELE, G.J. 1985. The use of a single complement fixation test
technique in bovine brucellosis, Johne's disease, dourine, equine piroplasmosis and
Q-tever serology. Onderstepoort J.Vet.Res., 52:279-282.
5. HENNING, M.W. 1956. Animal Diseases in South Africa 3d ed,
Johannesburg, South Africa: Central News Agency, pp.767-782.
6. LOSOS, G.J. 1986. Infectious Tropical Diseases of Domestic
Animals. New York:Churchill Livingstone, Inc., pp.182-318.
7. McENTEE, K. 1990. Reproductive Pathology of Domestic Animals.
New York:Academic Press, pp.204-205, 267-268.
8. MOHLER, J.R. 1935. Dourine of horses. U.S. Dept. of Agric.
Farmers' Bull., 1146:1010.
9. THEIS, J. H., and BOLTON, B. 1980. Trypanosoma equiperdum
movement from the dermis. Exp. Parasitol., 50:317-330.
10. WILLIAMSON, C.C. and HERR, S. 1986. Dourine in southern Africa
1981-1984: Serological findings from the Veterinary Research Institute, Onderstepoort. J.
S. Afr. Vet. Assoc., 57:163-165.
11. WILLIAMSON, C.C., STOLTSZ, W.H., MATTHEUS, A., and SCHIELE,
G.J. 1988. An investigation into altemative methods for the serodiagnosis of dourine.
Onderstepoort J. Vet. Res., 55:117-119.
R.O. Gilbert, B.V.Sc., M.Med.Vet,. College of Veterinary Medicine,
Cornell University, Ithaca, NY 14853-6401
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