Equine babesiasis: Epidemiology, control and chemotherapy

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FISCAL YEAR Figure 2

Percentage of positive

E I A I D tests, 1971-1984.

tories in Argentina, Brazil, Cuba, and Peru. In addition, a weak positive reference serum was prepared and distributed to any laboratory that requested it. The number of EIA ID tests performed in the United States increased from 82,777 in 1971 to a peak of 793,536 in 1977 and has since remained at about that level (Figure 1). There were 727,640 tests performed in 1984. The percentage of positive tests has decreased from 3.9 in 1972 to 0.38 in 1984 (Figure 2). Between 1972 and 1985, the states with the highest percentages of positive tests were Louisiana with 6.1 percent (20,947 of 340,973 tests), Arkansas with 5.1 percent (7,378 of 143,815), and Mississippi with 3.7 percent (4,579 of 123,903). (Figure 2.) The only western or northern state with greater than 1.0 percent positive tests was Oregon, which had a high prevalence from an Indian reservation. In 1984, 30 states had 10 or fewer positive tests and 10 had no positives.

The actual number of positive horses is about one half of the number of positive tests, as most of the positive horses are tested twice. The control of EIA by vaccines has been discussed. A vaccine against EIA has not been licensed by the USDA. Before licensing, the vaccine would have to be tested for safety, efficacy, and potency. Before an attenuated vaccine could be licensed, back passages would have to be performed with the virus to insure that there was no danger of reversion to a virulent form. In testing the efficacy, vaccinated horses would have to resist challenge with homologous and heterologous strains of the virus. The US program to controlEIA is based on restrictions on the movement of ID or CELISA test-positive horses and a requirement for a negative test prior to entry by 42 states. The slaughter of positive horses is not required. A program to standardize laboratory testing has been established by the USDA. Laboratories in other countries have participated in a similar program. The number of ID test-positive samples in the United States has decreased from 3.9 percent in 1972 to 0.38 percent in 1984.

REFERENCES 1. Coggins L, Noreross NL: Immunodiffusion reaction in equine infectious anemia. Cornell Vet 60:330-335, 1970. 2. Pearson JE, Knowles RC: Standardization of the equine infectious anemiaimmunodiffusion test and its application to the control of the disease in the United States. JAVMA 184:298-301, 1984.

EQUINE BABESIASIS: EPIDEMIOLOGY, CONTROL AND CHEMOTHERAPY Ralph C. Knowles

SUMMARY Equine piroplasmosis (EP) is a hemoprotozoan disease cased byBabesia caballi andB.equi. It is a tick-borne disease principally characterized by fever, anemia, and icterus. Clinically inapparent babesia carrier horses are important in the dissemination of the disease. Clinical episodes occur under two conditions: 1. When susceptible horse stock is moved into endemic EP areas; and 2. When inapparent babesia carriers are moved into nonendemic areas, then in the presence of certain ticks, babesiasis is spread to the susceptible horse population. Author's address: 27 Oak Avenue, Rehoboth Beach, Delaware 19971 USA Volume

8, N u m b e r

1, 1 9 8 8

Ticks are the principal vectors of equine piroplasmosis, additionally contaminated hypodermic needles have shown to spread B. equi among horses. In endemic EP areas, it has been shown that babesiasis can cause unthriftyness in foals. Control of babesiasis is principally directed at tick control. Various tickacidal sprays or dips can be used to break the life cycle of ticks. Chemotherapy, using certain aromatic diamidines, is an adjunct to tick control and also facilitates the international relocation of horses and other equidae. Objectives of chemotherapy are divided as follows: 1. In EP endemic areas, the therapeutic aim is to subdue the babesia parasites and leave the host horse in a state of premunition; and 2. In nonendemic areas, complete clearance of babesia organisms from the animal is the objective. Several aromatic diamadine

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pharmaceuticals are available to veterinarians. During recent years, horses and other equidae have become important in international commerce. Such commerce has focused attention on the international spread of certain infectious and communicable animal disease; among these is equine piroplasmosis (EP). Piroplasmosis is an infectious hemoprotozoan disease characterized by fever, anemia, icterus, and other signs arising from hemolysis caused by Babesia cabaUi or Babesia equi. The disease has been reported in horses, mules, donkeys, and zebras.s DISCUSSION Cause

The causative agents of EP are parasites of the family Babesidae. We have adopted the genus name Babesia according to the classification by Neitz. One the basis of his classification, the causative agents in solipeds are calledB, equi and B. caballi, which are one-celled, mononucleate unpigmented protozoa that multiply in RBC.4 Transmission Transmission of EP generally falls into 2 categories: tick transmission, usually called natural Iransmission, and transmission by humans using contaminated veterinary instruments. In the US, tick transmission ofB. caballi was demonstrated using the tropical horse tickDermacentor nitens? This trial provided conclusive evidence that transovarial transmission ofB. caballi occurs in Dermacentor nitens ticks. Serologic surveys of horses in Puerto Rico using the complement-fixation (CF) test showed that 89 percent of the equidae on that island carry antibodies against Babesia caballi. On the EP-enzootic island, most equidae are infested with tropical horse ticks but clinical piroplasmosis is seldom seen. It is believed that the following sequence takes place: A foal is born and has maternal antibodies against B. caballi. During most of the foul's life it is infested with tropical horse ticks, many of which are believed to carry B. caballi that they "share" with their horse. Thus the foal is believed to experience a subclinical episode of EP and only rarely shows clinical signs of EP. However, contrary to the previously described situation, if adult equidae that originated from EP-free areas are placed in pasture in EP-enzootic areas, such as Puerto Rico, and exposed to tropical horse ticks, clinical EP usually is evident in 14-21 days. This pattern was demonstrated in 1950 when horses originating from Missouri and Kansas were sent to Cuba. This also happened in Puerto Rico in 1964. Horses that were inapparent carriers ofB. caballi, when imported from Cuba into south Florida in 1959, were responsible for an outbreak of piroplasmosis in that state when tropical horse ticks transmitted the blood parasite to suscep62

tible horses. 4In 1978 B. caballi was experimentally transmitted by Dermacentor albipictus (transovarially) using ponies. 1 In 1977, a shipment of horses originating from Jordan, among which B. equi carders were present, showed evidence of transmission of EP when one hypodermic needle was used among the animals to inject a tranquilizing drug as they were prepared for transport. Levels of infection necessary to maintain an enzootic EP area in Florida depend on tick transmission. It is believed that transmission of EP by veterinary instruments, biting flies or mosquitoes is not common and does not perpetuate an enzootic area. The tropical horse tick, Dermacentor nitens, was fLrst described by Neumann in 1897 from specimens collected from horses in Jamaica and San Domingo. In 1901 the tick was reported in Guatemala, Venezuela, and Puerto Rico. Since then the tick has been reported in Texas, Guatemala, Panama, Costa Rica, Mexico, Cuba, Haiti, Trinidad, Colombia, and Argentina. Since 1908 D. nitens has been collected in Hidalgo, Nueces, San Patricio, Webb, and Willacy Counties in Texas. The tick is not permanently established in areas of the US where the average January temperature is less than 15.6°C (60 F). In May 1958, the tick was officially identified in Florida and is presently well-established in southern portions of the US. H D. nitens is found only in the Western Hemisphere and is a serious problem in many tropical and semitropical countries where it is established. It usually is found in the ears of equidae. In heavy infestations it may be found in the nasal diverticula, mane, perineal region, and along the ventral midline. The skin of a horse's ears often becomes greatly thickened, "crusty," and inflamed due to feeding of the ticks. The tropical horse tick is a one-host tick, ie, larval, nymph, and adult stages remain on the same animal during their development. The average time required for larvae to develop into engorged adults is 26 days. Although the horse is the preferred and primary host, the tick also has been collected from cattle, goats, sheep, and deer. In a Florida survey, D. nitens was found on horses 647 times, on cattle 55 times and once each on a human, goat, and deer. Collections from cattle have been more frequent in Puerto Rico. Although D. nitens had been suspected as a vector of EP a half century earlier, it was not until 1963 that it was demonstrated conclusively that this tick is a vector of the disease, transmitting B. caballi transovarially. 9 It is also reported that D. nitens transmits B. caballi hereditarily for 4 generations. Although it has been reported that Rhipicephalus sanguineus transmits B. caballi hereditarily for 4 generations and is widely spread in many parts of the US, it is seldom found on horses in this country? EQUINE VETERINARY SCIENCE

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D. nitens did not transmit B. equi transovarially in laboratory experiments at the USDA Animal Disease Parasite Laboratory at Beltsville, Maryland. t3 B. caballi may pass through four generations ofR. sanguineus and H. dromedarii fed on rabbits and dogs.7Infection ofD. nitens withB, caballi occurred only when uninfected ticks fed on a horse inoculated with blood from a donor horse that had parasitemia from a tickborne infection. 3 B. equi is transmitted by D. reticulatus, D. pictus, H. detritum, R. bursa and H. marginatum in Russia, by R. sanguineus in Central Asia, by H. excavatum, H. marginatum, R. sanguineus and H. dromedarii in North Africa, by R. evertsi in South Africa and by R. sanguineus in India, South Africa, Germany, France, and Brazil.

Geographic Distribution Generally, EP is recognized as a disease of tropical and subtropical parts of the world; however, it also is found in temperate zones. The important factor in the prevalence of EP is the presence of ticks that transmit the protozoa. The disease has been reported in southern Florida, US Virgin Islands, part of Asia, Russia, India, the Middle East, Europe, Africa, Australia, South America, Central America, Mexico, Philippine Islands, and numerous Caribbean islands. Clinical Signs The incubation period of naturai EP is 7-22 days. Horses acutely infected with EP may have fever, injected, blanched, or jaundiced mucous membranes, ventral edema of the chest and abdomen, and edema of the limbs.6 Respiratory signs may result from anemia and are intensified by pneumonia, m Subacute cases may only involve lassitude and inappetence. The EP-parasitized inapparent carrier commonly presents a special problem of diagnosis since outward signs of the disease are not evident.

Lesions Findings at necropsy indicate destruction of RBC and secondary effects of anemia. Hyperplasia of hemopoietic tissues in spleen, bone marrow, and liver may be evident, plus centrilobular necrosis in the liver as a consequence of anoxia. Excess fluid in peritoneal and pleural sacs may also be a feature. 1°

Diagnosis Of historical importance in considering a diagnosis of EP are possible exposure to ticks through hay, bedding, or pasture situations and residence or travel in tropical or subtropical areas of the world, especially areas known to be enzootic for EP. On certain occasions, contaminated veterinary equipment such as hypodermic needles can be a source of EP. Volume 8, Number 1, 1988

Since inapparent carriers live in a delicate balance with their blood parasites, stress such as from pregnancy, severe training schedules or transportation exhaustion exacerbates clinical signs of EP. Also, treatment of inapparent carriers against other disease entities with corticosteroids causes acute signs of EP. One should thoroughly examine the ears, false nostrils, mane, tall, foretop, and perineum of EP-suspect animals for ticks. Look for tick scars in the ears, which are evidence of past tick infestation. Piroplasmosis is confirmed in the laboratory by several procedures. Blood-film examination can be useful, but parasitemia is fleeting and negative results can be misleading. Subinoculation of susceptible experimental animals to reproduce piroplasmosis is impractical because of the expense involved. Complement-fixation testing is a practical aid to diagnosis. Submit 5 ml chilled, unpreserved serum free ofhemolyzed RBC to your State diagnostic laboratory; include a thorough case history. Such samples are forwarded to the National Animal Disease Center in Ames, Iowa, for complementfixation testing. The fluorescent antibody test for EP has been perfected in Australia, but the necessary antigens are not available in the US. Other tests have been reported but are not practical for clinical use. Treatment Babesiacidal treatments are only secondary to tick control campaigns in combatting EP. Babesiacidal treatment of horses in enzootic vs nonenzootic areas varies. When treating piroplasmosis in enzootic areas where re-exposure is probable, it is undesirable to completely cleanse the horse of the infection. There are several drugs that, at the proper dosage, depress the parasitemia and help effect remission of clinical piroplasmosis without removing the latent infection and relative immunity to reinfection (Table 1).t2 Horses or other equidae in residence or being prepared for shipment into nonenzootic EP areas should be given babesiacidal treatments to eliminate all Babesia from the animal. Total elimination of B. caballi and B. equi calls for greater dosage of babesiacidal drugs than does elimination of clinical

signs. Since 1961, the following babesiacidal drugs have been used experimentally in Florida and Puerto Rico: phenamidine, benenil, diampron and imidocarb. Imidocarb is the most effective and safest of all medications tried. In conjunction with the Burroughs Welcome Company, Animal Health Division, Research Triangle Park, NC 27709, a treatment regimen was developed to eliminate Babesia caballi and with lesser efficacy eliminate Babesia equi from horses and other

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TABLE 1 Selected Drugs Against Clinical Piroplasmosis ',1" Name

Daily Dosage

Days Administered

6,6-diquinolylurea dimethosulfate b

0.25 mg/lb SC divided b.i.d.

1 or 2

4,4'-diamidinodiozaminobenzene ~

1.5 mg/Ib SC

1 or 2

3,3'-diamidinocarbanilide di-isethionate d

2.0 mg/lb IM

1 or 2

3,3'-bis-(2-imidazolin-2-yl) carbanilide dihydrochloride =

1.0 mg/lb IM

1

=Usuallydo not eliminate premunizinginfectionat dosages shown. bLudobal, Bayer, Leverkusen,Germany ¢Berenil, Farbwerke-Hoechstaf,Frankfurt, Germany dDiampron,May and Baker, Dagenham, England qmidocarb, Burroughs Welcome and Co., London, England equidae as follows: 1. Animals are held in a tick-free environment. 2. The recommended treatment of imidocarb dipropionate at 2 mg/kg body weight every 24 hours for 2 treatments is administered. Each dose is given IM in at least 4 injection sites. This treatment eliminates B. cabaUi in nearly 100 percent of equidae treated. 3. The recommended treatment of imidocarb dipropionate at 4 mg/kg body weight every 72 hours for 4 treatments eliminates B. equi in 58 percent of equidae treated. Retreatment of animals withB, equi remaining in the blood should not be initiated before 30 days after the first treatment. Colic, transient salivation and purgation are common adverse effects of imidocarb treatment. These effects can be minimized by the use of atropine and similar preparations for colic therapy. Treated horses must be free of babesial antibodies to enter

certain countries. To accomplish this, time must be allowed for natural antibody "wash out." The complement-fixation test is performed at 30-day intervals to assess the presence of babesial antibodies. Control Control of EP is most effectively directed at killing ticks that transmit Babesia. The intensity of the effort against ticks ranges from application of parasiticides such as toxaphene (0.50 percent in cottonseed oil) or dioxathione (Delnav: Hercules, 0.15 percent in cottonseed oil) applied to the ears, mane, and tail of horses in EP-enzootic areas in farm- or areawide tick elimination programs. In the case ofB. caballi and the elimination of the tropical horse tick D e r m a c e n t o r nitens in a climate such as Florida, treatments consist of a wholebody spray (high-pressure spray) and hand treatment of the ears, false nostrils, mane, and tail using 0.15 percent dioxathione in cottonseed oil. Such treatments should be applied to all equidae on a premises every 21 days. While cattle can serve as hosts to D. nitens, they need not be treated to rid a premises ofD. nitens if diligence is used in treating all equidae.

REFERENCES 1. Frerichs WM, personal communication, 1978. 2. HolbrookAA, personal communication, 1969. 3. HolbrookAA et al: JProtozool 15, p 391, 1968. 4. HolbrookAA, et ah A m J Vet Res, 289, p 297, 1968. 5. KnowlesRC, et al: J Am Vet Med Assoc, 148, 407, 1966. 6. KnowlesRD: Proc 15th Ann Am Assoc Eq Pract, p 159, 1969. 7. La Page: Veterinary Parasitology, 2rid ed. Charles C Thomas, Springfield, IL 1968. 8. Maurer FD: J A m Vet MedAssoc 141, p 699, 1962. 9. Roby TO and Anthony DW: J Am Vet Med Assoc, 142, p 768, 1963. 10. Smith et al: Veterinary Pathology, 4th ed. Lea & Febiger, Philadelphia, 1972. 11. Strickland ILKand Gerrish BS: J A m Vet MedAssoc, 144, p 875, 1964. 12. Taylor,WM: Proc 17th Ann Am Assoc Eq Pract, p 165, 1971. 13. ThompsonPH: JAm Vet MedAasoc 155, 1>454,1969.

Coming up in the next issue of

The Journal of Equine VeterinaryScience... M o r e W o r l d E q u i n e Veterinary A s s o c i a t i o n Papers on "The H o r s e in International C o m m e r c e " FEI Involvement • Blood Typing • Electronic Identification • Health Regulations in the Federal Republic of Germany ° Regulatory Considerations from an Australian Perspective ° Origins, Scope and Operation of the Tripartate Group 64

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