Piroplasmosis

PIROPLASMOSIS (piroplasmosis), or tick-borne fevers, are diseases of animals caused by parasites of red blood cells belonging to the Protozoa. Specific vectors of the infestation from a sick animal to a healthy one are "pasture ticks" (families Ixodidae), which serve as the definitive hosts of the parasites. In the essence of the pathological process (pathogenesis), the mode of transmission of the infection, the character of immunity, and other aspects, animal piroplasmosis is analogous to human malaria. Initially, animal piroplasmoses were called "malaria-like diseases." In the USSR, piroplasmoses increase from north to south. In the tundras, reindeer piroplasmosis is observed; at the latitude of the Karelian ASSR and Leningrad Oblast, cattle piroplasmosis occurs; at the level of Moscow Oblast, horse piroplasmosis is added to it, and so on. In the North Caucasus, Crimea, and the Central Asian republics, several species of piroplasmosis are found in various domestic and wild animals. The territorial distribution of piroplasmosis naturally corresponds to the species composition of pasture ticks. The economic significance of piroplasmosis is very great. For many regions of the USSR, these diseases are highly devastating. Tens of thousands of horses, cattle, and sheep fall ill with them annually. Average mortality reaches 20–30% of the number of sick animals. Etiology. The causative agents of piroplasmosis are representatives of the families Piroplasmidae, Babesiidae, Theileriidae, and Anaplasmidae. For the systematics, morphology, and biology of Piroplasmida e, see Babesia. The family Theileriidae is characterized by the fact that the parasites multiply asexually (schizogony) in the endothelium of capillaries, in internal organs, in lymph nodes, and in bone marrow, forming special forms called "plasmodial spheres." Parasites residing in erythrocytes cannot cause infection upon reinoculation and are capable of further development only in the body of the tick. They have the shape of rings, spheres, pear-shaped formations, and rods up to 2–2.5 µ in size. Anaplasmidae in a stained state appear as small (0.2–1 µ) rounded "punctate" formations consisting seemingly of a single continuous nuclear substance. Due to the fact that in some cases inclusions can be found in the erythrocytes of sick animals that look very much like anaplasmas, various authors either completely deny the parasitic nature of anaplasmas or do not ascribe independent etiological significance to them, considering anaplasmas not as causative agents of the disease, but merely as companions of it. However, anaplasmoses are undeniably observed as quite independent diseases in several species of animals; for some anaplasmas, tick vectors have already been established, active immunization is performed, and so forth. Infection with all types of piroplasmosis under natural conditions occurs exclusively through tick bites. Susceptibility. Each animal species is subject to infection only by specific piroplasms inherent to it alone. Laboratory animals (rabbits, guinea pigs, white rats, and white mice) are insusceptible to any of the known piroplasmoses so far. Man is also considered insusceptible to piroplasmosis. Immunity. Observations and precise experiments have established that an animal that has undergone piroplasmosis acquires resistance to reinfection. Immunity has all the properties of "non-sterile immunity." As a rule, upon the animal's recovery, the number of parasites in the blood decreases and finally they are no longer visible under the microscope. However, reinoculation of the blood of a recovered animal into a susceptible one shows that virulent parasites persist in it for at least 1–2 years in the absence of any noticeable pathological phenomena on the part of the organism (Ehrlich's "non-sterile immunity," Schilling's "labile infection," Sergent's "premunity," etc.). In some types of theileriosis, immunity is sterile, meaning that recovered animals are not virus carriers (East Coast fever of cattle on the East African coast). Pathogenesis and pathological anatomy. Parasites, developing in erythrocytes, destroy them in large numbers and simultaneously cause general intoxication of the organism. With high fever and other general symptoms of infectious affliction, anemia develops. The liberated hemoglobin does not have time to convert into bilirubin in the liver; hemoglobinemia occurs, which in certain piroplasmoses manifests as hemoglobinuria. Protein is present in the urine. In the serous and mucous membranes of various organs, there are hemorrhages. The spleen enlarges to enormous sizes. Symptoms of the disease. The incubation period lasts on average 10–15 days (more rarely 20 days or more). The disease manifests as an elevation of temperature, anemia, jaundice, constipation alternating with diarrhea; in many piroplasmoses, hemoglobinuria is observed, giving rise to the name of the disease "bloody urine." In dairy cows and other nursing animals, milk production ceases. After 5–7 days, death ensues, or the animal gradually recovers. The most malignant are considered to be certain types of theileriosis (see below), in which mortality among the sick can reach 90% and higher; gonderiosis, on the contrary, produces almost no mortality unless accompanied by other piroplasmoses.

Epizootiology. Piroplasmosis is a strictly localized (endemic) disease whose season coincides with the period of parasitism of infectious ticks on livestock. Native animals using pastures are considered resistant to the infection. Becoming infected with piroplasmosis at a young age and suffering a mild form, they acquire "sterile immunity" which is maintained throughout their lives due to annual natural reinvasions in pastures. Animals brought from safe regions into unsafe ones and grazing on tick-infested pastures inevitably fall ill. Young animals tolerate the disease better than old ones. Immunity in animals may disappear if they are not exposed to infections in pastures for a long time (3-4 years). Recovery from one species of piroplasmosis does not confer immunity to another. In individual years, epizootics of piroplasmosis vary in the number of cases and virulence, which can be explained by the number of ticks on pastures, the presence of susceptible animals, etc. Prophylaxis. Preventive measures for piroplasmosis in farm animals can be built on two completely opposite principles: 1) prevention of piroplasmosis infection in animals by protecting them from the attack of infested pasture ticks, understanding such measures to include tick eradication, and 2) creation of resistance ("premunition") in the animal organism against piroplasmosis through illness and subsequent maintenance of this resistance by annual infections in pastures. In the first case, measures are directed toward combating the tick as a vector of piroplasmosis, while in the second case, the object of action is the animal organism. The fight against ticks, depending on their biological characteristics and other conditions, is carried out by various methods. In limited areas, ticks can be destroyed by thorough drainage of the soil, destruction (grubbing) of bushes, and systematic plowing of pastures for crops of grain and grasses. The method of regular "pasture rotation" can yield very good results. Reliable means for protecting livestock from piroplasmosis are arsenical baths (sodium arsenate; concentration of As₂O₃ in solution - 0.16%), used during the period of tick attacks on livestock every 4-5 days. Arsenical baths kill ticks or sterilize them; with regular bathing of livestock grazing in a certain area, it is possible to clear it of piroplasmosis vectors. Spraying, wiping, and manual destruction of ticks are less reliable. To obtain a greater guarantee, the use of baths is combined with a change of pastures. Smearing animals with odorous substances does not prevent tick attacks and consequently infection with piroplasmosis. Good results are obtained by housing animals indoors year-round (breeding studs) or during the piroplasmosis seasons. The weak point of all described preventive measures is that not only imported animals, but also those born in an unsafe area remain susceptible to piroplasmosis, and this is fraught with the danger of mass outbreaks if, for any accidental or unavoidable reasons, the livestock is subjected to attacks by infested ticks. The method of preventive vaccination against piroplasmosis has not yet yielded definitive results. As vaccination material, blood from young animals that have suffered from piroplasmosis not less than 3 months ago is used. Recovered livestock must be released annually onto unsafe pastures. Otherwise, their existing "premunition" may be lost. Piroplasmosis in individual animal species in the USSR. I. Equine piroplasmosis: a) "Northern equine piroplasmosis", or "spring disease of horses." Pathogen: Piroplasma caballi Nuttall et Strickland, 1910; vector: Dermacentor reticulatus F. in the imago stage and Dermacentor niveus Neumann. From 57° N lat. to the southern borders of the USSR. Mass outbreaks in spring (May-June), individual cases in autumn. An excellent therapeutic agent is Trypanblau (1-2.0 g intravenously in 100 cm³ of physiological NaCl solution; repeat after 24 hours). Prophylactic injections of this preparation at the end of the incubation period in horses subjected to attacks by infested ticks are useful. b) "Southern equine piroplasmosis", nuttalliosis. Pathogen: Nuttallia equi Laveran, 1901; the probable vector for the USSR is considered to be one of the species of Hyalomma. From 48° N lat. southward: Ukrainian SSR, Crimea, Kazakhstan, Caucasus, Turkestan, etc. Apparently proceeds more benignly than "Northern" piroplasmosis. Little studied; there are no specific therapeutic agents. c) Equine anaplasmosis has been detected in isolated cases. II. Piroplasmoses of cattle. Recently, the work of V. L. Yakimov and his co-workers in the USSR has established several new pathogens of cattle piroplasmosis (see below): a) "Southern cattle piroplasmosis" ("bloody urine", "chikhir", "hemoglobinuria", "Texas fever", etc.). Pathogen: Piroplasma bigeminum Smith et Kilborne, 1893; vector: larva of Boophilus annulatus calcaratus Birula, 1895. Crimea, Caucasus, and Central Asia. In the North Caucasus, it produces two outbreaks: April-May and July-August. The best therapeutic agent is Trypanblau. b) "Northern cattle piroplasmosis" ("bloody urine", "krovomochka", and others). Pathogen: Babesiella (Babesia) bovis (Babes, 1888); vector: Ixodes ricinus L. in all stages. Northern border - 60°. Cases from the end of May to September. Ichthargan (1-1.5 g intravenously) and Trypanblau are used for treatment. c) "Francaiellosis of cattle" (referred to by the general name piroplasmosis). Pathogen: Francaiella colchica Jakimoff, 1927; vector: Boophilus annulatus calcaratus B. North Caucasus, Crimea, and Turkestan. Epizootiologically close to "Southern cattle piroplasmosis", often observed together with it in the form of a mixed invasion. Trypanblau and ichthargan are ineffective. d) Piroplasmoses whose pathogens were discovered and described by Yakimov under the names Francaiella caucasica Jakimoff et Belavin, 1926, and Francaiella occidentalis Jakimoff et Bourzev, 1927; little studied, rarely encountered. Probable vector: Ixodes ricinus L. e) "Coast fever" ("East African Coast fever", "South African theileriosis of cattle"). Pathogen: Theileria parva Theiler, 1924. Vectors: ticks of the genus Rhipicephalus. Hemoglobinuria is absent; swelling of the lymph glands is characteristic. The disease is malignant and causes heavy losses. Preventive vaccinations and specific treatment have not been developed. Cases previously registered in the USSR under the name "coast fever" (Kamensky et al.) must be referred to f) "tropical piroplasmosis" ("Transcaucasian fever", "Transcaucasian theileriosis"), with the pathogen Theileria annulata Dschunkowsky et Luhs, 1904. Widely distributed in Central Asia, Transcaucasia, and the North Caucasus. Vectors, according to Dschunkowsky and Luhs, in Transcaucasia are the tick Boophilus annulatus calcaratus B.; for Turkestan, according to Kaluzo and Vernadskaya, Hyalomma dromedarii. A very malignant disease. g) "East Siberian theileriosis of cattle." Pathogen: Theileria sergenti Jakimoff et Dehtereff, 1903. Vector unknown. Primorsky Oblast. Benign. h) "Gonderiosis of cattle." Pathogen: Gonderia mutans Theiler, 1907; until recently classified in the genus Gonderia du Toit (1918) of the family Piroplasmidae; now, according to the mode of reproduction in internal organs, assigned to the genus Theileria Franca et Bettencourt - Theileria mutans Theiler, 1907; certain species of Rhipicephalus are considered vectors; widely distributed in the south of the USSR; has no economic significance since it does not cause fatal outcomes by itself. i) "Anaplasmosis of cattle" ("yellow fever"). Pathogen: Anaplasma marginale Theiler, 1910. Turkestan, North Caucasus; in the latter case, Yakimov discovered a distinct large species of anaplasms - Anaplasma rossicum Jakimoff et Belavin, 1926; vector, according to Yakimov, Boophilus annulatus calcaratus B. Often complicates and accompanies other piroplasmoses. Incubation period 30-60 days or more. Capable of causing high mortality among imported animals. III. Piroplasmosis of sheep and goats. Sheep piroplasmosis pathogens are also considered pathogenic for goats. In the USSR, exclusively in the south, 5 types of tick-borne fevers have been established in sheep. Mixed invasions are very frequently observed. a) "Sheep piroplasmosis" ("bloody urine of sheep"); pathogen: Piroplasma ovis Lestoquard, 1925; the vector in the USSR is considered to be presumably Rhipicephalus bursa Canestrini et Franzango. Treatment: Trypanblau. b) "Babesiellosis of sheep"; pathogen: Babesiella ovis Babes, 1892; vector is the same as for P. ovis. Both species are often found simultaneously, causing as it were a single epizootic. c) "Gonderiosis"; pathogen: Theileria recondita Lestoquard, 1929; vector unknown. Benign. Observed simultaneously with other piroplasmoses. d) "Theileriosis of sheep"; pathogen: Theileria ovis Lestoquard, 1914; vector unknown. The disease causes very high mortality; in the USSR, it apparently does not have a wide distribution. e) "Anaplasmosis of sheep"; pathogen: Anaplasma ovis Lestoquard, 1924; vector unknown. Usually complicates other piroplasmoses. IV.

IV. Piroplasmosis of swine. a) Piroplasmosis of swine, the causative agent Piroplasma trautmanni Knuth et du Toit, 1921; the vector in South Africa is considered by Trautmann to be Boophilus decoloratus C. L. Koch, 1844. Discovered in Kharkov (Dementyev). b) "Anaplasmosis of swine" discovered in Armenia (Prokopenko). The species of the parasite has not been established, and the vector is unknown. V. Piroplasmosis of reindeer. In the extreme north of the USSR, two species of piroplasmosis causing the so-called "splenic disease" have been established: a) Gonderia tarandi rangiferi (Kerzelli, 1909) and b) Françaiella tarandi rangiferi (Jakimoff et Kolmakoff, 1929). Ticks of the family Ixodidae have not yet been found on reindeer. The disease does not cause mass mortality. VI. Piroplasmosis of dogs has been recorded in various localities of the USSR, the causative agent is Piroplasma canis Piana et Galli-Valerio, 1895, the vector is Dermacentor reticulatus. Treatment: trypan blue. Anaplasmosis of dogs was established in 1913 by Yakimov in Turkestan. VII. Piroplasmosis of wild animals. On the territory of the USSR, the following have been established: a) in hares in Transcaucasia (Piroplasma leporis Dschunkowsky et Luhs, 1909); b) in field mice in Saratov Governorate (1909) and Transcaucasia (Theileria rossica Jakimoff et Sapronovitsch); c) in hedgehogs in Saratov Governorate (Nuttallia ninensis Yakimov, 1913); d) in foxes and wolves in Turkestan (Yakimov, 1913); e) in the little suslik (Citellus pygmaeus Pall.) in the Slomikhinsky district of the former Ural Oblast (Piroplasma golzovi Sassiuchin, 1930); the suspected vector is Rhipicephalus schultzei (Olenew, 1929). Susliks suffer from acute and chronic forms of piroplasmosis. Since piroplasmosis of susliks occurs in areas of plague epizootics among these animals, in some cases the pathological-anatomical picture provides a reason to suspect plague. A case of simultaneous infection of a suslik with piroplasmosis and plague has been recorded.