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Studies on East Coast Fever. II. Behaviour of the Parasite and the Development of Distinctive Lesions in susceptible Animals1

Published online by Cambridge University Press:  06 April 2009

E. V. Cowdry
Affiliation:
Anatomical Laboratory, Washington University, Saint Louis.
W. B. C. Danks
Affiliation:
Anatomical Laboratory, Washington University, Saint Louis.

Extract

The history of the ticks (Rhipicephalus appendiculatus) employed for transmission of East Coast fever is detailed in Part I. During the 1st day the ticks generally become attached and are partly held in place by a kind of cement substance (Fig. 1).

Penetration usually occurs at some time during the 2nd day, and the cellular elements of the corium quickly respond. There is a local swelling of the capillary endothelium, an infiltration with polymorphonuclear leucocytes and a slight increase in eosinophiles. More cement substance is produced which hardens about the edges. Some of it enters through the wound and spreads out in the corium along lines of least resistance (Fig. 2).

Later on the eosinophiles increase greatly in number and in turn give place to macrophages which ingest some of the cement substance. Mast cells also become more numerous. The area of reaction extends 2 or 3 mm. from the tip of the proboscis. Marked cytolysis of fibroblasts, of histiocytes and of the swollen endothelial cells occurs. The latter leads to haemorrhage (Figs. 6, 8, 9). The red blood cells and leucocytes are, however, not destroyed. They are sucked up by the tick, the leucocytes first because they accumulate before the haemorrhages take place.

Twenty-five of the sixty-six ticks examined were found to contain parasites in their salivary glands, but no parasites were seen in the sixty-six pieces of skin excised while the ticks were attached. Soon after the parasites enter the blood stream and spread throughout the system the corium of the skin is invaded by them like other parts of the body (Table III).

The medium-sized lymphocytes are the principal cells parasitised; but parasites are also found in lymphoblasts, large and small lymphocytes and occasionally in parenchymatous liver cells. We never saw them in vascular endotheial cells. For this reason we are unable to substantiate the view, which has apparently never been seriously questioned, that they undergo schizogony in this situation. The first agamonts were noted in lymphocytes in gland smears the day the fever first exceeded 103° F. The gamonts appeared about a day later and the intra-erythrocytic forms soon after. Taking the average of a number of cases: (1) The temperature first surpassed 103° F. on the 9·8th day after infestation with ticks. (2) The first Koch bodies within lymphocytes were observed on the 14·8th day, that is to say, 5 days after the fever commenced. (3) The first parasites within the red cells were noted 1·6 days later, on the 16·4th day after infestation.

The cycle which the parasite undergoes in changing from the agamonts to the intra-erythrocytic forms is illustrated in Diagram II (fully described on p. 36).

The alterations in the tissues caused directly or indirectly by the parasitic invasion were studied principally in specimens secured at autopsy from animals killed in extremis. The changes which apparently dominate relate to the lymphatic system. The medium-sized lymphocytes and to a less extent the small and large lymphocytes and lymphoblasts, first in the lymph glands and later in all parts of the body, become infested with Koch bodies which grow in their interior apparently without causing any severe injury. The distribu tion of Koch bodies is recorded in Table III, and their incidence in the lymph glands and in the liver in Tables IV and V. The evidence presented does not support the current conception that the parasites serve as a powerful stimulus to the multiplication of lymphocytes. The enlargement of lymph glands is caused more by oedema than by increase in their number. But there is a marked redistribution of lymphocytes. Their number is reduced in the lymph glands and in the peripheral blood stream and increased in the blood vessels of the liver and some other organs. Perivascular lymphocytic infiltrations are also a notable feature of the reaction in the liver, kidneys, adrenals and several other organs, but they are of rare occurrence in the nervous system. It is uncertain how far they are formed by the emigration of lymphocytes from the blood stream and by the proliferation of lymphocytes previously present perivascularly.

Small haemorrhages constitute a second alteration of importance. They are particularly prone to occur in the epicardium and endocardium, but may be found in almost any part of the body. Evidence is lacking that these haemorrhages play a part in the genesis of the perivasoular lymphocytic infiltrations. The latter are far more widespread and are chiefly observed in locations where haemorrhages are seldom seen.

Oedema is a third type of reaction. It is constantly found in the lymph glands and occasionally in the lungs, especially in the later stages of the disease.

Generally speaking, therefore, the lesions reported in this paper are acute in type. The functional activity of the several organs (except the lymph glands) has not been impaired sufficiently severely or over a time long enough to leave distinct structural changes in the parenchymatous organs; but the specimens examined were not collected from protracted cases of East Coast fever or from animals under suspicion of having undergone repeated attacks of the disease.

It is the parasites in the red blood cells which are capable of continuing the cycle if they are ingested by ticks able to act as vectors. We have recog nised three principal groups: (1) small spherical-ovoid parasites which are the first to make their appearance, (2) tailed parasites, and (3) plunip forms, both of which develop later and become more numerous than the spherical-ovoid parasites. Possible stages of transition are represented in Diagram I (p. 37). Though many parasites undergo differentiation and some probably divide, a variable number degenerate within the erythrocytes.

We question the validity of the genera into which the family Theileriidae are customarily divided on account of the inadequacy of the data on which they are based.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1933

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References

REFERENCES

Barron, E. S. G. and Harrop, G. A. Jr. (1929). Studies on blood cell metabolism. J. Biol. Chem. 84, 89.CrossRefGoogle Scholar
Bettencourt, A., França, C. and Borges, J. (1907). Un cas de Piroplasmose bacilliforme chez le Daim. Arch. Inst. Roy. de Bact. Camara Pestana, 1, 341.Google Scholar
Bevan, E. W. (1924). East Coast fever—the theory of latency. Trans. Roy. Soc. Trop. Med. 18, 328.CrossRefGoogle Scholar
Bruce, Sir David (1910). Amakebe. A disease of calves in Uganda. Proc. Roy. Soc. ser. B, 82, 35.Google Scholar
Brumpt, E. (1924). Les piroplasmes des bovidés. I. Les Theileries. Ann. Parasit. Hum. et Comp. 2, 340.CrossRefGoogle Scholar
Bulger, H. A., Dixon, H. H., Barr, D. P. and Schregardus, D. (1930). The functional pathology of hyperparathyroidism. J. Clin. Inv. 9, 143.CrossRefGoogle ScholarPubMed
Carpano, M. (1915). Piroplasmosi tipo “parvum” nei bovine del basso bacino del Mediterraneo. La Clin. Vet. 38, 497 and 553.Google Scholar
Carrel, Alexis and Ebeling, H. H. (1922). Pure cultures of large mononuclear leucocytes. J. Exper. Med. 36, 365.CrossRefGoogle ScholarPubMed
Christophers, S. R. (1906). The anatomy and histology of ticks. Sci. Mem. Med. and Sanit. Depts. Gov. of India, N.S. No. 23, 55 pp.Google Scholar
Cleland, J. B. (1910). A note on Eosinophile cells in the exudate from tick-bites on a horse. Proc. Roy. Soc. Med. 3, part 3, 42.CrossRefGoogle ScholarPubMed
Collaud, L. (1906). Beiträge zur pathologischen Histologic der Niere bei Rhodesian Redwater der Rinder in Südafrika. Inaugural Diss., Zürich, 36 pp.Google Scholar
Cooper, W. F. and Laws, H. E. (1915). Some observations on the practice and theory of dipping. Parasitology, 8, 190.CrossRefGoogle Scholar
Cowdry, E. V. (1926). Geographic distribution of spontaneous encephalitis in rabbits. J. Exper. Med. 43, 725.CrossRefGoogle ScholarPubMed
Cowdry, E. V. (1928). The microchemistry of nuclear inclusions in virus diseases. Science, 68, 40.CrossRefGoogle ScholarPubMed
Cowdry, E. V. and Ham, A. W. (1930). The life cycle of the parasite of East Coast fever in ticks transmitting the disease (Preliminary note). Science, 72, 461.CrossRefGoogle ScholarPubMed
Cowdry, E. V. and Ham, A. W. (1932). Studies on East Coast fever. I. The life cycle of the parasite in ticks. Parasitology, 24, 1.CrossRefGoogle Scholar
Dennis, E. W. (1932). The life cycle of Babesia bigemina (Smith and Kilbourne) of Texas cattle fever in the tick Margaropus annulatus (Say). Univ. of Calif. Publ. in Zoology, 38, No. 11, 263.Google Scholar
Du Toit, P. J. (1918). Zur Systematik der Piroplasmen. Arch. f. Protistenk. 39, 84.Google Scholar
Du Toit, P. J. (1931). Immunity in East Coast fever. Rep. Dir. of Vet. Serv. and Animal Husb. No. 17, part 1, 3.Google Scholar
Flexner, S. and Amoss, H. L. (1917). The relation of the meninges and choroid plexus to poliomyelitic infection. J. Exper. Med. 25, 525.CrossRefGoogle ScholarPubMed
França, C. (1913). Quelques considérations sur le genre Theileria et description d'une nouvelle espece de ce genre (Theileria stordii). Centralbl. f. Bakt. Orig. 67, 171.Google Scholar
Gonder, R. (1911). The development of Theileria parva, the cause of East Coast fever of cattle in South Africa. Rep. Gov. Vet. Bact. Pretoria, p. 69.Google Scholar
Gonder, R. (1911 a). Die Entwicklung von Theileria parva, dem Erreger des Küstenfiebers der Rinder in Afrika. Teil II. Arch. f. Protistenk. 22, 170.Google Scholar
Goodpasture, E. W., Woodruff, A. M. and Buddingh, G. J. (1931). The cultivation of vaccine and other viruses in the chorio-allantoic membrane of chick embryos. Science, 74, 371.CrossRefGoogle Scholar
Gray, C. E. and Robertson, W. (1903). Redwater in Rhodesia. Agric. J. of Cape of Good Hope, 21, 435.Google Scholar
Harris, W. H. (1932). Histopathological effects of Thorium dioxide on lymphatic glands of animals visualised by the Menville-Ané method. Proc. Soc. Exp. Biol. and Med. 29, 1049.CrossRefGoogle Scholar
Hegner, R. W. (1923). The effects of changes in diet on the incidence, distribution and number of certain intestinal protozoa of rats. Amer. J. Hyg. 3, 180.Google Scholar
Hegner, R. W. (1926). Biology of host-parasite relationships among protozoa. Quart. Rev. Biol. 1, 393.CrossRefGoogle Scholar
Hegner, R. W. and MacDougall, M. S. (1926). Modifying the course of infections with bird malaria by changing the sugar content of the blood. Amer. J. Hyg. 6, 602.Google Scholar
Hoeppli, R. and Feng, L. C. (1931). Histological reactions in the skin due to ecto-parasites. Nat. Med. J. of China, 17, 541.Google Scholar
Kleine, F. K. (1908). .Bemerkung zu Dr Mayer's Arbeit. Arch. f. Schiffs- u. Tropen-Hyg. 11, 494.Google Scholar
Knuth, P. and Du Toit, P. J. (1921). Tropenkrankheiten der Haustiere. Handb. d. Tropenkr. Leipzig:J. A. Barth, 2nd ed.6, 361.Google Scholar
Koch, R. (1897). Über die Viehseuchen in Deutsch-Ostafrika. Deutsch. Kolon.-Bl. 24, 719.Google Scholar
Koch, R. (1903). Report on Rhodesian red-water or African coast fever. J. Comp. Path. And Therap. 16, 273.Google Scholar
De Kock, G. and Quinlan, J. (1926). Splenectomy in domesticated animals and its sequelae, with special reference to anaplasmosis in sheep. Rep. Dir. Vet. Ed. and Res. Pretoria, Nos. 11 and 12, part 1, p. 369.Google Scholar
Lichtenheld, G. (1911). Beurteilung eines Befundes von Koch'schen Plasmakugeln in Niereninfarkten einer Elenantilope. Z. f. Infektionskr. d. Hausth. 9, 154.Google Scholar
Lucas, M. S. (1930). Results obtained from applying the Feulgen reaction to Protozoa. Proc. Soc. Exp. Biol. and Med. 27, 258.CrossRefGoogle Scholar
Maximow, A. (1928). Cultures of blood leucocytes. Arch. f. exper. Zellforsch. 5, 169.Google Scholar
Maximow, A. (1930). Textbook of Histology, 833 pp. (edited by Bloom, W.). Philadelphia: W. R. Saunders Co.Google Scholar
Maximow, A. and Bloom, W. (1932). The lymphocytes and plasma cells (revised by W. Bloom).. Special Cytology, 2nd ed., 2, 603. New York: Paul B. Hoeber.Google Scholar
Mayer, Martin (1910). Über das ostafrikanische Küstenfieber der Rinder. Arch. f. Schiffs- u. Tropen-Hyg. 14, 1.Google Scholar
Mettam, R. W. M. (1924). Snotziekte in cattle. Rep. Dir. Vet. Ed. and Res. Pretoria, Nos. 9 and 10, p. 395.Google Scholar
Meyer, K. F. (1911). Notes on the nature of Koch's granules and their rdle in the pathogenesis of East Coast fever. Rep. Gov. Vet. Bact. Pretoria, Union of South Africa, 1910, p. 56.Google Scholar
Montgomery, R. E. (1913). On bodies resembling Koch's bodies in the spleen of a topi (Damaliscus corrigum jimela). Ann. Rep. Vet. Path. Lab. Nairobi, 1911–12, 25.Google Scholar
Moskwin, J. A. (1929). Die Wirkung des Bisses der Zecke Ornithodorus papillipes Bir. auf die Haut der Versuchstiere. Centralbl. f. Bakt. etc., Abt. 1, Orig. 110, 208.Google Scholar
Mottram, J. C, Cramer, W. and Drew, A. H. (1922). Vitamins, exposure to radium and intestinal fat absorption. Brit. J. Exp. Path. 3, 179.Google Scholar
Nuttall, G. H. F. (1913). The Herter Lectures. III. Piroplasmosis. Parasitology, 6, 302.CrossRefGoogle Scholar
Nuttall, G. H. F. and Fantham, H. B. (1910). Theileria parva, the parasite of East Coast fever in cattle. Parasitology,. 3, 117.CrossRefGoogle Scholar
Nuttall, G. H. P., Fantham, H. B. and Porter, A. (1910). Observations of Theileria parva, the parasite of East Coast fever. Parasitology,. 2, 325.CrossRefGoogle Scholar
Nuttall, G. H. F. and Hindle, E. (1913). Conditions influencing the transmission of East Coast fever. Parasitology,. 6, 321.Google Scholar
Nuttall, G. H. F. and Strickland, C. (1908). On the presence of an anticoagulin in the salivary glands and intestines of Argas persicus. Parasitology,. 1, 302.CrossRefGoogle Scholar
Pawlowsky, E. N. and Stein, A. K. (1927). Experimentelle Untersuchungen über die Wirkung von Ixodes ricinus (Ixodidae) auf die Menschenhaut. Arch. f. Schiffs- und Tropen-Hyg. 31, 574.Google Scholar
Perla, D. and Marmorston-Gottesman, J. (1930). Further studies on Trypanosoma lewisi infection in albino rats. J. Exp. Med. 52, 601.CrossRefGoogle Scholar
Pfeiffer, L. (1891). Die Protozoen als Krankheitserreger, 2nd ed.Jena.Google Scholar
Robinson, L. E. and Davidson, J. (1913). The anatomy of Argas persicus. Part II. Parasitology, 6, 217.CrossRefGoogle Scholar
Ross, P. H. (1911). Nairobi Laboratory Reports for 1904–10. East Africa Protectorate, I.Google Scholar
Sabbatani, L. (1898). Fermento anticoagulante dell' Ixodes ricinus. Arch. Ital. de Biol. 31, 37.Google Scholar
Sawyer, W. A. and Lloyd, W. (1931). The use of mice in tests of immunity against yellow fever. J. Exper. Med. 54, 533.CrossRefGoogle ScholarPubMed
Schilling, Cl. (1930). Immunität bei Protozoeninfektionen. In Kolle and Wassermann's Handb. d. path. Mikroorg. 8, 95.Google Scholar
Schilling, Cl. and Meyer, K. F. (1930). Piroplasmosen. Handb. d. path. Mikroorg. 8, part 1, 1.Google Scholar
Schwetz, J. and Storck, N. (1930). Theileria (Gonderia) mutans et corps bleus de Koch. Bull. Soc. d. Path. exot. 23, 377.Google Scholar
Sergent, Edm. (1920). Étude morphologique du Piroplasma (Gonderia) mutans du Bœuf. Ann. Inst. Pasteur, 35, 193.Google Scholar
Sergent, Edm., Donatien, A., Parrot, L. and Lestoguard, F. (1929). Sur l'existence de corps en grenade dans le cycle évolutif de Gonderia mutans. Bull. Soc. Path. Exot. 22, 542.Google Scholar
Sergent, Edm., Donatien, A., Parrot, L., Planttureux, E. and Rougebief, H. (1927). La “fièvre de la cote orientale” et la Theileriose nord-africaine. Bull. Soc. Path. Exot. 41, 489.Google Scholar
Steck, W. (1928). Histological Studies on East Coast fever. Rep. Dir. Vet. Ed. and Res. Pretoria, Nos. 13 and 14, 243.Google Scholar
Strickland, C. (1915). Observations on the blood in East Coast fever of cattle. Parasitology, 8, 244.CrossRefGoogle Scholar
Taliaferro, W. H. (1928). Infection and immunity in bird malaria. Porto Rico Rev. Pub. Health and Trop. Med. 4, 155.Google Scholar
Teichmann, E. and Braun, H. (1911). Ueber ein Protozoentoxin (Sarkosporidiotoxin). Arch. Protistenk. 22, 351.Google Scholar
Theiler, Sir Arnold (1905). How long an area remains infected with East Coast fever. Transvaal Agric. J. 4, 700.Google Scholar
Theiler, Sir Arnold (1908). The influence of cold on ticks and Piroplasma parvum. Bull. Soc. path. exot. 1, 451.Google Scholar
Theiler, Sir Arnold (1911). The artificial transmission of East Coast fever. Rep. Gov. Vet. Bact. Pretoria, p. 7.Google Scholar
Theiler, Sir Arnold, Gray, C. E. and Power, W. H. (1915). Diseases transmitted by ticks. 10th Internal. Vet. Congress, London, 3, 806.Google Scholar
Theiler, Sir Arnold and Graf, H. (1928). Gonderia mutans or Theileria mutans. 13th and 14th reports Dir. Vet. Ed. and Res. Pretoria.Google Scholar
Theiler, Max (1930). Susceptibility of White Mice to the Virus of Yellow Fever. Science, 71, 367.CrossRefGoogle Scholar
Walker, J. (1930). Aids to Stockowners. Dept. of Agriculture, Kenya Colony, 158 pp.Google Scholar
Walker, J. and Whitworth, S. H. (1929). Artificial immunisation and immunity in their relation to the control of East Coast fever. Nairobi, Kenya: Government Printer, 18 pp.Google Scholar
Wenyon, C. M. (1926). Protozoology, 2, 7791563. London: Baillière, Tindall and Cox.Google Scholar
Zwick, W., Seifried, O. and Witte, J. (1929). Weitere Beiträge zur Erforschung der Bornaschen Krankheit des Pferdea. Arch. wiss. u. prakt. Tierheilk. 59, 511.Google Scholar