Abstract

2.7 Piroplasmoses and hard ticks

Piroplasms are parasites of pair- and unpair-hoofed animals, canids, felids, small mammals and birds, in the red blood cells (RBCs) of which they form pear-shaped merozoites. Their kinetes have an apical complex of rhoptries but wihout a conoid and divide by endodyogenia (internal division). The rhoptries of the daughter individuals are newly formed, whereas that of the mother cell is reduced (fig.2.59, page 121). In the phylum Sporozoa (Apicomplexa), they make up the order Piroplasmida in two families: Babesiidae and Theileriidae. They are transmitted only by hard ticks. Piroplasmosis is endemic predominantly in large herds of free-ranging cattle. The losses caused by these parasites threaten the protein supply of populations in the third world.

In vertebrates, Babesiae parasitize RBCs exclusively. In the tick, they propagate in muscle cells, peritracheal cells and oocytes, enabling transovarial transmission. Thus, the following generation of ticks is partially infective. The tick, which depends upon seasonally migrating wild pair-hoofed animals, becomes a reservoir host of the Babesiae. They propagate en masse in the large volume of blood of cattle and thus many ticks can become infected by a single vertebrate host (fig. 2.56, page 110).

In vertebrates, Theileriae propagate initially in the regional lymph nodes, than in bone marrow and in Peyer’s plaques of the intestine. They induce the infiltrated lymphoblastoid cells to divide again and thereby pass to the daughter cells: Theileriae thus increase their tissue substrate and preserve their host from immunological failure. They attack RBCs creating parasitaemias of high density only in order to develop gamonts for further transmission. In the vector tick, they propagate exclusively in type III acini of the salivary glands. There is no transovarial transmission (fig. 2.57, page 112).

Piroplasms, taken up by the ticks during a blood meal, develop into isogametes via variably shaped (Babesiae, fig. 2.56) or four nucleated symmetric (Theileriae, fig. 2.57) Strahlenkörper (male gamonts). After fertilization, the zygote is phagocytozed by the cells of the midgut. Here, it changes by endomonogenia to the first kinete, which enters the haemolymph of the tick. It becomes a multiplying body, which delivers the second kinetes. The latter divide by binary divisions to become sporozoites, which are infective for warmblooded animals.

In Babesia, the first kinetes in the haemolymph attack haemocytes and cells of the malpighian tubules and of the ovaries. In the latter, the stages are activated by a fresh blood meal and enter newly delivered egg cells. The second kinetes produced in other tissues enter the salivary gland cells and become sporozoites by repeated binary division (fig. 2.56, page 110).

In Theileria, the first kinetes in the haemolymph migrate to the salivary glands as soon as the tick has finshed its postfeeding moult. They attack the cells at the outlet of the type III acini. There, they change, via multiplying bodies and definitive endopolygenia, into sporontes. Induced by a new blood meal, sporogonia starts and sporozoites are transmitted by saliva (fig. 2.57, page 112).

The piercing apparatus of ticks consists of telescope-like chelizerae with terminal claws, a stiletto-like labrum and a hypostome with a dorsal food channel and ventral barb hooks. The pedipalps enclosing it carry sense organs. The salivary glands consist of grape-like arranged acini of three different types, each of which is constructed of a few cells with various functions (see chapt. 6.3, page 259 ff.).

To take a blood meal, the tick anchors itself by secretions of the salivary gland, which harden to form the stylostome. At the preparation phase, the tick rhythmically pumps secretions into the host’s tissue for its liquefaction. RBCs and tissue fragments are phagocytozed and blood plasma is endocytozed. This induces the growing phase of midgut cells. The blood meal is thickened and the liquid is returned back to the host via the haemolymph and the salivary glands. At the same time, the tick converts arachnidonic acid from the host to prostaglandins in its salivary glands; prostaglandins have immune-suppressive, coagulation-inhibiting and vasodilatory activities. In the subsequent extension phase, the tick rapidly engorges the main volume of blood (repletion) and later falls off by lysis of the stylostome. After each cycle of uptake and internal digestion, the phagocytozing intestinal cells are replaced by interstitial cells. The complete resorption of the blood meal takes weeks or months depending on the temperature. Faeces are discharged during feeding and, in larvae and nymphae, after each moult. Finally, the tick borrows into the ground and starts ovipositing. Each egg is covered separately by secretions from Gene’s glands protecting it from desiccation. The tick then dies, further protecting the delivered egg mass by its corpse (fig. 6.20, page 264).

Certain species of hard ticks give rise to paralyses because of toxins in their saliva: Tick paralysis. The pathogens of TBE (western tick-borne encephalitis) are zoonotic viruses transmitted by hard ticks, whereas those of Lyme’s disease/borelliosis are zoonotic spirochaetes.

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