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.
Babesia divergens, B. ovis and B. bigemina give rise to reddish urine (haemoglobinuria) and jaundice (icterus). Exitus is caused by the blockage of kidney function and the failure of the circulation. Infected calves of less than 9 months of age acquire at least a partially protecting resistence or premunition. Other babesiae include: B. canis in dogs, B. ovis in sheep and goat, B. felis in lion, leopard, puma and other felids, B. microti in mice (Box 2.3 above, page 108).
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).
Theileria parva, T. annulata and T. lawrenci give rise to watery mucous discharges of the nose and tear glands, dyspnea and, later on, bloody diarrhoea followed by anaemia but without icterus. Lethality is especially high in calves but less so in adult cattle, which acquire protective premunition. T. ovis and T. hirci attack goats and sheep (Box 2.3, below; page 108).
In vertebrates, Theileriae propagate initially in the regional lymph nodes, than in bone marrow and in Peyers 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 hosts 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 Genes glands protecting it from desiccation. The tick then dies, further protecting the delivered egg mass by its corpse (fig. 6.20, page 264).
Larvae, nymphs and imagos of hard ticks feed on blood (each of the stages only once). Piroplasms transmitted by the corresponding next stage are transmitted transstadially. In cases in which the parasites reach the next generation via the ticks ovaries, the transmission is generative, i.e. the piroplasms are transmitted transovarially. Three-host ticks change the host at each stage after feedig. In two-host ticks, the larva (which sometimes does not feed) and the nymph remain on the same host. In this case, piroplasms taken up by the nymph are transmitted only by the imago. In one-host ticks, the larva, nymph and imago remain on the same host and the piroplams (e.g. Babesia spec.) are exclusively transmitted transovarially.
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 Lymes disease/borelliosis are zoonotic spirochaetes.