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Endoparasites - Life Cycles

The life cycle of most parasites involve both immature and mature stages. The animal harbouring sexually mature parasites is called the definitive or principal host. Immature stages of some parasites must partially mature inside an animal of another species, such as an insect, a snail, or another mammal. These animals are called intermediate hosts. After such development, the immature parasite forms are infective to the principal host. All tapeworms (cestodes) and a few roundworms (nematodes) of dogs require intermediate hosts. These parasites are said to have indirect life cycles. Parasites that reproduce without an intermediate host have direct life cycles.

Immature forms of some parasites enter organisms called paratenic or transport hosts in which no development occurs. Paratenic hosts serve as a reservoir for the infective forms of the parasite. Principal hosts are then infected by eating all or part of the transport host. Once infective parasite forms have entered the principal host, they grow to maturity. The time from entry of the infective stage to reproductive maturity is known as the prepatent period.

Most parasites must develop partially before they are capable of infecting their principal host. There are six ways in which host animals can be infected by internal parasites:

  • Directly eating an infective larva or egg. Parasitic infection of the host often occurs after the ingestion of an infective larva or egg. Examples include Trichuris vulpis, Ancylostoma (not in NZ), Uncinaria (not significant in NZ) and Toxascaris (not significant in NZ).
  • Eating the intermediate host. In other cases, the principal host may ingest the intermediate host harbouring the infective stage. This is true of tapeworms such as Dipylidium caninum, whose infective larval form lives in fleas.
  • The parasite actively penetrates the principal host. Larvae of dog hookworms Ancylostoma caninum and Ancylostoma braziliense (not in NZ) and the intestinal threadworm Strongyloides (not in NZ) stercoralis may infect their hosts by skin penetration. Following infection, larvae are transported via the blood to the lungs before proceeding to their sites of predilection where they mature.
  • Becoming infected by means of the intermediate host. Mosquitoes, for example, carry infective forms of Dirofilaria immitis (not prevalent in NZ) in their mouthparts, and, when they feed on dogs, they release these infective immature parasites on to the skin and the larvae actively penetrate the bite wound to enter the bloodstream.
  • Eating the paratenic host. Dogs may become infected by ingesting tissues of the transport host containing infective immature parasites. This occurs with Toxocara and Toxascaris.
  • The parasite may be maternally transmitted. Some parasites, including Toxocara canis, Strongyloides stercoralis and Ancylostoma (not in NZ), may cross the placenta, infecting the foetal pups. These parasites may also pass via the milk of an infected bitch to her newborn puppies.

Knowledge of life cycles is important in controlling parasites. Sometimes control is possible by reducing contact with intermediate hosts. The frequency of parasite control measures is related to the length of time parasites take to complete their life cycles.


The most common roundworm parasites have similar direct life cycles. Females lay thousands of eggs, which pass out in the faeces of infected animals. If the environmental conditions of warmth and moisture are favourable, eggs deposited in the faeces will develop to the first larval stage (L1) and hatch in several hours. Alternately, as with Toxocara, Toxascaris and Trichuris, larvae may remain in the egg and develop until eaten and released. If deposited on dry ground or if temperatures are low, the eggs develop more slowly or will not survive. Hatched larvae can thrive on the ground, feeding mainly on bacteria.

Larval growth is limited by a rigid skin, or cuticle. Larvae increase their size through the process of moulting. When a first-stage larva grows to the limits of its cuticle, it develops a second, larger cuticle underneath the first, then casts off the old one to become a second-stage larva (L2). The L2 grows to its limits and moults again to become a third-stage larva (L3). The third-stage larvae will have the ability to infect dogs. Once inside the animal, infective larvae become established in the site of predilection appropriate to their species and develop into adult worms. Life cycles of nematodes infecting dogs often do not conform to the simple direct life cycles characteristic of may roundworm parasites of other species. Major differences occur in the development of infective larval stages and the patterns of migration these forms follow in the host.

Toxocara, Toxascaris and Trichuris nematodes are very common in dogs throughout the world. Infective larval forms develop outside the host of eggs. Toxocara and Toxascaris second-stage larvae inside eggs are infective. First-stage larvae of Trichuris are infective. Dogs may be infected by ingesting these eggs. Digestion stimulates the hatching of larvae. Infective larvae may also be acquired by dogs after first being ingested by transport or paratenic hosts, such as rodents. This occurs in the life cycle of Toxascaris, Toxocara and Spirocerca lupi. Paratenic hosts are specific for the nematode species. Spirocerca, for example, may use reptiles or birds as paratenic hosts. Ingestion and digestion of these organisms release infective larvae and the normal course of infection resumes.

Once inside the principal host, larvae may migrate through tissues before establishing themselves at the predilection site. Blood that is returned from body tissues to the heart is pumped to the lungs, so larvae that enter the circulation often pass through the lungs in a pattern known as tracheal migration. Infective larvae of Ancylostoma and Uncinaria may infect dogs by penetrating their skin and entering blood vessels. Circulation then carries them to the lungs. Here they often migrate out into the air spaces and travel up the airways to the trachea, where they are coughed up and swallowed. Development to adult stages is completed in the small intestine. Infective larvae of Toxocara, after being swallowed, penetrate the gut wall and enter blood vessels. They then follow a tracheal migration described above.

Another possible route of travel by infective larvae is somatic migration. In these cases, larvae that have entered blood vessels do not leave the circulation in the lungs but are carried in the blood to various tissues of the body. This may occur with Toxocara canis, Ancylostoma and Uncinaria. Larvae that reside in body tissues become inactive and development ceases. Toxocara larvae may survive in this state for 385days. Their activity is resumed, however, in bitches during late pregnancy. At this time, the larvae receive a stimulus that causes them to migrate to the uterus. After penetrating the uterine wall, they enter the foetuses. Puppies are then born with active larvae that migrate to the intestines by tracheal migration and become adult parasites. The invasion of foetal pups by nematode larvae is called prenatal infection. It may be lethal to puppies.

Indirect life cycles occur with some nematodes in dogs. An example is Dipetalonema reconditum. Dipetalonema reconditum lives in body cavities and connective tissues of the dog. They are viviparous giving birth to microfilariae (larvae) instead of eggs. These microfilariae cannot develop until they are taken up by a flea during feeding. Development to the infective stage occurs in the flea and this stage is then infused into the blood of the dog during subsequent feeding.


Adult tapeworms in the small intestine of the principal host grow by generating proglottides from the scolex. Proglottides mature and after fertilisation, become gravid (enlarged and filled with eggs). The enlargement of segments as they mature results in the characteristic widening of the tapeworm body toward its end. Gravid proglottides break off from the end of the tapeworm and pass in faeces.

Eggs are released as the proglottides decompose, either within the animal or on the ground in the faeces. With some species of tapeworms, eggs will not appear in the faeces even when a heavy infection exists. Rather, intact proglottides are found. Neither the proglottides nor the eggs can infect dogs. To become infective, eggs first must develop to the infective stage in intermediate hosts, such as arthropods or mammals. Because of the need for intermediate hosts, the life cycle of tapeworms is indirect.

The embryo that develops within the tapeworm egg is known as a hexacanth. When ingested by the intermediate host, it hatches and develops into an immature stage called a metacestode. Metacestodes of different tapeworm species show differences in structure. A metacestode is usually a fluid-filled cyst with one or more immature scolices (heads) growing on the inner lining. Infection of the principal host occurs when an intermediate host or part of the host tissue containing the immature metacestode is ingested. Digestion releases the scolices, which mature in dogs and become adult tapeworms.

Dog tapeworms of the genus Taenia use certain domestic animals as intermediate hosts. The metacestode may produce disease in these animals, as is the case with immature Taenia multiceps forms in sheep. Dogs are the principal host of Echinococcus granulosus. This adult tapeworm is of little importance to dogs, but its metacestode can grow in almost any mammal, including man. Disease may result; therefore, dogs infected with Echinococcus granulosus pose a serious health threat to man. The problems presented by tapeworm infections in dogs are discussed more completely under "Damage to Host".