The parasite Trichinella and its control of host muscle
Trichinella is a very important intracellular parasite. James Pagent first discovered Trichinella in humans in 1875 during a medical study. There are five species of Trichinella. Medically the most important is Trichinella spiralis. It is found worldwide and has the ability to infect a wide range of mammalian hosts.
Unlike many other species of intracellular parasites, such as Leishmania and Plasmodium, Trichinella does not kill the host cell. Instead it actively induces a series of modifications within the invaded cell ensuring the survival of both host and parasite.
Male and female Trichinella tend to live in the intestinal epithelium of mammals. Many L1 larvae are produced. These penetrate the intestinal wall and are transported via the bloodstream to striated muscle. Here they enter the cytoplasm and obtain nutrients via intracytoplasmic nutrition. Upon entering a muscle cell, the L1 larvae encounter a rigid arrangement of actin and myosin filaments. The parasite rearranges the cell contents in a co-ordinated manner, and in doing so transforms the muscle cell into a highly specialised nurse cell. The nurse cell acts in the same way as a placenta, secreting nutrients to the larva and exporting wastes.
The parasites initiate a form of population control by secreting a variety of antigens early in the developmental process. These antigens, whilst inducing a high level of protection, also restrict the numbers of developing larvae within a given area without inhibiting the development and survival of established parasites.
Transformation of the invaded muscle cell into a nurse cell typically takes 20 days and involves a number of morphological and biochemical reorganisations. The parasite induces the formation of smooth membranes and mitochondrial aggregates as a substitute for muscle-specific structures including myofilaments. This is followed by the enlargement of nuclei, which subsequently migrate to the centre of the cell. An additional change is the increased number of ribosomes, ER and golgi present, signalling the change in function of the complex from a contractile to a secretory cell. In addition, the nurse cell becomes encapsulated with a thick outer coat composed of collagen. This coat is continually shed in order to delay the host immune response. Infection is spread to other organisms when the muscle is eaten by predators or scavengers.
To date very little is known with regard to the molecular basis for these changes. It has been suggested however, that the secretion of antigens from the pharyngeal stichocytes of L1 larvae is responsible for maintenance of the nurse cell parasite complex. Since these antigens are not secreted until day 8 of the developmental process they are not thought to be involved in induction of nurse cell development.
It is proposed that these antigens interact with the hosts genome and either maintain or initiate the pattern of genome expression such that nurse cell development is completed.
These alterations in structure and functions can be detected clinically due to the onset of symptoms such as haemorrhaging under the skin, swelling under the eyes, cramping pains and diahorrea. In general, the severity of the infection is proportional to the number of infectious stages. Although Trichinella parasites can infect a wide variety of organisms it is only passed to humans through the eating of raw or uncooked flesh. Due to the implementation of stricter animal and food hygiene measures, Trichinella spiralis infections are less common. However, there remains a threat from infected rats, which may subsequently be consumed by farmyard animals such as pigs and horses.