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H. Sarcocystis Species 1. Introduction The taxonomy and identification of this genus has suffered in the past from confusion and a failure to link up the different life cycle stages to each other (Levine 1987), and studies on the sarcocysts in relation to an understanding of their life cycles and interrelationships have progressed along with those on Isospora and Toxoplasma, to which Sarcocystis is related (MARKUS et al. 1974; Levine 1987; BALL et al. 1989; ROMMEL 1989). However, much remains to be learned about this genus, including details of species concern- ed in zoonotic infections. In a review of intestinal protozoa infecting humans, Gotpsip (1985a) listed two species as infecting humans, S. hominis (for- merly Isospora hominis) and S. suihominis. These two species were also listed by HERBERT and SMITH (1987) and STEVENSON and HUGHES (1988), as having humans for their definitive host. However, in the latter discussion of sarcosporidiosis (sarcocystosis), STEVENSON and HUGHES (1988), while also listing two species, take a slightly different taxonomic approach, listing S. hominis and S. porcihominis (=S. suihominis) as species where the human serves as the definitive host and S. findemanni, where humans are believed to be the intermediate host and for which the definitive host has yet to be elucidated. The term “‘S. lindemanni” should thus be viewed as a collective term for several species of animal sarcocysts infecting humans as an inter- mediate, albeit dead-end host. Il. Life Cycle and Transmission The life cycles of the various species of Sarcocystis are believed to follow the same general pattern although differing in their definitive and inter- mediate host ranges. Descriptions of the life cycle of Sarcocystis are given by Markus et al. (1974), RomMet (1989) and Faver and ELasser (1991), and an outline of the general life cycle pattern as given in an excellent article by Herbert and SMITH (1987) is provided below and in Fig. 12.34. In the intestine of the carnivorous host (including humans and other pri- mates for S. hominis and S. suihominis), the coccidian stages are passed. The ingested tissue cyst in muscle is digested to release bradyzoites (cystozoites) which penetrate the goblet cells of the intestine and within 24 h differentiate into male and female gametes which after fusion form a zygote beneath the lamina propria. This develops to an oocyst and matures to produce two sporocysts, each with for sporozoites (Fig. 12.24). These oocysts pass out in the faeces of the host to infect a suitable intermediate host when ingested. In the case of S. hominis this intermediate host includes domestic live stock, especially cattle, and in the case of S. suihominis, itis the pig (HERBERT and Suri 1987; STEVENSON and HuGHes 1988). The stages in the definitive host, including humans, rarely cause problems, although a transient diarrhoea may occur (HERBERT and SMITH 1987). Endodyogeny intissue cyst in muscle. Intermediate host Fig. 12.34. Life cycle of Sarcocystis spp. (modified after RoMMet 1989) On ingestion by a suitable intermediate host, and this includes humans in the case of S. lindemanni, the mature oocysts excyst in the small intestine and penetrate the epithelium to settle in the endothelial lining of the arteries of various tissues, but especially lymphoid tissue, the intestinal tract and skele- tal muscle. Here, over the next 10 days, they undergo a process of nuclear division (endopolygeny) to produce meronts which intrude into he lumen of the blood vessel. These are then released and travel via the bloodstream to various sites throughout the body where they multiply by further endopoly- geny. These second-generation meronts develop about a month after infec- tion and are in their turn released and disseminated via the circulatory system, to be found either free in the blood or within mononuclear cells. Most of them, however, seem to be located in the mononuclear phagocyte system of the liver and visceral lymph nodes, where they may divide to form third- generation meronts. The second — and sometimes even third ~ generation meronts enter striat- ed muscle cells or nervous tissue in a wide range of organs. These developing forms become surrounded by a parasitophorous vacuole which becomes incorporated into the cyst wall that separates them from the host cell. The evsis. are, septate and initially contain stages, termed metrocvtes., which iniultiply by endodyogeny and mature into bradyzoites some 10 weeks post infection. Although the above life cycle is essentially as described for Sarcocystis in general by HERBERT and SMITH (1987) and RoMMEL (1989), it is probably applicable to the human definitive host in relation to S. hominis/S. suthomi- nis in the gut and to the human intermediate host for S. lindemanni in the tissues, especially the skeletal muscle — despite the fact that the life cycle of the latter species has not yet been elucidated (STEVENSON and HUGHES 1988). The overall transmission of sarcosporidiosis to humans thus depends on whether one is dealing with S. hominis/S. suthominis, for wl humans are the definitive hosts and for which infection involves the ingestion of infected meat of intermediate host animals (pork, beef etc), or with S. lindemanni, for which humans serve in the capacity of intermediate (albeit “dead-end” hosts and for which infection occurs by ingestion of faccally contaminated food or water infected with oocysts from the definitive host, whatever this may be for S. lindemanni. III. Distribution and Epidemiology It must be assumed that the distribution of human sarcocystosis is world- wide, as is the condition generally (HERBERT and SMITH 1987). Again, published reports probably reflect a lack of recognition and do not accurate- ly indicate the true distribution of the condition (GoLDsMID 1985a) ~ either intestinal due to 5. hominis/S. suihominis or extra-intestinal due to S. linde- manni. However, extra-intestinal sarcocystosis has been shown to be common in some areas of South-east Asia such as Malaysia (WoNG and PATHMANATHAN 1992). It would also seem reasonable to assume that both conditions will be found to be more prevalent in the Third World in areas where human sanitation and hygiene are poor and where meat inspection standards are not high.