Parasitology. Alan Gunn

species, the definitive host is a dog or other canine, whilst the intermediate hosts are cows and other bovids (Figure 3.14). The life cycle begins when an infected dog sheds free sporocysts or oocysts in its faeces. A cow must then consume the sporocysts/oocysts, and this usually happens through contamination of food or water. When the sporocyts/oocysts reach the cow’s small intestine, they release the sporozoites. The sporozoites then invade the gut epithelial cells and make their way to the blood vessels. The bloodstream then distributes them around the body. The parasites invade the endothelial cells of the blood vessels that serve many of the body’s organ systems. Within the endothelial cells, the parasites transform into merozoites and undergo four cycles of merogony (asexual reproduction). After each cycle, the newly formed merozoites are released, and these infect new endothelial cells downstream of the initial infection. After the last cycle, the merozoites invade skeletal and cardiac muscle cells. Occasionally, smooth muscle, the brain, and spinal cord are also infected. Within these cells, the merozoites transform into metrocytes or ‘mother cells’ each of which divides asexually to form a structure called a sarcocysts (Figure 3.15). With repeated asexual division, a sarcocyst steadily becomes larger and larger and in some Sarcocystis species may become big enough to be visible to the naked eye. Eventually, the globular metrocytes cease producing new metrocytes and form crescent‐shaped bradyzoites. The time taken for this depends upon the species of Sarcocystis but can be around 2 months. During this time, the sarcocysts are non‐infectious since only bradyzoites can transmit the infection. Completion of the life cycle requires a dog to consume flesh containing the bradyzoites. Digestion of the sarcocyst within the dog’s small intestine releases the bradyzoites, and these become motile. The bradyzoites initially invade the gut epithelial cells and then make their way to the lamina propria region where they transform into either male or female gametes. After gamete fusion, the parasites undergo sporogony to form oocysts that contain two sporocysts. The oocysts are therefore already sporulated when shed and each contains four sporozoites. The oocysts are shed into the lumen of the gut and passed with the faeces. The oocyst has a thin wall and often ruptures when one is preparing faecal samples for microscopy. Consequently, one normally sees sporocysts (16.3 × 10.8 μm) in faecal samples. Sarcocystis seldom causes serious pathology in its definitive hosts.

Figure 3.14 Life cycle of Sarcocystis bovicanis. 1: Digestion of a sarcocyst within the dog’s small intestine, releases bradyzoites that invade the gut epithelial cells and then make their way to the lamina propria region where they transform into either male or female gametes. After gamete fusion, the parasites undergo sporogony to form oocysts that contain two sporocysts. The oocysts are shed into the lumen of the dog’s gut and pass with the faeces. 2: A cow consumes the sporocysts/oocysts, and these release the sporozoites that invade its gut epithelial cells and make their way to the blood vessels. The parasites invade the endothelial cells of the blood vessels, transform into merozoites, and undergo four cycles of merogony. After each cycle, the newly formed merozoites infect new endothelial cells. 3: After the last cycle, the merozoites invade skeletal and cardiac muscle cells and transform into metrocytes, each of which divides asexually to form a sarcocyst. Eventually, the metrocytes cease producing new metrocytes and form bradyzoites. Completion of the life cycle requires a dog to consume flesh containing the bradyzoites. Drawings not to scale.

Figure 3.15 Transverse section through a sarcocysts of Sarcocystis muris in the trachea of a mouse.

      Human Sarcocystis Infections

      Humans are the definitive hosts for S. bovihominis, S. suihominis and several other species of Sarcocystis that we usually acquire from eating raw or poorly cooked meat. As definitive hosts to these parasites, we suffer from intestinal infections. The symptoms are non‐specific and typically include nausea and diarrhoea. The infections are usually self‐limiting and seldom serious.

      We can also act as intermediate hosts for some Sarcocystis species. For example, we can act as an intermediate host for Sarcocystis nesbitti although in most cases the species responsible is uncertain. The definitive hosts for S. nesbitti are probably snakes or other reptiles. Therefore, in common with the other species for which we are intermediate hosts, we are ‘dead end’ hosts because few animals have the opportunity to eat us. Presumably, we suffer accidental infections with the sporocysts/oocysts through contamination of food or water and the normal intermediate hosts are other species of primates. The symptoms of infection depend upon the site at which the sarcocysts grow and their abundance. Typically, they induce inflammatory responses that result in pain, fever, and swelling at the infected site. There are reports of regular outbreaks of human sarcocystosis amongst tourists visiting parts of Malaysia (Fayer et al. 2015). Whether these link to one or more species of Sarcocystis is uncertain.

      In intermediate hosts, the consequences of infection vary between species, the level of challenge, and the species of Sarcocystis parasitizing them. However, most pathology is usually associated with damage caused to the vascular epithelium during the second stage of merogony. Heavy infections of S. bovicanis in cattle can result in widespread haemorrhages afflicting virtually every organ in the body. This results in anaemia, emaciation, and the animal may become anorexic; abortion can occur in breeding cattle. The immune response results in lymphadenopathy and submandibular oedema whilst the hair at the end of the tail is often lost. Most infections in domestic livestock, however, are subclinical and not discovered until the sarcocysts are detected during meat hygiene inspections after the animal is slaughtered.

3.5.6 Genus Toxoplasma, Toxoplasma gondii

      This genus contains only one species, Toxoplasma gondii. However, it has a remarkable host range and can probably infect all mammals and birds.

This intracellular parasite was initially described from a desert rodent, the North African gondi (Ctenodactylus gondi) [sometimes spelled ‘gundi’ – vowels are not used in written Arabic, so some words appear in various spellings when translated into English] in Tunisia 1908, but the life cycle was not established until 1969–1970. The name Toxoplasma has nothing to do with toxins but derives from the curved shape of the tachyzoite stage of the life cycle (Figure 3.16). ‘Toxon’ (Tόξoν) is the Greek word for a ‘bow or something that is crescent shaped and ‘plasma’ ( πλάσμα) is Greek for ‘creature’. Since these humble beginnings, it has become apparent that not only does T. gondii have a cosmopolitan distribution but also it has perhaps the widest host range of any parasite.

The life cycle of T. gondii has two parts and three infectious stages (Figure 3.17). The two parts of the life cycle are the sexual cycle that occurs within cats and other felines that are the definitive hosts and the asexual cycle that occurs in the intermediate hosts – which are virtually any warm‐blooded animal, including us. The three infectious stages are the sporulated oocysts that contain the sporozoites, the tachyzoites, and the tissue cysts that contain bradyzoites: all three stages are infectious to both the feline definitive hosts and the intermediate hosts. Cats acquire their infection by consuming either sporulated oocysts passed in another cat’s faeces (e.g., through contamination) or an intermediate host containing the tachyzoites and bradyzoites. Following ingestion, the parasites invade the epithelial cells lining the cat’s