INTRODUCTION

Woese et al. first proposed that life on earth is composed of three primary divisions, or domains to which all organisms belong. These domains are named Archaea (or archaebacteria), Bacteria (or eubacteria), and Eucarya (or eukaryotes), with Eucarya being relatives (or descendants) of Archaea (Woese & Fox, 1977; Woese et al., 1990). This proposal was based on 16S ribosomal RNA sequences and later confirmed by the comparison of many protein sequences (Pohlschroder et al., 1997; Scamardella, 1999; Woese & Fox, 1977; Woese et al., 1990) . This proposal is currently widely accepted, although some sequence features and phylogenies derived from many highly conserved proteins are inconsistent (Gupta, 1998).

Prokaryotes and eukaryotes differ from each other in many respects, with the most important criteria of their distinction being the type of their cells; eukaryotes’ cells contain a membrane-bounded nucleus, while prokaryotes not (Gupta, 1998). Archaea resemble morphologically with bacteria (e.g both of them are prokaryotes), but they are evolutionary distinct from them and other prokaryotes and constitute a fundamentally different form of life (i.e., life’s third domain) (Gupta, 1998; Olsen & Woese, 1993; Pohlschroder et al., 1997; Woese & Fox, 1977; Woese et al., 1990).

Eukaryotes are organisms composed of one or more cells with nuclei which have inhabited Earth for approximately 1.2 billion to 1.8 billion years (Knoll et al., 2006). Eukaryotes dominate the visible landscapes of terrestrial and marine systems and are major players in biogeochemical cycling and cause numerous global diseases (e.g., malaria, African sleeping sickness, amoebic dysentery). Eukaryotes clearly differentiate from prokaryotes as all of eukaryotes share the main features of cellular architecture (e.g the complex intracellular compartmentalization) and the regulatory circuitry (Koonin, 2010). Plants, animals, fungi and protists are the most familiar eukaryotes (Tekle et al., 2009).

The small size of some of Eukaryotes has traditionally made these groups recalcitrant to study. In addition, their evolution exhibits a vast timescale that obscures evolutionary events during their origin and early diversification. However, advances in molecular techniques (e.g., multigene sequencing, genomics) are transforming our views on eukaryotic evolution (Tekle et al., 2009).

Protozoa are single-celled eukaryotes that commonly show characteristics usually associated with animals, most notably mobility and heterotrophy (Flynn et al., 2007; Pink et al., 2005). Protozoa combine cell and organism in one (Vickerman & Coombs, 1999). The kingdom Protozoa belongs to Protists that contains also algae, and lower fungi (Corliss, 2002). The term “protist” is often used instead of ”protozoa” because many protozoa have features in common with fungi or algae (Flynn et al., 2007).

They are a multiphyletic group of organisms, whose members differ in structure, morphology, biochemistry and genetics (Flynn et al., 2007; Scamardella, 1999) and their vast diversity of cellular organization provides an endless supply of material for biologists to investigate (Vickerman & Coombs, 1999). Protozoa adapt to changing environments by modifying form and function to achieve homeostasis (Vickerman & Coombs, 1999).

A few protozoa are important parasites (Pink et al., 2005) that are responsible for diseases of humans and other mammals, lower animals and higher plants (Vickerman & Coombs, 1999). Such protozoa experience devastating changes of environment during the course of their life cycles. Protozoa may leave the host to face the outside world before infecting another host or move directly from one host to another (e.g vector-transmitted parasites such as the trypanosomes, leishmanias and malaria parasites) (Vickerman & Coombs, 1999). In addition, some parasitic protozoa must avoid elimination by host defences, innate or acquired (Vickerman & Coombs, 1999).

Parasitic diseases are caused mainly by protozoa and continue to take an enormous toll on human health, particularly in tropical regions (Pink et al., 2005). Parasitic diseases also provoke crop damage and problems in livestock health (Adl et al., 2007).

EPIZOOTIC DISEASE AND ZOONOSIS

Epizootic (from Greek epi- upon + zoon animal) is a disease that occasionally occur at higher than normal rates in animal populations (in correspondence with the term epidemic applied to human populations) and it generally represent an unstable relationship between the causative agent and affected animals. High population density is a major contributing factor to epizootics (Encyclopaedia Britannica inc., 2001; Morens, 2003).

Even if both domestic and wild animals suffer from various parasites, wild animals seldom suffer massive deaths or epizootics because of the normal dispersal and territorialism of most species (L. S. Roberts et al., 2009). Domesticated animals, on the contrary, suffer from epizootics as they are usually confined to pastures or pens in great numbers year after year. This fact makes parasite eggs, larvae, and cysts become extremely dense in the soil and the number of adult parasites within each host becomes vast (L. S. Roberts et al., 2009). Coccidia, that are a diverse group of parasitic protozoa (Tenter et al., 2002), thrive under a variety of conditions in poultry flocks, in sheep (in wool) and in lambs, provoking severe economic losses (L. S. Roberts et al., 2009).

Ζoonosis is the human disease resulting from the transmission of parasites of wild and domestic animals to humans. Ζoonoses are quite common and consists an important hazard to public health (L. S. Roberts et al., 2009; Taylor et al., 2001).

THE PHYLUM APICOMPLEXA

The Apicomplexa are a large phylum of diverse obligate intracellular parasites (Morrissette & Sibley, 2002). These species are phylogenetically related and they constitute a major burden on human health, agriculture and economics. For example, this phylum contains parasites as Plasmodium spp. (the cause of malaria), Toxoplasma gondii, Cryptosporidium parvum (pathogens of immunocompromised individuals) and Theileria spp. Eimeria spp., as well as Isospora spp., Neospora spp. and Sarcocystis spp. that are parasites of considerable agricultural importance (Augustine, 2001; Dubey, 1999; Graat et al., 1996; Morrissette & Sibley, 2002; Wasmuth et al., 2009). The Apicomplexa phylum consists of around 6000 known species of protozoa (with potential number of species reaching 1.2–10 × 10⁶ species) infecting a wide range of animals from mollusks to mammals and man (Adl et al., 2007; Cavalier-Smith, 1993; Wasmuth et al., 2009).

Apicomplexan protozoan parasites share distinctive morphological features, cytoskeletal organization, and modes of replication, motility, and invasion (Morrissette & Sibley, 2002). Apicomplexans are generally slender, crescent-shaped cells with size that range from 4-9 microns long by 1 to 3 microns wide (Sibley, 2004). Ultrastructure of sporozoites and merozoites has the typical structure of Apicomplexa (Levine, 1973). They all possess an apical complex, that is a certain combination of structures, and help the parasites to enter into hosts (L. S. Roberts et al., 2009). Their cell cortex is comprised of several membranous layers and the underlying cytoskeleton (Sibley, 2004). Apicomplexans usually have no cilia or flagella. Generally, they have cysts (“spores”) that function in transmission, but in some that the cyst wall has been eliminated, the development of infective stages is completed within an invertebrate vector as sporozoites. Most apicomplexans contain an organelle called the apicoplast (Fast et al., 2001; Obornik et al., 2002; Toso & Omoto, 2007; Vaishnava & Striepen, 2006; Wasmuth et al., 2009) that is essential for parasite survival; it is involved in fatty acid synthesis and other critical metabolic pathways (Ralph et al., 2004; Vaishnava & Striepen, 2006; Waller & McFadden, 2005; Wasmuth et al., 2009). Apicomplexans are also characterized by various defining organelles involved in host cell attachment, invasion, and the establishment of an parasitophorous vacuole (that act intracellularly within the host cell) where proteins are stored and released through the apical complex at the anterior of the cell (Sibley, 2004; Wasmuth et al., 2009). Locomotor organelles in Apicomplexans are less obvious than in other protozoan phyla (L. S. Roberts et al., 2009; Sinden, 1985).

THE APICOMPLEXAN LIFE CYCLE

The apicomplexan life cycle is generally common to the phylum but there are striking differences between species, e.g some require a single host whereas others require sexual reproduction in the vector species for transmission. Coccidians, or coccidia, members of the subclass Coccidiasina of this phylum (that live in digestive tract epithelium, liver, kidneys, blood cells, and other tissues of vertebrates and invertebrates), present intracellular asexual reproduction, either as monoxenous species or oligoxenous species (according to the number of hosts required to complete their life cycles .Their life cycle is complex and may be broken down into three broad stages: sporozoite, merozoite, and gametocyte (L. S. Roberts et al., 2009; Wasmuth et al., 2009). Apicomplexans enters a host cell (infection) as sporozoites and then they becomes ameboid trophozoites that multiplie to form merozoites (merogony). Merozoites escape from the host cell and enter other cells to initiate further merogony or transform into gamonts (gametogony) that produce “male” microgametocytes or “female” macrogametocytes. Macrogametocytes develop directly into macrogametes and microgametocytes undergo multiple fission to form microgametes respectively. Fertilization produces zygotes, which after multiple fission produce sporozoite-filled oocysts (sporogony). In homoxenous life cycles all stages occur in a single host, although oocysts mature (sporozoite development is complete) in the oxygen-rich, lower-temperature environment outside a host and sporozoites are released when a mature oocyst is eaten by another host (L. S. Roberts et al., 2009). In heteroxenous life cycles, in some species merogony and a part of gametogony occur in a vertebrate host while sporogony occurs in an invertebrate and sporozoites are transmitted by the bite of the invertebrate; and in some other species sporozoites are infective to a vertebrate intermediate host, where they produce zoites that are infective to a carnivorous vertebrate host (L. S. Roberts et al., 2009).

THE FAMILIES EIMERIIDAE AND SARCOCYSTIDAE

The families Eimeriidae and Sarcocystidae of the phylum Apicomplexa represent a highly diversified group of intracellular coccidian parasites of vertebrate and invertebrate hosts (Jirku et al., 2002; Modry et al., 2001). Coccidian parasites are parasites that belongs to the suborder Eimeriina and subclass Coccidiasina (L. S. Roberts et al., 2009). They are parasites of great medical importance that’s why they have attracted substantially more attention than other coccidian groups (Jirku et al., 2002). Both of these families possess two sporocysts, each with four sporozoites per oocyst (L. S. Roberts et al., 2009). They are traditionally classified based on the number of sporocysts per oocyst but they can also classified based on the small subunit ribosomal RNA gene (SSU rRNA gene) (Modry et al., 2001). They represent the taxonomically most complex groups (Modry et al., 2001; Morrison et al., 2004). However, these families differ as the Eimeriidae is consisting of oocyst-forming coccidia, while Sarcocystidae is consisting of cyst-forming coccidia (Modry et al., 2001; Morrison et al., 2004).

THE LIFE CYCLE OF SPECIES OF THE FAMILY EIMERIIDAE AND SARCOCYSTIDAE

In the family Eimeriidae, micro- and macrogametes develop independently without syzygy; microgametocytes produce many active microgametes, which then encounter macrogametes (typically located within cells of a host’s intestinal epithelium). After syngamy, their oocysts develop resistant walls and contain sporocysts (one, two, four, or sometimes more), each with one or more sporozoites. Merogony and gemetogony occur within a host but sporogony typically occurs outside (L. S. Roberts et al., 2009; Tenter et al., 2002). Species of Isosporan and Eimerian genera of the family Eimeriidae have similar general life cycle (L. S. Roberts et al., 2009).

In family Sarcocystidae, the parasites are heteroxenous, with vertebrate intermediate hosts. Asexual development occurs in vertebrate intermediate hosts, whereas other vertebrates, mainly carnivorous mammals and birds, are definitive hosts. Oocysts from a definitive host sporulate and are swallowed by an intermediate host. Sporozoites released from oocysts infect various tissues and rapidly undergo endodyogeny to form merozoites, also known as tachyzoites which can infect other tissues such as muscles, fibroblasts, liver, and nerves. Asexual reproduction in these tissues (rather than in intestine) is much slower than in the original site, and the parasites develop large, cystlike accumulations of merozoites that are called bradyzoites. The cyst itself is called a zoitocyst, or simply a tissue cyst. A definitive host is infected when it eats meat containing bradyzoites or, rarely, tachyzoites or, in some cases, when it swallows a sporulated oocyst. When tissue cysts are ingested by a definitive host, bradyzoites invade enteroepithelial cells and undergo schizogony, then gametogenesis, and finally fertilization to produce oocysts (L. S. Roberts et al., 2009).

COCCIDIAN OOCYSTS AND SPOROCYSTS

Coccidian oocysts are remarkably constant in their morphology within a given species of the subclass Coccidiasina. The oocyst wall has two layers, an outer one that is electron dense and varies in thickness among coccidian genera, and an inner one that is 20–40 nm thick and not so dense. A membrane known as the veil surrounds the outer wall layer which contains mostly lipids and proteins, and is resistant to proteolytic enzymes and various chemicals (Belli et al., 2006). The oocyst wall helps the organism survive harsh conditions in the external environment. Oocysts of Isospora species resemble with oocysts of genera Toxoplasma, Sarcocystis, Levineia, Besnoitia, Frenkelia, and Arthrocystis (Belli et al., 2006; L. S. Roberts et al., 2009).

Sporocysts contain a sporocyst residuum that contains a large amount of lipid, an important source of energy for sporozoites when they stay outside a host. The sporocyst wall consists of a thin outer granular layer surrounded by two membranes and a thick, fibrous inner layer and an homogeneous Stieda body at one end of the sporocyst (plugging a small gap in the inner layer), which in some species is underlied by the substiedal body. When sporocysts reach the intestine of a new host, the Stieda body is digested, the substiedal body pops out, and sporozoites wriggle through the small opening thus created (W. L. Roberts et al., 1970).

ISOSPORA SPP

Isospora is an interesting genus of the protozoan phylum Apicomplexa which is consisted of enteric species that belongs to coccidian parasites. Isospora cause isosporosis which is a severe disease mainly in livestock. Isosporosis consists of an acute diarrhoea in humans and other mammals (Anantharaman et al., 2007). This genus less often infect humans; mainly infecting immunosuppressed or young individuals (Anantharaman et al., 2007; Lindsay et al., 1997; Sibley, 2011). Isosporans are known from all continents except Antarctica (Jirku et al., 2002).

Historically, Isopora species were considered to infect only the digestive tract of a single host species but now it is known that certain isosporans can produce encysted asexual stages in extraintestinal tissues of the host (Gardiner et al., 1989). The genus Atoxoplasma, homoxenous blood parasites of birds (N. D. Levine, 1982), has had a long and convoluted taxonomic history with Isospora but now is merged with Isospora (Barta et al., 2005). So the genus Isospora now includes species that have merogony in a variety of host cells, including a variety of blood cells as those of the intestinal epithelium, gametogony in the intestinal epithelium, and sporogony outside the host (Barta et al., 2005). These species show close affinity to the Eimeriidae, while other species of the genus Isospora from mammalian hosts are grouped together within Sarcocystidae (Modry et al., 2001; Morrison et al., 2004). Their current taxonomy is based on ultrastructural and life-cycle features, but also molecular evidence (based on the small-subunit ribosomal RNA gene sequence) (Jirku et al., 2002; L. S. Roberts et al., 2009). That’s why coccidians infecting mammals, formerly classified as Isospora species, are now considered members of genus Cystoisospora. So, parasites as the parasite infecting humans (frequently observed in the tropics) that was previously reported as Isospora belli, now is named Cystoisospora belli (Barta et al., 2005; Fletcher et al., 2012; L. S. Roberts et al., 2009; Samarasinghe et al., 2008) etc..

THE LIFE CYCLE OF SPECIES OF THE GENUS ISOSPORA

The life cycle of the species of Isospora which are referred to as Cystoisospora, may involve a transport host. So, when the transport host becomes infected by ingesting sporulated oocysts, it harbours a monozoic cyst (containing a single sporozoite) in various organs which is not pathogenic in the transport host but mildly pathogenic in definitive hosts. When this host is eaten by the final host, the sporozoite initiates the intestinal cycle (Gardiner et al., 1989).

C. Belli

The parasite C. belli is a parasite infecting humans frequently observed in the tropics (Barta et al., 2005; Fletcher et al., 2012; L. S. Roberts et al., 2009; Samarasinghe et al., 2008). This parasite can cause severe intestinal disease with fever, malaise, persistent watery diarrhoea, abdominal cramps, anorexia, weight loss and even death, especially in AIDS patients (Barta et al., 2005; Doumbo et al., 1997; Fletcher et al., 2012; L. S. Roberts et al., 2009) and other immunocompromised patients (Gruz et al., 2010; Guk et al., 2005; Kim et al., 2013; Koru et al., 2007; Lagrange-Xelot et al., 2008; Meamar et al., 2009; Perez-Ayala et al., 2011; Reeders et al., 2004; Resende et al., 2011; Velasquez et al., 2011), but also in indigenous populations in the United States (Fletcher et al., 2012). In AIDS patients, infection may be characterized by chronic diarrhoea, acalculous cholecystitis cholangiopathy, and extraintestinal infection (Resende et al., 2011; Velasquez et al., 2011). C. belli is often implicated in traveler’s diarrhoea, which is met in travellers to developing countries and has high levels of endemicity (Fletcher et al., 2012).

C. belli causes disease in several mammalian hosts, probably through the ingestion of mature sporulated oocysts in contaminated food or water. This infection is almost indistinguishable from cryptosporidiosis. Apart from C. belli, other Cystoisospora species are important causes of diarrhoea in domestic animals (Fletcher et al., 2012).

ISOSPORA SUIS (CYSTOISOSPORA SUIS)

Infections with intestinal coccidia are very important economically infections of intensively farmed mammalian livestock, and the costs of prevention and treatment are high (Mundt et al., 2006). Although several species of coccidia exist in pigs, only I. suis is recognised as a pathogen of economic importance (Fletcher et al., 2012; Mundt et al., 2006). I. suis was first described by Biester and Murray in 1934 (Worliczek et al., 2007). I. suis is a common intestinal parasite of piglets (Sotiraki et al., 2008; Worliczek et al., 2007) that can cause neonatal porcine coccidiosis (see below). Firstly, I. suis didn’t receive much attention as a pathogen of pigs until the increase of intensive pig breeding systems (Worliczek et al., 2007).

Nowadays, I. suis is one of the most prevalent parasites in intensive pig production. Recent investigations have shown that I. suis is the most frequent parasite found in piglets aged 7–14 days and that the presence of the parasite is associated with diarrhoea in over 50% of naturally infected animals (Scala et al., 2009) that lasts for three until seven days or nine days (Mundt, Joachim, et al., 2003; Worliczek et al., 2009). A study carried out in 12 European countries confirmed the presence of I. suis in 26% of litters and in 69% of the herds examined (Skampardonis et al., 2012). I. suis is spread worldwide with high prevalences in pig-breeding facilities independent of the farm management system and the farrowing facilities (Mundt et al., 2005).

Isosporosis represents a considerable problem worldwide as demonstrated also by various field studies (Mundt et al., 2005; Mundt et al., 2006; Sotiraki et al., 2008; Worliczek et al., 2010). The prevalence of piglet Isosporosis in different regions varies from 1% to 90% of farms (Karamon et al., 2008). The economic loss from Isosporosis is mainly due to this growth retardation (which can reach 20% in terms of weight loss) and decreased daily weight gain and can be extended into the post-weaning phase (Scala et al., 2009). It is noticeable that this disease is rarely seen in organic systems (Sotiraki et al., 2008).

NEONATAL PORCINE COCCIDIOSIS

Neonatal porcine coccidiosis is a disease which affects piglets up to the age of 3 weeks, mainly in the second to third week of their life (Worliczek et al., 2007). Neonatal porcine coccidiosis caused by I. suis comprises transient diarrhoea (non-haemorrhagic yellow to whitish diarrhoea) and dehydration in nursing piglets with subsequent decreased weight gain, poor nutrient absorption and poor performance (Mundt et al., 2005; Mundt et al., 2007; Sotiraki et al., 2008; Worliczek et al., 2010; Worliczek et al., 2007; Worliczek et al., 2009) and can cause significant economic losses. Affected piglets also present reduced and uneven weaning weights due to the reduced uptake of nutrients during a stage of intensive growth display, lower weight gain or even weight loss during and shortly after the period of diarrhoea (Worliczek et al., 2007). However, the disease shows a low mortality (Mundt et al., 2007; Scala et al., 2009; Sotiraki et al., 2008; Worliczek et al., 2010; Worliczek et al., 2007), except for cases with secondary bacterial infections (even though we don’t know the exact importance and the mechanism of such infections) (Sotiraki et al., 2008). In addition, Isosporosis seems to predispose the piglet to other secondary infectious agents such as E. coli, Clostridium sp. and rotavirus, which could considerably increase morbidity, mortality and management costs (Scala et al., 2009).

CLINICAL SIGNS AND PATHOLOGY

I. suis is a host-specific enteric parasite inhabiting the small intestines (mainly the jejunum and ileum) of pigs that causes fibrinous enteritis which mainly affects the middle and posterior part of the jejunum, described often accompanied with villous necrosis and atrophy (when the damage to the intestinal lining is extensive) (Mundt et al., 2007; Worliczek et al., 2010; Worliczek et al., 2009). Infection leads to damage of the mucosal surface in the jejunum and ileum and to non-haemorrhagic diarrhoea (Worliczek et al., 2007). The changes in the gut morphology reflect the clinical picture of the disease (Mundt et al., 2007). Diagnosis can be done from mucosal biopsy specimens (Koru et al., 2007; Velasquez et al., 2011) or by direct microscopic observation of the oocyst in faeces using acid-fast staining as the oocysts are quite large (20 to 23 μm by 10 to 19 μm) and morphologically distinctive. However, veterinarians frequently report difficulties in diagnosing the oocysts in the faeces maybe due to the high fat content (steatorrhoea) or because samples are taken during the non-patent stage of infection (Worliczek et al., 2007). Molecular techniques can also be used to augment diagnosis and the detection is more sensitive (Fletcher et al., 2012). Changes in haematological parameters during an infection with I. suis are not so clear, so they can’t be used as a test for this infection (Schlepers, 2010).

THE LIFE CYCLE OF ISOSPORA SUIS (CYSTOISOSPORA SUIS)

The life cycle of I. suis is completed within 5–6 days (Worliczek et al., 2010; Worliczek et al., 2007) and consists of three main phases: merogony (asexual reproduction), gamogony (sexual reproduction), and sporogony. The first two phases are located in host intestines and the third one in the environment (Karamon et al., 2008). Piglets are infected by ingestion of sporulated oocysts. After oral ingestion of them, the parasite (that is motile sporozoites released from the sporulated oocysts) invades the villus epithelial cells of the small intestines and develops intracellularly within a parasitophorous vacuole. Then it begins to reproduce asexually and sexually (Karamon et al., 2008; Worliczek et al., 2010; Worliczek et al., 2009). The meronts or gamonts are described as the pathogenic stages (Mundt et al., 2007; Worliczek et al., 2009). Meronts divide into many merozoites (with asexual reproduction) which infect next epithelial cells. Some of them transform to sexual stages (macro- and microgamonts) intracellularly and as a result of sexual reproduction, the oocysts arise (prepatent period lasts 5-7 days) (Karamon et al., 2008). Intracellular multiplication of the parasite leads to crypt hyperplasia and fusion, and atrophy and necrosis of the villi resulting in diarrhoea and reduced uptake of nutrients by the mucosa (Worliczek et al., 2010). The final stage of endogenous development is the oocyst which unsporulated exits the cell (released from the enterocytes) and is excreted with the faeces. The infectious stages (sporocysts containing sporozoites) develop in the environment within 1–3 days, depending on the temperature (Karamon et al., 2008; Worliczek et al., 2010; Worliczek et al., 2007); the sporulation rate increase with temperature, although the infective sporocyst stage was reached within 24 h at all temperatures (Langkjaer & Roepstorff, 2008). Unlike the closely related Eimeria, I. suis merogonies cannot be divided into generations, rather the meronts develop into different types (Worliczek et al., 2007).

TREATMENT AND PREVENTION

So as to control isosporosis, it is very important to identify the specific mixture of necessary conditions and events that are needed for the I.suis infection and determine the future course of the infection; such as the duration and level of exposure to the pathogen, the presence of animal- and herd-specific risk factors etc. (Sotiraki et al., 2008). Not all piglets in a litter or in a herd are equally affected (variation in the risk of occurrence of oocyst excretion, the level of excretion and the risk of diarrhoea) and this observation can also be made during experimental infections under highly standardised conditions (Mundt et al., 2006). So it can be assumed that the individual susceptibility to infection is very variable in outbred piglets and depends on their ability to respond to infection. Secondary bacterial infections or secondary infections with other enteric influence positively the morbidity of this disease, increasing the mortality. The age of the piglets upon infection also plays a role for clinical outcome under natural conditions, and this further adds to the heterogenic picture of isosporosis in a herd; younger animals are more affected than older ones (Sotiraki et al., 2008; Worliczek et al., 2009). However the mechanisms for this phenomenon are unclear (Worliczek et al., 2007). The infection dose and duration of exposure influences the intensity of the pathological changes (Worliczek et al., 2007).The factors varying at the litter level may affect the relation between the oocyst excretion pattern and clinical Isosporosis (Skampardonis et al., 2012). However, several aspects of the I. suis epidemiology have not been fully understood yet (Skampardonis et al., 2012) .

Control of this parasite is currently almost completely based on early routine treatment of piglets with toltrazuril, an anticoccidial triazin derivative (Scala et al., 2009; Sotiraki et al., 2008). Treatment with toltrazuril can decrease the prevalence of diarrhoea and the number of diarrhoea days. It can also contribute to a lower oocyst excretion and a higher gain than in infected pigs (untreated with toltrazuril) (Mundt et al., 2007; Schlepers, 2010; Worliczek et al., 2007). Notably, some results confirm that prophylactic treatment of piglets with toltrazuril (prevention) is the best option to control isosporosis in suckling piglets (Scala et al., 2009) as there is no real treatment versus an outbreak of isosporosis (confirming findings in experimental infections) (Scala et al., 2009; Schlepers, 2010). That means that after a pig show clinical signs of infections with I. suis, there are already tissue alterations, so a treatment is not still very effective (Scala et al., 2009; Schlepers, 2010). However, presently, metaphylaxis and specific therapy against Isosporosis in overt clinical forms with toltrazuril is recommended, since toltrazuril significantly reduces the shedding of oocysts and diarrheic symptoms in infected piglets (Scala et al., 2009). Certainly the correct treatment timing is very important issue so as the intervention get before the onset of diarrhoea and/or oocyst excretion which allows clinical or parasitological diagnosis and unfortunately I. suis has an extremely short life cycle (Mundt et al., 2007; Scala et al., 2009). The exact mode of action of toltrazuril is still not fully known (Mundt et al., 2007). It is believed that toltrazuril interferes with enzymes of the respiratory chain of the coccidian parasite and inhibits the pirimidine synthesis, without effecting the entry of the coccidians into the host cells (so there is development of immunity) (Greif, 2000; Harder & Haberkorn, 1989; Mundt et al., 2007; Schlepers, 2010).The use of sulphonamide drugs (coccidiostatic drugs for mammalian coccidia, mostly Eimeria spp. of cattle and rabbits) is not advisable (Scala et al., 2009).

Apart from prophylactic treatment with toltrazuril, hygiene measures are also advisable (Schlepers, 2010). Indeed, the impact of several managerial factors on the odds and the level of I. suis oocyst excretion are assessed. Such interventions could be used as preventing measures against Isosporosis alternatively or supplementary to medical control and that is very important because of the currently widespread use of anticoccidial compounds and the possible development of resistant parasites (Langkjaer & Roepstorff, 2008; Mundt, Daugschies, et al., 2003; Skampardonis et al., 2012) and the poor response to antibiotics of suckling piglets in the second week of life (typically infected by the scouring of farm). Unfortunately, even though hygiene measures may prevent disease outbreaks, the resistant oocysts cannot be easily inactivated (Worliczek et al., 2007). So, once I. suis has established itself on a farm, the infection is maintained (maybe through piglet-to-piglet transmission via contaminated farrowing pens, as sows are rarely found to excrete oocysts) (Sotiraki et al., 2008). Different approaches have been recommended to decrease the survival of I. suis oocysts in the environment and the risk of infection, such as changing microclimatic conditions in the farrowing pens or constructing perforated pen floors (Scala et al., 2009; Skampardonis et al., 2012). However, in large pig farms it is quite difficult to increase the days between litters and to maintain microclimatic conditions able to significantly decrease oocyst survival (Scala et al., 2009).

This research was previously published in the International Journal of Systems Biology and Biomedical Technologies (IJSBBT), 2(4); edited by Tagelsir Mohamed Gasmelseid, pages 49-62, copyright year 2013 by IGI Publishing (an imprint of IGI Global).

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