Protozoan Diseases in Farm Ruminants

Protozoa are ubiquitous throughout aqueous environments and the soil, and play an important role in their ecology. Protozoa occupy a range of trophic levels.They also play a vital role in controlling bacteria population and biomass. Farm animals are usually infected with several species of parasites and they are also confined to pasture or pens. Parasite eggs, larvae, and cysts are intense in soil. One of the most important aspect of animal protozoology is transmission to humans. These are called zoonosis. Some of zoonotic diseases are common and important to public health. This chapter is about of the etiology, epidemiology, pathogenesis, clinical findings, diagnosis, treatment and control of the pathogenic protozoa in farm ruminants.


Sheep and goats
In sheep and goats, babesiosis is associated with B. ovis and B. motası. Babesia ovis occur in Southern Europe, former Soviet State, Middle East and Asia. Rhipicephalus bursa has been shown to be a vector for B. ovis. Babesia motasi occur in Southern Europe, the Middle East, the former Soviet State, southeast Asia and Africa. The parasite transmitted by ticks of the genus Haemaphysalis (H. Punctata, H. Otophila), Dermacentor (D. silvarum) and Rhipicephalus (R. Bursa) ( Taylor et al., 2007).

Pathogenesis
Babesia spp. are a various group of tickborne, obligate, intra-erythrocytic Apicomplexan parasites infecting a wide variety of animals. Ticks are most often infected transovarially. The female tick becomes infected by the ingestion of parasites during engorgement. After it drops off the host, the babesial agents reproduce within the tick's tissues. Some of the reproducing organisms are incorporated within developing tick embryos, and the disease agents are transmitted to new hosts by the feding of ensuing tick larvae, nymphs, or adults (Zaugg, 2009).
B. bovis is the most pathogenic of the bovine Babesia. B. bigemina infections are not as virulent as those of B. bovis, however the parasites may infect 40% of the red cells (Taylor et al., 2007).

Cattle
Incubation period is 2-3 weeks. B. bigemina and B. bovis produce acute syndromes which are clinically indistinguishable, and are characterized by high fever (41˚C), anorexia, depression, weakness, cessation of rumination, and a fall in milk yield. Hemoglobinuria can be seen, the color of urine is dark-red to brown. Respiratory and heart rates are increased, and the red conjunctivate and mucous membranes change to the extreme pallor of severe anemia. Abortion ocur in pregnant animals (Radostits et al., 2000). Subacute syndrome also occurs in young animals, but fever is mild and hemoglobinuria is absent .
In cerebral babesiosis, hyperexcitability, convulsions, opisthotonos, coma, and death, may be observed in cattle infected with either B. bigemina or B. bovis, but especially with the B. bovis. Central nervous system signs are caused by brain anoxia resulting from severe anemia (Zaugg, 2009).

Sheep
In sheep develop fever and parasitemia within 2 to 4 days; the clinical signs of the disease include anorexia, listlessness, anemia, moderate jaundice and hemoglobinuria. In intact animals, hyperthermia returned to normal on the fourth day after the peak pyrexia, and parasitemia is eliminated within the course of the disease (Rahbari et al., 2008).

Diagnosis
Blood smears and clinical findingd are useful in acute cases of piroplasmosis, but are not sufficient in subclinical cases. The complement fixation test is used serological test for bovine babesiosis. The most commonly used tests are ELISA, PCR and a DNA probe, which can detect specific parasitemias at very low levels of infection (Radostits, 2008). Recently, the 'reverse line blot (RLB) is a versatile technique for simultaneous detection and identification of small ruminant piroplasm species, based on the recognition of specific gene regions by oligonucleotide probes (Nagore et al., 2004;Qingli et al., 2009;Inci et al., 2010;).
The control of the disease depends on effective quarantine to prevent the introduction of the vector tick. The control of ticks by dipping or spraying animals at risk with recommended acaricides. In routine surgery, Care should be taken to prevent accidental transfer of blood from one animal to another (e.g., castration, dehorning). In addition, in cattle, the selection and breeding of cattle which acquire a high degree of resistance to ticks is practiced. Widespread use of tick vaccines may also have a significant influence on the incidence of infection in cattle (Taylor et al., 2007;Radostits et al., 2008;Zaugg, 2009).

Etiology
Theileriosis is caused by Theileria spp. in cattle, goats, sheep and wild and captive ungulates (Radostits et al., 2000). Theileriosis is a hemoparasitic disease caused by protozoa of the genus Theileria (Apicomplexa). Theileria species affect domestic and wild ruminants, especially in Africa, Europe, Australia, and Asia (Allison and Meinkoth, 2010). The parasites are transmitted by tick. These parasites, undergo repeated merogony in the lymphocytes ultimately releasing small merozoites, which invade the red cells to become piroplasms. Theileriosis, have a variety of tick vectors which cause infections ranged from clinically inapparent to rapidly fatal (Taylor et al., 2007).
The list of theileria species is shown in table 2.

Bovine theileriosis
Bovine theileriosis is caused by at least six Theileria species (Table 2). In bovine, East coast fever caused by T. parva. The tick vector is Rhipicephalus appendiculatus. East coast fever generally ocur in cattle but also buffalo (OIE., 2004), and occurs in East Africa. ECF is prevalent throughout the wetter areas, but is absent from the wet highlands in the horn of www.intechopen.com Africa (Norval et al., 1991). In Africa, T. parva is a highly fatal disease in cattle Carlson, 2009a) and this disease is a great threat on the development of the livestock industry, with losses of about 10,000 cattle per year in Zambia (Nambota et al., 1994). In bovine, Tropical Theileriosis (Mediterranean coast fever), occurs in Mediterranean countries, Middle East, Indian and China, and is caused by T. annulata . The tick vectors are Hyalomma dentritum in north Africa and in the Mediterranean countries, H. dentritum and H. dromedaii in central Asia, and H. marginatum in India ( Taylor et al., 2007;Radostits et al., 2008). In endemic areas indigenous cattle are relatively resistant while modified cattle, especially European breeds, are highly susceptible (Taylor et al., 2007).

Organism
Theileria orientalis complex is a milder disease than East coast fever and Tropical Theileriosis, and called benign theileriosis in cattle . The tick vectors are Ambylomma variegatum, A. cohaerens, A. haebraeum, Haemaphysalis bispinosa that these vectors are the probable vectors in Australia (Taylor et al., 2007).
Theileia taurotragi has been described in cattle, antelope and eland. Geographical distribution of this disease is in Africa. The tick vectors are Rhipicephalus appendiculatus and Rhipicephalus pulchellus (Taylor et al., 2007).
Thieleria mutans has been seen in cattle and deer (Carlson, 2009a).
Theileria hicri is malignant theileriosis of small ruminants (Lawrence, 2004;), and is enzootic in North Africa, Middle East, China and India. The tick vectors are Rhipicephalus bursa and Hyalomma anatolicum (Taylor et al., 2007).
Theileria ovis is benign theileriosis in Africa . But in China Theileria ovis is a serious disease . The incidence and mortality rates of Theileria ovis in adult sheep and goats were have found 17.12% and 65.78%; 8.06% and 73.33% respectively in China (Shuzhen et al., 2002). In Turkey, prevalence of infection of T. ovis in sheep and goats were have been 64.19% and 12.36%, respectively ( Sayın et al., 2009). The tick vectors of disease are Rhipicephalus bursa in the Mediterranean and Rhipicephalus evertsi in Africa (Taylor et al., 2007).

Pathogenesis
Pathogenesis of different form of theileriosis is based on the production of schizonts in lymphocytes and piroplasms in erythrocyte. T. parva, T. annulata and T. hicri produce highly schizonts and piroplasma and are very pathogenic; T. mutans, T. buffeli, and T. ovis unusually produce schizonts but may cause varying degree of anemia when piroplasms are highly in red blood cells .

Clinical findings
Theileia spp. are classified in to 2 groups. In first group (T. parva and T. annulata), proliferate is seen in lymphocytes but in the second group (T. orientalis) it is seen in erythrocytes that causes hemolytic anemia (Magona et al., 2010).
In Theileria parva incubation period is approximately1-3 weeks . One or two days later, the first clinical sign is generalised swelling of the superficial lymph nodes, eyes, ears and submandibular regions. After few days there is anorexia, decreased milk production, loses condition, ceases rumination, rapid hearth beat, petechial haemorrhages under the tongue and on the vulva (Taylor et al., 2007). In cerebral theileriosis there are localized nervous signs and convulsions, tremor, salivation and head pressing .
In Theileria annulata, pyrexia, anorexia, enlargement of superficial lymph nodes, nasal and ocular discharges and salivation is the most common signs. Constipation is recorded in some cases. Respiratory distress, coughing and pulmonary oedema are seen ( Osman and Gaabary, 2007).
In Theileria orientalis clinical signs are associated with anemia, jaundice and lymphadenopathy (Taylor et al., 2007).
Clinical signs in Theileria velifera is not reported but in Theileria taurotragi mild fever and anemia are reported (Taylor et al., 2007).
In Theileria hicri which is very pathogenic in sheep and goats, in the acute form there is fever, inappetence, ceases rumination, weakness, enlargement of superficial lymph nodes, diarrhoea, jaundice, haemorrhage in submucous may ocur. In chronic form there is fever, inappetence, emaciation, anemia and jaundice (Taylor et al., 2007). Theileria hicri is not reported in Turkey (Sayın et al., 2009).

Diagnosis
Investigation of giemsa-stained blood smears and lymph node biopsy will reveal piroplasms in erythrocytes and schizonts in lymphocytes. For diagnosis, indirect fluorescent antibody test (IFAT) and indirect enzyme-linked immunosorbent assay (ELISA) are the most commonly used techniques. The ELISA tests is more sensitive than IFAT (Taylor et al., 2007;Radostits et al., 2008).

Treatment and control
Buparvaquone is the most effective drug and the recommended dose in cattle, sheep and goat is 2.5mg /kg BW (Taylor et al., 2007;Radostits et al., 2008).
In control of the disease use of genetically resistant breed, a judicious and selective application of acaricides at 3-week intervals and the use of vaccines are recommended .

Etiology
Sarcocystosis caused by Sarcocystis species in cattle, sheep and goats. The names of Sarcocystis species are according to their intermediate and final hosts (Taylor et al., 2007;Radostits et al., 2008). The list of sarcocystis species is shown in table 3.

Pathogenesis
Sarcocystis spp, are protozoon parasites with a requisite two-host life cycle. Sexual reproduction phase occur in the intestine of a carnivore (dogs, cats) later, cysts in the muscles of cattle, sheeo or goats. Sporocysts are shedded by carnivore's feces and then ingested by cattle, sheep, or goats. Then sporocysts hatch in the ruminant small bowel and invade the vascular endothelium during three phases of asexual reproduction. After third phase, merozoites enter the ruminant's muscle tissue and encyst as sarcocysts (Smith and George, 2009;Reilly et al., 2002).

Clinical findings
In cattle is usually asymptomatic, but in heavy infections and nonimmune cattle, clinical signs include fever, anorexia, anemia, weight loss, lameness, abortion and diarrhea (Taylor et al., 2007;Radostits et al., 2008). Neurologic signs are occasionally seen in cattle that include ataxia, tremors, muscular weakness, hypersalivation, blindness, opisthotonos and nystagmus Smith and George, 2009 ). In infections that caused by Sarcocystis bovicanis in cattle there is usually loss of hair at the end of the tail (Taylor et al., 2007).
In sheep and goats clinical signs may be asymptomatic. In heavy infections there is fever, loss of weight, anemia and weakness. Abortion may occur (Taylor et al., 2007).
In chronic infections clinical signs include poor weight gain, edema of the limbs, anemia and abortion ( Smith and George, 2009). Neurological disorder that is described in sheep caused by S. Tenella and S. Arieticanis . Neurological symptoms, such as depression, in coordination, hind leg paralysis and coma can be seen in Encephalitic Sarcocystosis (Ozmen et al., 2009).

Diagnosis
Generally Sarcocystis infections are diagnosed at meat inspection with grossly visible sarcocysts in the animala's muscle. When infection is very heavy in intermediate hosts, clinical signs and histological evidence of schizonts in the blood vessels of organs and the presence of cysts in the muscles at necropsy will be used for diagnosis (Urquhart et al., 1987).

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Indirect hemagglutination test (IHA) and ELISA test are used for serological diagnosis. In acute form of disease titers of antibodies are not high but 1week to 3 months later will be at diagnostic levels. For certain diagnosis immunohistochemistry, electron microscopy and PCR techniques are available .

Treatment and control
There is no effective treatment for sarcocystosis described in the literature (Urquhart et al., 1987;Radostits et al., 2008;Smith and George, 2009). Treatment of infected calves and sheep with salinomycin (4 mg /kg and 1-2 mg /kg BW; respectively) has been recommended. Amprolium 100 mg /kg, for 30 days reduces the severity of infection Smith and George, 2009).
After beginning nervous system symptoms in sheep, Encephalitic Sarcocystosis recovery has not been observed (Ozmen et al., 2009).
Control of disease is based on protection the food supply of ruminants. Feed bunk should be kept clean, also farm dogs and cats that have access to the feed or pastures should not be fed uncooked meat (Urquhart et al., 1987;Smith and George, 2009).

Etiology
Neosporosis caused by Neospora caninum in cattle, sheep and goats. Neospora caninum is a protozoan parasite of the phylum Apicomplexa in the family Sarcocystidae Matthewa, 2009

Epidemiology
The protozoa Neospora caninum is an important parasite that cause abortion in cattle, sheep and goats (Gumber et al., 2002). The majority of N. caninun-positive cattle prenatally infected via their dams. Transplacental transmission is considered the major route of transmission of N. caninum in cattle (Schares and Conraths, 2007).
In nonfatal infection in the fetus, the fetus is born with neurologic disorder (Smith and George, 2009).
N. caninum has a worldwide distribution, the prevalence of infection in cattle and sheep approaches 100% with a lower ( (Taylor et al., 2007;Radostits et al., 2008).

Pathogenesis
Definitive host: Dogs are the final host and sexual phase occur in them but, they are also intermediate host in prenatal infections (Taylor et al., 2007;Matthews, 2009 (Taylor et al., 2007;Radostits et al., 2008). Neospora caninum is a major cause of abortion in cattle, however, sporadic abortions can occur in beef cows that have been infected congenitally (Dubey et al., 2006;Taylor et al., 2007;Radostits et al., 2008;Matthewa, 2009 ).
Asexual phase has 2 stages: 1. Tachyzoites: Tachyzoites penetrate host cell like central nervous system, muscles, macrophages and other cells, where they divide rapidly. Tachyzoites can also be transmitted either with contaminated food and water or transplacentally to the fetus in pregnant animals. Tissue cyst containing bradyzoites that these are found only in the nervous system. After the asexual phase, sexual phase ocur in definite host. It results in production of oocysts, which is shed in the dog feces. 2. Tissue cysts (Taylor et al., 2007).
Infection in sheep and goats is infrequently .
Neurological symptoms are different because of the widespread distribution of the parasite in the central nervous system. Calves are born with neurological symptoms, which these symptoms initially are mild but after birth become progress. In calves with neurologic dysfunction clinical signs are included of unable to stand, unable to suckle, domed skull and torticollis (Smith and George, 2009).

Diagnosis
The diagnosis of neosporosis is based on the examination of maternal and fetal sera ideally combined with the examination of fetal tissues.
-Immunofluorescent antibody test (IFAT) and indirect enzyme-linked immunosorbent assay (ELISA) are used for diagnosis. -Histopathology of fetus: In histopathological examination of brain characteristic nonsuppurative encephalitis is suggestive of Neospora infection and also the lesions in the heart are characteristic for diagnosis (Gumber et al., 2002;Taylor et al., 2007;Matthews, 2009).

Treatment and control
At present, there is no effective treatment for bovine neosporosis.
Control of abortion in infected cattle depends on saving food and water sources and the grazing environment from feces of any animal. Aborted fetuses and placentas should be removed or incinerated. The feces of dogs should be prevented from contaminating animal foodstuffs.

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Congenitally infected cows are at high risk for abortion thus seropositive animals should be culling from a herd (Taylor et al., 2007;Radostits et al., 2008).

Etiology
Coccidiosis is a protozoan parasitic (genus Eimeria) disease that cause diarrhea in calves, lambs and kids .
There are 12 species of Eimeria in cattle but all of them may not be pathogenic ( Table 5).
The species that identified in sheep and goats is shown in

Bovine coccidiosis
Coccidiosis occurs universally in young animals normally in calves between 3 weeks and 6 months of age and caused important economic losses but also has been reported in cattle aged 1 year or more Ballweber, 2009). The disease occur in animals that kept in crowded and contaminated pens. The prevalence in calves is 46%, in yearling is 43% and in adult cows is 16% . Eimeria zuernii is the most pathogenic species that causing haemorrhagic diarrhoea (Taylor et al., 2007).

Sheep and goats coccidiosis
Coccidiosis in sheep and goats is caused by protozoa of the genus Eimeria. Coccidiosis is one of the most common, important and higher infection rates disease in lambs and kids that kept in small areas contaminated with oocysts . In

Pathogenesis
The pathogenesis of the disease is dependent on the destroy of the crypt cells of the intestinal mucosa because in the ruminant small intestine is very long and providing a high number of host cells and is a potential for parasite replication with minimal damage. Some E. species that invade the large intestin, cause pathological changes, specially when large numbers of oocysts are ingested in a short period of time (Taylor et al., 2007).
In healthy nonimmune animals when number oocysts ingested is low, the animals show no clinical signs of disease but in many oocysts condition, rupture and exfoliation of intestinal cells triggers intestin function and causes loss of blood, fluid, albumin and electrolytes into the intestin. Disaster of mucosal capillaries of intestin can cause to hypoproteinemia and anemia. Secondary bacterial infection may cause severe enteritis (Ballweber, 2009)

Clinical findings
In most clinical cases the temperature is normal or subnormal. Disaster of epithelial cells of intestine cause sometimes bloody diarrhea. Dehydration may occur but anemia occasionally may be seen. In severe infections, diarrhea which may be mucoid or bloody, tenesmus, abdominal pain, anorexia, dehydration and weight loss are the common clinical signs in coccidiosis Ballweber, 2009).
In the calves that infected with high number of oocysts may developed dysentery. Clinical coccidiosis occurs rarely in adult cattle .

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Coccidiosis in lambs is widely similar to that in calves, but dysentery do not usually ocur. In infected kids clinical signs are associated with watery diarrhea, dehydration, anorexia, and weight loss (Ballweber, 2009).

Diagnosis
Diagnosis is based on history, clinical and necropsy findings, and microscopic examination of feces. Acute coccidiosis can be diagnosed by direct examination of feces but in chronic coccidiosis that very low oocysts number are seen in feces, direct examination of feces may not be adequate (Navarre and Pugh, 2002).

Treatment and control
Coccidiostats drugs are used for treatment. All animals in the flock should be treated. Trimetoprim+Sulfadoxine (16-24 mg/kg) can be used for three days by intramuscularly in lambs and kids (Ozmen et al., 2004). Amprolium (10 mg/kg BW) for 5 days or 65 mg/kg BW one dose can be effective in calves . Diclazuril and toltrazuril are also coccidiocidal drugs (Matthews, 2009). Ghanem et al., (2008), suggested that toltrazuril is more effective than sulphadimine and amprolium in E. Bbovis and E. zuernii oocysts shedding in buffalo calves.
Because of the low serum vitamin C levels in lambs with coccidiosis, administration of vitamin C is suggested to be useful combined with the classical treatment .
Hygiene in the house, minimisation of predisposing factors, avoiding the overcrowding of animals in the pens, control of the pastures for parasite are important factors for the control of coccidiosis.

Etiology
Cryptosporidium are protozoan parasite with at least 13 species occuring in mammals, birds, and fish, but only 2 of these species are important in livestock animals (Taylor et al., 2007;Radostits et al., 2008). Cryptosporidium spp. are intracelluler protozoan parasites causing gastrointestinal disease and diarrhea, and they are important infection in young ruminants.
The list of cryptosporium specie is shown in table 8.

Epidemiology
Cryptosporidiosis occur primarily in neonatal calves, but also in lambs and kids . One major species, C. Parvum, infects both farm animals and humans (Jones et al., 1997). Cryptosporidiosis is a fairly prevalent disease in many countries, and the disease is one of the most economically important diseases especially in calves and kids in Turkey (Sevinc, 2004). Calves at 1-15 days are at the highest risk (El-Khodery and Osman, 2008). The higher percentage of oocysts excreted is observed in 7-day-old calves (Feitosa et al., 2008). Animals of all ages can be infected, but diarrhea occur only in young animals (Gunn et al., 2009). In young calves there is a significant relationship between season and infection (El-Khodery and Osman, 2008). Infection peaks occur in spring and autumn (Taylor et al., 2007). Castro-Hermida et al.,(2007), suggested that asymptomatic adult sheep and goats are the source of environmental contamination by C. Parvum.

Pathogenesis
Cryptosporidium parvum infection, cause a malabsorptive diarrhea (Navarre and Pugh, 2002). Cryptosporium life cycle consist of six developmental stages. After ingestion of the oocyt there is excystation, merogony, gametogony, fertilization, oocyst wall formation, and sporogony.In contrast to other protozoal agents, cryptosporidia do not require fecal excretion for sporulation to infective stages, and they sporulate in the intestine (Navarre and Pugh, 2002;Radostits et al., 2008). www.intechopen.com

Clinical findings
Infections that caused by Cryptosporidium andersoni, are usually asymptomatic, although depressed weight gain in calves and milk yields in milking cows have been reported (Taylor et al., 2007).
In Cryptosporidium parvum infections, clinical signs are characterised by anorexia, depression, weight loss, diarrhea, dehydration, high morbidity and possibly death because of dehydration. Cryptosporidium parvum can cause diarrhea in calves 5to15, and in lambs and kids 5to10 days of age (Navarre and Pugh, 2002;Radostits et al., 2008). Relapses of diarrhea are quite common, and Cryptosporidium parvum usually occurs as a component of mixed infections (Navarre and Pugh, 2002).

Diagnosis
Oocysts can be detected using Ziehl-Nielsen stained fecal smears Cryptosporidia can be diagnosed by fecal flotation. A number of molecular and immunological assays are available for diagnosis for example immunofluorescence (IF) or enzyme-linked immunosorbent assays (ELISA) (Taylor et al., 2007).
Cryptosporidiosis is a zoonotic disease, and human can become infected from handling infected animals or feces.

Treatment and control
There is no effective drug for treatment of cryptosporidiosis in ruminants (Navarre and Pugh, 2002).
Halofuginone has efficacy in calves with diarrhea due to Cryptosporidium parvum.
Halofuginone is reported to reduce oocyst shedding and the intensity of diarrhea. Oral dose of 0.1mg / kg BW daily for 7 days can reduce oocyte excretion (Klein, 2008).
Cryptosporidiosis in young animals should be treated with fluid therapy and correction of acid-base disturbance.
The control of disease is based on the minimize transmission between the source of the organism and young animals. During the course of the diarrhea, diarrheic young animals should be isolated from healthy animals . The best control of cryptosporidiosis comes from calves, lambs, and kids getting adequate immunity through colostrum after birth.

Etiology
Giardiasis is the infection caused by the flagellate intestinal protozoan, Giardia intestinalis, which is also known as G. duodenalis, or G. lamblia. Infection occur in a wide range of domestic and wild animals and also humans. G. intestinalis is a potential pathogen in www.intechopen.com livestock, causing diarrhea, weight loss, poor condition and lethargy (Hunter and Thompson, 2005). The parasite is a noninvasive and colonizes the mucosal surface of the small intestine.
The Giardia specie is shown in table 9.

Epidemiology
Giardia intestinalis is an important parasite in domestic ruminants also, in human with high levels of infection. Asymptomatic adult animals may act as healthy transporters and may be a source of environmental contamination and infection for young animals. Infection is commonly exhibited by the animals within 2 weaks of birth (Xiao, 1994). Diarrhea may be transient, but infected animals can continue to shed cysts for long times. Olson et al., (2004) reported a high levels of infection of Giardia in young livestock, specially calves. Giardia occur in both beef and dairy cattle, and studies have demonstrated prevalence rates of 100% (Xiao and Herd, 1994).

Pathogenesis
The pathogenesis of giardiasis is similar to cryptosporidiosis. The parasite cause diffuse injure to the small intestinal mucosal surface. Giardia infection cause a reduction in the height of the villus and microvillus, and loss of the absorptive surface area throughout the small intestine. If disease occur in animals, it is believed to result from nutrient malabsorption and due to diarrhea.

Clinical findings
Clinical signs of giardiasis include acute or chronic diarrhea, dehydration, weight loss, abdominal pain and reduction in weight gain. The diarrhea may be continuous or intermittent.

Diagnosis
Diagnostic methods for introduce of giardia include direct microscopy, fluorescent antibody staining, ELISA, and PCR (Gunn et al., 2009).

Treatment and control
Infected sheep and goats can be treated with fenbendazole (5-10 mg /kg) for 3 days (Navarre and Pugh, 2002). Fenbendazole (10 mg /kg BW daily for 3 days) and albendazole (20 mg /kg BW daily for 3 days), have been shown also to be effective in calves (Thompson, 2004;Radostits et al., 2008). Geurden et al., (2006), demonstrated the efficacy and safety of a 5 day treatment with paromomycin against an experimental Giardia infection in calves. Ozmen et al., (2006), suggested that five day treatment with Trimethoprim + Sulfodoxine and multivitamin complexes can be effective in the prevention and treatment of Giardia intestinalis in lambs and kids.
Re-infection frequently occurs if the sources of contamination are not eliminated and the frequency of transmission is high (Thompson, 2004).

Etiology
Besnoitia are protozoan parasite with classified 7 species, which only 2 of these species are important in livestock animals. Besnoitiosis is a emergent parasitic disease that caused by Besnoitia besnoiti in cattle, and Besnoitia caprae in goats. These parasites are in the family Sarcocystidae , and they are an obligate intracellular apicomplexan protozoan parasites (Majzoub et al., 2010

Epidemiology
Disease occur as outbreaks in tropical and subtropical countries and sporadically in other countries . Bovine besnoitiosis is common in Africa, Asia and in the South of Euroup ( Jacquiet et al., 2010), Caprine besnoitiosis in Kenya, Uganda, Iran, and Kazakhastan. In livestock, cattle and goats are intermediate host, and cats are their definitive hosts . It is thought that agent is transmitted mainly by hematophagous insects (Jacquiet et al., 2010).

Pathogenesis
Following infection in cattle or in goats, the tachyzoites proliferate in macrophages, fibroblasts, and endothelial cells and causing vasculitis. Subsequently they develop to form bradyzoite cysts in fibroblasts in the dermis, subcutaneous tissues, fascia, nasal and laryngeal mucosa (Taylor et al., 2007;Radostits et al., 2008). After developing cysts in the skin, painful subcutaneous swelling, thickening of the skin, alopecia, and necrosis can be occur (Taylor et al., 2007).

Bovine besnoitiosis
Clinical signs occur in two stages: acute and chronic. In acute stage clinical signs include fever, increase in pulse and respiratory rates, painful swelling on the ventral aspects of the body, edema of the skin, sometimes diarrhea, lacrimation and nasal discharge. In chronic stage, there is a severe dermatitis over most of the body .

Caprin besnoitiosis
Thickening of the skin over the lower limbs, around the eyes, nose, face and scrotum, alopecia in all of these areas, and white granular cysts in the sclero-conjunctiva can be seen (Oryan and Azizi, 2008).

Diagnosis
Besnoitiosis can be diagnosed by demonstration of B. bradyzoites in skin biopsy smears or scleral conjunctival scrapings .

Treatment and control
There is no known treatment for this disease (Taylor et al., 2007).
Control is effected by the elimination of infected animals and carriers, and early diagnosis ( Antonio Castillo et al., 2009 ).

Etiology
Toxoplasma gondii is a systemic coccidian, a universal parasite that causes rarely abortion in cattle but is a major abortifacient in sheep and goats Christensen et

Epidemiology
Toxoplasmosis is one of the most common parasitic infections of man and other warmblooded animals in most parts of the world (Hill et al., 2002). The disease is a major cause of ovine abortion in many countries (Christensen et al., 2009). Seroprevalence studies show high rates of infection in farm animals. Major importance of disease in farm animals is its zoonotic potential. Source of infection for sheep, and cattle is the oocyst passed in the feces of the cats. Cats shed oocysts by their feces. Cats infected by ingesting tissues of intermediate hosts .

Pathogenesis
The whole developmental process of Toxoplasma gondi requires two hosts, the definitive host, cat and the intermediate host (all warm blooded animals).

Clinical findings
There are a few reports of clinical toxoplasmosis in cattle associated with fever, dyspnea, nervous signs and abortion (Taylor et al., 2007).Toxoplasma is not significant in bovine abortion . In small ruminants, particularly in sheep clinical signs include fever, abortion, prenatal mortality in lambs, generalized tremor, and dyspnea (Taylor et al., 2007;Radostits et al., 2008).

Diagnosis
Diagnosis is based on the clinical signs, presence of the characteristic small white necrotic foci in cotyledons. ELISA test is also used to detect antibodies in fetal and maternal serum. Indirect fluorescent antibody test can be used for fluid collrcted from the fetal thorax or abdomen. Serological examination of dam can be used for diagnosis (Matthews, 2009).

Treatment and control
Combination of sulfamethazine (SMZ) and pyrimethamine (PMA) can be effective in pregnant ewes. The drugs are effective against the proliferating parasites in the acute stage of the disease . The combined dose of (SMZ) and (PMA) is administered over 3 days for 3 periods, commencing on days 110, 115 and 130 of gestation. SMZ is injected s.c. at an initial dose of 5 ml/ 10kg body wt on the first day of a given treatment priod with subsequent doses of 2.5 ml/10kg on each of the next 2 days. PMA is administered at 2 mg/kg on the first day and at 1mg/kg on the subsequent 2 days of each treatment period (Buxton et al., 1993).
Because the cats are the only definitive host of toxoplasmosis, it should be kept away from animals farm, and also feeding and drinking water should be prevented from contamination by cat feces. Aborted fetus and excreta, must be strictly disinfected.
It is important to reduce the risk for human disease associated with consumption of infected meat .

Etiology
Member of the genus Trypanosoma are lived in the bloodstream and tissues of cattle, sheep, and goats in all of the world. These are flagellated protozoal agents that produce a variety of very serious disease of human and animals, but many of them are nonpathogenic (Carlson, 2009b). Trypanosomosis is one of the most important diseases of animals and human. Most African species are transmitted by the tsetse flies (Taylor et al., 2007).
There are 7 species of Trypanosoma species in cattle, sheep, and goat but all of them may not be pathogenic (Table 12).
The most pathogens species in cattle are T. congolense and T. vivax. T. congolense and T. vivax caused severe disease in cattle, sheep, and goat but T. brucei brucei causes a subclinical infection in cattle, and severe disease in sheep, and goat . Trypanosoma evansi causes surra disease of cattle in India.
In Ethiopia the prevalence of infection in bovine which is caused by by T. species are reported as below: T. vivax 90.5%; T. congolence 4%; and mixed infection of T. vivax and T. congolence 5.5% (Mihret and Mamo, 2007).
T. theileri is nonpathpgeic and reported in Nourth Americabut occasionally occur parasitemia that causes fever, depression, and decreased milk production (Carlson, 2009b).

Pathogenesis
In African Trypanosomosis, after entering through the skin, parasite reach to the bloodstream via the lymphatic system. Infection characterized with parasitemia. Some trypanasoma spp. invade extravascular spaces such as the ocular aqueous humor and cerebral spinal fluid. Some trypanasoma spp. may produce hemolysin that causes anemia in the host. Then, phagocytic activity increased because of the massive erythrocyte failure. .

Clinical findings
Clinical findings are based on the speed of onset of anemia and the grade of organ impairment. Trypanasomosis can be acute, subacute, or chronic. In acute form abortion, drop in milk, depression, anorexia can be seen. Hyperemic mucous membranes and lacrimation also can be occur. In subacute form clinical signs include weight loss, enlargement of lymph nodes and dry hair coat. In chronic form dull, dry hair coat, inelastic skin, lethargy, pale mucous membranes and execise intolerance may be seen  .

Diagnosis
Diagnosis can be based on the clinical findings, presence of vectors, appearance of trypanasomes on a fresh blood smear, or a Giemsa-stained blood smear. Indirect fluorescent antibody test (IFA) and the enzyme-linked immunospecific assay (ELISA) test are used for diagnosis  .

Treatment and control
The most common drugs that is used for treatment of trypanosomosis are shown below. www.intechopen.com