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2. The epidemiology of helminth parasites

2.1 Introduction
2.2 Nematodes of the digestive tract
2.3 Nematodes of the lungs
2.4 Nematodes of other organs and tissues
2.5 Trematodes
2.6 Cestodes
2.7 Protozoa

2.1 Introduction

This section is devoted primarily to the epidemiology of the nematodes (roundworms), trematodes (flukes) and cestodes (tapeworms) of greatest economic importance.

2.2 Nematodes of the digestive tract

2.2.1 Life cycles

The most important and widely prevalent nematodes are the Trichostrongyle group (Haemonchus, Ostertagia, Trichostrongylus, Mecistocirrus, Cooperia and Nematodirus), Oesophagostomum and Bunostomum. The life cycles of most Trichostrongyles, Oesophagostomum and Bunostomum are similar: the cycles are direct, that is these nematodes do not require other animals to complete their life cycles.

FIGURE 2.1 The life cycle of gastro-intestinal nematodes

Adult nematodes inhabit the gastro-intestinal tract. Eggs produced by the female are passed out in the faeces. The eggs embryonate and hatch into first-stage larvae (L1) which in turn moult into second-stage larvae (L2) shedding their protective cuticle in the process. The L2 larvae moult into third-stage larvae (L3), but retain the cuticle from the previous moult. This double-cuticled L3 is the infective stage. The time required for the eggs to develop into infective larvae depends on temperature. Under optimal conditions (high humidity and warm temperature), the developmental process requires about 7 to 10 days. In cooler temperatures the process may be prolonged. Ruminants are infected by ingesting the L3. Most larvae are picked up during grazing and pass to the abomasum, or intestine, ex-sheathing the extra cuticle in the process. The L3 of the Trichostrongyle group penetrate the mucous membrane (in the case of Haemonchus and Trichostrongylus) or enter the gastric glands (Ostertagia). During the next few days the L3 moult to the fourth stage (L4) and remain in the mucous membrane (or in the gastric glands) for about 10 to 14 days. They then emerge and moult into a young adult stage (L5). Most Trichostrongyles mature and start egg production about 3 weeks after infection.

The parasitic part of the life cycle of Oesophagostomum requires about 6 weeks to complete. The infective L3 penetrate the lamina propria of the intestinal wall and the host response to the infection which surrounds the L3 results in the formation of fibrous nodules. The larvae emerge into the lumen of the intestine after about 2 weeks and mature in the following 4 weeks. In animals previously infected, the larvae may spend a prolonged period of time (3-5 months) in the nodules. Eventually many of the larvae will die and the nodules may become calcified.

The L3 larvae of Bunostomum infect ruminants when they are ingested or penetrate the hosts skin. Following skin penetration, the larvae are carried in the venous blood through the heart to the lungs, where they penetrate the alveoli, are coughed up and then swallowed, and so pass to the small intestine. Here they moult and mature 8-9 weeks after infection.

The infective larval stage of Trichuris is contained within the egg. The larva is released after the egg is ingested by the host.

2.2.2 Egg production

2.2.1 Life cycles
2.2.2 Egg production
2.2.3 Development and survival of infective larvae in the environment
2.2.4 Dissemination of infective larvae
2.2.5 Effect of climate on survival and development of infective larvae
2.2.6 Factors affecting the size of gastro-intestinal nematode infections
2.2.7 Pathogenesis of gastro-intestinal nematode infections
2.2.8 Toxocara vitulorum infections

Adult female nematodes produce eggs. The period between the infection of an animal by ingestion of infective L3 larvae and the first egg production by the adult female parasite is called the prepatent period. This period is different for different species of parasites, as shown in Table 2.1.



Prepatent period

Haemonchus placei (cattle)

3-4 weeks

Haemonchus contortus (sheep)

2 weeks

Ostertagia (sheep and cattle)

3 weeks

For most other gastro-intestinal parasites, the prepatent period is about 3-4 weeks.

Different species of nematodes have different egg-producing capacities as shown in Table 2.2. The individual female Cooperia, for example, produces many eggs but is not very pathogenic. Females of Trichostrongylus are quite pathogenic but produce few eggs. This means that the number of nematode eggs in a faecal sample is not an accurate indication of the amount of damage being done by gastro-intestinal parasites.



Daily egg production/female



Ostertagia, Trichostrongylus

100 200





Oesophagostomum, Chabertia


The number of eggs produced by an adult female nematode also depends on the level of immunity the host possesses to the intestinal parasites. In addition, adult female nematodes may increase their egg output around the time the host gives birth (parturition), especially in sheep and goats.

The number of eggs detected in the faeces also depends on the consistency of the faeces. Diarrhoeic faeces often contain lower numbers of eggs per gram than formed faeces, due to the effect of dilution.

In summary, the number of parasite eggs found in the faeces is influenced by:

· number of adult parasites established in the gastro-intestinal tract
· level of host immunity
· age of the host
· species of parasite
· stage of infection
· parturition
· consistency of the faeces.

2.2.3 Development and survival of infective larvae in the environment

The development of larvae in the environment depends Upon warm temperature and adequate moisture. In most tropical and sub-tropical countries, temperatures are permanently favourable for larval development in the environment. Exceptions to this are the highland and mountainous regions throughout the world, and the winters of southern Africa and Latin America where temperatures may fall below those favourable for the development of Haemonchus larvae.

The ideal temperature for larval development of many species in the microclimate of the tuft of grass or vegetation is between 22 and 26 °C. Some parasite species will continue to develop at temperatures as low as 5 °C, but at a much slower rate. Development can also occur at higher temperatures, even over 30 °C, but larval mortality is high at these temperatures.

The ideal humidity for larval development in this microclimate is 100%; the minimum humidity required for development is about 85%.

The survival of larvae in the environment depends upon adequate moisture and shade. Desiccation from lack of rainfall kills eggs and larvae rapidly and is the most lethal of all climatic factors. Larvae may be protected from desiccation for a time by the crust of the faecal pat in which they lie or by migrating into the soil. Infective larvae may survive for up to 6 weeks or even longer in the manure pats, which act as a reservoir of infections during dry periods. The development of infective larvae ingested by an animal during adverse environmental conditions may be temporarily arrested in the abomasal or intestinal mucosa. This suspension of development helps some nematode parasites survive the dry seasons. Of the three larval stages in the environment (L1, L2, and L3) it is the L3 which has a protective sheath, that is the most resistant to variations in moisture, temperature and sunlight.

2.2.4 Dissemination of infective larvae

The parasite's eggs develop into third-stage, infective larvae L3 in faecal material. To make themselves accessible to ingestion by ruminants, the larvae have to migrate or be transported from the faeces in which they were deposited on the ground to any nearby herbage. Such movement occurs in two ways: horizontal migration/transport and vertical migration/transport.

FIGURE 2.2 Survival and dissemination of larvae on pasture

The horizontal distance L3 will actively migrate does not usually exceed 5-10 cm. Suitable conditions for larval migration occur when rainfall or moisture disintegrates the crust of faecal material and larvae in this material are washed onto herbage. Invertebrates such as dung beetles may also play a role in the transport of larvae onto herbage. Once on the herbage, infective larvae migrate up and down blades of grass according to the amount of moisture on the grass. During rainfall and when dew is on the grass, larvae may migrate to the top of the herbage.

Following evaporation, the larvae migrate to the base of the herbage and even down into the soil. Heavy rain may wash larvae off the herbage and onto the ground. Larvae in water pools may infect drinking animals.

2.2.5 Effect of climate on survival and development of infective larvae

The development and survival pattern of infective larvae in the environment differs according to the climate. Three broad types of climate are found in tropical and sub-tropical regions:

· humid tropical climate
· savannah-type tropical and sub-tropical climate with a long dry season
· arid tropical and sub-tropical climate

The humid tropical climate characterizes much of West Africa as well as the regions surrounding Lake Victoria and parts of coastal eastern Africa. It is also the climate of much of southeastern Asia, central America and northern South America. This climate provides a more or less permanently favourable environment for the survival and development of parasitic larvae.

The savannah type tropical, sub-tropical and temperate climate with a long dry season is found in much of eastern, central and southern Africa, much of South America, and areas of western, central and eastern Asia. As the dry season progresses, the environment for larval development and survival changes from unfavourable to hostile, with populations of surviving larvae declining rapidly in open pastures and more slowly in wooded areas where ample shade is available. At the start of the rains, of course, this unfavourable environment is transformed rapidly into a favourable one for the larvae.

Arid tropical and sub-tropical climates characterize parts of western Asia, lowland Ethiopia, parts of Somalia and Sudan and much of northern Africa and the Sahel. This climate, with its sparse vegetation cover, is often permanently unfavourable for parasitic larval survival. Where vegetation exists, however, short periods of rainfall or irrigation can transform the environment rapidly into a favourable one for the nematode larvae, particularly the highly pathogenic Haemonchus.

2.2.6 Factors affecting the size of gastro-intestinal nematode infections

The size of any gastro-intestinal nematode infection depends on the following five main factors:

· The number of infective larvae L3 ingested by the host, which in turn is influenced by the climate, the amount of protection of larvae provided by vegetation, the livestock density and the grazing pattern of the ruminants present.

· The rate at which acquired resistance develops in the host, which is influenced by the species of the parasite and host, genetic factors, nutrition and physiological stress (e.g., parturition).

· The intrinsic multiplication rates of the species of parasites present which are controlled by the fecundity, pre-patent period and environmental development and survival rates of these species.

· Management, particularly grazing patterns.

· Use of anthelmintics, including the timing and frequency of administration.

2.2.7 Pathogenesis of gastro-intestinal nematode infections Effect of larval stages on the host Effect of adult worms on the host Effect of larval stages on the host

Considerable damage is caused by fourth-stage larvae (L4) of abomasal parasites (Haemonchus, Mecistocirrus, Ostertagia and T. axei). The L3 enter the mucous membrane or the glands in the wall of the abomasum within six hours of entering the host, and will usually stay in the mucous membrane or the glands for about two to three weeks. If large numbers of Haemonchus, Ostertagia and T. axei larvae enter the abomasum, the host will be affected by:

· reduced appetite
· reduced digestive capability of the abomasum

The larvae of Trichostrongylus in the small intestine may cause severe damage to the intestinal mucous membrane with similar effects. Under certain circumstances, larvae ingested at the end of a rainy season (in savannah-type climates) may remain inhibited in the abomasal wall during the dry season until the next rainy season or until the animal experiences stress, such as that produced when the animal is calving/lambing or sick. The inhibition will then cease, and the (L4) will develop into an adult worm. This development may be accompanied by destruction of the mucous membrane, the extent of which depends on the numbers of inhibited larvae emerging.

The (L4) of Haemonchus is a blood sucker in the abomasum. Animals infected with large numbers of larvae therefore may suffer from anaemia before the parasite eggs can be detected in the animal's faeces. Effect of adult worms on the host

Infections with gastro-intestinal nematodes usually involve several different species of parasites, which may have an additive pathogenic effect on the host.

Mixed infections comprising any of the species Haemonchus, Mecistocirrus, Ostertagia, Trichostrongylus, Bunostomum, Cooperia, Nematodirus, Oesophagostomum and Trichuris are common. The pathogenic effect of gastro-intestinal parasites may be sub-clinical or clinical. Young animals are most susceptible. The effect of these parasites is strongly dependent on the number of parasites and the nutritional status of the animals they are infecting. The following clinical signs may be seen:

· weight loss
· reduced feed intake
· diarrhoea
· mortality
· reduced carcass quality
· reduced wool production/quality

Severe blood and protein loss into the abomasum and intestine due to damage caused by the parasites often results in oedema in the submandibular region (a condition called bottle jaw). Some nematode species, especially those that suck blood, such as Haemonchus, Bunostomum and Oesophagostomum, are responsible for specific clinical signs. Haemonchus is the most pathogenic of the blood suckers and infections with large numbers of this parasite often result in severe anaemia in the host. Diarrhoea may not be a feature of Haemonchus infections. Blood losses from Bunostomum and Oesophagostomum infections may add to the severity of the anaemia.

2.2.8 Toxocara vitulorum infections Life cycle Pathogenicity of Toxocara infections

Although Toxocara vitulorum is an intestinal nematode, the life cycle and the epidemiology of this parasite is markedly different from that of the Trichostrongyle group described on the previous pages.

Toxocara vitulorum is a large ascarid-type parasite (20-30 cm) which has a world-wide distribution. The prevalence is, however, much higher in the tropics and it causes severe problems in young calves (cattle, buffalo) in Southeast Asia and parts of Africa. Life cycle

The life cycle is direct with possible prenatal infection and with neonatal infection through colostrum being the major route of infection for calves in Southeast Asia. The adult parasites which live in the small intestines are prolific egg producers and a very large number of eggs are produced every day. The thick-walled eggs are very resistant to adverse climatic and environmental conditions and may remain infective for a long period of time (several years).

Only if the infective eggs are ingested by young calves will the life cycle be completed. The Toxocara larvae penetrate the intestinal wall and migrate via the circulatory system to the liver and lungs where they enter the respiratory system. The larvae are coughed up and swallowed, returning to the small intestine where they mature and start egg production 3-5 weeks after infection.

If the infective eggs are ingested by older calves (more than 4 months of age) that possess immunity, the majority or all of the larvae that undergo somatic migration become arrested in organs and tissues. During pregnancy these larvae become reactivated and prenatal infection of the foetus is possible, but the majority of larvae are concentrated in the udder and new-born calves are usually infected through colostrum and milk. Following infection via this route, the larvae do not migrate in the hosts, but remain in the small intestine. This reduces the length of the prepatent period and eggs may be present in faeces 18-21 days after infection.

Whereas transmission through colostrum and milk is the major route of infection of calves in Southeast Asia, studies in the southern part of Africa have indicated that the ingestion of infective eggs from the environment is the most common route of infection there.

It is recommended that the local epidemiology of this parasite should be established for most efficient control. Pathogenicity of Toxocara infections

Migrating larvae may cause damage to the liver and lungs. The presence of the adult parasites in the small intestine is often associated with diarrhoea and reduced weight gain. In untreated cases and heavy infections, the mortality rate may be up to 35-40 percent of infected animals, and it is believed to be the most serious disease of buffalo calves in Southeast Asia. The parasites are expelled by 5 months of age.

2.3 Nematodes of the lungs

2.3.1 Introduction
2.3.2 Life cycles
2.3.3 Development and survival of infective larvae
2.3.4 Pathogenic effect
2.3.5 Factors influencing the epidemiology of lungworm infections

2.3.1 Introduction

Lungworms are widely distributed throughout the world but are particularly common in countries with temperate climates, and in the highlands of tropical and sub-tropical countries. The species of importance in ruminants belongs to two different families; the Dictyocaulidae and the Metastrongylidae. The Dictyocaulidae include Dictyocaulus viviparus in cattle and buffaloes, and Dictyocaulus filaria in sheep and goats. These worms are 5-10 cm long and live in the trachea and bronchi. The Metastrongylidae are represented by at least three species in small ruminants. Protostrongylus rufescens a small worm (1.5-3.5 cm) found in the bronchioles, Muellerius capillaris (1.2-2.5 cm) which are located in the alveoli, and Cystocaulus ocreatus (2-5 cm) found in the terminal bronchioles.

An infection of the lower respiratory tract by any of these nematode species may result in bronchitis or pneumonia, or both.

2.3.2 Life cycles

The Dictyocaulus species have a direct life cycle and the behavior of the free-living stages is similar to that described for the trichostrongyles of the digestive tract (see section 2.2.1). The infective larvae are ingested by the final host during grazing and the larvae migrate from the intestine to the lungs via the lymphatic system and the pulmonary blood supply. They emerge from the pulmonary capillaries and enter the alveoli, migrating to the bronchi and trachea where they mature. The prepatent period is approximately 4 weeks for D. viviparus and 5 weeks for D. filaria.

The Metastrongylus species have indirect life cycles that require a land snail as an intermediate host. The first stage larvae (L1) which are passed in the faeces infect snails by penetrating the foot of the snail, or by being ingested. The development of infective larvae in the snails takes approximately 2 weeks. The final host is infected by accidentally ingesting snails with their food. The released larvae migrate from the intestine to the lungs via the lymphatic system, similar to the route of the Dictyocaulus species. The prepatent period is 6-7 weeks.

2.3.3 Development and survival of infective larvae

Eggs laid by the female worms hatch quickly and the L1 larvae are coughed up, swallowed and appear in faeces.

For the Dictyocaulus species, the development into third stage larvae L3 takes a minimum of 5-7 days, but it may take longer depending on the ambient temperature and humidity. The Dictyocaulus larvae are generally more susceptible to adverse environmental conditions than are the larvae of the gastro-intestinal nematodes. Desiccation rapidly kills the larvae whereas moderate temperatures and high humidity will enhance their survival.

The L1 Metastrongylus larvae are fairly resistant to drying and the stages in the snails are well protected during adverse conditions. The infective larvae probably survive in the snails for as long as the snails live and for up to a week after the death of the snail.

2.3.4 Pathogenic effect

The pathogenic effect of lungworms depends on their location within the respiratory tract, the number of infective larvae ingested and the immune status of the animal.

During the early stages of a Dictyocaulus infection (the prepatent phase) the small bronchioles are blocked by exudate, which obstructs the airways, and this may result in the collapse of the lung tissue distal to the blockage. The adult nematodes (the patent phase) in the bronchi cause a bronchitis. Emphysema, pulmonary oedema and secondary infections are common complications in severe cases. After 2-3 months all or most of the adult worms are expelled.

The pathogenic mechanisms of the other lungworm species (Muellerius and Protostrongylus) is similar but they rarely produce serious effects. This may in part be due to their more restricted localization in the lungs. The formation of granulomas seems to be the predominant reaction following the infection with Muellerius and they are often found subpleurally in the caudal lung lobes.

Following infection, most animals develop varying degrees of immunity, but in the absence of reinfection the immunity may decrease, rendering the animal susceptible again.

The clinical signs of lungworm infection may range from moderate coughing, exacerbated during stress, to severe persistent coughing with marked increase in respiratory rates accompanied by respiratory distress. Animals may lower their head and stretch it forward. Severe infections in cattle are often accompanied by production losses.

2.3.5 Factors influencing the epidemiology of lungworm infections

The transmission and maintenance of these infections from year to year is dependent on some infected animals harbouring small numbers of adult lungworms for several months and thus serving as carriers. The carrier animals continue to contaminate the pastures, and the infection cycle is maintained in the population at risk. As a result, the number of infective larvae on pasture may reach levels that cause outbreaks of clinical disease. Larvae of some lungworm species may become inhibited in the lung tissue during periods of adverse climatic conditions (such as a dry season) and then mature at the beginning of the rainy season.

2.4 Nematodes of other organs and tissues

2.4.1 Filarial nematodes
2.4.2 Nematodes of the eye

2.4.1 Filarial nematodes Life cycles Pathogenicity of filarial nematode infections

The economic importance of filarial nematodes varies according to the species. The distribution and impact of these parasites is dependent on the availability of the intermediate hosts (various insect species).

The filarial nematodes which may cause disease and loss of productivity in ruminants, belong to the genera Stephanofilaria, Onchocerca, Parafilaria and Setaria. Life cycles

The life cycles of these parasites are similar to each other and are indirect, requiring insects as intermediate host for development and transmission. Stephanofilaria

The adult parasites live in the skin, where they cause an inflammation. Small papules develop and these coalesce to form larger crusty lesions. The female parasites produce microfilaria (first stage larvae) which remain with the adult parasites in the skin lesions. Several dipteran fly species act as intermediate hosts, with certain species predominating in a given geographical area. Adult flies ingest the microfilaria when they feed on the open lesions caused by the nematodes. Development into the third stage infective larvae occurs in the fly and takes from 10 to 25 days. The fly can then transmit Stephanofilaria to a new host. Onchocerca

These parasites are found in the connective tissue of their hosts. Their presence often results in the formation of hard nodules in which the nematode is coiled up. The location of the nodules in the host varies according to the species of Onchocerca and may be found in intra-muscular and subcutaneous connective tissue (Onchocerca dukei), in ligaments (Onchocerca gutturosa), intradermally (Onchocerca dermata and Onchocerca ochengi) and in the aorta (Onchocerca armillata). The parasites produce microfilaria which circulate in the blood stream. The microfilaria are picked up by biting insects (midges, black flies and others) and develop into infective third stage larvae. These are transmitted when the insect feeds on a new host.

FIGURE 2.3 Life if cycle of Onchocerca gutturosa Parafilaria

The adult parasites are located in subcutaneous nodules which are found primarily in the shoulder region and other dorsal areas of the body. When the female nematode invades the skin to lay eggs, it causes an inflammatory response and the nodules become enlarged. The penetration of the skin results in bleeding and these sites are known as bleeding points. Various species of dipteran flies become infected when they feed on the blood. The development into the infective third stage larvae takes 2-3 weeks in the fly. Transmission occurs when the flies feed on wounds. The maturation of the parasite in the final host may last 8-10 months. Setaria

These worms are commonly found in the peritoneal cavity of ruminants. They are 6-15 cm long. The microfilaria produced by the female circulate in the blood and are ingested by biting insects. Several species of mosquitoes and flies serve as intermediate hosts. Pathogenicity of filarial nematode infections

Although the prevalence of infections with these parasites may be high in some areas they usually only cause minor losses, with a few exceptions. In certain localized regions, Parafilaria species cause considerable losses at slaughter that result from the trimming of affected parts of the carcass. The major pathogenic effect of Setaria species occurs when the larvae accidentally migrate in the central nervous system of abnormal hosts, such as sheep and goats. The condition is known as endemic cerebrospinal nematodiasis and it is quite common in parts of Asia.

2.4.2 Nematodes of the eye Life cycle Pathogenicity of eyeworms

Thelazia species are common parasites of the conjunctival sac or lacrimal duct of cattle, buffaloes, sheep and goats. These worms are cosmopolitan in their distribution. Life cycle

The life cycle is indirect and several dipteran flies act as intermediate hosts. The flies become infected when feeding on lacrimal secretions which contains eggs or larvae. Development of the infective stage in the fly takes from 2 to 4 weeks. When the flies feed in the eye region of a host, infective larvae may be released into the eye. The transmission is seasonal in some areas, following the seasonal variation in the abundance of fly populations. Pathogenicity of eyeworms

These infections are common, but the majority of infections have no pathogenic effect on the host, apart from stimulating increased lacrimation from infected eyes. However, disease can occasionally occur in infected animals and an inflammatory reaction can be observed. In severe cases the cornea becomes cloudy, and the eye is swollen and covered with pus. Infections can be treated by injecting 2 ml of levamisole into the subconjunctival sac or by the use of eye ointments containing 4 % morantel tartrate or 1% levamisole.

2.5 Trematodes

2.5.1 Introduction
2.5.2 Trematodes of the liver
2.5.3 Gastro-intestinal trematodes
2.5.4 Pancreatic trematodes
2.5.5 Schistosomes (blood trematodes)

2.5.1 Introduction

All the trematode species which are parasitic in livestock belong to the subclass Digenea. In general, these trematodes (known commonly as flukes) are dorso-ventrally flattened, some being leaf-shaped and some long and narrow; the gastro-intestinal flukes have thick fleshy bodies. The schistosomes, which also belong to this group, are elongated and almost roundworm-like in appearance. The flukes that parasitize livestock are hermaphrodites (except the schistosomes) but they have the ability to reproduce asexually and multiply in aquatic or amphibious snails, which they require as intermediate hosts in order to complete their life cycles. Most flukes are very discriminating in their choice of snail as intermediate host and the geographic distribution of trematode species is dependent on the distribution of suitable species of snails.

This section describes the ecology and epidemiology of the flukes of greatest economic importance.

2.5.2 Trematodes of the liver Fasciola hepatica and Fasciola gigantica Dicrocoelium dendriticum

Fasciola hepatica is leaf-shaped and may reach a size of 30 x 30 mm. It occurs in the bile ducts of a large number of ruminants, equines, pigs, rabbits and other animals and is cosmopolitan in its distribution. Fasciola gigantica resembles F. hepatica but is easily distinguished by its characteristic shape and larger size. It is common in Africa, the Indian sub-continent, Central and Southeast Asia, and other sub-tropical and tropical areas of the world. Mixed infections with the two flukes may occur.

Dicrocoelium dendriticum is a small fluke, 6-10 mm long and 1-3 mm wide. It has an elongated lances-like body and inhabits the bile ducts of livestock and rodents. It occurs in Asia, North Africa, Europe, North America and rarely in South America. Fasciola hepatica and Fasciola gigantica Life cycles

Fasciola hepatica and F. gigantica have similar life cycles. The adult flukes inhabit the bile ducts of the final host (cattle, buffaloes, sheep, goats). The hermaphroditic parasite produces eggs which are expelled with the bile into the intestine and shed in the faeces. The eggs embryonate and hatch in water or wet pastures, releasing a free-swimming miracidium. The ciliated miracidia actively seek and penetrate suitable intermediate hosts and undergo several stages of development by asexual multiplication. Five to seven weeks after infection of the snail the tadpole-like motile cercariae emerge from the snail and swim until they make contact with herbage. They then encyst on blades of grass close to streams or in low-lying damp pasture areas. Infection of the final host occurs by ingestion of herbage contaminated with the encysted metacercariae. After ingestion, the young flukes are released from the cysts in the small intestine. They penetrate the intestinal wall and migrate through the abdominal cavity and the liver capsule into the liver parenchyma. Following the penetration of the capsule the immature flukes migrate through the liver tissues for about 6-8 weeks and then enter the bile ducts where they mature and commence egg production.

FIGURE 2.4 Life cycle of Fasciola gigantica Life cycle of the intermediate snail host

The important Lymnaea species of snails involved in the transmission of fascioliasis vary in their geographical distribution in the world. The habitat requirements of the intermediate hosts of the two most important liver flukes differs slightly. The intermediate hosts for F. hepatica are amphibious snails that live close to the edge of slow moving or stagnant water whereas those transmitting F. gigantica live in deeper water and are close to being true aquatic snails in their behaviour. They can, however, adapt to an amphibious existence in adverse conditions. The optimum temperature range for development of the snail is 15-26 °C, when rapid production of snail egg masses occurs. These eggs hatch within two weeks and the resulting snails mature a month later. Thus one snail can produce several thousand descendants within a period of 10-12 weeks. No development and no reproductive activity takes place at temperatures below 10 °C, but snails may survive adverse conditions for months buried in the mud. Egg production

The prepatent period for F. hepatica is about 8-12 weeks and 10-14 weeks for F. gigantica.

The egg-producing capacity of the liver flukes is very high and each fluke may produce 5,000-20,000 eggs per day throughout its life. The factors which influence the egg production of Fasciola species are not well understood, but include the level of nutrition of the parasites in the bile ducts, and this can be influenced by crowding of flukes and reduced blood intake when bile ducts calcify in cattle. The eggs are carried through the bile to the gall-bladder, which may serve as a reservoir of eggs for a considerable time. Eggs are expelled from the gall-bladder when it contracts during digestion, and large numbers of eggs are released during these contractions. This means that the number of liver fluke eggs in a faecal sample is not an accurate indication of the number of parasites in the liver, nor of the amount of damage being done to the host.

The factors which influence the number of parasite eggs in faeces are similar to those listed for nematodes (see section 2.2.2). Development and survival of eggs and miracidia

Light is essential for the embryonation and hatching of eggs and this process does not take place while the eggs are in the faecal mass. For development to start the eggs need to be washed out of the manure by rain or surrounding water. Eggs are rapidly killed by desiccation, but they may survive for months in moist faeces; manure pats may thus act as a reservoir of the infection for a considerable length of time. The embryonation of eggs also depends on suitable temperatures and the availability of oxygen. In most tropical and sub-tropical countries, temperatures are permanently favourable for the embryonation and hatching of the eggs and larvae. Exceptions to this are some highland and mountainous areas.

The time taken for development to be completed is temperature-dependent; this is about 6 weeks at 15 °C and 10 days at 22 °C. The ideal temperature for development is between 20 and 25 °C. At temperatures above 25 °C (up to approximately 35 °C) development takes place at an ever increasing speed but the mortality rate of embryos will increase at higher temperatures. No development takes place below 10 °C.

The miracidia do not survive for more than approximately 24 hours following their release from the egg and their survival depends on locating a snail within this period. The swimming pattern of the miracidia is guided by numerous factors including phototaxis and chemotaxis. When a snail is located the miracidia penetrate the snail. Development and survival of larvae in the intermediate host

Following penetration of the snail, the miracidia transform into sporocysts; through several stages of development and asexual multiplication, one miracidium may produce 600-4,000 cercariae. The development in the snail is temperature-dependent and at optimum temperatures cercariae may be shed from the snail as early as 5 weeks after infection. At lower temperatures the development rate slows down and at temperatures below 10 °C no development takes place. The larval stages may survive in the snails for several months and this is often the mechanism for persistence of the infection from season to season. Development and survival of the metacercariae

Survival of the motile cercariae emerging from the snail depends on their ability to locate a suitable object on which to encyst within 1 hour. When contact is made with blades of grass the cercariae lose their tails and encyst, becoming metacercariae. These are the infective stages to the final host. The metacercariae are relatively resistant to unfavourable climatic conditions and may survive for as long as a year under conditions of high humidity and moderate temperatures. Many die during prolonged periods of drought, freezing or very high temperatures. Infection of the final host

Infection of the final host occurs by ingestion of encysted metacercariae on herbage, or less commonly by ingestion of suspended metacercariae in drinking water. Once ingested, the young flukes encyst in the small intestine, penetrate the gut wall and traverse the abdominal cavity to reach the liver capsule and the liver tissue. The immature flukes migrate in the liver parenchyma for 6-8 weeks before entering a bile duct where they mature and commence egg production. Pathogenicity of liver fluke infections

Fascioliasis in ruminants ranges in severity from a devastating highly fatal disease in sheep to an asymptomatic infection in cattle. The severity of pathological manifestations usually depends on the number of metacercariae ingested over a period of time and the relative susceptibility of the animal. In sheep, acute fascioliasis occurs seasonally and is manifest by anaemia and sudden death. Deaths can occur within 6 weeks of infection. Cases of chronic fascioliasis occur in all seasons and the clinical signs may include anaemia, reduced weight gain, decreased milk production, unthriftiness, submandibular oedema and possibly death in sheep. In contrast, even heavily infected cattle may show no obvious clinical signs, but some production losses may be evident.

Under natural conditions there is little evidence of any acquired immunity to fascioliasis in sheep and the effect of additional infections is additive as far as pathogenicity is concerned. This is evident at post-mortem examination where a succession of developmental stages may be found. Cattle seem to be less susceptible than sheep, and following the first infection immunity develops, reducing the migration of immature flukes in subsequent infections. The development of fibrosis of the liver, the calcification of the bile ducts and acquired immunity may be responsible for the elimination of the infection which occurs in some animals. Effect of immature flukes on the host

The migration through the intestinal wall appears to be non-damaging to the host but the penetration of the liver capsule by a large number of young flukes results in an inflammatory response of the capsule (peri-hepatitis). The subsequent simultaneous migration of many immature flukes through the liver parenchyma causes severe destruction of liver tissue, especially during the last 2-3 weeks before they enter the bile ducts. This may result in bleeding into the abdominal cavity which can be severe enough to cause sudden death of the animal (acute fascioliasis). With smaller numbers of migrating immature flukes, the liver damage may be considerably less and clinical signs may even be absent. During the reparatory phase following fluke migration, the liver tissue may show varying degrees of fibrosis. Effect of adult flukes on the host

After 6-8 weeks of migration in the liver tissue the young flukes enter the bile ducts. Their blood sucking activities irritate the lining of the ducts, resulting in an inflammatory response and the associated blood loss results in anaemia. Considerable thickening of the bile duct walls occurs with the result that these protrude markedly from the surface of the liver. In cattle the ducts often become calcified giving rise to the name "pipe-stem liver". The inflammatory effect is not limited to the bile ducts. Irritation of the ducts and obstruction of the bile flow may cause severe fibrosis of the liver. Seasonal transmission and epidemiological patterns

Moisture is the critical factor determining the presence and extent of snail habitats, which serve as transmission foci for liver flukes. Temperature is an important factor affecting the rate of development of snails and of the stages of the parasite outside the final host. The interaction between moisture and temperature determines the survival and reproduction rate of the snails and the parasites.

The liver flukes have a versatile survival strategy; certain stages of the parasites and their intermediate hosts have a relatively well-developed ability to persist through adverse weather conditions such as drought and freezing. Thus persistence of infection from one season to the next may occur by several mechanisms: as adult flukes in mammalian hosts, as eggs on pasture, as larvae developing in snails and as metacercariae encysted on herbage. Dicrocoelium dendriticum Life cycle

The life cycle is unusual for flukes in that this parasite does not require an aquatic environment at any stage in the development. The adult flukes live in the bile ducts and eggs are passed in the faeces. The eggs are small, operculated, dark brown and typically flattened on one side. Two intermediate hosts, a terrestrial snail and an ant, are required for the completion of the cycle. The eggs are ingested by the first intermediate host, the snail, when it feeds on manure. A miracidium hatches out which undergoes asexual multiplication and further development in the snail. Cercariae are released from the snail and different species of ants eat these. Metacercariae are formed in the ant and the final host is infected by accidentally ingesting the infected ants. After excysting in the gut of the final host young immature flukes enter the liver via the main bile ducts and mature in the smaller bile ducts. Development and survival of larvae in the intermediate hosts

Miracidia hatch out in the snail after it has ingested embryonated eggs. The miracidia migrate in the snail and transform into sporocysts, the first stage of asexual multiplication. Numerous cercariae develop from a single miracidium. The cercariae emerge from the snails clumped together in masses called "slime-balls", in which several hundred cercariae are held together by a sticky material which adheres to the vegetation. The slime-balls are ingested by ants, and metacercariae develop in the abdominal cavity of the ants. Some of these may enter the central nervous system of the ant resulting in behavioural changes. These changes render the infected ants more susceptible to ingestion by grazing animals. The rate of development in the snail is usually slow, and lasts 3 months or more. Pathogenicity of Dicrocoeleum dendriticum

The young flukes migrate directly up the biliary duct system of the liver. There is no penetration of the gut wall or the liver capsule as in Fasciola and no migration in the liver tissue. The effect on the liver depends on the number of flukes and the duration of the infection. Massive long-lasting infections may cause hypertrophy of the bile ducts and progressive fibrosis of the liver. Clinical signs and loss of production are rare in cattle; however, older sheep may suffer reduced milk production and loss of weight. Sheep production can be unprofitable in areas with a high prevalence of the infection. Factors affecting the epidemiological pattern

The eggs of D. dendriticum are relatively resistant and may survive for months in soil and faeces. In addition the intermediate hosts are not restricted to aquatic environments and both snails and ants may be widely distributed over pastures. The infection is often maintained in wildlife, which may serve as a source of infection to livestock.

2.5.3 Gastro-intestinal trematodes Life cycles Pathogenicity of paramphistomes Factors affecting the epidemiological pattern

A large number of gastro-intestinal trematode species (paramphistomes) have been described. They are usually thick, short (4-12 mm), fleshy, maggot-like worms. They may infect all ruminants but young calves and lambs are the most susceptible. The infections are very common in Africa, Asia, Oceania, Eastern Europe, Russia and some of the Mediterranean countries. Not all the species are pathogenic, but clinical outbreaks of paramphistomiasis have been caused by Paramphistomum microbothrium (Africa), Cotylophoron cotylophorum (Asia), P. ichikawar, C. calicophorum (Australasia) and P. cervi (Europe). Life cycles

Paramphistomes require an aquatic snail as an intermediate host and the pre-parasitic stages of the life cycle (miracidia and stages in the snail) are very similar to those of F. hepatica and F. gigantica described earlier.

The metacercariae encysted on the herbage are ingested and young flukes are released in the duodenum of the final host. They attach to - or invade - the duodenal mucosa, usually in the proximal 3 m of the gut. The immature flukes re-emerge/detach from the mucosa 10-30 days after initial infection and migrate towards the rumen and reticulum, where they attach to the mucosa and mature into egg-producing adult parasites. The pre-patent period is reported to vary from approximately 56 days in cattle to around 70 days in sheep and goats. The parasites appear as reddish/pink clusters between the papillae of the rumen and reticulum. Adult paramphistomes may survive for many years in the rumen of the host. Pathogenicity of paramphistomes Effect of larval stages on the host

The size of the paramphistome burden is the most important factor determining the degree of small intestinal damage and the possible clinical effects. The immature flukes may be responsible for severe damage while embedding in and penetrating the mucosa. This causes bleeding and necrosis in the gut wall. If present in sufficient numbers the damage may be responsible for clinical signs. Affected animals are listless, with reduced appetite and increased thirst. A profuse foetid diarrhoea develops which may be accompanied by anaemia, oedema and emaciation. Severe cases lead to death in a few days, especially in young calves and lambs. Effect of adult flukes on the host

Little if any pathogenic effect is associated with the presence of the adult flukes in the rumen and/or reticulum, even though large numbers may be present. Localized destruction of rumen papillae may be seen, but this appears to have no measurable effect on the host.

Two species of the genus Explanatum (Gigantocotyle) develop to maturity in the bile ducts and cause severe fibrosis. Factors affecting the epidemiological pattern

The infection of cattle, sheep and goats with paramphistomes is very common. These parasites may survive for years, so there is a virtually constant source of infection for successive generations of snails. The intermediate hosts (snails of the genus Planorbidae and for some species Lymnaeidae) are extremely adaptable and prolific breeders, which ensures a widespread availability of the snails within infested areas. Massive asexual multiplication of the parasites in infected snails and the survival of snails for several months may result in the shedding of large numbers of cercariae. Infected snails may also survive in mud for months.

Clinical outbreaks of paramphistomiasis are usually confined to the drier months. During this period, the snail population becomes concentrated around natural sources of water and as these areas may provide the only dry season grazing, animals may become heavily infected. Older animals, especially cattle, seem to acquire immunity to the infection.

2.5.4 Pancreatic trematodes Life cycles Pathogenic effect

Several Eurytrema species have been found in the pancreatic ducts of sheep, goats, cattle and buffaloes in eastern Asia and Brazil. Their length varies from 8-16 mm. Life cycles

The pancreatic flukes have two intermediate hosts. The eggs are passed in the faeces and ingested by different species of land snails. A miracidium is released and asexual multiplication and development takes place in the snails. Cercariae are released onto herbage where they are ingested by second intermediate hosts, grasshoppers and crickets. The final hosts become infected accidentally by ingesting the infected insects. Immature flukes migrate from the small intestine to the pancreas via the pancreatic ducts. The prepatent period is 80-100 days. Pathogenic effect

The presence of flukes in the pancreatic ducts cause an inflammation and destruction of the ducts. The severity varies according to the number of parasites. In cases of massive infestations, severe fibrosis of the pancreas occurs resulting in atrophy of the organ. Reduced weight gain or weight loss are usually the only clinical signs observed.

2.5.5 Schistosomes (blood trematodes) Life cycle Pathogenic effect Factors affecting the epidemiological pattern Nasal schistosomes

Schistosomes are elongate, sexually differentiated (an exception among the trematodes) flukes which live in the circulatory system of their hosts. The flattened male carries the female in a special ventral groove. The males are 4-22 mm and the females from 12-28 mm in length. Several different species exist. These include Schistosoma bovis in central, eastern and west Africa, the Mediterranean area and the Middle East; S. mattheei in central, southern and eastern Africa; S. intercalatum in central Africa; and S. japonicum in the Far East (a species infecting humans but which may also cause schistosomiasis in ruminants and other host species). S. nasalis is found in the veins of the nasal mucosa of livestock in the Indian subcontinent. Infection rates of 40-50% have been reported in buffaloes and cattle. It will be described in section Life cycle

Like many of the other trematodes, Schistosomes require an aquatic or amphibious snail as an intermediate host in order to complete their life cycle. The adult parasites live in the mesenteric veins of the final host. During the period of egg-laying, the female parasite enters the small vessels of the gut wall. The eggs, which have a sharp spine, penetrate the wall, enter the intestinal lumen and are passed out in the faeces. Different snail species act as intermediate hosts. The development in the snail is similar to that of other trematodes. The infective forms released from the snails are free-swimming, fork-tailed cercariae. Infection of the final host takes place when the animal is drinking from a contaminated water source. Infection occurs either via skin penetration by the parasite, or by penetration of the digestive tract after ingestion of cercariae with the water. The immature flukes migrate through the lungs and the liver to the mesenteric veins, where they mature. Pathogenic effect

The effects of schistosome infections of livestock are not easily recognized and the non-specific clinical signs are often overlooked by farmers. Infections may, however, result in severe clinical signs. The infections are often manifest by acute intestinal signs, 7-9 weeks after infection (the time when the females produce large numbers of eggs which penetrate the gut wall). The mucosa of the intestine is severely damaged and the animal develops profuse, sometimes bloody diarrhoea, dehydration and loss of appetite. Anaemia and general loss of condition may also be seen. The intensity of the pathogenic effects depends on the duration of the infection and the number of Schistosomes present. Signs associated with chronic hepatic disease may develop when eggs are washed back to the liver by the portal circulation during their penetration of the gut wall. The eggs become lodged in the liver and an intense immunological response results, followed by the formation of a granuloma. A large proportion of the liver may be destroyed and the liver function severely disturbed. Factors affecting the epidemiological pattern

Schistosomiasis is closely associated with large permanent water bodies such as ponds, lakes and marshy pastures. A key determinant in the epidemiology of this infection is the relative abundance of the intermediate hosts and their ability to develop and survive in the environment. Contamination of water with schistosome eggs results when animal defaecate in the water while drinking or if manure is used for feeding fish in ponds. As sheep and goats are reluctant to enter water, cattle are largely responsible for the transmission of the important schistosome species. Cattle become infected through skin penetration and the oral route, whereas sheep and goats generally become infected by drinking contaminated water. The type of watering facilities used by domestic stock is therefore a crucial factor in the maintenance and transmission of the infection. Nasal schistosomes

The adult parasites live in the blood vessels of the nasal mucosa. They are present in abscesses and granulomas that are full of eggs; these pass out in the nasal secretions and exudate. The development of the free-living stages, the stages in the snail and the transmission to the final host are similar to the processes in other schistosomes. Infected animals show varying degrees of sneezing, snoring and discharge from the nostrils.

2.6 Cestodes

2.6.1 Introduction
2.6.2 Cestodes with ruminants as the final hosts
2.6.3 Cestodes with ruminants as the intermediate hosts

2.6.1 Introduction

Cestodes in ruminants can conveniently be classified into two distinct groups; one in which ruminants act as the final host (the intestinal and hepatic cestodes) and one in which cattle, buffaloes sheep and goats act as the intermediate hosts for the larval stages (Cysticercus, Coenurus and hydatid cysts) of various tapeworm species. In the latter group, the adult parasites live in the small intestines of domesticated and wild carnivores (Taenia ovis, T. hydatigena, T. multiceps, Echinococcus granulosus) and man (T. saginata).

2.6.2 Cestodes with ruminants as the final hosts Intestinal tapeworms Hepatic tapeworms Intestinal tapeworms

This group comprises species of the genera Moniezia (cosmopolitan), Thysaniezia (Africa) and Avetellina (Africa, Asia). Life cycles

The life cycles of these tapeworms are indirect and herbage mites of the family Oribatidae act as intermediate hosts. The mites, which are soil-inhabiting, surface during the night and early morning to feed on manure. During their feeding they accidentally ingest eggs of the intestinal tapeworms present in the manure, and the larval stage called a cysticercoid develops in the mites. Ruminants become infected by ingesting herbage containing mites carrying the infective stage of the parasite. Pathogenesis of intestinal tapeworms

Lambs, kids and calves under six months old are commonly infected. Light to moderate infections are considered to be non-pathogenic. Heavy infections have been reported to cause poor growth and diarrhoea in lambs. Whether the intestinal cestodes are directly responsible for production losses is still a controversial issue and the pathogenicity of these parasites has not yet been established conclusively. Hepatic tapeworms

Stilesia hepatica (Africa) occurs in the bile ducts of ruminants and is very common in certain parts of Africa. It is believed that certain antelope species act as a reservoir of this infection. Life cycle

The life cycle is similar to that described for the intestinal tapeworms; ruminants become infected by ingesting infected herbage mites. The parasite occurs in animals of all ages. Pathogenicity of Stilesia hepatica

This parasite is considered to be non-pathogenic, and no clinical signs are associated even with heavy infections. Affected livers may show signs of mild cirrhosis with some thickening of the bile ducts. The economic importance of this infection results from the condemnation of affected livers at meat inspection.

2.6.3 Cestodes with ruminants as the intermediate hosts Muscular cysticercosis Abdominal cysticercosis Coenurosis of the brain Hydatidosis Muscular cysticercosis Bovine cysticercosis

This is caused by the presence of the vesicular larvae Cysticercus bovis in the striated muscles of cattle. Bovine cysticercosis has a cosmopolitan distribution being particularly common in certain parts of Africa. Life cycle

Cysticercus bovis is the larval stage of T. saginata, a tapeworm of man. Tapeworm segments containing thousands of eggs are passed in faeces or shed from the intestine of a parasitized individual. If the eggs are ingested by a receptive intermediate host, the embryos migrate through the blood stream and become disseminated throughout the body. Usually only the embryos which reach the striated muscle tissues will develop further, but viable cysts have been identified in other organs and tissues. Development takes 3-5 months and the majority of cysts remain viable (and thus infective) for 1-2 years. Man becomes infected by ingesting live cysts in raw or undercooked meat. Following infection of man an adult tapeworm develops in the intestine within 3 months. Infection of animals

Cattle become infected when they ingest the eggs of T. saginata. Poor standards of personal hygiene of infected human populations is responsible for the spread of cysticercosis. In some societies such as nomadic pastoral people there is a high risk of animals becoming exposed to infected faeces. Abnormal eating habits of cattle due to certain mineral deficiencies (pica) may result in cravings that increase the exposure through the ingestion of faeces. The survival of the eggs is strongly influenced by climatic conditions. Under wet and moist conditions, eggs may survive for months, exposing animals to a source of infection for a prolonged period of time. Eggs are very susceptible to dry conditions and are rapidly destroyed during the dry season. Pathogenicity of bovine cysticercosis

The cysticercus appears as a small (6-10 mm) oval vesicle which is at first semitransparent. These lesions are known as beef measles. The majority of cysts will gradually undergo degenerative changes resulting in loss of transparency, and this is followed by caseation and calcification.

Not all striated muscles are infected to the same degree. It appears that the parasite has preferred muscle sites for development (predilection sites) and these are usually the myocardium, the tongue, the masseter and the shoulder muscles.

The development and presence of cysts in bovines is generally not clinically apparent. The importance of this parasite is its public health significance and the resultant losses encountered during meat inspection when infected carcasses are condemned. Ovine cysticercosis

This is caused by the presence of the vesicular larvae Cysticercus ovis found in the striated muscles of sheep and goats Ovine cysticercosis is common in many countries of the world. Life cycle and pathogenicity

Cysticercus ovis is the larval stage of T. ovis, a tapeworm of dogs and other carnivores. The development cycle is similar to that of C. bovis. Although the cysts are found in the muscles of sheep, this parasite is not considered of public health importance because man cannot become infected with T. ovis. The most common sites of infection are the heart and the diaphragm, but other muscle groups may also be affected. The detection of the cysts usually results in condemnation of the meat for aesthetic reasons. Some reports indicate that massive infestations can kill animals. Abdominal cysticercosis

Abdominal cysticercosis of ruminants is caused by C. tenuicollis, the larval stage of T. hydatigena, a dog tapeworm. This parasite is cosmopolitan in its distribution.

FIGURE 2.5 Life cycle of Cysticercus ovis Life cycle

The adult tapeworms live in the small intestines of dogs and other carnivores and segments containing numerous eggs are passed in the faeces. After disintegration of the segments, eggs can be disseminated by wind and by insects contaminating the pasture. Ruminants then become infected by ingesting eggs. The embryos penetrate the wall of the digestive tract and migrate to the liver, where they migrate through the liver surface to enter the abdominal cavity. The fully developed cyst is a large (5 cm or more in diameter), soft, semi-transparent bladder within which the invaginated head of the tapeworm is clearly visible. The final host becomes infected by ingesting the-cysts.

FIGURE 2.6 Life cycle of Cysticercus tenuicollis Pathogenicity of abdominal cysticercosis

The developed C. tenuicollis has no pathogenic effect while situated in the abdominal cavity. When many embryos migrate simultaneously through the liver clinical signs may be seen. The migration may cause severe destruction of liver tissue and the pathology seen in the liver may be similar to that observed in liver fluke infections. Coenurosis of the brain

Cysticercus cerebralis is the cystic larval stage of T. multiceps, a tapeworm of dogs and other wild carnivores. The coenurus develops in the brain of sheep. This parasite is cosmopolitan in its distribution but not very prevalent. Life cycle

Egg-filled segments of T. multiceps are passed in the faeces of dogs. When sheep ingest the eggs, the embryos migrate via the circulatory system to the brain and spinal cord where the cystic stage, the coenurus, develops. The cyst takes 6-8 months to develop and at maturity may be up to 5 cm in diameter. The cyst is characterized by numerous invaginated tapeworm heads. The final host becomes infected by ingesting the cyst.

FIGURE 2.7 Life cycle of Coenurus cerebralis Pathogenicity of Coenurus cerebralis

The pathogenic effect is that of a space-occupying lession and the resulting pressure applied to the brain by the cyst during its development. The clinical signs depend on the size and site of the Coenurus in the brain. These include uncoordinated movements of the legs and abnormal positioning of the head. Affected animals may become blind in one or both eyes and indifferent to food and water. This can result in emaciation and eventual death. Hydatidosis

Hydatidosis or larval echinococcosis is the cystic stage of Echinococcus granulosus, a very small tapeworm of dogs and other canids. This parasite has a cosmopolitan distribution and is very common in parts of Africa, Latin America and some countries of Southeast Asia. Life cycle

There are several types of life cycle involving different mammalian species. One cycle involves domesticated ruminants and dogs; another cycle involves wildlife species, for example the warthog-lion cycle in Africa. Other cycles involve domesticated animals and wildlife, such as the dromedary camel-jackal cycle in some regions of sub-Saharan Africa.

The gravid segments of the E. granulosus tapeworm are excreted in the faeces of dogs and the eggs released from the segments are very resistant to adverse climatic conditions. They may be carried by wind in dust or be mechanically transported by flies. Following ingestion of the eggs by the intermediate hosts, which include man, domesticated animals and numerous wild mammals, the embryos emerge and migrate to the blood stream through which they are carried to various organs and tissues in which the hydatid cysts develop. Hydatid cysts are most commonly found in the liver and the lungs. The embryos grow slowly into large fluid filled cysts, 5-10 cm or more in diameter. Hydatid cysts are lined with a thin layer of germinal epithelium. After 5 months this germinal layer is capable of producing tapeworm scolices, which can be found individually in the fluid of the cyst as "hydatid sand". It also produces brood capsules which consist of several scolices held together by a thin membrane. Part of the germinal epithelium may occasionally form daughter cysts with a germinal layer of their own. In some cysts the germinal layer does not produce infective protoscolices and brood capsules; these cysts remain sterile. The final host acquires the infection by eating viscera containing fertile hydatid cysts. Cysts maintain their infectivity for several weeks after the death of the intermediate host and carrion feeders are therefore considered important in disseminating this infection. Pathogenicity of hydatid cysts

The effects of hydatid cysts depend on the organs in which they are situated and the number of cysts present. It is generally considered that hydatid infections of ruminants are not clinically important and disease due to the presence of hydatid cysts in ruminants is rare. Occasionally numerous large cysts may cause respiratory problems when they are situated in the lungs; digestive disturbances and ascites may be seen associated with heavy infections of the liver. The major significance of Echinococcus granulosus is the risk of human infection.

FIGURE 2.8 Life cycle of Echinococcus granulosus

2.7 Protozoa

Coccidia are protozoan parasites; most species infecting cattle, sheep and goats belong to the genus Eimeria. All Eimeria species parasitize the intestinal epithelium of infected animals. Older animals Usually become immune to infection but often remain carriers of coccidia and continue to pass oocysts in the faeces. Young animals become infected by ingesting sporulated oocysts in contaminated food and water. The parasites usually migrate into the intestinal mucous membrane, where oocysts are produced which pass out in the faeces. Successive infections in young animals may cause the animals to excrete large numbers of oocysts and this excretion will heavily contaminate kraals and watering places. The multiplication of the parasite in the intestine causes damage to the mucous membrane. The severity of this damage depends on the number of oocysts ingested. Clinical signs are usually seen only in young animals. A prominent sign of clinical coccidiosis is diarrhoea, which is sometimes bloody. Affected animals have poor growth rates; severely affected animals may die.

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