CHAPTER 2: DISEASES CAUSED BY HELMINTHS

Helminthosis is considered to be a major cause of mortality and sub-optimal productivity in goats and sheep in traditional farming systems in sub-Saharan countries. Helminths cause direct losses due to deaths and indirect losses due to reduced productivity through reduced feed intake and liveweight gains and, decreased quality of skins, wool or mohair. Furthermore, they render animals more susceptible to other infections.

Aetiology

Helminthosis is a widespread infection of small ruminants in the sub-Saharan region. Nematodes, trematodes and cestodes are the three major classes of parasitic helminths of economic and zoonotic importance affecting goats and sheep in this region.

The most common species of nematodes associated with parasitic gastro-enteritis in small ruminants in most sub-Saharan countries are Haemonchus contortus, Oesophagostomum columbianum and Trichostrongylus colubriformis. Trichostrongylus axei, Bunostomum trigonocephalum, Cooperia curticei, Trichuris ovis, Trichuris globulosus, Strongyloides papillosus, Gaigeria pachyscelis and Chabertia ovina also contribute to the syndrome. In winter rainfall and cool highland areas, Ostertagia circumcincta and Nematodirus filicollis are also involved in the pathogenesis of parasitic gastro-enteritis in goats and sheep. Lungworms such as Dictyocaulus filaria, Muellerius capillaris and Protostrongylus rufescens cause parasitic bronchitis particularly in young animals.

Fasciola spp, Paramphistomum spp and Schistosoma spp are the main trematodes infecting goats and sheep. Fasciola gigantica is the commonest species associated with fasciolosis in most sub-Saharan countries. Fasciola hepatica has also been shown to be a significant cause of fasciolosis in highland areas of Kenya, north-eastern and south-western Tanzania, Ethiopia, Lesotho and the Republic of South Africa. Clinical paramphistomosis in small ruminants is caused by Paramphistomum microbothrium. Schistosoma bovis is the main cause of clinical schistosomosis in small ruminants although Schistosoma mattheei has also been implicated.

Stilesia hepatica and Moniezia expansa are the common parasitic cestodes encountered in goats in the sub-Saharan region. S. hepatica causes biliary fibrosis and is an important cause of liver condemnations in abattoirs in Kenya and Tanzania. M. expansa infection is very common in kids and heavy infection with the parasite causes unthriftiness. The significance of Stilesia globipunctata and Avitellina centripunctata infections in small ruminants in sub-Saharan Africa has not been well documented. The presence of other cestodes such as Echinococcus granulosus, Taenia ovis (metacestode, Cysticercus ovis), Taenia multiceps (metacestode, Coenurus cerebralis) and Taenia hydatigena (metacestode, Cysticercus tenuicollis) in tissues or organs leads to condemnation of the affected tissues/organs. The migration of Coenurus cerebralis through the brain can cause meningo-encephalitis while the presence of many hydatid cysts in the lungs may be associated with respiratory problems.

Epidemiology

Gastrointestinal nematodes

The epidemiology of gastrointestinal nematode infections is influenced by climatic factors (particularly rainfall and temperature), management systems used for the animals, host factors and parasite factors.

Climatic factors: Rainfall or moisture is the most important factor which influences the survival, development, dissemination and availability of free living stages of helminths. Moisture facilitates horizontal and vertical migration of nematode larvae on the environment. Some workers have demonstrated that dung beetles may also transport larvae up and down the herbage. Higher worm burdens and outbreaks of parasitic gastro-enteritis in goats and sheep in this region are encountered during or immediately after the end of the rainy season. Temperature also influences the development of nematode larvae and the optimal temperature for the development of most trichostrongylid larvae is 22-30°C. No development of trichostrongylid larvae occurs below 5°C while temperatures above 40°C are lethal. Some trichostrongylid larvae such as T. colubriformis and O. columbianum are known to be resistant to desiccation and this ability enables them to survive under extremely low or high temperatures.

Gastrointestinal nematodes can survive harsh conditions by hypobiosis or arrested development of larvae (usually L3 or early L4) within the host. In the absence of hypobiosis nematodes survive in hosts during the hot and dry season as adults. The humid tropical climate is favourable for the survival, development and transmission of gastrointestinal nematodes throughout the year.

Management systems: Management systems for the animals have a strong influence the epidemiology of gastrointestinal nematodes. High stocking density increases the contamination of the environment with nematode eggs or larvae and thus makes the infective stages to be more accessible to susceptible animals. High stocking rates and intensive management with little or minimal rotational grazing, are associated with high pasture contamination and outbreaks of clinical helminthosis. On the other hand, low stocking rates and extensive management systems in the traditional husbandry systems preclude a built-up of high worm burdens. The concentration of animals at watering points particularly during the dry season may also result in massive contamination of pastures with eggs or larvae leading to outbreaks of parasitic gastro-enteritis. Tethering of goats and sheep during the wet season which is common in many agro-pastoral societies has been reported to result in increased environmental contamination with infective larvae and incidence of clinical disease. Outbreaks of parasitic gastro-enteritis in such systems have been reported in Tanzania, Nigeria, Kenya and Cameroon. However, if tethered animals are moved each day to fresh ground and the number of animals in the area is small, the risk of helminthosis is reduced.

Similarly, if animals are totally confined and fed on helminth free diets the risk of helminthosis is reduced.

Anthelmintic treatment reduces the prevalence and severity of gastrointestinal nematode infections and may significantly influence their epidemiology. However, the effectiveness of anthelmintic treatment regimes depends on a thorough knowledge of other factors which influence the epidemiology of nematodosis. Indiscriminate use of anthelmintics may result in the development of resistant nematode strains and this problem is increasing in importance across the sub-Saharan region.

Host factors: The incidence rate and severity of infection with gastrointestinal nematodes can also be influenced by host factors such as age, breed, nutrition, physiological state and presence or absence of intercurrent infections. For instance, kids and lambs are known to be more susceptible than adults and there is a tendency for the worm burdens in goats and sheep to decrease with increasing age. Some breeds of goats and sheep are known to be genetically resistant to gastrointestinal nematodes infections than others. It has been demonstrated in Kenya that the Small East African (SEA) goats are more resistant to H. contortus infection than their crosses with the Toggenburg and the Galla goats. The Red Maasai sheep have also been found to be more resistant to H. contortus infection than the Merino, Dorper, Corriedale, Romney Marsh and Hampshire sheep. The West African Dwarf goats and sheep are also known to be resistant to gastrointestinal nematodes.

The physiological status of the animal may influence its susceptibility to gastrointestinal nematode infections. Hormonal changes during late pregnancy and lactation lower the resistance of the host to nematodes and consequently result in the establishment of higher worm burdens. Prolactin and glucocorticoids are considered to be modulators of periparturient egg rise in goats and sheep. The increase in the fecundity of adult worms already in the alimentary tract and non-specific immunological loss of resistance by the does and ewes as a result of stress associated with lambing and kidding are also considered to be responsible for the 'post parturient rise' in faecal egg count in does and ewes. On the other hand, oestrogens have been found to be responsible for the resistance of female hosts to gastrointestinal nematodes.

Poor nutrition lowers the resistance of the animal thus enhancing the establishment of worm burdens and increasing the pathogenicity of the parasites. Consequently, worm burdens tend to be higher in poorly-fed than in well-fed animals. Malnutrition during the dry season has been found to lower the resistance of goats and sheep to H. contortus infection in Sierra Leone, Nigeria and Kenya resulting in heavy mortalities while restricted feeding due to tethering during the rainy season has been associated with high nematode burdens and mortality of goats in some parts of Tanzania. Intercurrent infections and other stress factors also enhance the establishment of higher worm burdens.

Parasite factors: The intrinsic multiplication rate of the nematode species determines the rate of establishment and size of nematode burden in the host. The multiplication rate is determined by the fecundity of the adult worms, the prepatent period and the survival and development rate of the parasite in the environment. For example, H. contortus and O. columbianum have a high biotic potential such that establishment of these nematodes occurs very rapidly as long as environmental factors are favourable. Trichostrongylus spp has a lower biotic potential and hence its establishment is slower.

Lungworms

The epidemiology of lungworms is similar to that of gastrointestinal nematodes. A damp and cool environment is very suitable for the development of D. filaria and the third stage larva (L3) is resistant to cold. The sporangia of a fungus (Pilobolus spp) and dung beetles facilitate the spread of D. filaria larvae. Under adverse (dry) conditions the larvae may be inhibited in the lungs. Some animals may harbour adult worms in the lungs and act as carriers which continue to contaminate the pastures and maintain the infection in the environment. Muellerius capillaris and Protostrongylus spp have indirect life cycles, with land snails and slugs acting as the intermediate hosts. Therefore, factors which influence the epidemiology of the intermediate hosts will determine the epidemiology of the parasite as well. Moisture is considered to be an important factor determining the survival and availability of land snails and slugs.

Trematodes

As in nematode infections, climate, management systems, parasite and host factors influence the epidemiology of trematode infections in goats and sheep. However, unlike gastrointestinal nematodes, trematodes have indirect life cycles and intermediate hosts play an important role in their epidemiology. Therefore, factors determining the availability, development and survival of intermediate hosts in the environment will also influence the level and severity of trematode infections.

The intermediate host for F. gigantica is the aquatic snail, Lymnaea natalensis although L. truncatula has also been found to serve as an intermediate host of F.gigantica in East and Central African highlands. The optimum temperature range for the survival and development of L.natalensis is 15-26 °C while temperatures below 10 °C inhibit the development and reproductive activity of the snails. L. natalensis requires permanent water bodies with abundant vegetation such as lakes, slow-moving rivers, irrigation ditches and water tanks. Clean, clear and unpolluted water is the most favourable habitat for L. natalensis.

Light, suitable temperature (20-25 °C) and availability of oxygen are essential for the embryonation and hatching of Fasciola spp eggs. No development occurs below 10 °C and higher temperatures (>35 °C) result in death of the larvae. The humid environment of most sub-Saharan countries is favourable for the embryonation and hatching of Fasciola spp eggs throughout the year. The development of miracidia in the snail host is also temperature- dependent. Faeces and manure pats can act as reservoirs of the infection. It has been found that the concentration of animals at watering points during the dry season is a favourable factor for the transmission of F. gigantica leading to outbreaks of fasciolosis.

The epidemiology of Paramphistomum microbothrium is similar to that of F. gigantica although other species of snails such as Planorbis spp and Bulinus spp may serve as intermediate hosts.

The epidemiology of Schistosoma spp is similar to that of F. gigantica and Bulinus spp is the common intermediate host for S. bovis and S. mattheei in Africa. In Tanzania, Bulinus africanus is the main intermediate host for S. bovis.

Cestodes

The cestodes, M. expansa, S. hepatica, S. globipunctata and A. centripunctata have indirect life cycles and the intermediate host are the soil-inhabiting oribatid mites such as Oribatula spp, Galumna spp and Peloribates spp. Birds may involved in the dissemination of tapeworm eggs.

Transmission

Gastrointestinal nematodes

The adult nematodes inhabit various regions of the gastrointestinal tract. Females lay eggs which are passed out with faeces of the host. The eggs embryonate and hatch into first (L1), second (L2) and third (L3) larvae, the latter being the infective stage. Animals are infected with Haemonchus spp, Trichostrongylus spp and Oesophagostomum spp by ingestion of L3 with pastures. After ingestion, the L3 of Haemonchus spp and T. axei develop through the fourth (L4) and fifth (L5) stage larvae and mature into adults in the abomasum while the maturation of T. colubriformis and Oesophagostomum spp occur in the small and large intestines respectively.

The third stage larvae of Bunostomum spp and Strongyloides spp enter the host mainly by skin penetration although infection through ingestion is also possible. After skin penetration they are carried into the venous circulation through the heart and the lungs. The larvae penetrate the alveoli, are coughed up and then swallowed. They pass to the small intestine where further development and maturation occur. The larva of Trichuris ovis is contained within the egg and the infective L1 is released when the egg is ingested by the host. The prepatent period for most gastrointestinal trichostrongyles is about 21 days.

Lungworms

Adult Dictyocaulus spp are found in the trachea or bronchi where eggs are produced. The eggs are coughed up and swallowed. Hatching of eggs occur in the air passages or in the intestines and it is the L1 which is found in host faeces. Under suitable conditions of temperature and moisture, the L1 hatches into L2 and L3. Infection is acquired through ingestion and the L3 migrate through the intestinal wall and enter the mesenteric lymph nodes where they moult into (L4). The L4 passes through the lymphatic and venous circulation to the heart and then through the pulmonary circulation to the lungs where they enter the alveoli. Maturation occurs in the bronchi or trachea and the mature worms start to produce eggs. Adult M. capillaris is found in the alveoli and pulmonary parenchyma while P. rufescens lives in the bronchi and their life cycles are similar to that of Dictyocaulus spp.

Trematodes

Adult Fasciola spp lay eggs in the bile ducts and the eggs are transported to the gall bladder through the bile. When the gall bladder contracts the eggs enter the duodenum and then are expelled from the host with the faeces. Under optimum conditions of temperature and moisture the eggs hatch into miracidia. The latter actively penetrate snail hosts and develop through the sporocyst, redial and cercarial stages. The cercariae leave the snail hosts, encyst onto herbage just below the water level and become metacercariae, which are the infective stage. The metacercariae are ingested by grazing animals with infected herbage or water. They excyst in the duodenum, penetrate the intestinal wall and pass through abdominal cavity (or sometimes through the blood stream) to the liver where they penetrate the liver capsule. The immature flukes migrate in the liver parenchyma and then enter the bile ducts where they mature and start to produce eggs. The prepatent period of F. gigantica in goats is about 90-100 days and may be shorter under heavy infections.

The transmission of Paramphistomum spp is similar to that of Fasciola spp. However, after excystation and attachment in the duodenum, the immature paramphistomes migrate up the alimentary tract and finally attach to the epithelium of the rumen and reticulum. The prepatent period is 4-5 months.

The life cycle of Schistosoma spp is similar to that of Fasciola spp but when the eggs are passed out in the faeces of the host they already contain a miracidium which hatches shortly if environmental conditions are optimum. There are no rediae or metacercarial stages in the life cycle of S. bovis. The cercaria is the infective stage and infection occurs through skin penetration or ingestion. The cercariae are carried through the lymphatic and blood systems to the mesenteric veins where they mature and commence to produce eggs 6-8 weeks after infection.

Gastrointestinal cestodes

The adults worms are found in the small intestine of goats or sheep. Proglottids and eggs are passed out in the faeces of the infected animal. In the environment, the eggs may be ingested by oribatid mites where they develop into cysticercoids. The cysticercoids which are the infective forms are produced in 1-4 months depending on temperature. Ruminants are infected by the ingestion of the infected mites with herbage. The prepatent period is 5-6 weeks.

Clinical and Pathological Features

Parasitic gastro-enteritis

The major parasites associated with parasitic gastro-enteritis in small ruminants in sub- Saharan Africa are H. contortus, T. colubriformis and O. columbianum. Other nematodes of lesser importance are T. axei, B. trigonocephalum, T. ovis, Cooperia spp, and S. papillosus. O. circumcinta and N. fillicolis are important in cooler highland areas. Due to the differences in their predilection sites and pathogenetic mechanisms, gastrointestinal nematodoses present with differing clinical and pathological features. However, most commonly in field infections the clinical and pathological features of parasitic gastro-enteritis are due to the additive pathogenic effects of several nematodes.

Haemonchosis

Haemonchosis is considered to be the most economically important disease of goats and sheep in Africa. The pathogenesis of haemonchosis is related to the blood sucking habit of the parasite. Three syndromes; hyperacute, acute and chronic haemonchosis occur in goats and sheep.

Hyperacute haemonchosis occurs when there is a sudden massive challenge of susceptible animals with infective larvae resulting in severe blood loss due to haemorrhagic gastritis. The syndrome is of short duration and is characterised by sudden death although in some animals dark coloured faeces may be seen before death. Faecal egg count of up to 400,000 may be encountered in the affected animals.

Hyperacute haemonchosis has limited gross pathological features due to sudden death, although a large number of immature or young adults may be found on the abomasal mucosa at post mortem examination. There are also multiple erosions and petechiae of the abomasal mucosa and minimal expansion of the bone marrow. However, hyperacute haemonchosis is not very common in field infections.

Acute haemonchosis occurs when animals are exposed to a continuous challenge from eggs leading to gastritis associated with hypoproteinemia and generalised oedema. Other signs include weakness, pallor of the mucous membrane, lethargy or agalactia which may lead and starvation death of kids. Dark coloured faeces are often observed. Self-cure may occur at any stage of the disease. The syndrome is more common when young susceptible animals become infected.

Pathologically, acute haemonchosis is characterised by a pale and watery carcass. The abomasal mucosa is petechiated and oedematous with many parasites on its surface and contents. There is a marked expansion of the bone marrow throughout the medullary cavity which may extend up to the epiphyses.

Chronic haemonchosis is the common form of field infection. The syndrome is caused by gradual intake of infective larvae and the course of disease may take 2-6 weeks. It is a chronic gastritis with chronic blood loss and abomasal dysfunction leading to weakness, progressive weight loss, rough hair coat and stunted growth. Chronic haemonchosis is aggravated and often confused with malnutrition.

At necropsy, chronic haemonchosis is characterised by pallor carcass, hyperplastic thickening of the abomasal wall, chronic expansion of the bone marrow and resorption of the cancellous and cortical bones. In terminal stages the bone marrow reverts to white due to exhaustion.

The clinical pathology of haemonchosis includes lowered packed cell volume, haemoglobin concentration, erythrocyte counts and serum iron.

Trichostrongylosis

Trichostrongylosis is commonly a disease of young animals. The penetration of larvae and adult worms into the intestinal mucosa results in desquamation of the latter causing a malabsorption syndrome and hence, a protein-losing gastroenteropathy and hypoalbuminemia. Heavy infections cause an acute enteritis which is characterised by dark- coloured diarrhoea and foul smelling faeces. There may be sudden death without evidence of anaemia or emaciation but weakness of the legs is a frequent feature. Most commonly, trichostrongylosis is a chronic wasting disease characterised by loss of appetite, emaciation, loss of weight, dry skin, diarrhoea, oedema and atrophy of skeletal muscles or mycocardium.

At necropsy, the acute disease is characterised by a swollen and haemorrhagic or catarrhal intestinal mucosa and, worms may be found in the mucosal scrapings. The chronic disease is characterised by an emaciated carcass, fatty degeneration and, a thickened, inflamed and ulcerated intestinal mucosa. Histopathologically, chronic infection with T. colubriformis is characterised by marked villous atrophy, flattening of the intestinal mucosa and osteoporosis. The clinical pathology is characterised by hypoalbuminaemia, hyperglobulinaemia and hypophosphataemia.

Oesophagostomosis

The pathogenicity of O. columbianum is related to the migration of larvae in muscularis mucosa of the large intestine resulting in a fibroblastic response around the larvae forming fibrous nodules. The extensive nodular formation interferes with digestion, absorption and bowel movements. Mucoid diarrhoea or sometimes constipation, emaciation, general weakness, dry skin, prostration and death are the common clinical features. The diarrhoea often coincides with the emergence of larvae from the nodules. The nodules are frequently invaded with pyogenic bacteria which cause suppuration. Rupture of the nodules may cause peritonitis and multiple adhesions.

At post mortem examination, the most severe form of the disease is characterised by ulcerative colitis. The adult worms cause thickening of the bowel wall, congestion and production of excessive amount of mucus. In primary infection, adult worms are found in the lumen of the large intestine where they are often covered with mucus and there may be few nodules. In superinfection, there is an extensive nodular formation with marked emaciation and severe fatty degeneration. Abscesses with greenish or yellowish pus may also be present.

Bunostomosis

Bunostomosis is characterised by progressive anaemia, emaciation, weakness or paresis, submandibular oedema, dark coloured faeces, prostration and death. At post mortem examination there is hydrothorax, hydropericardium and pin-point haemorrhages in the small intestine or blood in its content.

Other gastrointestinal nematodes

Other gastrointestinal nematodes such as Cooperia spp, T. ovis and S. papillosus have limited pathogenicity. Their clinical and pathological features are often masked with the more pathogenic species. However, heavy challenge with these parasites particularly in young animals may be associated with anorexia, weight loss, moderate anaemia and inflammation of the intestinal mucosa.

Parasitic bronchitis

Parasitic bronchitis (verminous pneumonia) caused by D. filaria and M. capillaris is more common in kids or lambs under 6 months than in other age groups. Adult D. filaria cause alveolar and bronchiolar irritation leading to coughing, dyspnoea and loss of body condition. Secondary bacterial infection may lead to toxaemia.

At necropsy, there is pulmonary oedema and emphysema with consolidation of some parts of the lung. The bronchioles are filled and may be blocked with exudate. Bronchoectasis frequently accompanies secondary bacterial infections. In M. capillaris infection, nodular circumscribed and raised grey or greyish white patches are observed especially on the dorsal and lateral aspects of the diaphragmatic lobes. Consolidation of the ventral portion and antero-ventral aspects of the diaphragmatic lobes is frequently observed. There may also be fibrinous strands which are adherent to the thoracic wall and a frothy fluid may be expressed from cut lung surface.

Histopathologically, eggs, larvae or adult worms are found in the air passages and in the interalveolar spaces. Mucopurulent exudate containing inflammatory cells such as lymphocytes, fibrocytes, mononuclear phagocytes, eosinophils and foreign body giant cells fill the bronchial and alveolar lumina. The inflammatory cells may also be found in the blood vessels accompanying bronchioles. Thickening of the interalveolar connective tissue, erosion of bronchiolar epithelium, mucosal hyperplasia, peribronchial lymphoid hyperplasia and epithelialisation of the alveoli are common features.

Trematode Infections

Fasciolosis

F. gigantica infection is associated with a clinical disease in goats and sheep even when the fluke burden is light. It has been found that as few as 42 flukes can cause clinical fasciolosis in goats. The disease is more severe in goats than in sheep. Three syndromes; acute, subacute or chronic fasciolosis may occur.

Acute fasciolosis occurs when there is an acute traumatic hepatitis caused by the migration of larvae through the parenchyma leading to extensive destruction and marked haemorrhage. The haemolytic crisis results in progressive weakness, pallor of the mucous membranes, enlargement of the liver and abomasal distension. Anorexia, paresis prior to death and anasarca are observed in terminal stages of the acute disease in goats. At necropsy, acute fasciolosis is characterised by the presence of a blood-tinged fluid in the peritoneal cavity, fibrinous exudate covering the liver surface, hepatomegaly and numerous haemorrhagic and friable tracts in the liver parenchyma. The gall bladder is also enlarged. Immature flukes can be expressed from the cut liver surface. Adhesion of the liver to the diaphragm or other internal organs may occur.

Subacute fasciolosis is associated with ingestion of a large number of metacercariae over a long period of time. The syndrome is characterised by anorexia, rough hair coat, slight abdominal distension, pallor of mucous membranes, disinclination to move and emaciation.

Chronic fasciolosis is a persistent wasting disease characterised by emaciation, anaemia and submandibular oedema. At post mortem examination, fibrosis and thickening of the bile ducts resulting from cholangitis is evident. The bile ducts may be blocked with flukes and desquamated epithelial cells. The damaged parenchyma becomes indurated and flukes may be seen in the bile ducts with granulomata often being observed around fluke remnants. Calcification of the bile duct walls which is commonly observed in cattle is not a feature of fasciolosis in small ruminants. F. hepatica produces a disease similar to F. gigantica.

The clinical pathology of acute fasciolosis is characterised by a normochromic anaemia, eosinophilia, hypoalbunaemia and elevation of plasma glutamate dehydrogenase and gamma- glutamyl aminotranspeptidase. The two enzymes are very sensitive indicators of the liver damage. Plasma sorbitol dehydrogenase and aspartate aminotransferase are also elevated. The elevation of plasma aspartate aminotransferase is more notable in the fourth week of infection coinciding with the migration of the immature flukes in the liver.

Paramphistomosis

This is an acute enteritis caused by the migration of the immature flukes in the duodenal mucosa and is characterised by profuse and foetid diarrhoea, dehydration, loss of body condition, weakness, pallor of the mucosae and submaxillary oedema. In some countries, outbreaks of the disease have been reported to occur during the dry season following concentration of animals at watering points and subsequent massive contamination of the environment with fluke eggs.

At post mortem there is a marked haemorrhagic enteritis with large numbers of the parasites on the mucosa or contents of the duodenum and upper ileum, subcutaneous oedema, gelatinous fatty degeneration. Extensive catarrhal or haemorrhagic duodenitis or jejunitis with destruction of associated glands and lymph nodes are the main histopathological features. Young flukes may be found embedded in the duodenal mucosa. There is a marked fall in total plasma proteins due to increased leakage of plasma albumin.

Schistosomosis

Intestinal and hepatic forms of the disease are distinguished. The intestinal syndrome is related to the damage caused by passage of large numbers of eggs in the intestinal mucosa and is characterised by diarrhoea or dysentery, dehydration, anorexia, loss of weight and profuse, foetid or intermittent diarrhoea, submandibular oedema and anaemia. Neuralgical signs may be observed in the chronic form of the disease. The hepatic syndrome occurs when eggs are washed back to the liver by portal circulation during penetration of the intestinal wall resulting in hepatic damage. The clinical and pathological features of the hepatic syndrome resemble those of fasciolosis

Pathologically, the intestinal form of the disease is characterised by petechiae or ecchymoses and granulomata in the gastrointestinal mucosa and, oedema and pallor of the carcass. In the hepatic syndrome there is hepatic infarction, portal fibrosis, thrombosis and dead parasites may be expressed from the cut vessels. There may also be hydrothorax, hydropericardium and ascites.

Cestode infections

The pathogenic effects of Moniezia spp are limited and the parasite is considered to be non-pathogenic. However, heavy infections in young animals may cause anorexia, weight loss, moderate anaemia, inflammation of the intestinal mucosa and sometimes obstruction of the intestines. S. hepatica occurs in the bile ducts of small ruminants and its economic importance is associated with condemnation of the affected livers. Migration of C. cerebralis in the brain may cause meningo-encephalitis while massive numbers of cysts of E. granulosus in the lungs may cause respiratory problems. Other cestodes have limited clinical significance in small ruminants.

Diagnosis

Diagnosis of helminthosis is based on history, epidemiological, clinical and pathological findings and laboratory analysis of appropriate samples. The most commonly used laboratory methods for diagnosis of gastrointestinal nematodes are faecal egg counts, faecal cultures, determination of infective larvae on herbage and worm counts at post mortem.

Nematodes

Faecal egg counting is the most common antemortem means of diagnosis of nematodosis and is based on the assumption that the size of worm burden in animals may be accurately deduced from faecal egg counts. Faecal egg counting is a cheap and easily performed technique. The McMaster technique is a rapid, easy and most commonly used method in quantitative analysis of nematode egg counts in the field and in epidemiological surveys. However, the number of nematode eggs or larvae in faeces is influenced by several factors such as the biotic potential of the nematode species, resistance of the host, developmental stage of the parasite, season of the year, quantity and consistency of the faeces passed and, sensitivity of the diagnostic method used. Therefore, the interpretation of faecal egg counts should take into account these factors.

Faecal cultures are based on the fact that the infective larvae of different genera of nematodes differ morphologically hence their examination permits a specific diagnosis of nematode infections. However, faecal culturing is a slow process and does not take into consideration the differences in fecundities of different nematode species.

Estimation of number of infective nematode larvae on pastures provides an indication of the level of infection to which grazing animals are exposed. The technique is useful in the diagnosis and prognosis of a nematode infection on farm and in epidemiological investigations. However, the larval population in herbage is affected by rainfall, herbage cover and stocking density. The method and time when herbage samples are taken may also affect the number of larvae recovered. These factors should be considered when interpreting the significance of the number of infective nematode larvae recovered from pastures. Tracer or sentinel animals can be used alone or in conjunction with herbage larvae determination to provide an indication of the availability of infective larvae on pastures. The use of tracer animals is more reliable than herbage sampling but it is limited by its cost.

Post mortem worm counting permits identification of adult worms and a direct count of worms present in an animal thereby providing a precise assessment of the worm burden. Post mortem worm counting is considered to be the most accurate method of diagnosis of helminthosis, however, it is also expensive.

Other helminths

Patent Fasciola spp, Paramphistomum spp and Schistosoma spp infections can be diagnosed by faecal egg and post mortem worm counting. Examination of eggs in faeces is most commonly used in routine diagnosis of chronic fasciolosis but a more precise assessment of the fluke burden of an animal can be made by post mortem examination and identification of immature and mature flukes.

Monieziosis and stilesiosis can be diagnosed by demonstration eggs or proglottids in host faeces whereas, the adult worms can be found in the small intestine or bile ducts at post mortem examination.

Other methods used in the diagnosis of helminth infections include immunodiagnosis and enzyme assays. However, these methods are used where laboratory facilities are adequate and are of limited use in direct field investigations of helminthoses. Helminthosis especially haemonchosis closely resembles trypanosomosis but the mortality rate is higher in haemonchosis than in trypanosomosis and, in addition, the demonstration of trypanosome in circulation can rule out haemonchosis. However, it should be borne in mind that concurrent infections of helminthosis and trypanosomosis in the field is very common.

Treatment

Many anthelmintics which are effective against different species of helminths affecting small ruminants have been developed. Benzimidazoles, imidazothiazoles, tretrahydropyrimidines, organophosphates and ivermectins form the major classes of anthelmintics.

The following benzimidazoles are used to treat gastrointestinal nematodes, lungworms and some tapeworms; albendazole (5.0-10 mg/kg), fenbendazole (5.0-7.5 mg/kg), mebendazole (12.5 mg/kg) and oxfendazole (4.5-5.0 mg/kg), oxibendazole (15 mg/kg), parbendazole (20 mg/kg) and thiabendazole (80 mg/kg). Oxibendazole is not effective against Trichostrongylus spp while parbendazole is not effective against Bunostomum spp. Fenbantel and thiophanate are effective against gastrointestinal nematodes, lungworms and anoplocephalid tapeworms. The imidazothiazoles, tetramisole (15 mg/kg) and levamisole (7.5 mg/kg) and the tetrahydropyrimidines, morantel (7.5 mg/kg) and pyrantel (15 mg/kg) are also used to treat gastrointestinal nematodosis. The organophosphates; coumaphos, haloxon, trichlorfon, naphthalophos and dichlorvos have also been used to treat parasitic gastro-enteritis in small ruminants. Ivermectin 0.2 mg/kg is very effective against gastrointestinal nematodes and immature stages of lungworms in goats.

Triclabendazole (10 mg/kg), rafoxanide (5.0-10.0 mg/kg), brotianide (10-15 mg/kg), nitroxynil (8-15 mg/kg), diamphenetide (80-120 mg/kg) and niclofolan (4-8 mg/kg) are effective against both the immature and mature stages of Fasciola spp while oxyclozanide (15 mg/kg) has been found to be effective against the adult stages only. Albendazole and oxfendazole are also effective against Fasciola spp.

Niclosamide (90 mg/kg), brotianide (15 mg/kg ) and closantel have been shown to be effective in treating paramphistomosis whereas, praziquantel (15 mg/kg) and trichlorfon are the drugs of choice for the treatment of schistosomosis.

Niclosamide (80 mg/kg), resorantel (75 mg/kg), praziquantel (15 mg/kg), bunamidine (25- 50 mg/kg), cambendazole (25-35mg/kg), albendazole (5 mg/kg), mebendazole (10 mg/kg) and fenbendazole (10 mg/kg) have been in use against cestodes. Benzimidazoles are particularly effective against anoplocephalid tapeworms.

The routes of administration and the dosage forms of various anthelmintics are documented in detail in standard textbooks of veterinary pharmacology and parasitology. It is worth noting that the pharmaceutical industry in most sub-Saharan countries is underdeveloped and hence, most drugs for use in small ruminants are manufactured in the developed countries and their efficacies have been tested mainly in sheep than in goats. Therefore, it is always important to adhere to the manufacturers' instructions before using them.

Control

The control of helminthosis is designed to eliminate or reduce the prevalence of helminths and improve the productivity of the livestock industry. The eradication of helminthosis in animals is difficult and the aim of control is therefore to limit the infection by minimising the challenge to an economically justifiable level. It is therefore important to accurately assess the cost-benefit effectiveness of any helminth control programme if production from the animals is to be optimised. Effective control of helminthoses can be achieved by judicious use of anthelmintics and good management. The methods of control of helminthosis can be grouped into three main categories;

Control by use of anthelmintics : This method aims at eliminating the parasitic stages of the parasite in the host thus preventing the discharge of eggs and larvae into the environment. Chemoprophylaxis is extensively used in the control of helminthosis throughout the world. Since the species of helminths and epidemiological factors vary from one place to another, the strategies for anthelmintic treatment will vary between different agro-ecological zones within a country. It is therefore recommended that the frequency of treatment should be determined by the epidemiology and biology of the dominant parasite, the stocking rates of the particular area and the benefits accrued from the control regime adopted.

In Nigeria, for example, some workers recommend treatment at the end of the rainy season because the helminth burdens in small ruminants tend to be higher during these times. Others recommend anthelmintic treatment in the early dry season in order to eliminate the declining worm burdens and because there will be no recrudescence of worm population due to resumed development of inhibited larvae. In Cameroon, some workers have found that treatment at the beginning or middle of the rainy season will keep the worm burdens throughout the year at a minimum level. In Kenya, some workers have recommended treatment just before the beginning of rains because helminth burdens are found to be higher during the dry season while others recommend a four weekly treatment interval. In southern Tanzania, a single anthelmintic treatment at the end of the dry season has been found to minimise worm burdens during the rainy season while in the northern part of the country treatment at the beginning and end of the dry season has been recommended. Other studies conducted in Tanzania, have shown that treatment of goats two weeks after the onset of rains and at a four-weekly interval during the rainy season minimises pasture contamination with helminth eggs thereby reducing the number of infective larvae on pastures during the dry season.

In small-holder farming systems where worm burdens are generally low, treatment of clinical cases may be more practical, economical and acceptable by farmers than mass treatment. Furthermore, small farmers unlikely to spend their meagre income to purchase drugs for regular treatment.

It should also be remembered that frequent use of anthelmintics interferes with the development of immunity of animals against helminths and indiscriminate use of anthelmintics can lead to the selection of drug resistant helminths. Anthelmintic resistance has been reported to occur in goats and sheep in Kenya, Tanzania and South Africa and, it is likely to be a serious problem in many other countries.

Control through management: This method aims at reducing the contact of susceptible animals with infective larvae. Control of helminthosis by good management is considered to be more sustainable than the use of anthelmintics and may be the most practical method for use by small-holder farmers who cannot afford to purchase expensive drugs. Rotational grazing, separation of animals according to age groups, alternate grazing by different species of hosts, adjustment of stocking rates, improvement of nutrition and better housing systems are the common management manoeuvres employed in the control of helminthosis in most countries.

(i) Rotational grazing is commonly used in modern production systems but is of limited used under communal grazing systems. However, a rigid rotational grazing system may delay the development of premunity in animals. Grazing of kids or lambs ahead of adults prevents them from acquiring heavy worm burdens from pastures contaminated with helminths eggs or larvae from the adult animals.

(ii) Alternate grazing by different host species depends on the degree of cross-transmission of parasites between host species. Alternate grazing of cattle and small ruminants is practised in some ranches in South Africa, Kenya and Zimbabwe. Although this practice may reduce the overall burden of the species in question, the reduction may not be sufficient for efficient parasite control.

(iii) Reducing the stocking rates reduces pasture contamination with helminth eggs or larvae thereby reducing the acquisition of heavy worm burdens by animals.

(iv) The use of parasite-free forage, slatted-floor housing systems and raised feed or water troughs has been found to be effective in minimising infections of animals with helminths. Provision of adequate nutrition also lessens the pathogenic effects of helminths on animals.

Control by breeding resistant stocks: This method is based on genetic resistance of different breeds of animals to helminth infections. The resistance of indigenous breeds of goats and sheep to hemonchosis compared to exotic or crossbred ones is well documented. Breeding of resistant stock can be possibly adopted as a long term strategy for the control of helminthosis. Presently, this method of control of helminthosis is not widely used in sub- Saharan countries but it still has a great potential if well pursued.

Control by immunisation: Vaccination for helminth control is based on the ability of some helminths to stimulate an immune response that can persist after infection. It has been demonstrated that vaccination of adult sheep with X-irradiated H. contortus larvae confers immunity to subsequent challenge. However, little work has been done regarding the control of helminthosis in small ruminants by immunisation in the sub-Saharan region.

In general, the ideal approach towards an effective control of helminths in small ruminants is the integration of the several methods because each method has its own advantages and disadvantages.

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