Veterinary Parasitic Diseases Note.pdf

PARASITIC DISEASES HELMINTHS NEMATODES TREMATODES CESTODES I. TREMATODES 1. HEPATIC DISTOMIASIS OR HEPATIC FASCIOLOSIS OR LIVER ROT OR FLUKE...

PARASITIC DISEASES HELMINTHS NEMATODES TREMATODES CESTODES I. TREMATODES 1. HEPATIC DISTOMIASIS OR HEPATIC FASCIOLOSIS OR LIVER ROT OR FLUKE DISEASE It is a parasitic infestation of most of the domestic animals caused by the various genera of flukes and characterized by either acute or chronic hepatic insufficiency. Etiology: ❖ Fasciola hepatica: Present in the bile duct of sheep, goat, cattle, buffaloes, pigs, elephants, dog, horse, cat and man. It is leaf like and having broad shoulders. It measures about 13 mm x 13mm. ❖ Fasciola gigantica: Similar to F. hepatica, but it is bigger in size and having narrow shoulders. It measures 25-75 mm x 12mm. ❖ Fascioloides magna: Recorded in the liver of cattle, sheep, bison, deers and it measures about 23-100 mm x 11-26 mm. ❖ Dicrocoelium dendriticum: Occurs in the bile duct of sheep, goats, cattle, pigs, deers, dog, donkey and man. Epidemiology: 1) Occurrence: Occurrence of this disease is worldwide. It is very common in areas where irrigation channel, tanks, ponds, are present in good numbers, because in these the intermediate host of flukes lives. Because of this fact flukes are not common in Bidar district. However, it is present in animals purchased from neighboring states like A.P. and Maharashtra and also sheep gone for grazing to far of places during summer. All age groups are susceptible, young ones are more susceptible and severe form of the disease occurs when compared to adults. It causes severe economic loss which may be due to; 1) Mortality 2) Decrease in production which may vary from 8-20%. Decrease in milk production. 2) Transmission: Ingestion of metacercariae May be also congenital. Life cycle: The adult flukes are present in the bile ducts. They lay eggs and these  2 eggs are passed through the bile into intestine, and thrown out of the body through, the faeces. These eggs under suitable environmental conditions develop, into miracidium which penetrate into the intermediate host i.e. snail (Lymnea spp), and develops into sporocyst. The sporocyst develops into radia and radia gives rise to cercaria. The cercaria comes out of the snail and forms a cyst around it called metacercaria. These metacercaria are found attached to the leaves of the water plant and floating in water. When the animals are taken to tanks, ponds and channels for ingesting along with water metacercaria are also ingested, which goes to the intestine and the cyst breaks open releasing the immature fluke. This will reach the bile duct in any one of the following ways: 1) These can penetrate through the wall of the intestine and get into peritoneal cavity, then it penetrates through the liver capsule and then migrate through the liver parenchyma and gets into the bile duct. 2) From the intestine it will get into the portal vein and through this parenchyma it will get into the liver and migrating through this parenchyma it will reach the bile duct. In the bile duct they mature and become adults and start laving eggs. The above life cycle is characteristic of F. hepatica. F. gigantica - similar to F. hepatica F. magna - Life cycle is same but in cattle it forms cyst in the liver and hence the fife cycle may not be completed. But in sheep it is similar to F. hepatica. Dicrocoelium dendriticum - Here 2 intermediate hosts are present. The first intermediate host is the snail. Where in miracidium gets into the snail and forms sporocyst and then cercaria (there is no radia stage from sporocyst) is formed which are thrown out of the snails in the form of “slime balls” which are eaten by the ants (2nd IH) and develops into “metacercaria”. Final host gets infected by eating such ants in the feed. The cercaria is released in the intestine and crawls through the bile duct opening and migrates through bile into the gall bladder. Pathogenesis: Acute Fasciolosis: The immature flukes burrow and migrate through liver parenchyma leading to destruction of parenchyma. In addition, they feed on the hepatic cells. Due to these things damage to the blood vessels results in haemorrhages and bleeding. If too many immature flukes are migrating through liver it may cause sudden death due to the above damages. Chronic Fasciolosis: Due to the migration of immature flukes the hepatic cells are destroyed and are replaced by fibrous tissue leading to cirrhosis of liver. The  3 small bile duct undergoes thickening and hardening due to the constant irritation caused by the flukes. Later on deposition of calcium in the wall of bile ducts can occur. Because of these things the bile ducts become more prominent and this condition is known as "piped stem liver". In fasciolosis, anaemia can occur, and the causes of anaemia are: 1) The flukes suck blood at the rate of 0.2 ml per fluke per day. 2) May be due to haemorrhages and internal bleeding. 3) Suppression of the bone marrow 4) Destruction of the RBCs. In fasciolosis, obstructive jaundice can occur. Because the conjugated bilirubin formed in the liver is not excreted into the intestine through the bile, since bile duct is obstructed by the flukes. Hence, conjugated bilirubin gets into the circulation and stains the mucosa and serosa yellow coloured. Due to the liver damage, albumin is not synthesized in good amount leading to hypoproteinaemia. This result in decrease in the osmotic pressure of blood leading to seepage of fluid part of blood into the cavities, in s/c tissues especially of intermandibular space i.e. bottle jaw. Clinical findings: Acute: Young claves and lambs can die without showing any clinical signs. In some, the signs noticed are anorexia, pale mucous membranes, dullness, weakness, edema of the throat and conjunctiva. Upon palpation of the last two intercostal spaces of the right side, the animal evinces pain and enlargement of the liver can be noticed. Many will die and can show the symptoms of passing of blood or bloody discharge from the anus and nasal cavity. Chronic: 1) Alternating diarrhoea and constipation, dehydration, weakness, sunken eyeballs. 2) Bottle jaw. 3) Pale mucous membrane 4) In adults decrease in milk production. In sheep wool may fall off. Emaciation and some may have jaundice. In very chronic cases debility and emaciation are common and the animal appearing like having skin and bone appearance. Course: Acute - Up to 2 day to- several days. Chronic - Months (2, 3, 4 months to 1 year). Necropsy findings: Acute: Liver is enlarged, haemorrhages and blood clots on the liver and fluke burrowing tracts most common. Serous fluid in peritoneal cavity. Lot of flukes in liver.  4 Chronic: Liver is small, hard and shrunkened. The bile ducts are prominent, hard and thickened "pipe stem liver". Flukes in the bile ducts. Such livers are condemned for human consumption. Diagnosis: 1. By clinical signs 2. Faecal examination: The liver fluke ova are big in size, the operculum and embryonic mass are indistinct. The eggs are yellow coloured. 3. Serological tests: Indirect IPT, Indirect FAT and ELISA are used. 4. Vanden Berg test: Direct test will be positive. 5. Urine analysis: a) Test for bile pigment is positive. b) Test for urobilinogen is negative since it is not formed Differential Diagnosis: (1) Amphistomosis - By faecal examination - foul smelling faeces and the ova having a knob with distinct operculum and embryonic mass. (2) Salmonellosis: Fever, diarrhoea, dysentery. (3) Johne's disease: Non responding chronic diarrhoea, thick pea soup type of faeces. No fever. By faecal examination one can rule out this disease as ova are not detected. (4) Parasitic diarrhoea: Faecal examination - reveals the presence of various types of nematode ova. Treatment: - I. To eliminate the flukes administer any one of the following anthelmintic. 1. Carbon tetrachloride (CCl4 or CTC) available as 450 ml chemical. Dose: Calf: l-2 ml; Adult cattle: 3-5 ml; Lambs: 0.5-4 ml; Sheep: 1-3 ml; and Dogs: 1-5 ml. Route: orally, mixed with butter milk and drench, it. It is effective against mature flukes. This drug has been administered parenterally i.e. i/m or s/c either alone or mixing with equal quantity of liquid paraffin. Dose: - 1 ml/9 kg. b. wt. with a maximum of 30 ml, 10-15 ml/site i/m. CTC toxicity: CNS depression, drowsiness, inco-ordination, cardiovascular collapse. It is also hepatotoxic. This may be due to administering CTC with fat where it is quickly absorbed. It may also be related to hypocalcaemia. This toxicity is commonly noticed in weak and debilitated animals, when such animals are presented, first treat with calborol and liver extract for 1-2 weeks and then administer CTC. If Nicotinic acid is available administer 2 gms of nicotinic acid and then after one hour administer CTC.  5 2. Hexachloroethane: It is available as - 1) Avlothane (ICI) 500 gm & 3 kg packet. 2) Fairmethaine - 30 gms and 1 kg packet. 3) Hexathane (Sarabhai) 30 gm & 500 gm sachet. Dose: 220 mg / kg. b. wt. (Calf: up to 15 gms. Yearlings to adult: 30 - 45 gms and Sheep: 5-15 gms.) Effective on immature flukes. 3. Hexachlorophene Distodin (Pfizer) available as 100 mg tabs Flukin (AR-Ex) 100 mg tab Flukin forte (AR-Ex) 1 gm tab Dose: 10-20 mg/kg b. wt., for all species. Route: Orally in a banana or as electuary or roti. 4. Nitroxynil - Trodax (M&B) 34% solution, available as 10 ml, 50 ml vial. Dose: 10 mg/kg. b. wt. Route: s/c. This drug will stain wool and should be careful enough to prevent it. Also it will stain milk so avoid using in lactating cow. 5. Oxyclozanide: Zanil (Imkemex) it is a 3.4% w/v available as 1 litre container. Dose: 10-15 mg/kg. b. wt. orally. Nilzan (Imkemex) it contains Tetramisole - 3%, oxyclozanide 3%, w/v (50ml, 100ml. 1 litre size container) Dose: 0.33 ml/kg. b. wt. It is effective against adult worm. Distodin fluke bolus (Pfizer) 1 gm/bolus 6. Hetol @ 125 mg/kg b. wt. It is effective against adult worm. 7. Freon – Dose: Cattle: 100 mg/kg Sheep: 330-660 mg/kg It is effective against adult flukes. 8. Bithional - Cattle: 30-35 mg/kg orally. 9. Phenacetin - 150 mg/kg. for 2 days orally to sheep. 10. Distoject - contains Nitroclofene. Cattle: 3 mg/kg. i/m. 11. Acedist - 6.5 - 33 mg/kg. Effective against adults. 12. Clioxanide - 40 mg/kg. Orally- effective against both mature and immature flukes.  6 13. Niclofolan - 2-3 mg/kg orally effective against mature flukes, can be used for i/m route also. 14. Rafoxanide (Ranide l0 g packets, 20% powder) - 7.5 mg/kg orally, also half the dose s/c. 15. Diamphenitide - 100 mg/kg b. wt. orally - effective against immature flukes. 16. Rafoxanide + Levamisole: Available 17. Albendazole 2.5% suspension i.e. 25 mg/ml used @ 10 mg/kg b. wt., orally. 18. Closantel: Available as Zycloz (Sarabhai Zydus) in 30 and 100 ml containers and the concentration is 15% (150 mg/ml). The dose is 15 mg/kg b. wt., orally for flukes. 19. Triclabendazole: effective against immature and mature flukes and available as – (a) Endex 8.75% suspension (Novartis) – 60 and 250 ml bottles containing 5% Triclabendazole and 3.75% Levamisole hcl. The dose recommended is 2 ml/10 kg b. wt., for sheep and 1 ml/5kg b.wt., for cattle. (b) Endex 19.5% (Novartis) – 30, 60, 250 ml bottles containing 12% Triclabendazole and 7.5% Levamisole hcl. (c) Fasinex bolus – 250 (Novartis) – Containing 250 mg of Triclabendazole and the dose is 1 bolus/25 kg b.wt., in sheep and goats. (d) Fasinex 900 bolus (Novartis) and the dose is 1 bolus/25 kg b.wt., in cattle and buffaloes. II. To overcome dehydration, lactated ringers with dextrose can be given i/v III. Liver extracts like Belamyl, Beekom-L is given orally IV. To overcome anaemia, haematinics are used - Imferon Calf: 3 ml, Heifer - 5 ml and Adult cow/buffalo: 10 ml, i/m on alternative days for 5 days. Prevention and Control: 1. The suffering animals are identified and treated with the recent anthelmintic mentioned above. 2. To eliminate the source of infection the following can be done: A) To eliminate the snails: To kill the snails various chemicals have been used which are known as Molluscicides. 1) Copper sulphate: effective at 26 ppm. It can be applied to marshy lands at the rate of 9 kgs of CuSo4. 2) Frescon - N - trityl – morpholene - 0.25- 0.5 ppm. 3) Sodium pentachlorophenate - 6 ppm. 4) Bayluscide (Bayer) - 0.35 ppm.  7 5) Copper pentachlorophenate - 4.5 kg/acre. Characteristics of Molluscicides: 1) It should be very effective at very low concentration. 2) It should be cheap and commonly available. 3) It should not produce adverse/harmful effect to water faunae, animals and human beings. It is very difficult to get a chemical with the above property hence one or other draw back will be present. Lot of work has been done by WHO in African countries by using molluscicides for the control of snails in Human Schistosomosis. B) By rearing of Ducks. These ducks will eat the snails. This is highly impracticable because ducks may be used for meat purpose by the human beings. C) Hand picking and destroying of snails. It is practically impossible to eliminate all the snails and the cost of labour is very high. D) Biological control: Any one of the following may be tried: a) Hydrophilus triangularis - water scavenger beetle. b) Dyticus marginalis. c) Spherodema rusticum- giant water bug. d) Lamprophorus tenebrosa - Larva of Firefly. These will eat snails at the rate of 1-5 snails/day. The practical utility of the above is questionable because of the chances of above acting as pests to well grown crops cannot be ruled out. 2. AMPHISTOMOSIS (Immature Amphistomosis, Intestinal Amphistomosis, Stomach fluke disease) It is a parasitic infestation mainly of cattle caused by various genera of amphistomes and characterized by severe enteritis. Etiology: Paramphistomum - P. cervi, P. orthocoelium P. gotoi P. epiclitum Cotylophoron - C. cotylophorum Calicophoron - C. calicophorum Ceylonocotyle - Cey. streptocoelium Cey. thapari Gastrothylax - G. cruminifer  8 Fischoederius - F. elongatus F. cobaldi Carmyerius - C. spatiosus C. gregarius Gigantocotyle - G. explanatum They are flukes and they measure about 5-13 mm in length X 2-5 mm in breadth. They are light red in colour. The mature flukes are found in the rumen and the immature flukes are found in the intestine. Epidemiology: 1) Occurrence: World wide. Mainly a disease of cattle and buffaloes and also recorded from sheep and goat. It can cause mortality of 40-60% resulting in good economic loss. Commonly occurring disease. Severe form of the disease is seen in yearlings but can occur in any age group and any sex and breed. Immature Amphistomosis: This name is given because the immature flukes are harmful and the mature flukes are not harmful. Intestinal amphistomosis: This name is given because immature flukes present in the small intestine brings about the pathological changes and thus the disease occurs. Stomach fluke disease: Since the adult amphistomes are present in the stomach viz., rumen and reticulum originally thought of as producing the disease. 2) Transmission: By ingestion of contaminated feed and water especially of tanks, ponds and channel water. Life Cycle: The adult flukes in the rumen lay eggs and will be passed through the faeces. Under suitable environmental conditions further development of egg occurs and the eggs hatches releasing the miracidium. The miracidium penetrates the snail like Indoplanorbis exustus, Lymnaea spp. Bulinus sp., Planorbis planorbis and develops into sporocyst → radia → cercaria. The cercaria comes out of the snail develops into metacercaria which will be found on the leaves of water plants and also floating in water. When the animals ingest water and water plants, the metacercaria are ingested and goes to intestine. From the intestine they migrate into the rumen through the oesophageal groove. In the rumen they develop into adults and start laying eggs. Pathogenesis: The immature flukes which are in the intestine are harmful. They attach to the intestinal mucosa and pluck the mucosa. This results in ulcer formation and bleeding or haemorrhages. These damages results in diarrhoea → dehydration → haemoconcentration → shock → death. Clinical findings: Diarrhoea which is profuse, foul smelling faeces and contains mucosal shreds. Symptoms of dehydration, anorexia, depression, bottle jaw, some may collapse and die. In some loss of weight, weakness, and emaciation is seen.  9 Sometimes immature flukes are passed in the faeces. Necropsy findings: Atrophy of muscles, s/c edema, excess of fluid in peritoneal cavity, serous atrophy of fat, - due to mal-nutrition, or mal-absorption are seen. Haemorrhages in small intestine, ulcers and thickening of mucosa of small intestine and plenty of light red coloured adult flukes in the rumen and reticulum are characteristics of this disease. Diagnosis: 1) By signs of diarrhoea, foul smelling faeces. 2) Faecal examination, in the early stages eggs are not seen and also we may see immature flukes in the faeces. Differential Diagnosis: 1) Fasciolosis: Faecal examination and finding the characteristic ova. 2) Johne's disease: Thick pea soup like faeces, not responding to treatment. 3) Salmonellosis: Fever, diarrhoea, dysentery. Treatment: Very similar to fasciolosis. To over come etiological agent any one of the following drugs can be used: 1. Carbon tetrachloride 2. Hexachlorophene Refer Fasciolosis for dose and route of 3. Hexachloroethane. administration 4. Niclosamide - Niclosan, 500 mg tab Niclex - powder (Alved) 75% w/w Niclex bolus (Alved) 1 gm bolus; dose is 90 mg/kg, b. wt., orally. 5. Bithional. 6. Methyridine. 7. Yomesan. 8. Resorantel. Supportive therapy: a. Kaolin pectin preparation or Astringent mixture. b. To overcome dehydration - lactated ringers and dextrose. Prevention and Control: Similar to fasciolosis. 3. ANIMAL SCHISTOSOMOSIS (a) NASAL SCHISTOSOMOSIS (NS) (Nasal granuloma, snoring Disease) It is a parasitic disease mainly of cattle caused by a blood fluke i.e., Schistosoma nasale and it is characterized by snoring, nasal discharge and nodular or cauliflower like lesions in the nasal cavity. Etiology: Schistosoma nasale previously known as Schistosoma nasalis. It is a  10 blood fluke. It is found in the nasal veins of the nasal cavity. Males and females are present. The males measures about 6.3 -11 mm and female 5-11 mm. The male is having a gynaecophoric canal and in this canal the female is carried during copulation. Epidemiology: 1) Occurrence: It is a disease of the Indian subcontinent i.e., this disease occurs in India, Pakistan, Srilanka, Burma (Myanmar) and Philippines. It is a very common disease of our country and even in Karnataka. It is mainly a disease of cattle and to an extent buffaloes. This disease has been recorded for the first time in sheep by the AICRP on Nasal schistosomiasis, Bangalore centre. Later on by Tamil Nadu AICRP on NS and latter on recorded from goats also. Minimum age of infestation in cattle is 6 months and 11 months in buffalo (and above). There is no variation in breed or sex. Economic importance: The economic loss is due to- 1. Reduction in the working capacity of animals. 2. Reduction in milk yield. 3. Mortality due to NS is very low and very rare. 2) Transmission: The infective stage of the parasite is the cercaria which actively penetrates the skin, the oral and nasal mucosa. Life Cycle: The adult flukes are present in the nasal veins and lay eggs. These eggs are passed out of the body through the nasal discharge. These eggs develop under suitable environmental condition and hatches releasing the miracidium. The miricidium enters the intermediate hosts i.e., snails - Indoplanorbis exustus and develops into sporocyst I which gives rise to sporocyst II. This gives rise to cercaria. There is no matacercaria formation. The cercaria is the infective stage which actively penetrates the skin or oral mucosa or nasal mucosa when the animal ingests water from tanks, ponds and channels. Then they enter circulation and through circulation go to nasal veins and localize in these veins. They develop into adult flukes and start laying eggs. Pathogenesis: The adult worms are harmless. The harmful effects are produced by the eggs. The egg in the nasal cavity undergoes development and will have miracidium which secretes proteolytic enzyme which comes out of the pores of egg shell. These enzymes damage the wall of veins resulting in the rupture of venules/veins. Then the eggs enter the surrounding tissue and around this there will be infiltration of eosinophils, neutrophils and macrophages. These proteolytic enzymes act on these cells and bring about degenerative changes of these cells resulting in formation of ray like structures. This is known as actinobody  11 formation- means pseudo tubercle. Later on lot of neutrophils, lymphocytes and monocytes gets into the site which results in small abscess formation. Later on ripening of the abscesses occurs leading to breaking open of abscess releasing the ova into the nasal discharge. To these areas granulation tissues grows and fills up the area resulting in nodule or cauliflower like lesion. Usually small nodules form, then these coalesce together to form cauliflower like growths. Clinical findings: 1) Nasal discharge - serous, mucous, mucopurulent, serosanguineous, blood & blood clots also can be seen. 2) Sneezing. 3) Snoring which can be heard even from a distance and is due to obstruction of nasal passage. 4) Nodules or cauliflower like lesions in the nasal cavity. This type of lesion may not be present in some animals but commonly seen in most of the animals. 5) Decrease in working capacity, decrease in milk production and in advanced cases dyspnoea can be seen. Course: It is a chronic disease and without treatment it is probably present throughout the life of animal. Necropsy findings: Nodules or cauliflower like lesions in the nasal cavity. Diagnosis: 1) By symptoms of snoring and nasal discharge. 2) By lesions- nodules or cauliflower like lesions in the nasal cavity. 3) By examination of the nasal discharge and demonstrating the presence of eggs. The nasal discharge is collected by using an instrument called Vaulkman's scoup. The scraping should be done until slight bleeding occurs. Then the nasal scrapings can be examined in two ways or preserved in 10% formalin and submitted to a laboratory. (1) Direct examination: A small quantity of discharge/scrapings is placed on a slide and 2 drops of 10% Sodium or potassium hydroxide is added. Then the contents are mixed and a coverslip is placed and examined under the low power of microscope. (2) Indirect examination: The nasal scrapings is transferred into a glass centrifuge tube and 3-5 ml of 10% sodium or potassium hydroxide is added. Then the contents are boiled and cooled. Then centrifuged at 2000 - 3000 rpm for 5 minutes and the supernatant is discarded. Mix the sediment and transfer a small quantity on a slide and put a coverslip. Examine the slide under the low power of  12 microscope. If Napoleon hat shaped or Boom rang shaped eggs are seen then it is positive for nasal granuloma. 4) Intradermal test: Jagannath and co-workers of Veterinary College, Bangalore devised this test in 1988. In this test the antigen from S. japonicum is injected intra dermally at the ventral aspect of the base of the tail. If erythema and wheal of about 0.7 to 2.7 cm in size occurred within 10-20 minutes, then it is considered as positive. Differential Diagnosis: NG should be differentiated from Rhinosporidiosis. It is a disease, which is recorded commonly in foreign countries like Australia, U.S.A., previously has been also recorded in our country now a day (Tamil Nadu). It is caused by a fungus called Rhinosporidium seeberi and this disease is very similar to NG and the double walled endospores are detected in the nasal discharge microscopically. Treatment: To eliminate the fluke any one of the following can be used: 1) Anthiomaline (M&B) - Lithium antimony thiomalate 6% available as such and Anthiomaline (M&B) as a 50 ml vial. Dose: - 15-20 ml deep i/m administered 3-4 times at an interval of 3 days i.e., twice a week for 2 weeks. Even can be used on alternate days for 3-4 times. Some Veterinarians have tried i/v route also. Side effect: It causes painful swelling at the site of injection which can be overcome by fomentation. 2) Antimosan (Bayer) - 50, 500 ml container. It contains penta sodium antimony biscatechol - 3:5 disulphonate. Dose is 20-40 ml/animal, any route i/v, i/m or s/c, 3 times at an interval of 3-4 days. Now not available in our country. 3) Neguvon (Bayer) - It is an ectoparasiticidal agent and available as a powder of 1 kg packet but not available in our country. This drug has been tried by the AICRP, Bangalore centre as follows: i) 30 mg/kg b. wt daily for 8 consecutive days orally as drench. It was toxic. ii) 40 mg/kg, b. wt. - for 4 consecutive days orally - also toxic. iii) 40 mg/kg. b. wt. 4 times administered on alternative days was found better. Here the animals behaved as though they have recovered from this disease i.e., no nasal discharge, no nodules, no snoring for only 1-3 months and then again animals exhibited the clinical signs of the disease. That means it produces a temporary curative effect. Recurrence of the disease was noticed within 1-3 months. iv) 50 mg/kg, b. wt. - 4 times at an interval of 3 days. The effect was similar to iii.  13 v) Topical application (a) the powder was mixed with small quantity of water and made into a paste and was applied and rubbed to nasal lesion every day for 10 days. (b) An ointment was prepared with Vaseline and applied to the lesions once a day for 10 days. These methods were also toxic to animals. 4) Ambilhar (Ciba) - It contains Niridazole. It is a drug used for human schistosomosis and it was available as tablet. Dose: 25-50 mg/kg was not effective; 75 mg/kg b. wt. daily for 7 days was toxic. 5) Sodium antimony tartarate (SAT): It is available as a chemical in powder form. It is administered after preparing a 2% solution in 10% Dextrose saline. Dose: 1.5 mg / kg body weight. Route: Administered as a slow i/v. injection. The solution is drawn into a 20 or 30 ml syringe. The 18 gauge needle is inserted into the jugular vein of a cow and fixed the needle. Check whether the needle is exactly in the vein or not. Then the syringe is connected, and few ml of blood is withdrawn into the syringe. Then 2-3 ml slowly is injected and then few ml of blood is withdrawn into the syringe. Again 2-3 ml is injected. This procedure is repeated until all the solution is injected. Schedule: In Bangalore, in one schedule, it was administered twice a day for 2 consecutive days and was found to be slightly toxic. Then this schedule was modified and the drug was administered once a day for 4 consecutive days and this method was not toxic and the animals recovered from disease. 6) Potassium antimony tartarate - available as Tartametic (Ethicare) as 2% and 4% solution, 25 ml vial. Dose: route & schedule of administration is similar to sodium antimony tartarate. Adverse reaction to Sodium and Potassium antimony tartarate: If by chance perivascular infiltration of the drug occurs then it causes severe irritation and swelling of the region. The swelling goes on increasing and it appears as though another head is growing in that region. This swelling will be hard and mostly fibrous. The antimony preparation should not be used in cows which are in advanced stage of pregnancy even though they are suffering from NS. Because – i) They are highly irritant resulting in swelling which may be responsible for fever resulting in abortion. ii) Delaying the treatment for 3-4 months will not cause the death of the animal. 7) Praziquantel: @ 5 mg /kg. b. wt. orally, reduced the EPG. 8) Muraleedharan K and Rajashekar C. published a research paper in 1996 in the Indian Veterinary Journal (73(3): 265-269) entitled Comparative efficacy of some Anthelmintics against nasal schistosomiasis in cattle and the findings are:  14 Oxyclozanide @ 10 mg/kg b. wt., orally, once a week for 3 weeks – best Levamisole @ 7.5 mg/kg, s/c once a week for 3 weeks - 2nd best Rafoxanide @ 7.5 mg/kg, orally once. Ivermectin @ 0.2 mg/kg b. wt. (1 ml/ 50 kg) s/c once. Lithium antimony thiomalate @ 15-20 ml per animal, i/m, once a week for 3 weeks. Complete cure was not noticed and reduction in EPG and lesions was observed. Prevention and Control: 1. Identify the infected animals and treat them. 2. Eliminate the source of infection. (a) Give tap or well water to the animals. Because such water does not contain the cercaria, it is not possible practically. So store the pond or tank or channel water for 24-48 hrs and then allow the animals to ingest the water. This method makes the water free from cercaria because they will not survive in such condition for 24-48 hours. (b) To eliminate the source of infection, we have to eliminate the intermediate hosts i.e. snails. This method is very similar to the one mentioned in fasciolosis. (c) Guppy fish method: Lebistus reticulatus which is commonly kept in the aquarium, to keep the water clean because it ingests the excreta. One guppy fish will ingest 48% of the miracidium in one hour. Thus reducing the no. of miracidium entering the snail and the no. of cercaria coming out of the snail. In addition, one guppy fish will devour 1000 cercaria per hour. This method was developed by Dr. K, Muraleedharan, Dr. S. Prasanna Kumar and Dr. K. S. Hegde (1975) who was awarded the Dr. K. M. Nair's memorial award for the best Research paper published in IVJ, in 1975. Very easy to breed the guppy fish, very economical, not harmful. (b) OTHER SCHlSTOSOMES OF DOMESTIC ANIMALS 1. Schistosoma bovis: It occurs in the portal and mesenteric vessels of cattle, sheep, goats and sitatunga in Southern Europe, Southern Asia and Africa. The affected animals become anaemic, lose condition and show alternate diarrhoea and constipation, gradually wasting away until death takes place. The faeces contains blood and mucous and the eggs can be found in them in large numbers. A characteristic feature is the marked grey pigmentation of the lungs and liver. On microscopic examination there is pigment in the liver and numerous eggs may be found, surrounded by cellular infiltration and fibrous tissue. The intestine  15 shows the presence of eggs in its wall in the form of grey clusters or thickenings which are opaque and grating to the knife. The mucosa usually shows small haemorrhages and sub mucosa may be thickened. 2. S. spindale: Present in the mesenteric vein of cattle, goats, sheep and dog in India and Sumatra. The eggs are passed in the faeces but sometimes also in the urine. The eggs are elongate, flattened on one side and have terminal spine. 3. S. indicum: Present in the portal, pancreatic, pelvic, hepatic, and mesenteric veins of sheep, goats, cattle, equines and camels in India. The eggs cause nodules in various organs and cirrhosis of the liver with debility especially in horses. The eggs are oval with a terminal spine. 4. S. suis: Present in the pig and dog in India. It may be identical with S. incognitum. 5. S. japonicum: Present in the portal and mesenteric vessels of man as well as cattle, horse, sheep, goat, dog, cat, rabbit and pig in the Far East. The eggs are passed in the faeces. They are short, and oval, and may have a small lateral spine or knob. The main clinical sign is diarrhoea and the faeces contains mucous and blood. Abscesses in the liver and intestine. Ascites is usually present.  16 II. NEMATODES 1. ASCAROSIS (a) CANINE ASCAROSIS It is one of the common parasitic infestations of all the domestic animals. It is a parasitic disease of dogs caused by Toxocara canis and Toxascaris leonina and characterized by signs of pneumonia and enteritis. Etiology: Toxocara canis: It is a round large worm. Males measure about 10 cms and females 18 cms in length and occur in the small intestine. Toxascaris leonina: A long round worm, males 7 cms and females 10 cms in length. Occurs in the small intestine. Epidemiology: 1) Occurrence: Recorded throughout the world. It is a very common parasitic infestation of dogs. Puppies are highly susceptible when compared to adults and many can die. 2) Transmission: By ingestion of eggs containing second/third stage larvae. - Transcolostral - Transplacental Toxocara canis: Life Cycle: The adult worms are present in intestine and they lay eggs. One adult female worm can lay up to 200,000 eggs in a day and these eggs are passed in the stool. The eggs develop, under suitable environmental condition. The larva moults to become second stage larvae. The eggs containing the second/third stage larva is the infective stage. The animals when they ingest contaminated feed and water or by licking skin of animals containing the eggs, swallow this stage. It goes to the intestine and the egg hatches and releases the second / third stage larva. This larva penetrates the intestinal mucosa gets into the portal vein and goes to the liver. From the liver it goes to the heart and enters the circulation. In adult dogs or bitches somatic migration occurs, where in the third stage larva goes to the various tissues like liver, heart, kidney, muscles and remains in these tissues. Hence this stage is (3rd stage) lying dormant. Further development does not occur in these tissues. When the bitch is in 42nd day of gestation some of the larvae are withdrawn from these tissues into the circulation. These larvae pass through the placenta and get into the developing foetus. They remain in the liver of the foetus. This type of transmission is called as transplacental transmission. After the birth of the puppies, some of the larvae are secreted along with the colostrums. When pups suckle the colostrums, the 3rd stage larvae get into the  17 intestine and through the portal vein into the liver. This type of transmission is known as ‘Transcolostral transmission’. These larvae go through blood to the heart and through circulation into the lungs. In the lungs, by rupturing of the capillary, the larvae enter the alveoli or parenchyma of alveoli. Here they moult to become the 4th stage larvae. These migrate into the bronchiole and then into bronchi to the trachea. From trachea, it goes to the larynx and then to the mouth and reswallowed; through the esophagus goes to the stomach and then to the intestine, In the intestine, they moult to become the 5th stage larva and become adults. These develop to become mature worms and the female starts laying eggs. The pups under 5 weeks of age if they ingest the eggs containing 2nd stage larva it goes to the intestine and gets into the portal vein and goes to the liver. From liver, it goes to the heart and then to the lungs (4th stage). From the alveoli it migrates to the larynx and then to the mouth and reswallowed. It gets into the stomach and then goes to the intestine. If the pups are more than 5 weeks of age and above and if they ingest the eggs containing the 2nd stage larva, the somatic migration seen in adult dog will be seen in such pup also. Toxascaris leonina: Life Cycle: The eggs containing the 2nd stage larva when it is ingested it goes to the intestine. Here it hatches and larva comes out. The moulting of larvae takes place and complete development of worm into the adult occurs in the intestine itself. Pathogenesis: Because the larvae are present in the liver and lungs, damage to these organs occurs. In the liver, it causes formation of milky white spots and hence it is called as ‘white spotted liver’. In the lungs, damage to parenchyma occurs with haemorrhages, pneumonic changes are also seen. In the intestine it causes mild form of enteritis and also due to the accumulation of large number of adult worms in the form of bundle will result in intestinal obstruction, intussusception or intestinal perforation resulting in the death of pups. Clinical findings: Some pups may die without showing symptoms, which may be due to intestinal obstruction. Occasional vomition, diarrhoea, dehydration, weakness, emaciation, unthriftiness, rough hair coat, pot belly and symptoms of pneumonia like coughing is also seen. Stunted growth can be seen in pups. Vomition can result in aspiration of the material into the respiratory system, leading to aspiratory pneumonia. Nervous signs are also seen; i.e., restlessness, incoordination, etc. These symptoms may be due to the irritation of the nerve endings of the intestinal  18 mucosa by the worm. Necropsy findings: Refer to pathogenesis. Diagnosis: By faecal examination. Treatment: Drug of choice is Piperazine. Dose: 100-300 mg/kg. This drug is given orally. The first dose is given when the pups are 2-3 weeks of age, as the larvae have developed into the adult worms. Because the drug is effective against mature worms only. The drug is not effective against immature worms and migrating larvae. Then repeat the drug at 6 and 8 weeks of age to kill all the worms. Piperazine compounds available in our Country Piperazine hydrate : Piperazine phosphate : Piperazine citrate 100 mg : 104 mg : 120 mg (More effective) Mechanism of action of Piperazine: It is having a narcotizing effect on worms resulting in detachment of the worms from the mucosa and along with the peristaltic movement of the intestine the worms are thrown out in the faeces. Piperazine Compounds: - 1) Helmacid Liquid (Glindia): It is a 45% solution of piperazine hydrate. Container size: 115 ml and 450 ml bottle. Dose: 4-5 ml /10 kg b. wt. In all spp. of large animals. 1 ml/5 kg b. wt. in dogs and cats. Better to avoid piperazine in cats as it may cause adverse effects. 2) Helmacid Tablets: Piperazine hydrate 260 mg/tab. 3) Helmacid with Senna granules: It produces laxative and purgative effect also. Available as 10 gm sachet. 4) Antepar (Burrough's Wellcome): 40% piperazine citrate solution and the container size is l00 ml and 450 ml bottle. 5) Antepar Tablets: Contains 500 mg of piperazine per tablet. 6) Piperex (Sarabhai): 35 and 225 gms containers available. Along with this 9 gm spoon is also available. 7) Verban Liquid (Cyanamid): 56.3% solution of Piperazine hexahydrate. 120 ml, 450 ml bottles and 4.5 liter jar available. 8) Vermex Liquid (Pfizer): This contains Piperazine hexahydrate. 100 ml, 500 ml, 4.5 liters containers available. 165 mg/ml. 9) Helmavet (Minumix Pharmaceuticals): 45% piperazine hydrate solution 100 ml and 500 ml bottles. 10) Piperazine Liquid (HAL): 450 mg/ml. It contains piperazine 45%, 500 ml  19 and 4.5 liter jar available. Many other companies also prepares this product The following drugs also can be used: 1) Chinapodium oil - 0.1 ml/kg b. wt., orally 2) Diethyl carbamazine citrate - 50 mg/kg b. wt., orally 3) Thiabendazole - 300-500 mg/kg b. wt., orally 4) Tetramisole - 10 mg/kg b. wt., orally 5) Pyrental tartarate - 5-7 mg/kg b. wt., orally 6) Dichlorovas - 12-15 mg/kg b.wt., orally 7) Neguvon - 75 mg/kg tid for 2 weeks 8) Avlon/Tetracap - 0.l ml/lb b. wt., orally 9) Fenbendazole - 5 mg/kg b. wt., orally (old) 20-50 mg/kg b. wt.(new) for 5 days 10) Nitroscanate - 50 mg/kg b. wt 11) Mebendazole - 10 mg/kg, bid, orally 12) Levamisole - 7.5 mg/kg b. wt., orally 13) Albendazole - 5-10 mg/kg b. wt., orally. (b) FELINE ASCAROSIS Toxocara cati: It occurs in the small intestine of the cat and members of the wild felidae family. Infection occurs by the ingestion of 2nd stage larvae. The life cycle is almost similar to T. canis. Mouse may act as intermediate host and will have the 2nd stage larvae. Second stage larvae may be found in the tissues of earthworms, cockroaches, chickens, sheep and other animals fed infective eggs. Visceral larva migrans: Mainly caused by the larvae of T. canis though the larval stages of T. leonina, T. cati. Capillaria hepatica (of rodents) and Lagochilascaris minor (of wild felines) etc. have also been incriminated. It is characterized by the chronic granulomatous lesions in the inner organs of children like liver, lungs, brain and sometimes eye. (c) SWINE ASCAROSIS It is caused by Ascaris suum. Life Cycle: It is almost similar to Toxocara canis. Here the disease is characterized by severe dyspnoea which is called 'Thumps' (Rib cage raising and falling) and blockage of bile ducts and hence obstructive jaundice may be noticed. Necropsy findings: Milky white spotted liver is very characteristic lesion and it is nothing but a chronic granulomatous inflammation with white necrotic material.  20 Treatment: 1) Piperazine (citrate) - 100-300 mg/kg b. wt., and given orally in the feed. 2) Sodium Fluoride - (old drug) 100-150 mg/kg b. wt. and administered in the feed. 3) Hygromycine - (old drug) 6000 IU/lb. of feed. This is extensively used as feed additive and used for the period of 60 days. 4) Levamisole - Effective against both immature and mature worms - 7.5 mg/kg b. wt., orally or i/m, s/c. 5) Tetramisole - 15 mg/kg b. wt., orally. It is effective against both mature and immature worms. 6) Parbendazole - 30 mg/kg b. wt., orally. 7) Fenbendazole – 5-10 mg/kg b. wt., orally. 8) Cambendazole - 20 mg/kg b. wt., orally. 9) Morantal tartarate - 5 mg/kg b. wt., orally. (d) BOVINE ASCAROSIS Bovine ascarosis is caused by Toxocara vitulorum (Neoascaris vitulorum). Etiology: It is caused by Toxocara vitulorum (Neoascaris vitulorum). The males measure up to 25 cm x 5 mm and the females 30 cms x 6 mm. The cuticle is not as thick as that of other large ascarids and these worms therefore have soft, translucent appearance. The eggs are sub globular, provided with a finely pitted albuminous layer and measure 75-95 by 60-75. Epidemiology: 1) Occurrence: They occur in small intestine of calves of cattle and buffaloes. They cause the severe form of the disease in young calves of 1-4 months of age. However, calves above 6 months of age are faecally negative which may be due to the 3rd larvae lying dormant and may be also such calves may be immune to this parasitic disease. Buffalo calves suffer from severe form of the disease when compared to cattle calves. Previously it was considered as the number one cause of calf mortality in buffalo calves, causing considerable economic loss to the dairy farmers. Mortality can range from 25 to 50%. Now due to regular deworming with piperazine salts, the occurrence is reduced. However, it is still a big problem in buffalo calves of Bidar. 2) Transmission: It is very similar to that of Toxocara canis. Transplacental and transcolostral is very common and it may vary from place to place. In Bidar it appears to be transplacental transmission, which is playing a major role since  21 repeated examination of the colostrums and milk from cows and buffaloes immediately after parturition until 2 weeks after parturition were negative for the 3rd stage larvae. Life cycle: It is also very similar to that of T. canis. In some places both transcolostral and transplacental transmission can occur and in some places it can be any one of these methods of transmission. Pathogenesis: This is also very similar to that of T. canis. It appears that worm load plays an important role. It appears that liver may be significantly affected. Depending on these above factors, clinical signs vary from one buffalo calf to the other. The changes can be mild, moderate and very severe. In advanced cases intestinal obstruction due to forming of bundles by the adult worms in the intestine can lead to death of the calf. The exact reason is not known, however the possibility of toxemia playing a major role cannot be ruled out. Whether the toxaemia is due to the toxins of the worms or toxins liberated by the intestinal bacteria or toxins due necrosis of intestine after the obstruction ? Further detailed work on these aspects is very much essential. Clinical findings: Depending on the severity, three forms of the disease are observed: 1. Mild form (Grade I): The buffalo calf will be in a standing position and will not exhibit much of the clinical signs. Here at the most, one can observe mild diarrhoea. Faecal examination will be positive. 2. Moderate form (Grade II): In this form, the buffalo calf will be slightly anorectic, slightly weak, rough hair coat, pot belly and slightly depressed. Slight to moderate diarrhoea may be present. Slight loss of weight may also occur. Worms can be noticed in the faeces. Faecal examination will be positive. 3. Severe form (Grade III): In this form, the buffalo calf will be recumbent, anorectic, markedly depressed, weak and subnormal temperature is very characteristic. Usually the animal has not passed the faeces from 1-3 days indicative of constipation. In addition, conjunctival mucous membranes are very much congested/cyanotic, shallow respiration and weak heart beats occurs. The faeces will be pasty, brown in colour and slightly foul smelling. Necropsy findings: These are very similar to Toxocara canis. In advanced cases, the entire length of the intestine especially colon will be filled with worms. Diagnosis: 1. By clinical signs. 2. Faecal examination.  22 3. Examination of colostrums and milk up to a period of 15-20 days after parturition can reveal the 3rd stage larvae. Treatment: Mild and moderate form of ascarosis responds well to anthelmintic treatment. Supportive therapy may not be required. However, severe form of ascarosis requires anthelmintic as well as supportive treatment. Even inspite of vigorous supportive therapy, many of the buffalo calves will succumb to severe form of ascarosis. The following anthelmintics can be used: 1. Piperazine @ 100-300 mg/kg body wt., orally. 2. Tetramisole @ 15 mg/kg body wt., orally. 3. Levamisole @ 7.5 mg/kg body wt., orally, s/c, i/m. 4. Fenbendazole @ 5-10 mg/kg body wt., orally. 5. Albendazole @ 10 mg/kg body wt., orally. 6. Mebendazole @ 10-20 mg/kg body wt., orally. 7. Ivermectin @ 0.2 mg/kg body wt., s/c, orally. The following supportive therapy can be tried for severely affected calves: 1) Fluid therapy: 5% Dextrose, DNS, Lactated Ringer’s solution, Arolyte-M can be administered @ 1-2 bottles, i/v. 2) Camphor-in-oil: 1-2 tablets of camphor is crushed and mixed in 5 ml of ground nut oil and administered @ 0.5 -1.0 ml s/c and 0.5 -1.0 ml i/m. to a calf. This may be beneficial to overcome hypothermia. Corticosteroids: Dexamethazone @, 0.5-2.0 mg/kg, body wt. i/v, i/m may help in over coming toxaemia and hypothermia. 3) Calcium preparations: Administer 20-30 ml of calcium borogluconate or Mifex (Ca, Mg, P, Dextrose) i/v or s/c with caution. It may be useful to overcome hypothermia. 4) Antibacterial agents: May or may not be useful. Use of gentamicine, ampicillin, amoxycillin, OTC etc., may be beneficial. Prevention and control: 1. Proper disposal of faeces. 2. Administering of an anthelmintic in the advanced stage of gestation is very essential. Here the drug effective against 3rd stage larvae is required. This will over come the transplacental and transcolostral transmission. However such drugs are not available for use in buffaloes and cows. However, in sows levamisole has been found to be effective against 3rd stage larvae in pregnant sows. 3. Following regular deworming schedule is a must. Administering of any one  23 of the anthelmintic mentioned under treatment when the calves are of 1 month, 2 months, 3 months and 4 months of age is very essential. This will save lot of calves. 2. HOOKWORMS OF DOMESTIC ANIMALS (a) ANCYLOSTOMOSIS It is a disease of dogs caused by Ancylostoma caninum, Uncinaria and Necator spp., characterized by poor growth, and clinical signs of anaemia. Etiology: 1) Ancylostoma caninum are gray to red coloured worms, females are slightly longer than males and males measures about 10-12 mm in length and females measures about 14- 16 mm. Both have well developed buccal capsule and 3 pairs of ventral teeth. 2) Ancylostoma braziliens: Found in small intestine of dog, cat, foxes and human beings. 3) Ancylostoma tubaeformis: Found in cats. 4) Ancylostoma duodenale: Common in man and also occurs in dogs and cats. 5) Necator americanus: Common in man. 6) Uncinaria stenocephala: Dogs, cats and foxes. Epidemiology: 1) Occurrence: It occurs through out the world. All breeds of dogs are equally susceptible and young ones are highly susceptible when compared to adults. It is one of the commonly occurring parasitic disease of canines wherein many severely affected dogs can die. 2) Transmission: Infective larvae enter the final host either by penetrating the skin or by ingestion of contaminated feed and water. Life cycle: Life cycle is direct. The eggs hatch and parasitic larvae are produced in about a week. There are 2 free-living larvae. (a) Non parasitic stage larvae which is very sensitive to desiccation. (b) Infective larvae which is capable of entering the body by penetrating the skin. Second stage larvae (50 larvae infective) penetrate the skin and get in to the blood, then carried to the heart and later on to lungs. Larva stays in the lung capillaries for a while become 4th stage larvae and enter the alveoli by rupturing and penetrating capillaries. Larvae crawl up in respiratory tract, coughed off and then swallowed. It develops and moults after reaching intestine and becomes adult and lays eggs. An infected pup can pass as many as 5 million eggs / day.  24 (2) Sometimes larvae directly get in to the GIT and becomes adult with out migration. (3) Sometimes larvae in the circulation may get through placenta to the foetus and may develop prenatal infection, and this is transplacental transmission. This is questioned by many workers. (4) Transcolostral transmission: Larvae in the milk for 20 days after whelping are recorded. Pathogenesis: Migrating larvae does not cause much damage and only adult parasites are harmful as they are active blood suckers and cause severe anaemia. The mechanisms of anaemia are: (1) Sucking of blood by parasites (0.8 ml / parasite/ day) (2) Hemorrhages in the intestine, it is observed, that the parasite produces a type of anticoagulant which is responsible for haemorrhages. Anaemia does not occur as long as iron in body reserve is present. When its reserve is depleted it results in microcytic hypochromic anaemia. (3) Malabsorption: - Impaired absorption of iron from the intestine. (4) Disturbances in hemopoiesis (not confirmed). Clinical findings: Puppies may die without showing any symptoms. At the age of 2-3 weeks it remains alive, shows the signs of severe anaemia and coma. Other dogs show signs of anemia - weakness, pale visible mucous membranes, increase in heart rate, emaciation; ascites (hypoproteinaemia), dry skin, stunted growth, mild diarrhoea, melaena (black coloured faeces) and itching of skin. Necropsy findings: Anaemia, cachexia is well marked, pale mucous membranes, ascites, Intestine is congested, oedematous, haemorrhages and lot of worms embedded in its lumen. Red-bite marks of intestine are very important lesions. Diagnosis: (1) Faecal examination. Egg may appear in different shape. It should be differentiated from coccidial oocyst and Dipylidium caninum egg. Coccidial oocysts are very small where as Dipylidium egg/brood capsule is very large. (2) Occult blood test of faeces will be positive. Differential Diagnosis: This disease should be differentiated from the diseases which causes anaemia, like: (1) Acute leptospirosis: High fever, haemoglobinuria, jaundice, demonstration of organism in urine. (2) Chronic nephritis: Normocytic normochromic anaemia.  25 (3) Coccidiosis: Dysentery and oocyst in the faeces. (4) Canine babesiosis: High fever, haemoglobinuria, demonstration of organism inside the RBCs. (5) Canine Ehrlichiosis: Detection of organism in the cytoplasm of mono nuclear cells. Treatment: (1) Disophenol (2, 6, Di-iodo 4-nitro phenol) was available as Ancylol - 10 ml vial, 1 ml containing 45 mg. It was a commonly used injectable anthelmintic. Dose: 1 ml /4.5 kg body weight/(10 mg/kg. b. wt. and 0.2-2 ml/dog, s/c). Now a days it is mostly not available. (2) Tetrachloro ethylene (Tetracap) 0.2 ml/kg orally. Should be administered after overnight fasting. A saline purgative (MgSo4 + NaCl) is administered after the giving the Tetracap. (3) Bephenium hydroxy naphthoate (Alcopar, Burroughs Wellcome) is administered @ 15-20 mg/kg and repeat after 6-10 days. Very bitter to taste. (4) Thiabendazole: 300-500 mg/kg orally. (5) Mebendazole 22 mg/kg, daily, orally for 5 days. (6) Pyrental: 6-15 mg/kg, orally commonly used in human beings. (7) Albendazole: 5-10 mg/kg body weight (old dose); now a days used @ 25-50 mg/kg b. wt. (8) Panacur 50 - 100 mg/kg. body weight orally. (9) Nitroscanate 50 mg/kg. body weight, orally. Supportive treatment: To over come anaemia - 1) Blood transfusion is done in severe anaemia. 2) Haematinics like Imferon (1-2 ml/dog, i/m, 3-4 times at an interval of 1-2 days) and Ferrous sulphate( 1-2 tablets/dog/day for 20 days) are used. To over come metabolic acidosis and dehydration sodium bicarbonate and lactated Ringer's solution is used. Prevention and Control: (1) Keep the floor dry. (2) Treat the floor with sodium borate at the rate of 10 lbs/100 sq. feet or 1% sodium hypochlorite solution. This treatment kills the larvae or exposes the sheath of egg so that larvae cannot survive in the environment Sodium borax should not be applied to the lawns as it damages it. (3) Proper disposal of stool. (4) The following vaccines have been tried: a. Killed.  26 b. X-irradiated vaccine. c. Attenuated vaccine (5, fluro uracil can be used). The vaccines are not commercially available in India. (5) Administration of fenbendazole every day 15 days before whelping and 5-7 days after whelping / 40th day of gestation to 14 days after whelping @ 50 mg/kg, b. wt. orally. (b) HOOKWORMS OF SHEEP AND GOAT (1) Bunostomum trigonocephalum: Common one is Bunostomum trigonocephalum which is present in small intestine of sheep and goats and it is similar to Ancylostomosis. Treatment: Thiabendazole 75 mg/kg, orally. All other broad spectrum anthelmintics used for Strongyle sp. are used here also. (2) Gaigeria pachyscelis: Similar to Bunostomum and found in sheep and goat of India and Africa. (c) HOOK WORMS OF CATTLE Bunostomum phlebotomum: Similar to Ancylostomes. Mainly occurs in cattle and rarely in sheep and goat. Treatment: Thiabendazole 50-110 mg/kg, orally. All other broad spectrum anthelmintics used for Strongyle sp can be used here also. 3. CANINE SPIROCERCOSIS It is caused by Spirocerca lupi and characterized by the development of nodules in the oesophagus, stomach and aorta of dogs, fox, wolf and jackals. Etiology: Spirocerca lupi - it is a nematode, it is bright red in colour and spiral in shape and, male measures about 30-50 mm and females 50-80 mm. Transmission: - Ingestion of intermediate host i.e. coprophagus beetles and also due to numerous transport hosts (paratenic host) like amphibians, reptiles and birds. Infective stage is the 3rd stage larvae. Life cycle: The embryonated eggs are laid in the oesophagus or stomach and are passed in the faeces. These eggs are ingested by Coprophagus beetle and in the beetles, larva are encysted in the tracheal rings (L3). These beetles are ingested by the transport host i.e., mainly by birds i.e. chickens. When the dog eats the beetles or transport host the larva (L3) gets into the stomach and penetrates the wall of the stomach and reaches the gastric and gastro epiploic artery. Through the wall of these arteries they get into the coeliac artery and then migrate to the aorta. They may remain in aorta or they may bypass the connective tissue through tunnel like  27 structures between the nodule of aorta and oesophagus and gets into wall of the oesophagus and then into the stomach. When they are in the oesophagus or stomach they become adults and then start laying eggs. Pathogenesis: Migrating larvae produces haemorrhages, inflammatory reaction, purulent streaks or abscesses and these heal up and lead to stenosis of aorta. Later on, chronic granulomatous inflammation sets in leading to formation of nodules in the oesophagus and stomach. These nodules can unite together to form pedunculated mass. Due to this, difficulty in ingestion of food and also repeated vomition occurs. Nodules can break open abruptly leading to massive internal bleeding which is often fatal. Sequelae: 1) May cause oesophageal sarcoma. 2) Hypertrophic pulmonary osteo arthropathy. Some larvae can get into long bones - thickening of bones. 3) Pyaemic nephritis. 4) Spondylitis of adjacent thoracic vertebrae (cervical spondylosis) 5) Aplastic anaemia. Clinical findings: Depends on place of nodules: Stomach - persistent vomition and no food remaining in the stomach. Oesophagus - Comes in the way of deglutition and also due to pressure on trachea, difficulty in respiration. Loss of weight, emaciation, weakness, and in oesophageal sarcoma animal will die of severe emaciation. Sometimes sudden death - due to rupture of nodules present in pulmonary aorta - thoracic cavity filled with lot of blood. In prolonged cases, there may be enlargement of long bones. Necropsy findings: Nodules in stomach, oesophagus and aorta. If the aorta is ruptured then clotted blood is found in thoracic cavity. Diagnosis: 1) By symptoms of persistent vomition, weakness and emaciation. 2) Faecal examination: Eggs are small, transparent, capsule shaped, oval, containing larva. 3) X-ray of long bones- pulmonary osteo arthropathy. Treatment: (A) Any one of the following anthelmintic can be used:  28 (1) Diethyl carbamazine citrate: Drug of choice since long time and administered @ 25 mg/kg body weight orally for 4-10 days. The preparations available are- 1) Hetrazan (Lederle) l00 mg/tab. 2) Lorcid (Vets Pharma) - 400 mg/tab. 3) Caricide 4) Banocide (2) Disophenol (Ancylol) -1 ml/4.5kg b. wt., s/c is effective. (3) Recently levamisole and albendazole have been found to be effective. (4) Avermectins: Also has been used. (B) Surgical therapy is also not of much use. Prevention and control: Control of intermediate hosts may be of use in prevention of the spirocerca infection. 4. CANINE HEART WORMS It is a parasitic disease of dogs, cats, foxes and wolves caused by Dirofilaria immitis and are characterized by malfunctioning of the right side of the heart, leading to passive venous congestion, ascites and hydrothorax. Etiology: It is caused by the filarial worm, Dirofilaria immitis. The male worms are 12-16 cms and the female worms are 25-30 cms in length. Epidemiology: 1) Occurrence: Heart worms have been recorded through out the world in dogs, cats, foxes, wolves etc. It can occur in any age group. 2) Transmission: The third stage larva is the infective stage and is transmitted by the bite of all the three types of mosquitoes namely Anopheles, Culex and Aedes. Life cycle: The adult worms are found in the right atrium, right ventricle and pulmonary artery. The adult female lays the first stage larva known as the microfilaria. The larvae get into the circulation and will be found in the peripheral blood. When the mosquito sucks the blood the first stage larvae get into the mosquito and further development takes place. This larva moults twice to become the third stage larva which is the infective stage. When such mosquitoes suck the blood from a dog, they introduce the third stage larvae. In the subcutaneous tissue and muscular tissue further development of larvae occurs for a while. Then they get into the blood and through circulation these larvae are carried to the right side of the heart. Within 1-2 months they become adults. Pathogenesis: The larvae in the subcutaneous tissue cause dermatitis and itching. The larvae and the adult worms in the heart causes the blood flow from right  29 auricle to right ventricle to pulmonary artery to lungs will become irregular and there will be back flow of blood leading to passive venous congestion which is characterized by ascites, anasarca, etc. The worms cause rugose or villose endarteritis of the pulmonary artery resulting in the formation of the thrombus. This can cause infarction, necrosis and fibrosis. Clinical findings: In some animals sudden death can occur which may be due to intra vascular haemorrhages and there may be renal haemosiderosis. Commonly the disease is characterized by chronic cough which will be exaggerated exercise. Weakness, pot belly, rapid breathing and upon exercise the dog may collapse and die. Upon auscultation heart murmurs can be heard. ECG will indicate inverted T wave. Necropsy findings: Ascites, hydrothorax, hypertrophy and enlargement of the right side of the heart and lot of adult worms are seen. Diagnosis: 1. By symptoms / clinical signs. 2. By blood examination: Any one or all the methods mentioned below can be used to demonstrate the microfilaria in the blood of dogs. The blood is collected during the activity of the mosquitoes i.e., evening and night wherein good number of microfilaria will be present in the peripheral blood: a) Direct method: Place a drop of blood on a slide and place a coverslip and examine under the low power of the microscope. The moving larvae can be demonstrated. b) Make a blood smear and stain with Giemsa and examine under the microscope to demonstrate ‘S’ shaped larvae. c) Modified Knott’s method: 1 ml of blood is placed in a centrifuge tube and then 9 ml of 2% formaline is added and the contents are mixed. Then centrifuged for 5- 10 minutes at 1000-1500 RPM. The supernatant is discarded and the sediment is mixed. Then a drop of the sediment is placed on a slide and a drop of 1: 1000 Methylene blue solution is added and the contents are mixed. Then a coverslip is placed and examined under the microscope for the blue coloured larvae. 3. Serological test: ELISA has been used. Treatment: To eliminate the worms, various drugs have been used. Since the drugs have to be used for a prolonged period of time, it will end in toxicity or adverse reaction. Any one of the following drugs can be used: 1. Thiacetarsamide sodium (Caparsolate): It contains 20% arsenic and is available as a powder. A 1% solution is prepared with water for injection and administered  30 @ of 1.0 mg/lb body weight as a slow i/v injection, b.i.d. for 2 days. It's effect is only on the adult worms and does not have any effect on the microfilariae. It is the drug of choice for heart worms and is not available in our country. Note: 1. Perivascular infiltration is highly irritant and will result in huge swelling. 2. To overcome the toxicity, administer the antidote. The antidote is Dimercaprol (BAL) and it should be administered at the rate of 4 mg/lb body weight per day in 4 divided doses. Also corticosteroids can be administered. 3. Diethyl carbamazine citrate: can be used @ 25 mg/kg body weight per dose, orally, t.i.d. for 3-5 weeks. The effect of the drug is only on the microfilaria. It sensitizes the microfilaria so that it is readily phagocytized by the macrophages. 4. Antimosan (Bayer): This is an old drug which is not available in our country now. The schedule to be followed is : a) First course is for 6 days @ 0.5 ml/10 kg weighing dog, slow i/v, i/m, s/c daily. b) Give a break for 7 days. c) Start a second course @ 1.0 ml daily for 6 days. d) Give a break for 7 days. e) Start the third course @ 1.5 ml daily for 6 days. The drug temporarily sterilizes the female worm. Only the cumulative effect is fatal to the worm. 5. Levamisole: Recent studies have given highly encouraging results in treating heart worms with levamisole @ 11 mg/kg, b. wt., orally, for 5-6 days. Levamisole: 6 mg/kg b. wt., orally is commonly used dose in dogs. Prevention and Control: All the efforts should be made to eliminate the intermediate host i.e, the mosquitoes. Various ectoparasiticides should be used to eliminate the mosquitoes. Identify the infected animals and treat them with the anthelmintics mentioned above. Some have used the prophylactic dose of the anthelmintic during the mosquito breeding season.  31 5. LUNGWORM INFESTATION (a) VERMINOUS PNEUMONIA OF CATTLE (Lung worm infestation, Verminous bronchitis, Husk, Hoose) It is a parasitic disease of cattle caused by Dictyocaulus viviparus and is characterized by pneumonia. Etiology: It is a round worm and the males measure about 5 - 5.5 cms and the females about 6-8 cms in length. Epidemiology: 1) Occurrence: Reported from many parts of the world. It is very common in U.K. and U.S.A. In our country it is commonly recorded in hilly areas. This worm is highly host specific as only the cattle are affected. Cattle of all the age group can be affected but calves of 4-10 months of age are commonly affected with the severe form of the disease. This disease is commonly seen in warm, wet summer months. 2) Transmission: is by ingestion of contaminated feed and water. The infective stage is the third stage larva. Life cycle: The adult worms are present in the bronchioles and alveoli and they lay eggs. These eggs are coughed up and reswallowed. Then they pass through the g.i. tract and while passing through the g.i., tract the eggs are hatched and the first stage larvae will be passed in the faeces. Under moist environmental conditions, the larvae develop and moult twice to become the third stage larvae and this is the infective stage. When the animal ingests the infective stage, it will get into the small intestine. Then they will penetrate the intestinal wall and get into the mesenteric lymph nodes. Here the third stage larva moult to become the 4th stage larva. Then it gets into the lymphatic and goes to the heart and then into the lungs. In lungs they get into the alveoli and develop into the mature worm and starts laying eggs. Pathogenesis: The migrating larvae damage the intestine and lungs and haemorrhages are seen. When they will be in the bronchi, there will be inflammation resulting in accumulation of neutrophils and eosinophils leading to the obstruction of the air passages and emphysema develops. Damage to the intestine can result in diarrhoea. Clinical findings: This condition can be acute or sub-acute one. 1. Acute type: This type commonly occurs in adult cattle. Calves also can be affected. Initially there will be fever of 104 -105°F, nasal discharge, increase in heart and respiratory rate; the breathing will be shallow and hurried. Coughing  32 will be loose and husky. There will be increase in vesicular murmurs and bronchial tone. Because of emphysema, crackling sounds can be heard. There will be marked reduction in the body weight. Later on there will be marked dyspnoea characterized by open mouth breathing, grunting and cyanosis. Finally the animal collapses and dies. The course of the disease is 3-4 days. The mortality is 75-80 per cent. 2. Sub-acute type: This form is commonly seen in calves. Initially, before the onset of respiratory signs, there will be diarrhoea. The temperature may be normal or slightly elevated. The respiratory rate can be 60-70 per minute. There will be paroxysms (violent and uncontrolled) of coughing and loss of gain in weight. The course of the disease can be 3-4 weeks. Then there will be disappearance of the signs and these animals will have the badly damaged lungs and will be highly susceptible to bacterial infections. Stunted growth can be there for several months. Necropsy findings: Areas of consolidation (atelectasis) can be seen. Emphysema is also seen which can be alveolar and interstitial. There will be oedema of the septa. In the bronchi and bronchioles there will be pus and larvae and adult worms can be seen. Histopathology: Alveolar epithelialization and hyaline membrane formation are very characteristic of this condition and these changes are irreversible. Diagnosis: 1. By symptoms 2. By faecal examination for the presence of larvae. 3. Serological test like CFT is used for the diagnosis. 4. Intradermal allergic test also has been used. Differential diagnosis: All the types of pneumonia should be considered under the differential diagnosis. Whenever an animal is not responding to sulpha and commonly used antibiotics then one should suspect for Verminous pneumonia. Treatment: 1. To eliminate the lungworms any one of the following anthelmintics can be used: a) Tetramisole: It is available as Nilverm (AIL) and Curaminth (Sarabhai) as a 30% powder and the container size is 6 gms and 100 gms. The dose is 15 mg/kg body weight of the active ingredient. b) Levamisole: It is available as Helmonil (Alved) in the form of a tablet, bolus, 30% powder and an injectable solution (182 mg/ml). The dose is 7.5 to 8.0 mg/kg  33 body weight orally or i/m, s/c. It is very effective and is the drug of choice for lungworms. Also many companies are preparing this drug. c) Diethyl carbamazine citrate: It is available as a tablet like Caricide (Cyanamid, 400 mg), Uni carbazon (Unichem, 50 mg), Hetrazan (100 mg), Unicarbazon forte (250 mg) and as an injectable like Unicarbazon 2 ml amp. and Unicarbazon forte 5 ml amp. containing this drug, chlorpheniramine and Prednisolone. The dose used is 20 mg/lb. body weight i/m or 100 mg/lb. body weight in 3 divided doses, orally. This drug is effective against adolescent worms. Recently the following drugs have been used for the treatment of lung worms in all the species of domestic animals, and are found to be very effective: 1. Ivermectin : Used @ 0.2 mg/kg body weight, s/c. 2. Fenbendazole : Used @ 5-7.5 mg/kg body weight, orally. 3. Albendazole : Used @ 5-10 mg/kg body weight, orally. 4. Oxibendazole : 2.5-5.0 mg/kg body weight, orally. 2. Also antihistaminics like Avil @ 3-5 ml/calf, i/m can be used. 3. Administer corticosteroids like Dexamethazone @ 10 mg/calf or 20 mg/adult, i/m. Prevention and Control: 1. Proper disposal of faeces. 2. Avoid grazing of animals on wet pastures. 3. Vaccinate the animal with any one of the following: a) X-ray irradiated vaccine: This vaccine is prepared by IVRI, Izatnagar, UP. This vaccine contains the third stage larvae of the lung worm exposed to the X-rays. It is administered orally at an interval of 6 days twice. The larvae gets into the intestine and then into mesenteric lymph nodes and stays there. Here it triggers the immune response. It gives 90 -100 % protection. b) Triethylene malamine attenuated vaccine: This vaccine contains the third stage larvae exposed to this chemical. Thus the larvae lost its pathogenicity. To preserve this vaccine is difficult and hence not commonly used when compared to the first vaccine. (b)VERMINOUS PNEUMONIA OF SHEEP AND GOATS Etiology: It is due to: 1. Dictyocaulus filaria which is very similar to D. viviparus 2. Mullerius capillaris. 3. Protostrongylus rufescense. For number 2 and 3 the life cycle is indirect and needs snails and slugs as intermediate host. They cause nodules in the lung parenchyma.  34 Treatment: It is very similar to cattle. (c) VERMINOUS PNEUMONIA IN PIG Etiology: 1. Metastrongylus apri. 2. Metastrongylus salmi. 3. Metastrongylus pudendotectus. Life cycle: is indirect, as earth worms act as intermediate host. These lungworms transmit hog cholera and swine influenza viruses. Treatment: is very similar to cattle. (d) VERMINOUS PNEUMONIA IN HORSES AND DONKEYS Etiology: Dictyocaulus arnfieldi which is very similar to D. viviparus. It occurs commonly in donkeys when compared to horses. It produces mild form of the disease. Treatment: is very similar to cattle. 6. PARASITIC GASTROENTERITIS (Parasitic diarrhoea) It is a parasitic infestation of almost all the domestic animals caused by various species of Trichostrongylus, Ostertagia, Nematodirus, Cooperia etc., and it is characterized by gastroenteritis. Etiology: Cattle Sheep & Goats Name of the parasite Abomasum Small intestine Abomasum small intestine I. Trichostrongylus sp. Trichostrongylus axei + - + - T. colubriformes - + + - T. longispicularis - + - + II. Ostertagia sp. O. ostertagi - - + - O. circumcincta - - + - O. trifurcata - - + - III. Cooperia sp. C. punctata - + - + C. onchophora - + - + C. pectinata - + - - C. curticei - - - + IV. Nematodirus sp. N. spathiger - + - + N. battus - + - + N. filicollis - + - + N. helvetianus - + - - These worms are nematodes and they are short and thick worms.  35 Epidemiology: 1) Occurrence: Present throughout the world. They cause severe economic loss which may be due to - (1) Stunted growth - they utilize the nutrients. (2) Mortality. (3) Anaemia (Trichostrongylus) not so severe. Young ones are highly susceptible and severe form of disease is seen. 2) Transmission: It is due to ingestion of contaminated feed and water which contains 3rd stage larva. Life cycle: The adult worms are present either in abomasum or small intestine and lay eggs. They are passed in the faeces and under suitable environmental conditions, the larvae develop and moult twice to become the 3rd stage larva. These are ingested by the animals which go to abomasum or small intestine and develop into the adults. Pathogenesis: Some of the larvae can get into the gastric glands and may destroy them. Hence the hydrochloric acid secretion is reduced. The normal pH of abomasal fluid is 2.5-4.5 and in this condition there will be increase in pH and it may be around 6. Due to this change, indigestion occurs. Also formation of pepsin is reduced resulting in improper digestion of proteins. Some of the pepsinogen get into blood and its level increases in the blood. These worms also cause abomasitis and enteritis which results in increased motility of gastro intestinal tract. All the above changes cause diarrhoea → dehydration → haemoconcentration. Because of these changes, there will be hypoproteinaemia i.e., total plasma proteins (TTP) will be decreased from its normal value of 7-7.5 gms to 4-5 gm %. This results in anasarca. Ostertagia also can cause microscopic nodules in the gastro-intestinal tract. Clinical findings: Diarrhoea and the faeces may be dark green in colour and may or may not be foul smelling. Rough hair coat, anasarca, stunted growth, and decrease in gain in weight, weakness and emaciation, are seen. Constant mortality in a dairy farm can be seen which is very important. Necropsy findings: Abomasitis, enteritis and presence of large number of worms. Diagnosis: 1. By symptoms /clinical signs. 2. By faecal examination: By morphological characteristics of eggs it is very  36 difficult to identify the worms into various genera and hence they are classified as strongyle ova. 3. Biochemical, TPP - 4-5 gm% Blood pepsinogen level is increased. Differential Diagnosis: 1. Colibacillosis - Young ones under 2 weeks, fever and chalky white diarrhoea. 2. Salmonellosis - Any age group, usually young ones, fever, diarrhoea and dysentery. 3. Viral gastroenteritis - R.P. and B.V.D. Oral lesions, fever, diarrhoea and dysentery. 4. Parasitic - Fasciolosis, Amphistomosis, Coccidiosis. Faecal examination reveals the characteristic ova, or oocyst. 5. Johne's disease - No fever, thick pea soup like diarrhoea and not responding to treatment and it is a chronic disease. Treatment: A) To overcome the gastro-intestinal parasites any of the following broad spectrum anthelmintics can be given. 1. Phenothiazine: Chemical name is Thiodiphenyl amine. Also known as Dr. Roger's product. It is a very old product, used extensively for a long period of time. Now a days it is not commonly used even though it is cheap. It is available as "Phenovis" (EEL) 95% dispersible powder - 3 kg tin (Rs. 300/-). It is a green powder. Dose: Cattle - 10 gm/45 kg bodyweight with a maximum of 79 gms/animal and administered orally. Sheep and goats: 5-20 gms depending on the size of animal. Horse: 3-5 gms/45 kg, body weight orally - through naso-gastric tube or as an electuary. Metabolism: Half of the drug administered remains in the gastro-intestinal tract and produces its effect. The other half of the drug gets converted into phenothiazine sulphoxide by the action of certain enzymes in the mucosa of gastro-intestinal tract and gets absorbed. It goes to the liver and converted into leucophenothiazone and leucothional. These go to the kidney and get filtered in the urine. Then they get oxidized and forms into phenothiazone and thional. These oxidized products are brown colouring dyes which imparts brown or reddish brown colour to the urine. Phenothiazine sulphoxide can get into the anterior chamber of eye and when it is exposed to ultraviolet rays i.e., sunlight, it causes keratitis, ulceration, blindness within 36 hours. Such type of reaction can occur in non pigmented skin  37 leading to photosensitization. Eventhough it has been extensively used for long period of time, now a days it is not commonly used because: (1) Photosensitization - Keratitis, dermatitis. (2) In anaemic and debilitated animals it has been shown to cause lysis of RBCs. (3) In advanced stage of pregnancy, it may cause abortion. (4) In sheep, when this drug is administered, due to spilling of urine on the wool, the colour of wool is changed to brown or reddish brown which is very difficult to remove. Horses are highly susceptible to toxicity. To prevent the toxicity and its side effect in all the species of domestic animals, it is better to administer the drug in the evening and not to expose the animal to sunlight for 1-2 days which will be not that easy. 2. Benzimidazole compounds: These compounds bind to tubulin and disrupt the nutrient uptake. (a) Thiabendazole: [2-(4-thiazolyl) benzimidazole] and when it is administered it is readily absorbed and excreted. The mechanism of action is it acts on the enzyme Fumerase reductase of the worm and hence the energy to the worms is not available. It is a broad spectrum anthelmintic wherein it is effective against many species of nematodes. It has got a very good effect on mature worms and moderate effect on immature worms and also ovicidal effect. Dose: Cattle, sheep and goats – 50 -100 mg/kg body weight, orally. Availability: Thiabendazole (MSD) 75% powder in 100 gm and 1 kg containers. Thiabendazole bolus – 2 gms Thiabendazole tablets – 0.5 gm Thiabendazole solution - 450 ml, 10 ml = 3.33 gm Thiabendazole premix 250 gm and 1 kg tin (b)Cambendazole: Chemical name is (isopropyl 1,2-(4-thiazolyl)-5- benzimidazole carbamate and is not available in our country. Dose: 20-25 mg/kg body weight orally. (c)Fenbendazole: The chemical name is [Methyl 5-(phenyl thio)-2- benzimidazole carbamate] and it is a broad spectrum anthelmintic wherein it is effective against various nematodes and Moneizia spp. It was introduced as Panacur (Hoechst) 25% powder; container size of 6, 60 and 120 gms., Panacur tablets of 150 mg and bolus of 1.5 gm. Dose: 5-10 mg/kg body weight, orally for large animals and 25-50 mg/kg body weight for dogs. (d) Parbendazole: The chemical name is [Methyl 5-butyl-2-2-benzimidazole  38 carbamate] and is available as Helatac premix (SKF) in 480 gm tin/jar as 4% powder and along with it a 7.5 gm spoon is also provided. Dose: Cattle – 30 mg/kg b. wt., orally. Sheep – 15-30 mg/kg b. wt., orally. Pigs - 25-30 mg/kg b. wt., orally either in feed or as electuary. Precautions: a. The cow’s milk should not be used for human consumption for 3 days after administration. b. This drug should not be administered to pregnant ewes during the first two months of gestation, because it can cause teratogenic effect. (e)Albendazole: Broad spectrum anthelmintic, effective against strongyles, flukes, and tapeworms. Available as "Analgon suspension" (Wockhardt) 70 ml bottle, 1 litre, 4.5 litre, 25 litres can. 25 mg of albendazole/ml of suspension Albomar (Glindia) – 2.5 suspension; 30 ml, 120 ml, 2500 ml suspension. Albomar - powder 250 gms and 50 gms. It is a 15% powder Valbazan (SKF) available as 30 gm sachet, powder and tablets of 150 mg and bolus of 600 mg. Dose: 5-10 mg/kg, b.wt., orally. 6. Oxibendazole Dose: 10 mg/kg b. wt., orally. 3. Imidazothiazoles: a) Tetramisole: Broad spectrum anthelmintic and a very safe drug in all the large animals. It is also an immunopotentiating drug and it potentiates the CMI response. There are no contraindications in sheep and goat. It is a d-form (dextro rotatory). It is available as "Nilverm" (ICI) which is a 30% powder (out of 100 gm powder 30 gm active ingredient). 10 gms and 100 gm container. Dose: 15 mg of tetramisole/kg, b. wt. 35-50 mg of Nilverm/kg b. wt., readily dissolves in water hence administer as drench. b) Levamisole: It is an l-form of tetramisole i.e., levo rotatory. It is a broad spectrum anthelmintic wherein it is effective against many nematodes, mites etc. It is also having immunopotentiating effect. It is used in human being, sheep, goat and all species. It is also used along with vaccine especially in Clostridium chauvoei, Cl. septicum, etc. It potentiates the CMI response and also it increases the humoral immune response. It is also used along with H.S. vaccine and got good response.  39 This is also quite safe in large animals but not extensively used in dogs because it causes side effects like vomition, tremors, salivation, bone marrow disturbances. Mechanism of action: Levamisole blocks the metabolic pathway responsible for formation of ATP. It produces muscarinic and nicotinic like effect. Available as Helmonil (Alved, Madras) powder 30% powder. 10 gms, 50 gms, 100 gms and 1 kg tin. Helmonil tablets – 150 mg/tab Helmonil bolus Helmonil injectable 10 ml, 30 ml vial 182 mg of levamisole Hcl/ml of inj. solution Kalmisole (KAL) - 75 mg/ml. "Lemasol" (Ranbaxy) available as 10% powder, 20 gm and 100 gm. Available as 50 ml vial, 75 mg/ml. "Wormal" soluble powder (Microlabs) 20 gm, 50 gm, 500 gm. 30% powder, 300 mg of levamisole hcl/gm of powder. Dose: 7.5 mg/kg, b. wt., orally or i/m or s/c. 4. Tetrahydropyrimidines: (a) Pyrantel tartarate: This drug causes nicotinic like effect. Here acetyl choline gets accumulated and hence paralysis of worm occurs. (b.) Morantal citrate (Broad spectrum) "Banminth II (Pfizer) available as 4% solution, container size 100 ml. 500 ml, 4.5 litre. Available as tablets. 118.8 mg/tab. Available as Banminth forte bolus- 1.188 gm/bolus. Dose: 10 mg/kg, b. wt. or 1 tab/20 kg, b. wt. or one bolus / 200 kg, b. wt. Contraindication: This drug should not be administered within 72 hours after the administration of CCl4 other wise, severe mortality will occur. Broad spectrum means - These anthelmintics are effective against various species of Trichostrongylus, Haemonchus, Bunostomum, Trichuris, Ostertagia, Cooperia, Nematodirus. All are not effective against Ascaris but few anthelmintics, like Fenbendazole, Albendazole, Levamisole are effective against Ascaris of dog, swine, cattle and buffalo. 5. Ivermectin inj. (Ivomac 1 ml, 7 ml, 20 ml and oral suspension (Dynamic Pharma) 1% w/v -cattle 1 ml/50 kg s/c, sheep 0.5 ml/25 kg.  40 It is a broad spectrum anthelmintic having effect on many nematodes and also ticks, lice, mites. The mechanism of action involved is it interferes with nerve transmission by opening the chloride channels. Contraindications: Not to be injected in horses. Not to be used in pregnant cows one month before parturition. Toxic to Collie and other related breeds of dogs. Moxidectin, Doramectin, administered @ 0.2 mg/kg b. wt., in sheep, cattle i/m. 6. Thiophanate wettable powder (M&B) - Thiophanate 70% w/w 10g, l00 g, 1 kg. Effective against mature and immature worms and also ovicidal. Dose: 70 mg/kg b, wt., orally. 7. Febantel – 7.5 mg/kg b. wt., orally. 8. Netobimin – 7.5 mg/kg b. wt. 9. Oxfendazole – 4.5 mg/kg. b. wt., for cattle and sheep. Schedule of deworming: 1st dose at 1-2 months of age. 2nd dose at 2-3 weeks after the first dose. Repeat once in 3 months until they are one year of age. The first dose is given at 1-2 months of age because by that period the adult worms will be found in the g.i. tract. Majority of the anthelmintics are effective against mature worms. The second dose is given after 2-3 weeks because the immature worms were not eliminated by the anthelmintic and by allowing 2-3 weeks these worms will become mature, so that, they are also eliminated. For the animals which are one year and above regular deworming is done once in 3-6 months. If an adult animal is suffering from parasitic infestation, the anthelmintic is administered twice at an interval of 2-3 weeks. This schedule holds good for both trematodes and nematodes. B) To overcome anaemia, administer haematinics. C) To overcome dehydration and metabolic acidosis give lactated ringers i/v. D) To overcome hypoproteinaemia give protein rich feed and if necessary administer Hermin (Alembic) it contains essential amino acids. 200 ml bottle Dose: As much as possible. To over come hypoglycaemia and supply energy administer 1-2 bottles of 5-10% dextrose i/v. E) To reduce diarrhoea, administer "Neblon" or Kaolin pectin preparation. F) Give mineral vitamin mixture for 3-4 weeks; Lactivet, Nuvimin forte - old name now known as Supplivite - M (Sarabhai). These animals suffering from heavy parasitic infestation will take many  41 weeks to return to normal condition after treatment. Prevention and Control: 1. Sustained release intra-ruminal devices (boluses) have been used – a) Ivermectin – 1 bolus – 135 days - cattle b) Fenbendazole – 1 bolus – 140 days – cattle c) Morantel tartarate – 1 bolus – 90 days - cattle d) Oxfendazole 5 or 6 times, releases anthelmintic once in 3 weeks - cattle. e) Albendazole – 100 days – sheep 2. Pour-on : 10 mg/kg b. wt. in cattle but not in sheep. 3. Rotational grazing: (a) Here the grazing land (pasture) is divided into different plots. Animals were grazed in the first plot for few days and then moved on to the second plot. This is done to cover all the plots. This will eliminate the source of infection. (b) Rotating the species of animals (c) Mixed grazing (d) Using different age groups. 4. Management practices like – (a) Avoid overcrowding. (b) Proper disposal of faeces. (c) Keep water and feed troughs above ground level. (d) Maintain high plane of nutrition. (e) Keep the barn dry. 5. Follow regular deworming schedule. To avoid resistance to the anthelmintic better to follow: a) Rotate the chemical group annually. b) Use the effective drug. c) Do not under dose. d) Use the minimum number of doses. Some of the anthelmintics like Closantel and Disophenol have been used which will be in the body for a prolonged period of time. Closantel is an endectoparasiticidal agent and when it is administered orally, it will be absorbed and will be protein bound in the blood and will remain there for about 60 days. When the worms suck blood this will enter into the worm and kill them. Hence such anthelmintics are now a days preferred for the prevention and control of worm infestation in animals. 6. Vaccination ~ x-ray irradiated vaccines have been tried, but commercially not available.  42 7. HAEMONCHOSIS It is a severe parasitic infestation of cattle, sheep and goat caused by Haemonchus sp. and is characterized by anaemia and anasarca. Etiology: (1) Haemonchus contortus (2) Haemonchus placei Both found in the abomasum of cattle, sheep and goats. They are short, thick round worms-about 1-2.5 cm in length. They are called as "Barber's pole" worms. Occurrence: This parasitic infestation has been recorded in many parts of the world and also occurs in our country. Ruminants are commonly affected and in sheep it is a big problem. Young ones are very susceptible and good number can die of this parasitic infestation. They suck lot of blood from abomasum which is similar to the hook worm - anaemia, weakness, emaciation, pale mucous membrane, and lack in growth rate. Symptoms of anaemia is seen, and in chronic cases the animals will be very much emaciated i.e., hide bound condition i.e., skin and bone appearance. The PCV and TRC will be very low. Transmission: Life cycle, diagnosis, treatment and prevention and control are very similar to parasitic diarrhoea. Hypobiosis occurs with H. contortus and outbreaks of the disease may occur in sheep that have been placed inside. Under field conditions larvae may become hypobiotic in the autumn and winter and remain so until spring, when they mature and commence egg laying. Hypobiosis appears to be related to cold stress on the larvae. A great deal of effort has been devoted to determining the conditions in which haemonchosis occurs in sheep so that outbreaks can be predicted and preventive measures taken. Bioclimatographs have been produced for different geographic areas and it has been accepted that months which have a mean temperature of 180C with rainfall over 5.25 cm. are those in which outbreaks may occur. Thus outbreaks are more likely to occur in wet hot conditions where cold nights are not encountered. Lambs on a low protein diet are less able to withstand the pathogenic effects of infection. The cobalt status of sheep is also important in haemonchosis, animals on a cobalt deficient diet being less susceptible to the effects of infestation with H. contortus. Hay free rations have been shown to inhibit fertile egg production, the inhibition being overcome by the addition of 5% alfalfa.  43 8. EQUINE STRONGYLOSIS (Red worm infestation) It is a parasitic infestation of horses caused by various species of Strongylus, Triodontophorus and Trichonema and characterized by anaemic and colicy signs and debility. Etiology: Strongylus vulgaris, Strongylus edentatus and Strongylus equinus are known as large strongyles which suck blood. Triodontophorus and Trichonema are called small strongyles which will not suck blood. Epidemiology: 1) Occurrence: It occurs throughout the world. They are the most commonly occurring parasites of the equines viz., horses, donkeys and mules. The young ones are highly susceptible when compared to the adults wherein there will be failure of young horses to grow properly and the less efficient performance of working horses. These parasites cause colicy signs which are very common in horses and lot of importance has been given to this parasitic infestation. It can kill the animals as a result of pathological changes due to Verminous mesenteric arteritis and even considered as one of the emergency conditions of the horse. 2) Transmission: Since Strongylus vulgaris it is a very common parasite, its details are given below: transmission is by ingestion of 3rd stage larvae. Life cycle: The adults are found in the caecum and colon and lay eggs. These are passed in the faeces. Under suitable environmental conditions, the larvae develop and moult twice to become 3rd stage larvae. Upon ingestion, it goes to the intestine and penetrates the mucosa and gets into the mesenteric arteries. They will enter the tunica intema of the artery and crawls through this artery and goes to the aorta. It may be circulated to renal, hepatic, cerebral and coronary artery. Latter they will come back to caecum and colon and become adults and start laying eggs. Pathogenesis: 1. They suck blood and causes anaemia. 2. They cause arteritis. 3. They produce aneurysms and even nodules. Because of this, the lumen of the blood vessels is decreased and blood supply to the part of the intestine is decreased. Latter on the b