Anaemia causing Helminthes Parasite in Ruminants

Alok Kumar Singh1#, Snigdha Shrivastava2,G. Daniel Risheen3, Shalini Tiwari4, and 5Birendra Pratap Singh

1Department of Veterinary Parasitology, College of Veterinary Science & A.H., Rewa
2Ph.D. Scholar, Department of Veterinary Medicine, COVSc& A.H., Rewa
3Department of Animal Husbandry, SHUATS, Prayagraj
4B.V.Sc & A.H., Students, College of Veterinary Science & A.H., Rewa
5Teaching Associate, Animal Husbandry Diploma College, Rewa

Helminthes aredescribed as the parasitic worms belonging to phylum platyhelminthes and nemathelminthes.These parasites cause severe economic losses to the animal owners/farmers by affecting the health of the animals by their blood sucking habit principally leading to anaemia.

  • Anaemia can be referred to the condition when there is reduction in the amount of haemoglobin per unit of blood with or without reduction in red blood cells.
  • List of helminthes parasites causing anaemia in ruminants and details about important parasites
S. No.Name of parasiteSite of predilection
1.Fasciola hepaticaLiver
2.SchistosomabovisPortal and mesenteric veins, urogenital veins
4.Bunostomum phlebotomumSmall intestine
5.OesophagostomumradiatumLarge intestine
6.AgriostomumvryburgiSmall intestine

1.Fasciola hepatica:

These are the leaf shaped, grayish brown flat worms, commonly called as liver fluke, mature in bile ducts. The intermediate host is snails of genus Lymnaea. The definitivehost picks up the infection by ingestionof contaminated grasses containing encysted metacercariae. Principal pathological lesions are seen in liver parenchyma or in bile ducts causing extensive damage of liver parenchyma and marked haemorrhages and in chronic cases hepatic fibrosis is seen.

Clinical signs:

  • In acute cases suddenly sheep dies, blood tinted froth from nostrils
  • Anaemia
  • Hypoalbuminaemia
  • Sub mandibular oedema (i.e. bottle jaw condition)
  • In cattle, digestive disturbances such as constipation is more often seen
  • Reduced milk yield
  • Decreased SNF content in milk 


  • By faecal examination (Eggs in faeces, appear as brownish yellow having indistinct operculum and embryonic cells).

Prevention and control:

  • Elimination of snails by use of molluscicides  such as CuSO4
  • Also done by biological control(by duck rearing)
  • Improving the drainage, to prevent snail habitat
  • Treatment of infected host by suitable anthelmintic
  • Avoiding the grazing of livestock around water bodies
  • Six to seven months old calves immunized with 3 doses of irradiated metacercariae
  • Fencing should be done near the pond/ water logged area

2. Schistosomabovis:

These parasites occur in portal and mesenteric veins of ruminants. Definitive host gets the infection through active skin penetration of the cercariae. Pathogenesis includes; acute intestinal syndrome and chronic hepatic syndrome. Severe haemorrhagic lesions and edema are seen on small intestine mucosa in acute intestinal syndrome and due to host’s cell mediated immune response to schistosome eggs there is hepatic syndrome, in which the inflammatory cells surrounds the egg, later the egg is destroyed and healing is accompanied by deposition of collagen and fibrous tissue formation, giving liver appearance of ‘clay-pipe stem’ fibrosis.

Clinical signs:

  • In acute cases diarrhoea is seen along with dehydration and anorexia.
  • There may be coughing due to migration of schistosomula
  • Anaemia and hypoalbuminaemia seen
  • Loss of weight
  • Decrease in production
  • In chronic cases animals are emaciated and blood picture shows eosinophilia,anaemia and hypoalbuminaemia
  • Neurological signs maybe seen sometimes


  • By faecal examination (Eggs in faeces, appear as spindle shaped).

Prevention and control:

  • Control of intermediate host i.e. snail population
  • In humans- to avoid skin penetration of cercariaby wearing boots, using repellants such as;dibutylphthalate and benzyl benzoate.

3. Haemonchuscontortus:

It is one of the most pathogenic parasites occurring in abomasum of ruminants and commonly known as ‘wire worm’ or ‘Barber’s pole worm’. Anaemia is the principle feature causing the disease as the average blood loss is 0.05 ml/parasite/day. The development of anaemia occurs in three stages, in the first stage, PCV falls rapidly and serum iron level remains normal. In the second phase, PCV maintained at steady and increase in plasma iron level. And lastly, in the third phase, there is rapid drop of PCV due to dyshaemopoiesis.

Clinical signs: It includes three types

(i) Hyperacutehaemonchosis

  • It is seen when animal is exposed to sudden massive infection and severe anaemia may observed
  • Dark colouredfeaces seen
  • Death of the infected animal due to sudden blood loss

(ii) Acute haemonchosis

  • Generally occurs in young animals, in this anaemia is followed by hypoproteinaemia and oedema leading to bottle jaw condition.
  • Chronic haemonchosis
  • Most commonly seen, resulting in 100% morbidity but mortality is low.
  • Infected animals become weak, unthrifty and emaciated.
  • Anaemia and hypoproteinaemia is less severe.


  • On the basis of clinical signs
  • High faecal egg count
  • Identification of larvae in faecal culture (i.e. larvae of haemoncus has ‘kinked’ in tail).

Prevention and control:

  • By grazing management; provision of clean water and safe pastures to the animals.
  • Alternate grazing by other species of host.
  • Ploughing, reseeding and burning of pastures
  • Keep goodnutritional management of the animals
  • Strategic use of anthelminthics
  • Infected animal should be treated and isolated from healthy herd
  • Worm refugia; it ensures that a level of genes remain sensitive to dewormers
  • Use of alternate herbal dewormer
  • Barbervaxis a suitable vaccines, against this parasites

4. Bunostomum phlebotomum:

These are the parasite present in small intestine mainly in duodenum of cattle, grayish white in colour with hooks at anterior ends and commonly called as cattle hookworms. The infection in host occurs through mouth or skin.

Clinical signs:

  • Young animals are more susceptible
  • Affected animals may be diarrhoeic and emaciated
  • In severe cases bottle jaw condition is present due to submandibular edema
  • In calves, when skin penetration by larvae occurs foot stamping and itching is seen


  • By faecal examinationi.e. eggs, are bluntly rounded with relatively thick sticky cells

Prevention and control:

  • Pasture management for control of infective larvae
  • Water trough should be treated with salt and kept clean
  • Bedding must be kept dry
  • Faeces should be removed frequently

5. Oesophagostomumradiatum:

Commonly known as ‘Nodular worms’, adult worms are slender and whitish in colour. In animals having no previous exposure to the parasite, there is no reaction by the larvae migration into mucosa whereas in presensitized animals, there is marked inflammatory reaction around the parasite and focus become encapsulated by fibroblasts. Later on, the nodules may become calcified or the worm may come out leaving a small opening which may discharge pus into the lumen.

Clinical signs:

  • In acute form- causes the inflammation of intestine and affected animals passes black foetiddiarrhoeicfaeces
  • In chronic form- in the entire length of intestine there is formation of nodules referred as pimply gut
  • Intermittent diarrhea seen
  • Occurrence of emaciation and anorexia


  • By faecal examination (faeces may show forth stage larvae in acute cases or eggs)
  • Also done byfaecal culture; the infective larvae have sheath and long whip like tail

Prevention and Control:

  • Antihelminthic therapy with broad spectrum antihelminthics
  • Pasture management
  • Maintain hygienic condition
  • Infected animal should be treated and isolated from healthy herd