SCHISTOSOMOSIS IN LIVESTOCK
This family is primarily parasitic in the blood vessels of the alimentary tract and bladder. The schistosomes differ from other flukes in that the sexes arc separate, the small adult female lying permanently in a groove, the gynaecophoric canal, in the body of the male.
AETIOLOGY AND HOST
S.bovis- Cattle, sheep and Goats (Rest of Asia)
S.indicum- Cattle, sheep and Goats
S.spindale- Cattle and Goats
S.nasalis- Cattle, Buffaloes and Goats
S.incognitum- Pigs and dogs
INTERMEDIARY HOSTS
Snails like planorbis, indoplanorbis and Lymnea.
LIFE CYCLE
Eggs are passed out which hatches immediately to release miracidia. They penetrate, or are ingested by, the IMH snail. After 5-17 weeks furcocercus cercaria emerge from the snail. (Radia and metacercarial stages are absent in the life cycle). The furcocercus cercaria are the infective stage which, after release from the IMH penetrate the skin of host (within 1-2 days). After penetration they become schistosomula and travel via systemic circulation to reach liver, where they become sexually mature and travel to mesenteric veins. Prepatent period is 6-7 weeks.
PATHOGENESIS
Disease is entirely due to deposition of eggs in the mesenteric veins and their subsequent penetration of intestinal mucosa. Localisation in portal vessels may also cause disease associated with hepatic insufficiency.
The female in the mesenteric vein inserts her tail into a small venule and since the genital pore is terminal, the eggs are deposited, or even pushed, into the venule. Aided by their spines and by proteolytic enzymes secreted by the unhatched miracidia, they penetrate the endothelium to enter the intestinal submucosa and ultimately the gut lumen. Haemorrhagic lesions in the mucosa of the intestine are caused by their movement in the lumen.
The wall of the intestine appears greyish, thickened and oedematous due to confluence of the egg granulomata and the associated inflammatory changes. In the liver there is also evidence of egg granulomata and of portal fibrosis provoked by eggs which have been swept into small portal vessels
CLINICAL SYMPTOMS
- spindale
Intermittent diarrhoea with specks of blood and mucous in feces, anaemia and progressive weakness, constipation and diarrhoea alternatively are seen. Chronic hepatic syndrome with neurological signs like ataxia and incordination is also reported. Severe cases have typical “Rice gruel diarrhoea” characterised by profuse, watery, whitish faeces with specks of blood.
- nasalis (Nasal schistosomosis)
In parts of the India sub-continent Schistosoma nasalis occurs in the nasal mucosal veins of cattle, buffalo and horses. In heavy infections there is a copious mucopurulent discharge, snoring and dyspnoea. The main Pathogenic effects arc associated with the eggs which cause abscess formation in the mucosa. Fibrous granulomatous growths occur which may occlude the nasal passages. Rhinitis with mucopurulent discharge, Dyspnoea and snoring, Fibrous tissue proliferation and sanguineous nasal discharge are common. Nasal mucosa may appear studded with small abscesses containing ova. Infection is confirmed by the presence of the spindle-shaped eggs in the nasal discharge.
DIAGNOSIS
This is based mainly on the clinico-pathological picture of diarrhoea, wasting and anaemia, coupled with a history of access to natural water sources. The relatively persistent diarrhoea, often blood stained and containing mucus, may help to differentiate this syndrome from Fasciolosis. The demonstration of the characteristic eggs in the faeces or in squash preparations of blood and mucus from the faeces is useful in the period following patency but less useful as egg production drops in the later stages of infection.
TREATMENT
Tartar emetic 1-2mg/kg Bwt slow i/v (Max-300mg/cow) as 2% soln. Repeated after 24 hrs or a week two more times.
Praziquantel 25-50mg/kg Bwt orally
Anthiomaline- 2.5-5mg/Kg B wt. 1/m. Repeated on alternate days or weekly once for two more times.
CONTROL
Allow dung to ferment which can kill off the larvae
Molluscicides
Management
