Endemic Moist Eczematous Syndrome in Cattle a Laboratory Outbreak Investigation in Jhapa District of Nepal
Endemic Moist Eczematous Syndrome in cattle a Laboratory outbreak investigation In Jhapa District of Nepal
Dr.Kedar Karki
M.V.St.
Preventive Veterinary Medicine
Vet. Officer
Central Veterinary Laboratory
Abstract
An endemic hyperemic moist eczematous syndrome was reported in Cattle and Buffaloes in Jhapa district of Nepal throughout month of September soon after prolong spell of drought followed by heavy rainfall causing water logging total 56 cattle and buffalo had been affected and out of which 12 animal died. Rest of ill animals had been treated with five%of Antidegnala liquor and Penta-sulphate. Straw and Skin samples revealed Penicillium sp.Fungus.
Key word: Endemic hyperemic moist eczematous syndrome, Cattle and Buffaloes, Jhapa district, Nepal, Antidegnala liquor and Penta-sulphate, Penicillium sp.Fungus, postmonsoon.
Review of Literatures:
Facial eczema is a disease of sheep and cattle which occurs in warmer districts of the North Island throughout late summer and autumn and is responsible for significant production losses in some years. It is caused by a fungus, Pithomyces chartarum, which proliferates on dead plant material in pasture under warm, humid conditions. The minute spores of this fungus include a substance, sporidesmin, which produces severe toxic effects in the liver. The appearance of livers of affected animals varies, according to the severity of the damage, from slight mottling with light patches to gross discoloration, distortion, and atrophy of large areas. Often the severely damaged portions are surrounded with new liver tissue. As a result of this harm the functions of the liver are impaired. Blockage of bile ducts might stop the excretion of waste substances in the bile for example, accumulation in the fat and skin of bile pigments, derived from the normal breakdown of old red corpuscles, produces the jaundice or yellow staining generally seen in the carcasses of affected sheep. Of certain significance is the loss of capability to excrete the substance phylloerythrin. This is formed in the digestive tract of ruminants by means of the degradation of chlorophyll and is absorbed from the intestine and carried to the liver, where it is normally excreted in the bile. If this excretory mechanism is upset, phylloerythrin passes into the bloodstream which supplies the whole of the body. Phylloerythrin belongs to a class of flourescent pigments which are capable of generating the skin sensitive to sunlight, causing reddening, intense itching, swelling, and scab formation. It is these effects, normally showing on the face of affected animals but also on other unpigmented skin exposed to light, such as the teats and udders of cows, which give rise to the well-liked name “facial eczema”. These skin effects are, even so, secondary to the a lot far more significant impairment of liver function.The fungus, Pithomyces chartarum, grows only on dead or dying plant tissues, not on the living leaf. Hence the amount of the fungus in a pasture is related to some extent to the quantity of this dead material, or litter, present. Growth of the fungus, and its production of spores, is strongly influenced by climate and environmental factors. Temperature, humidity, and the time throughout which the litter remains wet appear to be particularly essential. This explains the typical, despite the fact that not invariable, association of the illness with a period of warm, wet weather, frequently following a dry spell throughout which grass growth has ceased and litter has accumulated in the herbage.The toxic substance, sporidesmin, has been isolated from cultures of the fungus and its chemical structure determined. A single dose of one-thousandth of an ounce is sufficient to kill a lamb of about 60 lb live weight. Sporidesmin itself does not appear to accumulate in the liver, but its effects are cumulative, so that repeated tiny doses are as powerful as a single huge dose. Even with a single dose, the full sequence of changes takes some time to develop. Hence photosensitisation typically does not happen until 10 to 14 days soon after the animal received the toxin, and it could be even further delayed. Both the chemical nature of sporidesmin and its effects on tissues present unusual features which have not however been fully studied.Facial eczema (FE) is a type of sunburn (at times known as photosensitisation) affecting exposed areas of pale skin of cattle. It is caused by a poisonous substance referred to as “sporidesmin” that causes liver damage. Sporidesmin is produced on pasture plants, such as rye grass, by a fungus known as Pithomyces chartartum. This fungus is widely distributed and occurs naturally within dead plant material at the base of standing pasture.
FE has been recorded in sheep and cattle on mainland south eastern Australia.
Signs of illness
The disease could be observed in stock between a number of days and several weeks following choose-up of sporidesmin from the pasture. The toxin is absorbed from the intestine and reaches the liver, where it causes severe harm to bile ducts and liver cells. All the outward signs of FE result from the liver damage caused by sporidesmin.
The signs of FE range from mild photosensitisation (sunburn) to severe jaundice and death, depending on the amount of sporidesmin consumed. Sunburn is the most consistent sign, and generally affects the exposed areas of the skin of the face, ears, teats, and vulva, and areas of skin lacking dark pigmentation, ie. areas covered by white hair. The skin over these areas becomes reddened, and then goes crusty and dark. It eventually peels off leaving huge raw areas, which are susceptible to infections. The sunburn is often accompanied by watery swelling of the underlying tissues. Jaundice (yellowing of mucous membranes) is usually observed at this stage.
Affected animals lose weight rapidly. Most animals recover from the acute phase, but tend to be unthrifty, typically taking a lot of months to regain condition. Some by no means recover, and either die or are culled. In dairy cattle, the udder and teats are typically severely affected, and milk production drops sharply. Loss of weight and general illness are usually severe, and death, even though uncommon, can occur up to months soon after the initial liver harm occurs.
• initial dullness, lethargy and anorexia
• variable onset of jaundice and photosensitisation .
• some animals could die with out either becoming observed
• photosensitisation:
o sheep – non wool skin which includes muzzle, ears, face, escutcheon
o cattle – non black pigmented areas such as teats
o deer – generalised
• some animals develop chronic ill-thrift
• some progress to a hepatic encephalopathy
• dullness, depression
• tremor, recumbency
Epidemiology
Animal elements
• sheep, cattle, deer susceptible
• horses resistant
• evidence for genetic resistance in sheep
Plant/environmental aspects
• fungus grows on the dead leaf litter of pasture
• most frequent pasture is perennial rye grass, but can occur on other species
• requires warmth and humidity to promote rapid fungal growth and sporulation
• typical weather conditions involve autumn break rains following dry summer, many days of consistent warmth (TºC>15.5ºC) and high humidity (>80%)
• fungus concentrates toxin in spores which might be distributed all through whole pasture sward
• most toxic part of pasture is base of sward
Occurrence
Outbreaks of FE generally happen when weather conditions suitable for rapid fungus growth and spore production are combined with abundant dead, recently killed plant material, which favours fungal growth. The fungus requires warm, humid weather and light rain (or irrigation) for growth. This is most likely to be a difficulty in autumn when the summer has been hot and dry, the pasture nicely eaten back, and rains fall when the ground is still warm. In such conditions both pasture and grass grow rapidly.
The fungus producing sporidesmin is typically not visible to the naked eye. It multiplies by producing millions of spores which are coated with the toxin sporidesmin. Freshly produced spores are the most toxic if fungal growth stops soon after a change in the weather, the residual spores on the pasture lose their toxicity inside one or two weeks.
The fungus will grow on most pasture plants, but it grows very best on perennial ryegrass. It grows in the dead pasture litter at the base of the plants. When the fungus reaches toxic levels, animals grazing short pasture at high stocking rates are at greatest risk.
Pathogenesis
• sporidesmin toxin concentrated in spores that are ingested by animal
• sporidesmin absorbed, removed by liver and concentrated into biliary method
• toxin participates in reduction/autoxidation processes to form superoxide radicals
• these radicals destroy membrane integrity and induce a necrotising obliterative cholangitis – obstructive jaundice develops
• accumulation of phylloerythrin outcomes in photosensitisation
Clinical Pathology:
Hematological findings of samples from clinical case pretreatment:
Species of animal RBC WBC PCV%HB
OX 4*10 millionmmc 7.2*10 mm3 23 7.6
C.calf 4.6*10 millionmmc 8.2*10 mm3 28 9.3
C.calf 4*10 millionmmc 7.8*10 mm3 24 8
C.calf 4.5*10 millionmmc 8.2*10 mm3 27 9
Normal 5*10millionmmc 4-12*10mm3 28-42 8.five-13.five
Hematological findings of samples from clinical case post treatment:
Species of animal RBC WBC PCV%HB
Ox 7.2*10 millionmmc 4.6*10mm3 28 9.three
Ox 8.5*10 millionmmc 5*10mm3 30 10
Calf 9*10 millionmmc 5.five*10mm3 33 11
Calf 8.6*10 millionmmc 5*10mm3 30 10
Ox 7.9*10 millionmmc 4.8*10mm3 29 9.6
B.bull 9.five*10 millionmmc 6*10mm3 36 12
Mycobiota of Straw and fodder forage:
Revealed the growth of fungus Penicilliun spp in mycological medium on laboratory culture
Treatment
Use of 5% of Anti-Degnala liquor 5-19ml s/c or i/m alternate day 4 times a week has been found to be successful. Alternately orall use of Penta-sulphate is seems to be useful.
Importantly, affected animals should be sheltered from direct sunlight if probable. In dairy herds, affected cows ought to be dried off and shifted to low-risk pasture to guarantee recovery and satisfactory future production.
Prevention and control
Despite the fact that the basis of prevention of FE is stock management, one of the difficulties in preventing FE is predicting the occurrence of the illness.
Identify prospective issue pastures and deal with them just before high risk periods.
Throughout high risk periods or in the course of an outbreak, the following actions could assist to reduce the intake of toxic pasture:
• Shift stock to the longest pasture feasible, and try to stay away from quite close grazing.
• Avoid paddocks cut for hay or late-topped. These are most likely to be much more toxic since of higher quantities of pasture litter. If topping need to be carried out, ensure topped material is removed.
• In general, paddocks sheltered by windbreaks or hills are more hazardous and need to be avoided.
• It is believed that warmer northern slopes may possibly carry higher spore numbers and really should be avoided in favour of cooler southern slopes throughout outbreaks.
• Feed hay or other supplements to preserve ground feed and minimise close grazing of pasture. Do not push stock to eat into the base of the sward where spore concentration is highest.
• Summer-growing crops are typically safer than pastures, and stock should be given as considerably access to these as feasible where they are available.
• On irrigated farms, if pasture is short and grazing pressure is heavy, farm irrigation might be useful if utilised right away.
• Alternate grazing between native and improved pastures if feasible.
Conclusion:
High doses of zinc can be utilized to reduce liver harm and production losses, even so this need to be administered at the time of, or just before, animals ingest sporidesmin. Every day drenching, in-feed and drinking water have been utilized to administer zinc. Slow-release intra-rumen zinc boluses are also employed overseas, but are presently not available in Australia. There are possible side effects with prolonged zinc dosing and these ought to be discussed with your veterinarian.
Monitoring of pastures by undertaking spore counts is utilised in some countries to supply an early warning system.
References:
• Facial Eczema :Signs of diseaseOccurrencePrevention and controlTreatmenthttp://www.dpiw.tas.gov.au/inter.nsf/WebPages/JBRN-6X95LG?open – was last published on 16 June 2007 by the Department of Primary Industries and Water.
• Facial eczema (FE)by Dr Marjorie Orr – veterinarian, veterinary pathologist and lifestyle farmer
• FACIAL ECZEMA:Methods of Prevention: by Norman Trevor Clare, M.SC., Chief Bio–chemist, Ruakura Animal Study Station, Hamilton. New Zealand Journal of Agriculture, Vol. 105 (1962), “Further Progress in Facial Eczema Research” Smith, J. D., Clare, N. T., Lees, F. T.
• FACIAL ECZEMA:Sheep and Cattle Disease: by Norman Trevor Clare, M.SC., Chief Bio–chemist, Ruakura Animal Analysis Station, Hamilton. New Zealand Journal of Agriculture, Vol. 105 (1962), “Further Progress in Facial Eczema Research” Smith, J. D., Clare, N. T., Lees, F. T.
• Facial eczema of sheep and cattle:Robin van der graaff,Attwood Could,1998 AGO0822,Data note,Department of main industries, © The State of Victoria, 1996 – 2007.This document was published on 31/05/2006 12:48:13.
• Facial Eczema Production Animal Clinical Toxicology http://vein.library.usyd.edu.au/links/pact/facialeczema.html 2008 feb 24.
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