Endemic Moist Eczematous Syndrome Lab Outbreak in Nepal

By: Dr.Kedar Karki

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 during month of September after prolong spell of drought followed by heavy rainfall causing water logging total 56 cattle and buffalo were affected and out of which 12 animal died. Rest of ill animals were treated with 5%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 during late summer and autumn and is responsible for serious 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 contain 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. Frequently the severely damaged portions are surrounded with new liver tissue. As a result of this damage the functions of the liver are impaired. Blockage of bile ducts may prevent 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 commonly seen in the carcasses of affected sheep. Of particular importance is the loss of ability to excrete the substance phylloerythrin. This is formed in the digestive tract of ruminants through 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 making the skin sensitive to sunlight, causing reddening, intense itching, swelling, and scab formation. It is these effects, generally 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 popular name "facial eczema". These skin effects are, however, secondary to the much more serious 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 amount 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 during which the litter remains wet appear to be particularly important. This explains the typical, although not invariable, association of the disease with a period of warm, wet weather, often following a dry spell during 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 small doses are as effective as a single large dose. Even with a single dose, the full sequence of changes takes some time to develop. Hence photosensitisation usually does not occur until 10 to 14 days after the animal received the toxin, and it may be even further delayed. Both the chemical nature of sporidesmin and its effects on tissues present unusual features which have not yet been fully studied.Facial eczema (FE) is a type of sunburn (sometimes called photosensitisation) affecting exposed areas of pale skin of cattle. It is caused by a poisonous substance called "sporidesmin" that causes liver damage. Sporidesmin is produced on pasture plants, including rye grass, by a fungus called 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 disease
The disease may be seen in stock between several days and several weeks following pick-up of sporidesmin from the pasture. The toxin is absorbed from the intestine and reaches the liver, where it causes severe damage 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 usually 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 large 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 often seen at this stage.
Affected animals lose weight rapidly. Most animals recover from the acute phase, but tend to be unthrifty, often taking many months to regain condition. Some never recover, and either die or are culled. In dairy cattle, the udder and teats are often severely affected, and milk production drops sharply. Loss of weight and general illness are often severe, and death, although uncommon, can occur up to months after the initial liver damage occurs.
&bullinitial dullness, lethargy and anorexia
&bullvariable onset of jaundice and photosensitisation .
&bullsome animals may die without either being observed
&bullphotosensitisation:
osheep - non wool skin including muzzle, ears, face, escutcheon
ocattle - non black pigmented areas including teats
odeer - generalised
&bullsome animals develop chronic ill-thrift
&bullsome progress to a hepatic encephalopathy
&bulldullness, depression
&bulltremor, recumbency

Epidemiology
Animal factors
&bullsheep, cattle, deer susceptible
&bullhorses resistant
&bullevidence for genetic resistance in sheep
Plant/environmental factors
&bullfungus grows on the dead leaf litter of pasture
&bullmost frequent pasture is perennial rye grass, but can occur on other species
&bullrequires warmth and humidity to promote rapid fungal growth and sporulation
&bulltypical weather conditions involve autumn break rains after dry summer, several days of consistent warmth (T?C>15.5?C) and high humidity (>80%)
&bullfungus concentrates toxin in spores which may be distributed throughout whole pasture sward
&bullmost toxic part of pasture is base of sward
Occurrence
Outbreaks of FE typically occur 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 problem in autumn when the summer has been hot and dry, the pasture well 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 normally 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 after a change in the weather, the residual spores on the pasture lose their toxicity within one or two weeks.
The fungus will grow on most pasture plants, but it grows 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
&bullsporidesmin toxin concentrated in spores that are ingested by animal
&bullsporidesmin absorbed, removed by liver and concentrated into biliary system
&bulltoxin participates in reduction/autoxidation processes to form superoxide radicals
&bullthese radicals destroy membrane integrity and induce a necrotising obliterative cholangitis - obstructive jaundice develops
&bullaccumulation of phylloerythrin results in photosensitisation
Clinical Pathology:
Hematological findings of samples from clinical case pretreatment:
Species of animalRBCWBCPCV%HB
OX4*10 millionmmc7.2*10 mm3237.6
C.calf4.6*10 millionmmc8.2*10 mm3289.3
C.calf4*10 millionmmc7.8*10 mm3248
C.calf4.5*10 millionmmc8.2*10 mm3279
Normal5*10millionmmc4-12*10mm328-428.5-13.5
Hematological findings of samples from clinical case post treatment:
Species of animalRBCWBCPCV%HB
Ox7.2*10 millionmmc4.6*10mm3289.3
Ox8.5*10 millionmmc5*10mm33010
Calf9*10 millionmmc5.5*10mm33311
Calf8.6*10 millionmmc5*10mm33010
Ox7.9*10 millionmmc4.8*10mm3299.6
B.bull9.5*10 millionmmc6*10mm33612
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 possible. In dairy herds, affected cows should be dried off and shifted to low-risk pasture to ensure recovery and satisfactory future production.
Prevention and control
Although the basis of prevention of FE is stock management, one of the difficulties in preventing FE is predicting the occurrence of the disease.

Identify potential problem pastures and deal with them before high risk periods.

During high risk periods or during an outbreak, the following actions may help to minimize the intake of toxic pasture:
&bullShift stock to the longest pasture possible, and try to avoid very close grazing.
&bullAvoid paddocks cut for hay or late-topped. These are likely to be more toxic because of greater quantities of pasture litter. If topping must be carried out, ensure topped material is removed.
&bullIn general, paddocks sheltered by windbreaks or hills are more dangerous and should be avoided.
&bullIt is believed that warmer northern slopes may carry higher spore numbers and should be avoided in favour of cooler southern slopes during outbreaks.
&bullFeed hay or other supplements to preserve ground feed and minimise close grazing of pasture. Don't push stock to eat into the base of the sward where spore concentration is highest.
&bullSummer-growing crops are generally safer than pastures, and stock should be given as much access to these as possible where they are available.
&bullOn irrigated farms, if pasture is short and grazing pressure is heavy, farm irrigation may be valuable if used immediately.
&bullAlternate grazing between native and improved pastures if feasible.
Conclusion:
High doses of zinc can be used to reduce liver damage and production losses, however this must be administered at the time of, or before, animals ingest sporidesmin. Daily drenching, in-feed and drinking water have been used to administer zinc. Slow-release intra-rumen zinc boluses are also used overseas, but are currently not available in Australia. There are potential side effects with prolonged zinc dosing and these should be discussed with your veterinarian.
Monitoring of pastures by undertaking spore counts is used in some countries to provide an early warning system.

References:
&bullFacial Eczema :Signs of diseaseOccurrencePrevention and controlTreatment - was last published on 16 June 2007 by the Department of Primary Industries and Water.
&bullFacial eczema (FE)by Dr Marjorie Orr - veterinarian, veterinary pathologist and lifestyle farmer
&bullFACIAL ECZEMA:Methods of Prevention: by Norman Trevor Clare, M.SC., Chief Bio-chemist, Ruakura Animal Research 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.
&bullFACIAL ECZEMA:Sheep and Cattle Disease: by Norman Trevor Clare, M.SC., Chief Bio-chemist, Ruakura Animal Research 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.
&bullFacial eczema of sheep and cattle:Robin van der graaff,Attwood May,1998 AGO0822,Information note,Department of primary industries, ? The State of Victoria, 1996 - 2007.This document was published on 31/05/2006 12:48:13.
&bullFacial Eczema Production Animal Clinical Toxicology 2008 feb 24.



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