An investigation of endemic outbreaks of wet lab eczematous syndrome in cattle in Jhapa district of Nepal
Background:
Service District Jhapa won the incidence of the syndrome reported similar to those described as Degnala disease. A total of 56 affected cattle, of which 12 of them died during treatment with antibiotic drugs and other support. In the field observation in the area of the outbreak all the sick animals had a lesion moist eczematous hypernic throughout the body, and tail, thigh, legs, udder, testicles with normal temperature and the animals showing symptoms were apitite.All Eczematous diagnosed syndrome endemic wet and were provided treatment and sulphate penta antidegnala liquor.
Review of literature:
facial eczema is a disease of sheep and cattle produced in the warmer districts of the North Island in late summer and autumn and is responsible for production serious losses in some years. It is caused by a fungus, Pithomyces chartarum, which grows in the dead plant material in pasture under warm, humid conditions. The spores of this fungus minutes contain a substance, sporidesmin, which produces severe toxic effects on the liver. The appearance of the livers of affected animals varies, depending on the severity of the damage, mottled with light patches of light discoloration gross distortion, and atrophy of large areas (Dr. Marjorie). Often severely damaged parts are surrounded by new liver tissue. As a result of this damage liver functions are impaired. Obstruction of the bile ducts may prevent the excretion of waste substances in the bile, for example, the accumulation in the fat and skin of bile pigments, derived from normal breakdown of old red blood cells, causes jaundice, or yellowing frequently in affected sheep carcasses. 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 in the intestine and liver, where it is excreted in the bile normal. If this mechanism of excretion is annoying, phylloerythrin into the bloodstream which supplies the whole body (Norman Trevor). Phylloerythrin belongs to a class of fluorescent pigments that are able to make the skin sensitive to sunlight, causing redness, intense itching, inflammation and crusting. Are these effects, in general, showing the faces of the affected animals, but also in other unpigmented skin exposed to light, such as the teats and udders of cows, which give rise to the popular name "facial eczema." These effects are the skin, however, secondary to the much more serious condition function.The liver fungi, Pithomyces chartarum, grows only on dead or dying plant tissues, not in the resume. Therefore the amount of the fungus in a pasture is related to some extent the amount of this dead material, or waste, present. Fungal growth and spore production is strongly influenced by climate and environmental factors. Temperature, humidity, and time during which the waste remains moist seem to be particularly important. This explains the typical but not invariable association of the disease with a period of warm and humid, often after a drought period during which growth has ceased grass and debris has accumulated in the toxic substance herbage.The, sporidesmin, has been isolated from cultures of the fungus and its chemical structure determined. A single dose of one thousandth of a gram is enough to kill a lamb of about 60 pounds of body 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 complete sequence of changes takes some time to develop. Hence the photosensitivity usually does not occur until 10 to 14 days after the animal received the toxin, and may be further delayed. Both the nature sporidesmin chemistry and its effects on tissues unusual characteristics that have not yet been fully studied.Facial eczema (FE) is a type of sunburn (a sometimes called photosensitivity) affecting exposed areas of pale skin of cattle. It is caused by a poisonous substance called "sporidesmin" causing liver damage. Sporidesmin occurs on pasture plants, including rye grass, by a fungus called Pithomyces chartartum. This fungus is widely distributed and occurs naturally in the dead plants at the base of grass standing.
FE has been recorded in sheep and cattle in south eastern mainland Australia. Deg Nala disease, which causes necrosis and gangrene of the parties who depend on cattle and buffaloes (Bubalus bubalis) is known to exist in India and Pakistan, as a number of cases arising were recorded a current of monsoon rainfall in the area of Murdike (Sheikhpura District), near Deg Nala in Pakistan (Shirlaw 1939). Widespread disease has been informed of the rice-growing areas of India and Pakistan (Irfan, 1971, Kalra et al., 1972; Irfan and Maqbool, 1986), which caused considerable economic losses.
Signs of illness
The disease can be seen in action several days to several weeks after the collection of grass sporidesmin. The toxin is absorbed in the intestine and reaches the liver, where it causes serious damage to the bile ducts and liver cells. All external signs of liver damage resulting FE caused by sporidesmin.
Signs of mild photosensitization range Fe (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 skin of the face, ears, nipples and vulva, and areas of the skin lacks pigmentation, ie. areas covered by the white hair. The skin in these areas becomes reddened, and then goes crusty and dark. Over time, leaving off large raw areas, which are susceptible to infection. The sunburn is often accompanied by watery swelling of the underlying tissues. Jaundice (yellowing of the mucous membranes) is often seen in this stage.Affected animals lose weight rapidly. Most animals recover from the acute phase, but tend to be unthrifty, taking often several 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. The weight loss and malaise are often severe and death, although rare, may occur even months after injury initial liver occurs. The clinical symptoms observed are initial clumsiness, lethargy and anorexia, the onset of jaundice and photosensitization variable. some Animals can die without being observed, photosensitization: sheep – including the skin of untreated wool muzzle, ears, face, livestock escutcheon – non-pigmented areas black, including teats, deer – Generalized, some animals develop chronic bad second hand, some progress to hepatic encephalopathy clumsiness depression tremor, prostration (Norman Trevor). Factors.sheep animals, cows, deer, sensitive and resistant to the horses, the evidence of genetic resistance in cattle sheep plant / environmental factors, the fungus grows in the litter of dead leaves of grasses, grazing is the most common perennial rye grass, but can occur in other species, require heat and humidity to promote rapid fungal growth and sporulation, typical weather conditions involving rain fall break after of a dry summer, several days of constant heat (T º C> 15.5 º C) and humidity (> 80%), the fungus toxin is concentrated in the spores that can be distributed across the prairie grasses most toxic part of the pasture is the base of the pasture (http://vein.library.usyd.edu.au/links/pact/facialeczema.html).
Appearance
Outbreaks usually occur when weather conditions suitable for fungal growth and rapid production of spores are combined with abundant dead plant freshly killed, which favors the growth of fungi. The fungus requires warm, humid weather and light rain (or irrigation) for growth. This is more likely to is a problem in autumn when the summer has been hot and dry, well-fed grass back, and autumn rains when the soil is still warm. In such conditions, both grass and grass growing rapidly.
The fungus producing sporidesmin not normally visible to the naked eye. It multiplies by producing millions of spores which are coated sporidesmin with the toxin. newly produced spores are the most toxic, and if it stops the growth of fungi after a change in climate, the residual spores grasses lose their toxicity in one or two weeks.The fungus grows on the most grass, but grows best on grass. It grows on dead pasture litter at the base of plants. When the fungus reaches toxic levels, animals grazing short pasture at high stocking densities are at greater risk (http://vein.library.usyd.edu.au/links/pact/facialeczema.html).
Research Objective:
(A) determine the exact cause of the syndrome.
(B) Evaluation of the isolated fungi of rice straw to feed cattle in the area.
(C) Assessment of hematological clinical animal and treatment.
(D) Evaluation of treatment with liquor Antidegnala / Sulphate penta systemic mycoses
Clinical Pathology:
Hematologic results of samples from clinical cases pre-treatment:
The species of animals% HB RBC WBC PCV
OX millionmmc 4 * 10 * 10 23 7.6 7.2 mm3
10 millionmmc C.calf * 4.6 8.2 * 10 28 9.3 mm3
C.calf 4 * 10 * Millionmmc 10 24 8 7.8 mm3
C.calf 4.5 * 10 * 10 27 9 millionmmc 8.2 mm3
Normal 5 * * 28-42 4-12 8.5-13.5 10millionmmc 10mm3
Hematologic results clinical signs of post procedure:
The species of animals% HB RBC WBC PCV
Ox * 7.2 * 10 4.6 28 9.3 millionmmc 10mm3
Ox 8.5 * 10 5 * 10mm3 millionmmc 30 10
Calf 9 * 10 * 10mm3 millionmmc 5.5 33 11
Calf 8.6 * 10 * 10mm3 millionmmc 5 30 10
Ox 7.9 * 4.8 10 * 10mm3 millionmmc 9.6 29
B.bull millionmmc 9.5 * 10 6 36 12 * 10mm3
Normal 5 * * 28-42 4-12 8.5-13.5 10millionmmc 10mm3
Mycobiota straw and fodder fodder:
Revealed the growth of Penicillium species in the middle of mycological culture laboratory
The treatment provided
Use of 5% of liquor Anti Degnala s 5-19 ml / C or I / m 4 alternate days twice a week has been found to be successful. Or oral Penta-sulphate was given.
Results and Discussion:
All animals were treated with the previous preparation eczematous lesion disappeared within a week and animal health returned to normal. Under the landscape marshy area of land, wet weather hot and humid tropical farming practices of feeding rice straw seems to be the source of the invasion by opportunistic fungi is evident from the proliferation of fungi in the laboratory mycomedia.The increase of total white blood cell count and decreased hematocrit, hemoglobin in the blood of clinically ill animals and response to treatment indicates that any change in the weather conditions are suspected new condition of the disease is likely to also occur in cattle should be evaluated
Conclusion:
The disease is strongly associated with feeding rice straw containing multiple dark spots. This observation is in agreement with the findings of previous researchers (Irfan and Maqbool 1986) who reported that the straw and mushroom fungus-infested carpets of various species in different combinations, when mixed with fresh rice straw is not infected, the disease causes. Saprophytic fungi that infest rice straw to produce mycotoxins vasoconstriction has produced disease lesions (Irfan et al., 1984). The increased severity of the disease in buffalo compared with cows that may partly be due to the high susceptibility of this species. Therapeutic trials with an antidote (a penta-sulphate mixture) given orally, and a vasodilator (nitroglycerin ointment) applied locally in the lesions out the highest percentage (90%) cure rate. This cure rate was broad agreement with the results of Schöntal (1980) who reported a cure rate of 80% with a penta-sulphate mixture. Just as this observation was noted whole animal was treated with injection of anti liquor Degnala penta sulfate followed by total recovery. The same way there was a significant increase in the count total white blood cells and decreased hematocrit and hemoglobin in the clinical phase syndrome treatment there was marked increase in both PCV and increased hemoglobin and counting of cells and normal leukocytes also support that this syndrome was attributed by the infestation of fungi in the rice straw fed to these animals. If the proper management of forage dry during the rainy season can be conducted to minimize losses due to moisture endemic eczematous syndrome. Others, if timely treatment of animals is if you start using alcohol or anti Degnala sulfate penta minimize losses should be analyzed in
References:
• Facial Eczema: Signs of diseaseOccurrencePrevention and controlTreatmenthttp: / / www.dpiw.tas.gov.au/inter.nsf/WebPages/JBRN-6X95LG?open – Was published last June 16, 2007 by the Department of Primary Industries and Water.
• Facial eczema (FE) by Dr Marjorie Orr – veterinary pathologist and lifestyle farmer
• Facial eczema: Methods of prevention: Norman Trevor Clare, M.Sc., Head of the Bio-chemist, Ruakura Animal Research Station, Hamilton. New Zealand Journal of Agriculture, vol. 105 (1962), "More Research Advances in facial eczema" Smith, JD, Clara, NT, Lees, FT
• Facial eczema: disease of sheep and cattle: 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 the investigation facial eczema" Smith, JD, Clara, NT, Lees, FT
• facial eczema of sheep and cattle: Robin van der Graaff, Attwood May 1998 AGO0822, Information note by the Department of Primary Industries, © The State of Victoria, 1996 – 2007.This document was published on 31/05/2006 12:48:13.
• Production Animal Clinical Toxicology http://vein.library.usyd.edu.au/links/pact/facialeczema.html facial eczema February 24 2008.
• Arora, SP (1980): The use of radioactive selenium for studies on Deg Nala disease. J. Nuclear Agri. Biol 9, 11-13.
• Irfan, M. (1971): The clinical and pathology of Gr Nala disease in buffaloes. Vet. Rec 88, 422-424.
• Irfan, M., A. Maqbool (1986): Studies on Deg Nala disease in cattle and buffalo. Pak. Vet. J. 6, 87-93.
• Irfan, M., A. Maqbool, M. Ashfaque (1984): Importance of molds, fungi and mycotoxins in food and feed. Pak. Vet. J. 4, 187-192.
• KALRA, DS, KC Bhatia, Gautam OP, Chauhan SL (1972): A dark disease (possibly Deg Nala disease) in buffaloes and cattle. Studies on its epizootiolgy, pathology and etiology. Haryana Agri. J. Univ Res 2, 256-264.
• Shirlaw, JE (1939): Deg Nala disease in buffaloes. An account of the injury and the condition essential. Indian Vet. SCI. Anim. Husban. 9, 853-864.
• Schoental, R. (1980): Keep your animals Deg Nala disease. J. Nuclear Agri. Biol 92, 27-28.
Acknowledgements:
I like to make my thanks to Dr.Poornima Manandhar SVO / Central Vet.Laboratory Director, Dr. Dilip Sapkota SvO / Head of Jhapa District Livestock Services for their contribution in raising sanples and information required during the outbreak and continue to treatment.As and I would like to thank Mr. Prakash Devkota, Bahadur Kunwar Mr.Bal Vet.Tech CVL and Mr.Yam B. Subba Vet.Tech. DLSO Jhapa for their help in field and laboratory work
About the Author
Senior Vet.Officer,Central Veterinary Laboratory Kathmandu Nepal M.V.St. Preventive Veterinary Mrdicine
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