Eating Disorders

Clinical and epidemiological Moldy corn poisoning Udayapur district, Nepal

Clinical and epidemiological poisoning moldy corn in Udayapur district, Nepal
1. Dr.Kedar Karki
Senior. Vet. Officer
Dr.Poornima SVO Manandhar
Central Vet. Laboratory. Tripureswor Kathmandu Nepal
Abstract:
A clinical epidemiological investigation of Acute sudden death syndrome due to which 31 mules from a herd of 9oo died within the period of 12/07/2006 to2006-10-21 in the District Udayapur Nepal. These animals were used for Transportation Construction Quality in the hilly region of Nepal. On rout these animals were fed only whole maize and grame.Normally healthy animals began to die suddenly. Initially suspected for acute bacterial disease and treated with broad spectrum antibiotics and vaccinated with the observation vaccine.On close flock of bacterial food orders showed these animals fed grain during the rainy season was found 20% moldy in appearance. In the post-mortem examination of severe acute congestion and hemorrhage in the liver, lungs, heart, spleen, intestinal mucosa found.Histopathological were examining tissues of these organs revealed infiltration of mononuclear cells in the tissue of the code the chronic nature of the use of condition.Continous apparently 15-20% moldy grain (maize, gram) was used as food. On analysis laboratory samples of grain was rated 60-110CFU/gm containing Penicillium spp of fungus. When remaining herd still using food treated with the same toxin binding (Toxicurb, varishta), liver tonic like Biolive, hepatocare, digevet, Promin mixture of minerals and immunocare controlled the mortality rate may be a sign of the disease syndrome being caused by moldy corn poisoning similar to condition Equine findings Encephalomalacia.Laboratory and the response of treatment indicates that during the rainy season and immediately after the rainy season, food grain storage will be detrimental equine species. During this period care should be taken to feeding grains to this animal if treated with a binder of toxins, and herbal immunomodulater will reduce the chances of producing the syndrome.
Keyword:
Equinelukoencephalomalcia, moldycorn, hepatocare, Varishta, Toxicurb.bioliv, Immunocare, mule, Nepal, Penicillium.

History: The Udayapur DLSO reported the death of all periodic mules 31 adults during seeding o63/2/16-o63/7/6.With symptoms as abnormal behavior, aggression, changing habits, Abnormal proprioceptive positioning, abnormal pupillary reaction to light, agalactia, Anorexia, ataxia, blindness, circling, colic, coma, cyanosis, decrease in the amount of stool, stool present, Constipation, Decreased bowel sounds, decreased thirst away, hypodipsia, adipsia, dehydration, difficulty prehending chewing food, confused, dull, dysmetria, dysphagia, dyspnea, salivation, excitement, weakness, head pressing, shaking his head, head, face, ears, jaw weakness, droop, head, face, ears, jaw, nose, nose, swelling, head, face, neck, tongue hypoesthesia, Hemoglobinuria or myoglobinuria, hyperesthesia, jaundice, inability to standing, increased respiratory rate, mydriasis, opisthotonus, paraparesis, Petechiae or ecchymoses, Propulsion, Red or brown urine, reluctant to move, Seizures or syncope, edema of the skin, sudden death, sweating, tetraparesis, weak language, trembling, shaking, Underweight, poor condition, thin, gaunt, unthriftiness, failing economy, loss of weight
Death within 10-15 minutes after collapsing on the ground. These herds have been treated with antibiotics and vaccinated against anthrax during this period, mortality unchecked. On a field investigation, obtaining a history and completing a physical examination, he was discovered that the horses were fed cracked and moldy corn.

Review of literature:
Penicillium mold is probably the pathogen second most common grain mold. It can be caused by several species of Penicillium, including P. oxalicum and P chrysogenum. Penicillium species are well adapted to survival in many types of storage facility. Kernel infection can occur in the field or in storage. Symptoms range from development mold outside the internal discoloration ("Blue Eye") of the embryo. Symptoms caused by Penicillium are easy to confuse with those caused by Aspergillus glaucus. Mushrooms most mycotoxin producing a class of chemical compounds called secondary metabolites. These compounds a wide range of biological activities including antibiotic (antibacterial and antifungal), acute and chronic toxicities (plant, animal and human), and growth hormone and regulation (plants and animals). It is not uncommon that more than one kind of grain pathogen mold to be present in a single storage tank and many mold pathogens can be active in the same environmental conditions providing the possibility of having more than one mycotoxin produced in a batch of contaminated grain. The nature of the toxic effects caused by mycotoxins varies. Some mycotoxins cause acute (ie immediate effect), where a certain organ (eg, liver, kidney) loses complete or partial function; other mycotoxins cause chronic poisoning (ie long term) resulting in symptoms such as weight loss and reproductive dysfunction. Still others mycotoxins impair the immune system predisposing the affected animal to a variety of infections or other ailments. For some mycotoxins damage is not permanent and affected animals can recover from the ingestion of contaminated food if the food is removed. (Jim Stack,).
Equine leukoencephalomalacia commonly called "Moldy corn poisoning," is a disease of the central nervous system that affects horses, mules and donkeys. It is commonly associated with feeding moldy corn over several days to several weeks. The clinical associated with the neurological form of Equine leukoencephalomalacia horses include apathy, drowsiness, pharyngeal paralysis, blindness, circling, trouble backing, staggering, hyper excitability, seizures and eventual recumbency. However in some cases, sudden death may be the only clinical signs observed. Once the animals show neurological signs, death usually occurs within 48-72 hours. If an animal survives the acute syndrome, neurological deficits are observed. A recovered horse is sometimes called a model "because of the loss of his intelligence. Histologically, there may be diffuse vacuolization hepatocytes, fatty degeneration, centrilobular necrosis with inflammatory cells, proliferation of bile ducts, bile stasis, increased mitoses in the hepatocytes, or periportal fibrosis. leukoencephalomalacia equine neurological disease is usually fatal, rapid progression of horses (and other equids) caused by ingestion of fumonisin. Horses showing these signs usually become recumbent and comatose in 1-10 days and may clonic convulsions, tonic, before she died. In some cases, frantic behavior such as head pressing, agitation, hyper excitability, profuse sweating and delusion can be observed. It is characterized by a liquefaction necrosis of the white brain. Liver damage can also occur. The extent of the contamination of raw corn with fumonisins varies with geographic location, agronomic and storage practices, and the vulnerability of plants to fungal invasion during all phases of growth, storage and processing. The levels of fumonisins in raw corn are also influenced by environmental factors like temperature, humidity and precipitation during pre-harvest and harvest periods. High levels of fumonisins are associated with hot and dry weather, followed by periods of high humidity. High levels of fumonisins may also occur in raw corn that has been damaged by insects. Horses with rabbits, are the species most susceptible to the toxic effects of fumonisins. Ruminants, mink and poultry are more resistant than horses, rabbits, catfish and pigs for fumonisins. Onset of clinical signs may occur 1-21 weeks after eating food containing fumonisin, but occur usually within 2-9 weeks. Time of onset depends on the concentration of fumonisin in the feed. Clinical signs of fumonisin poisoning in horses are usually related to liquefaction necrosis of the white matter of the brain and progressive ataxia, depression, anorexia, delirium, aimless wandering, recumbency, coma and death. Death can occur from 24:00 – one week after onset of clinical symptoms. At autopsy, lesions in the cerebral cortex can vary from zero to multifocal areas of hemorrhage and necrosis, the presence of cavitation necrosis liquefaction. Histologically, there are multifocal areas of necrosis liquefaction in the cerebral cortex with infiltration of macrophages. The differential diagnosis include rabies, equine encephalitis, equine herpes virus, botulism, a head injury, hepatoencephalopathy, and meningoencephalitis Bacterial (Dr. Steve Hooser, Dr. Duane Murphy 2003).
Material and Methods:
Mule breeding population Udaypur:
A 900 Total mules are used for the transport of domestic carriers in the mountainous district of Mule Society since BS2060.A total of 50 members are involved in this are generally bissunes.Mules fed dried whole corn kernels Grame. These grains are generally purchased from small market that part of it is used in domestic production. These grains are having mold upto15-20% and are not treated before the meal.

Preliminary Field Investigation:
The postmortem examination of Mule death revealed severe congestion of liver, lung, Speen, heart, liquid serosangqinus cavity.Haemorrhage thoracic stomach mucosa. Preliminary question sudden death was suspected of moldy grain poisoning.
For the bacteriological culture of smear, collection, blood.
Liver, lungs, spleen, heart tissue for histopathology.
Blood for bacteriological, parasitological examination.
Liver, lungs, spleen, heart, intestine for toxicological
. Fecal samples for endoparasite examination.
Serum for serological examination.
Fodder: Maize, Grame for the identification of culture mycological quantitification were collected.
Mules in herds have been provided with toxinbinder, adaptogen, immunomodulater, vitaminBcomplex that treatment and preventive measure.

Laboratory Investigation:
Bacteriological culture of the sample tissue, blood stem: revealed no growth of bacteria. Blood parasite toxin in tissue Negative.Chemical: negative. Intestinal parasites Joint Strongyels spp.
Penicillium, Aspergillus, Candida spp on mycological media.
6 * 10-110 * 10 CFU / g Penicillium colonies recorded in samples food.
Histopathological changes: Liver,: fatty degeneration of cells hepatocytes.Mononuclear infiltration in the form of few nodules.
Lungs: perivascular cuffing. Infiltration of mononuclear cells in the form of nodules.
Kidney: Deep medullary region reveals infiltration of cells mononuclear.
Rate: The number of white blood cells seems to be increased in the area of white pulp. Suggestive of chronic / viral.
Serum sample:
Tested positive for Japanese encephalitis (Elisa)
Treatment and Control Measure recommended:
Advised for proper drying grain before feeding. 2% copper sulfate to be mixed in the grain before feeding. toxinbinders commercial Varishta, 1kg/tone Toxicurb @ Grain for 15 days with liver tonic, Immunomodulaters, Vitamin B complex

Results and discussion:
Approximately 15-20% moldy corn infestated with Penicillium spp being fed regularly to these sudden but herd.Intermitent acute death during post rainy season suggest the death due to fungi changes toxin.Histopathological in the tissues of the lungs, liver, kidney are similar to results of other workers. Histologically, a center of necrosis with no structure recognizable will be observed. The transition between normal and necrotic tissue often show hemorrhage, edema, congested blood vessels and neuronophagia. In animals with the hepatotoxic syndrome, livers will be swollen and a diffuse yellow-brown. Irregular nodules and pale foci can be seen in the parenchyma liver. (Dr. Steve Hooser, Dr. Duane Murphy 2003). Pathogenicity of Fusarium has revealed that it causes hepatic congestion with mild triaditis, pulmonary congestion, and splenic lymphoid hyperplasia (Karki 2003). Furthermore, a positive response to treatment with toxinbinder, adaptogen, immunomdulater confirm Sudden death due to poisoning from moldy corn. Further monitoring of the conclusion of this investigation is suggested.
Conclusion
Results of this survey indicates that the feed grain and moldy ingredients are infested with toxic fungus appears as health hazard for new livestock and the use of poultry.Simultonious toxinbinder, adaptogen like livertonic, and drugs mineralmixture Immunomodulaters promises to minimize the risk to the health of livestock and poultry production should be considered.
References:

1: Moldy CORN POISONING HORSES: (Equine LeukoencephalomalaciaMark Russell, PhD, Department of Animal Sciences Don Scott, PhD, Department of Botany and Pathology Plant William Hope, DVM, Department of Clinical Veterinary Extension SciencesCooperative ServicePurdue UniversityWest Lafayette, IN 47907, BOLETIM TÉCNICO http://www.micotoxinas.com.br/ No. 15 – Accessed 21/06/2007
2: Poisoning FINAL DIAGNOSIS-Moldy Corn (Leucoencephalomalacia Equine fumonisin toxicity) in horses: Dr. Steve Hooser, ADDL Toxicologist Dr. Duane Murphy, ADDL Pathologist Spring 2003 Newsletter http / / www.addl.purdue.edu/newsletters/2003/Spring/finaldx.shtml. Accessed on 21/06/2007

3: the harmful effects of mycotoxins prevent the impact of your horse's health and performance.Mycotoxins in Equine Feed,: By Trevor K. Smith, Ph.D., PAg www.ecmagazine.net/…/mycotoxin2.jpg Accessed 06/21/2007

4: Grain Molds and Mycotoxins in corn: Jim Stack Extension Research Plant Pathologist Division of the Institute of Agriculture and Natural Resources at the University of Nebraska-Lincoln cooperating with the counties and the U.S. Department of Agriculture.http: / / cbc.homestead.com / Archives.html, Accessed 21/06/2007
Five: Toxocurb: www.polchemgroup.com.
6: Varishta: www.varshagroup.com
7: Evaluation of Fusarium graminearum pathogenicity in mice. Kedar B. Karki: pp14, Vetcon 2003, 7th Conference National Veterinary 2003, Nepal Veterinary Association.
Acknowledgement:
We would like to thank Dr.Rebti Man Shrestha, veterinary Chief Dr.Salina Manandhar, Dr.Binaya Kumar Karna, Dr.Pragya Koirala Veterinary Officer and all laboratory technicians for their help in laboratory work and investigative work.

About the Author

Senior Vet.Officer,Central Veterinary Laboratory Kathmandu Nepal M.V.St. Preventive Veterinary Mrdicine

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