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Veterinary World, Vol.1, No.4, April 2008
History
The DLSO Udayapur reported the periodicdeath of total 31 adult mules during
12-07-2006 to21-10-2006
with showing symptoms like twisting ofhead, star-grazing position, excessive sweating,aimless biting to inanimate objects. Death within 10-15 minutes after collapsing on the ground. Theseherd were being treated with antibiotics andvaccinated against anthrax during this period withunchecked mortality. On field investigation, obtaininga thorough history and completing a physicalexamination, it was discovered that the mules werebeing fed cracked and moldy corn.
Review of Literatures
Penicillium 
grain mold is probably the secondmost common grain mold pathogen. It may becaused by several species of
Penicillium 
, including
P. oxalicum 
and
P. chrysogenum 
.
Penicillium 
speciesare well adapted to survival in many types of storage
Clinical-Epidemiological Investigation of MoldyCorn Poisoning due to
Penicillium spp 
in mulesat Udayapur District, Nepal
Kedar Karki
1
and Poornima Manandhar
2
Central Veterinary LaboratoryTripureswor, Kathmandu, Nepal
Abstract
A clinical epidemiological investigation of Acute sudden death syndrome due to which 31 mules from aherd of 900 died within the period of 12-07-2006 to 21-10-2006 in Udayapur District Nepal. Theseanimals were being used for good transportation work in hilly region of Nepal. On rout these animalswere being fed only whole maize and gram. Normally healthy looking animals started dying suddenly.Initially suspected for acute bacterial disease and treated with broad-spectrum antibiotics and vacci-nated with bacterial vaccine.On close observation of herd their feed stuff revealed grains fed to theseanimal during rainy season was found 20% moldy in appearance. On Postmortem examination acutesevere congestion and hemorrhages in liver, lung, spleen heart, intestinal mucosa were found. Histo-pathological examination of tissue from these organs revealed infiltration of mononuclear cell in tissueindicative of chronic nature of condition.Continous use of apparently 15-20% moldy grain (maize, gram)was used as feed. On laboratory analysis of sample of same grain was found to be containing
6
10
-110
10
CFU/gm
of
Penicillium 
spp of fungus. When remaining herd still using same feed treated with toxin binder(toxicurb, varishta), liver tonic like bioliv, digevet, mineral mixture promin and immunocare controlled themortality may be indicative of the disease syndrome being caused by moldy corn poisoningsimilar tocondition Equine Encephalomalacia.Laboratory findings and response of treatment indicates that duringrainy season and immediately after rainy season feeding of stored grains are going to be detrimental toequine species. During this period care should be taken to feeding grains to this animal if treated with anytoxin binder as well as herbal immunomodulater is going to reduce the chances of occurring this syn-drome.
Keywords:
Clinical-epidemiological investigation, Moldy Corn poisoning,
Penicillium Spp 
., Mule, Nepal,
facility. Kernel infection can occur in the field or instorage. Symptoms range from external molddevelopment to internal discoloration (“Blue Eye”)of the embryo. Symptoms caused by
Penicillium 
areeasy to confuse with those caused by
Aspergillus glaucus 
. Mycotoxins most fungi produce a class ofchemical compounds called secondary metabolites.These compounds have a wide range of biologicalactivities including antibiotic (antibacterial andantifungal), acute and chronic toxicities (plant,animal, and humans), and hormone and growthregulation (plants and animals). It is not unusual formore than one species of grain mold pathogen tobe present within a single storage bin and many grainmold pathogens can be active under the sameenvironmental conditions providing for theopportunity to have more than one mycotoxinproduced in a lot of contaminated grain. The natureof the toxic effects caused by mycotoxins varies
1. Veterinary Officer,2. Senior Veterinary OfficerRESEARCH
Veterinary World, Vol.1(4): 107-109107
 
Veterinary World, Vol.1, No.4, April 2008
greatly. Some mycotoxins cause acute toxicities (i.e.,immediate effect) where a certain organ (e.g., liver,kidney) loses complete or partial function; othermycotoxins cause chronic toxicities (i.e., long-term)resulting in symptoms such as weight loss andreproductive dysfunction. Still other mycotoxinsimpair the immune system predisposing the affectedanimal to a variety of infections or other ailments.For some mycotoxins damage is not permanent andaffected animals can recover from ingestion if thecontaminated feed is removed from the diet.(
Jim Stack).
Equine leukoencephalomalacia commonlycalled “Moldy Corn Poisoning”, is a disease of thecentral nervous system that affects horses, mules,and donkeys. It is commonly associated with feedingof moldy corn over several days to weeks. The clinicalsigns associated with the neurologic form of Equineleukoencephalomalacia in horses include apathy,drowsiness, pharyngeal paralysis, blindness, circling,difficulty backing, staggering, hyper excitability,seizures and eventual recumbency. However, insome cases, sudden death may be the only clinicalsign observed. Once animals show the neurologicalsigns, death usually occurs within 48-72 hours. Ifan animal survives the acute syndrome, neurologicaldeficits are observed. A recovered horse issometimes referred to as a “dummy” because of itsloss of intelligence. Histologically, there may bediffuse vacuolization of hepatocytes, fattydegeneration, centrilobular necrosis withinflammatory cell infiltrate, bile duct proliferation, bilestasis, increased mitotic figures within thehepatocytes, or periportal fibrosis. Equineleukoencephalomalacia is a generally fatal, rapidlyprogressing neurologic disease of horses (and otherequids) caused by ingestion of fumonisin. Horsesshowing these signs will usually become recumbentand comatose in 1 to 10 days and may show clonic-tonic convulsions before dying. In some cases, franticbehavior such as head pressing, agitation, hyperexcitability, profuse sweating and delirium may beobserved. It is characterized by liquefactive necrosisof the cerebral white matter. Liver lesions can alsooccur. The extent of contamination of raw corn withfumonisins varies with geographic location,agronomic and storage practices, and thevulnerability of the plants to fungal invasion duringall phases of growth, storage, and processing. Thelevels of fumonisins in raw corn are also influencedby environmental factors such as temperature,humidity, and rainfall during pre-harvest and harvestperiods. High levels of fumonisins are associatedwith hot and dry weather, followed by periods of highhumidity. High levels of fumonisins may also occurin raw corn that has been damaged by insects.Horses, along with rabbits, are the species mostsensitive to the toxic effects of fumonisin. Ruminants,mink and poultry are more resistant than horses,rabbits, catfish and swine to fumonisin. Onset ofclinical signs can occur from 1-21 weeks afterbeginning eating feeds containing fumonisin, butgenerally occur within 2-9 weeks. Time of onsetdepends on the concentration of fumonisins in thefeed. Clinical signs of fumonisin poisoning in horsesare usually related to liquefactive necrosis of thewhite matter of the brain and include progressiveataxia, depression, anorexia, delirium, aimlesswandering, recumbency, coma and death. Death canoccur from 12 hours-1 week after onset of clinicalsigns. At necropsy, lesions in the cerebral cortexcan range from none to multifocal areas ofhemorrhage and necrosis, to the presence of largecavitations of liquefactive necrosis. Histologically,there are multifocal areas of liquefactive necrosiswithin the cerebral cortex with infiltration ofmacrophages. Differential diagnoses should includerabies, equine encephalomyelitis, equine herpesvirus, botulism, head trauma, hepatoencepha-lopathy, and bacterial meningoencephalitis (Dr. SteveHooser, Dr. Duane Murphy 2003).
Material and Methods
Mule population and Husbandry in Udaypur:
Atotal 900 mules are being used for domestic goodtransportation to hilly district under Mule TransportersSociety. A total of 50 members are being involved inthis bissunes.Mules are generally fed on dry wholemaize,grame grains. These grains are generallypurchased from market only small part of it is utilizedfrom domestic production. These grains are havingmoldiness upto15-20% and are not processedbefore feeding.
Preliminary Field Investigation:
Post-mortemexamination of dead mules revealed severecongestion of liver, lung, speen, heart,serosanginousfluid in thoracic cavity. Haemorrhage in stomachmucosa. Preliminary cause of sudden death wassuspected for moldy grain poisoning. For bacterio-logical culture of smear, swab,blood. Liver, lung,spleen, heart tissue for histopathology. Blood forbacteriological, parasitological examination.Liver, lung, spleen,heart,intestine fortoxicologicalanalysis. Fecal samples for endo-
Clinical-Epidemiological Investigation of Moldy Corn Poisoning due to Penicillium spp in mules
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