a) I ‘ENTEROTOXAEMIA® This is primarily an infectious disease of tuminants that Se Enlerotovaemia has been reported from canile sheep, lambs, (2G from countries like Australia, UF apan. Newzealand and North America (Radostits, Enterotoxacmia is_an_impo: Population caused by Clostidium erjringens i cla ani Epsilon toxing._The discas 1s co! Kile: ier disease in poals and has been reco ppal. ulshrestha er al, Chakrabarty et af, 1980 ; Tarbela am! A recen| +0 acat, 181; Harbels saa & 1990; Pal et al, 170). . The sTise du in guat (Prabhakar: ef @ ot 1). h Preduced in goats (PEzS39 DNA-DNA Characterisation of Clostndan inges has been made through int plasmids hybridization. DNA proheswen Served from multicopy reeombina tying searched genes (D b 53). All sabe ef mae 19 ices ct al. 1993) the isolate: ridized es showed, charact) . MuU-toxin and INA DNA sialidase pens zpon DNA hybridization with 13 © perfringens gene bes hes Y eofringes Probes (Phukan et als TIRE emerges type A_used to produce a traasicnt diarrhoea and it subsides within 12 2 On the other hand twpe-D cetcrotoxaemia and death nal Uransmission as also been £6 etal, 2000) repo disease has heey experimentally iB since bacterin vaccine is nut satisfactory, - Loxoids (Etlotogy + a \ Clostridium Perfringens Type—A ~The exact role of type—< in relation ‘odisease in cattle, calves, and lambs is not clear, It produces toxin. Enteroto? roemic jaundice is seen in sheep and cattle. This is characterized by intense icterus, hacmoglobinacmia and hacmoglobinuria, The affected animal will show respi. Atory distress and bloody bein5 setinention (schofield —_— aid — a 7 orserid foun fen A TARLO, yy _ bee 5s Ulmonary 25) Mary emphysema may excut due 10 8YP* Synonym produces a di The organi? a W sc ban ase has bee reported in cole rw a Vaenb jab, ae and cal cs a.P ‘The toxin produces Crganinn protaces 6 lon toxin 2 ect tae inal enter ard ep’ neural Have’ characterised \ i wande cd by abdc pain, seman ates WANICKINg Peraeute Cyr sal ood to se Cait will Lead to sudden cat without showing APY clinical manifestation (eadontits ot a, 2009) ecrotie arcas, SUTTO he Sanall necrotic AER rounded by 7oxe of hacmortbages at2 #0 tia iheinreainal mucosa. ThEIE Henbirgement of mesenteric ynph nodes UY is enlarged and (riable. iyiapaosis can be made based on changes in the intestinal muco#> and "tion of toxin by mouse inoculation text, Oral and gystermic antibiotics may be tried but the Ireatment xpcios does not yield eatisfactory response. Antitorin if available may be given $008 ‘after birth, Immunization of ewe prior to lambing may prevent lamb dyscntt: demo Synonym fy affects the shery at and cattle. I produces haemorrhasic enteratoeseria hich js. acute disease of young calves, Tt produces bo Excess feeding of milk causing, intestinal stasis favour a and fo vwxin Tnultiphcation of the organisms and therehy production of toxin, The ¢ signs include abdominal pain, weakness, depression, failure to nurse hacmarthagic thatrhoca, intestine particularly in the jejunum and There is also necrotic and be noted in the epicardium, ‘The lesions are found in the small leu characterized by hacmorrkagic changes. whcrdie changes 5inall hagmorrhagiclestons may thymus and diapheagen Priagnasis 1s made based on history, slatian of tain, presence of gram posi reaonsteation of rin in the intestinal contest Oral antibiotics (tetracyeline, chlortetracycline, For control, immunization ‘of calves with antitoxin soon after bir sudden death, haemorrhagic enteritis, tive bacilli in the intestinal smear and penicillin) may be wsed. sugested. Two injections of toxoids are necessary at one mosth apart. Cow should be immunized one to three month prior to parturition. Sheep my be ed V—CD (BAIF) vaccine. ft is primarily a disease of sheep but cattle and goals are occasionally affected, It produces @ toxin, The young sheep and calves arc affected. th is |Enterotoraemig There jg as gor. myocardial fy lille reddening of abomasal mucosa, 8UB“CFis, 3 become tin enerEaB?. The C.N.S, may be affected. FOF is found in thy Once? ™AY show the signs of glycosuria. In shee ‘he goneal pleural and pericardial sac. iB the disease is known as pulpy kidney diss35® 4 gic ™” may jum, . IP ing ai ; - minutes, he air, fall in the ground go into convulsion 9 ; jo 7 fesio®™” re Sheep that dic suddenly may not show any pos: morle™ nde sdem Agi i, i ii i i i = orrhagic lesions arc scen in the peritoneum, epicer dint gnc Kid diephra P Diragm, abomasum and duodenum. There is st fteni: change: velop in: es develop in 3 to 4 hours following death. Brow! Pormalised anaculture is used for vaccinati =P 5 ed ‘ tion of 1; v. Spectrum antibiotics like Chlortetracyctine may be used f extent losiridium wetchi type-—D vaccine (BAIF) can be uscd 2gainst SherP- ‘Clostridium pertringens type—E ii 1 There is fata | Clostridium perfringens type E produces @ and f toxin. infection leading to death, There is haemorrhagic chanzes in U Clostridium perfringens type—F The organism produces potent toxin and causes di lamb (Bosworth, 1943). It is not certainly known to be any fatal discascs of animals. REFERENCES he intestine. oca in calves and 2 causative accnt of Roxworth, 1. (1943). J. Comp. Pathol. Therap. $3: Chakrabarty, A.K. ef af, (1980). Indian Vet. J. ct al, (1992) ; Ann, Med. Vet. 136 : 53 Daube, GMALIGNANT OEDEMA Nisan acute infections dis and is characterized by fever ¢ the wound (Sinit} h, 1976). Distribution The disease is str in those regions where t Etiology ASC ue | septicu” Nedemat, 1 ii" mn © woundscaused by Clostrid arow Ming, well ‘Ous and emphysematous § buted throy UghouL the Worl he soil is, heavily contami, ., c is mor ithe prewalea orcs. ated with bacterial Hae His aa anacrabie gram posit vism meas A in length. Though cr ; of oedema, uring 0.4 too -6 64 in width and a DEEN Considered ay the primary ie Gt lous and em, tion but other organisms like c h chavoci, TEens, Ch nov, rdelli are aly associated wil malignant reanism produces tun "Sins viz @andB toxin. Hyaluronidase and Collaginase are aley Produced by ih. organisms. Susceptible hosts . The disease ig Fecorded in caute, Sheep and goat, Mode of transmission — tis a soil borne infection, The Organisms are common inhabitants of alimentary tract. Organisms Bain access through surgical or ace’ Castraction, docking, Parturition injurig, a infection . It is Sporadi ie disease and and Punctured Wound. idental Wounds. may Pathog enesis io? MEMENL the faring up of multiptictiog is favoured due to abrasion the acelerated ndition, Due to The Swelling ia, hen the arked OXaemia Te is Sedematous "™B 10 Gedema. There teen ® Malignant Ocedena hyperacmia of conjunctival mucosa and sins of toxemia, Foul smelling discharges are drained through the wounds Lateran, the exelled area became cold. Gas formation cause the wound to break with easing of serosanguinenis materials. Swelling may sometime be located in the head god intermandibular space, Death usually occurs within 24-48 hours die to touemia Lesions Lesions are mostly observed at the site of wound. There is oedematous and emphysematous swelling, Gangrene of the affected tissues and gelatinous blood stained uid are abyerved on the wound. Mood tinged fluid may be observed in the peritoneal, pericardial and pleu Diagnosis Tt is based on: © History of injury and wound. © Clinical signs. It has to be differentiated from black quarter @ Inblack quarter, there is deep muscle involvement and muscles become necrotic. . e@ FAT. { Treatment | It is very difficult to recognise the disease in tie initial stage in the field + condition. But, massive dose of crystalline pericillin throush intravenoas route ‘ followed by procaine penicillin through intramuscular route will be a rational approach. Tetracycline may also be used. Control @ Proper cleanliness and hygienic measures will reduce the chance of infection. @ Both surgical and accidental wounds should be properly treated. @ The area of contamination should be adequately disinfected. @ The dead carcases should be disposed properly, They should be burnt or burried and soaked with lime. e Formalized bacterin may be uscd. Vaccination should be done as a routine measure in enzootic ari REFERENCES Smith, L.D. (1976). The pathogenic anacrobic bacteria 2nd Ed. Charles Thomas, Spring ticld IL, :Be OMS NOD -i Da Mabel 27 BOTULISM > Ig- \o-Vo af hh wns, Mir Synonyms. Limber qech + li Wisa toeeaol Ch as jmals and birds eaused by th ingestion of toxin OF Ch by E irds ewused by the ingestion, 4 of ani hotutinun —9 soil saprophyte and common inhabitant of digestive tract of animals (Smith et at, 1988) Distribution The disease is world wi to country. Type—B has bee indidtribution. ‘The type may vary from country irded in the soil of Belgium, Denmark, England, Netherland and Switvverland whereas Type-C and D have been recognized in the soil of North America, Australia, Europe and certain parts, of Africa, The disease has been reported fram mast of the tropical countries, sooy The disease is cauccd by Clostridium botulinum, It is an anacrobic, larg, bacillus measuring 4-8 fe x F=L.5a. In young culture the organisms appear gram negative. The organisms may he seen as singly or pair or short chains. The orranism is anarchic and prow in common media, The organism does not grow in animals body but can proliferate in de ying animal matter, I may also grow on vegetable decaying matte Spores are highly resistant and can survive for a long periad in decaying carcases. The organisms may remain as normal inhabitant in the intestine of cattle and sheep. The: type of toxins which are liberated by Cl. botatinumn, Toxins type A, B, E and F have been shown to be pathogenic for mammals, The C toxin has been further divided to type Ca and Type Cb, The organism is not able to produce toxin in the alimentary tract of animals, Prefarmed toxin is the sole source of intoxication. Susceptible hosts * Horse, cattle, sheep, goat, chick, duck, goose, lurkey, pheasants, water fowls and man are susceptible, Dog is rarely affected, But, incidence of death in dog owing to motor paralysis has been recorded. This is due to ingestion of garbage toxin (Kirk and Bistener, 1915). . Mode of transmission © Clostridium botulinum is a common inhabitat of the alimentary tract of ry tract o herbivorous animals.eal 485 Botutisr © The p ° — nals jant eng BEt8 contaminated with excreta of ae aovmponee P jaan” multiplies in the decaying sninat and UE put Materials, «at's body: The organisms ‘da not Produce toxin within the anima! low Preformed toxin is the main source of disease transmission. soil with In some parts of Africa, United State: nd Austealia Ah Phospharous content hasbeen Considered to have co-relation Wit fh the disease, This is due nq the fact that phosphorus deficien from pica (depraved appre 4 result of which they chew am farcase, bones and debris Bet the chance to ingest tOxim Ie may have Dead tortoise has been incriminated toxie ih some areas. caby dead and chance to get the problem by drinking water contaminated bY and silage OMPosed carcases of fowl and other ani, Decomposed hay ® May also act as source i © . ay becom: of infection Blood e1 83), Horse ™: alfected by eating hay and eet (Blood er af., 1983) uid exudating from 88¢ Contaiminated by toxic Hui decomposed cat or rat care, es, Man may became infected by ‘or other meat products, Decompo: factor, sw and the deer . m, sausages ‘ating imperfectly preserved ha: ontributory Sed vegetables may also act asc Pathogenesis . The toxicity vanes in different species of animals, The ingested toxin is readily absorbed and get disseminated throughout the body and ultimately reaches the nerves. The heurotoxin exerts the effect by localization in the peripheral nervous system. This ultimately pives tise to various clinical signs Altributable to motor Rerve paralysis (Payling, Wright, 1955). Clinical findings The disease appear as per-avute, bation period varies from 2 to 6 sted. There is no rise oftemperat or complete paralysis of muscles of k incu inge: Acute, sub-acute or chronic form. The doys depending on the amount of tox ure, The cardinal manif estation is partial neamotion. The affected animal initially shows stiff gait, marked inclination to lie down and difficulty to raise its body, Then the animal lies On sternum with legs folded Underneath the body, With the progression of the disease the animal fails to hold its head in the normal Position and head rests on the flank region. There js Profuse sali ‘ation. The animal is unable to chew and swallow and the excessive Salivation is due to Paralysis of the muscle of pharynx and throat, The longue Protrudes from mouth and paralysed, Recovery seldom occurs. The discase ends fatally. Lesions There is no characteristic macrosco Diagnosis / ve . . ebased on clinical findings and neg: (a) Inthe field, diagnosis can be made based on elinica Post mortem lesions. PIE OF Microsconic Lesions.And Viet Ai, (ny tn the Habioetory, enigerted fad samy We teated angered frvadd be naceratead miced with equal tating, ‘Che mbataire is Wen ee nteitiged dad thea bet je injected Wt Bie eBe tay dete rinine the gateaenen Uae erate junnecerd qpuleeagilye ate bepd ne ernie (re) Vor isolation! nf causal crganican matetial ie nit aad ind wh tutes comtninitt freed birth and reat geartilee The tutes are ther peate? iy vanes toate at wrt fen Me hue Then es planes We nett at yc. npn’ Alter ulnnt 4 days, the culture tai 15 10807 fot tonicity YY [nae ulations bn guinetp (A) ‘Torin can fhe demensteated lig ebeeteplirs is and PAG (1) Identification of tarin as tie canelusive eAdenee if thie, Sioa Treatment ied. Mo reliable treatment je wvailable, » Antitann it, amitable ca" he tHe Control “ Por this, the {olen can he adopted: Mood, DC. Honk Society. Kirk, WW, and Bistener, and emergeney (rcatrncn laylings Weight, G, (1955). Proc. Sah Prevention bs the i yest method of control Access 10 contaminated foods and cancanes are 10 DE avoided as far as practicable, Cale and sheep yeazings phosphors deficient P provided with adequate phosphorus. When the above metlinds a6 difficult t ‘Type speeiticot unbined bival ed in India and can he REFERENCES _ astute, should be i, to ve This » follow vaccination ent toxoid can be used. brought from abroad. resorted toroid is not prepar at, A963). Veterinary Medicidle. 6th Ed. The English Language gf. (1975). In, Handbook of Veterinary procedurcs 1, 2nd Fd. W.B, Saunders Co., Philadelphia. Symp. of the Soc. gen. Microbiol. Cambridge Univ, Uren. ‘ ih, DM etal, (1988). In. Bovine Medicine and Surgery. Vol-I Edt. Amstutz. ULN,, American, Vel. Pub, Inc, U.S.A. P, 240.[29 | INFECTIOUS NECROTIC HEPAT ITIS Synonym. Black disease, . + tis an acute localized infection of liver which is characteriseo © toxacmio- pistribution The disease is world wide in distribution, Etiology soued The disease is caused by ‘in, . ; ‘pe associate! With invasion of liver by liver Moke cry nae, The disease a Cysticercous tenuiculis may help the disease process” 31 The FF” Susceptible hosts It is primarily a disease of sheep but it may b infreat ii f freq! pig and horse. The well developed animals are moet euseeptible- ently in cattle, Mode of transmission The organism may remain in the soil as normal flora. ! through ingestion of vegetative cells. Organisms pass through intestinal and reach the portal circulation and lodge in the liver. The transmission may take place from one farm to the other via infective sheep- The spores may spread and contaminate the pasture through irrigation. infection occurs 1 wall Pathogenesis ‘ The Ch. novyi spores localizes in the liver when a favourable anaerobic condition is created duc to invasion of liver fluke. Duc to migration of liver fluke, there is heavy destruction of liver tissues and thus the organisms get the opportunity to proliferate and liberate toxin. As a consequence there is extensive necrosis of liver. Clinical ‘findings The affected animals may dic without showing any previous signs. There is high tise of temperature, dullness and recumbency. There is abdominal pain and periorbital oedema (Blood et al., 1983). Lesion Liver shows necrotic changes. The name black disease has been applied because the liver appears black as a result of Capillary blood vessels congestion.= Infectious Necrotic Hepauus Liver tutes migration is evident. Pericardi . 1 cavity er Me pa . Pericardial, pleural and peritoneal show blood tinged Muid. P Diagnosis ‘the diagaotis is made based on history, clinical sig s changes in the liver. Picees of liver may be subjected to histopathological examinating, The confirmative diagnosis can be made py isolation of Clortidinm organism from liver lesion and demonstration of preformed toxin in the liver and peritoneal fluid (Williams, 1976). ns and characteristic Treatment No effective treatment is available. Penicillin may be tried. Control 1. Attempts should be made to control liver fluke infestation by destroying, the snail population. . ; be extended in an cnzootic area. 2. Periodical antifluke treatment ma: 4, Dead animals should be properly disposed by burning. * . 4. Vaccine: Alum precipitated toxoid provide immunity for 45 months. REFERENCES * — 1933), Veterinary Medicine. 6th Ed. the English Language Blood D.C., etal, ( Honk Society. P. 546. Sci. Industr. Kes. Aust. Pamphlet No. 19. Turner, A.W. (1931), Counc, Vida, 0 M. (1976), br, Vet. J. 132 : 221,