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This organisms is the cause of Blackleg in ruminants.It occurs throuhout the world. In Indonesia it occurs at: Yogya, Solo, Madiun East Java.

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Presentation on theme: "This organisms is the cause of Blackleg in ruminants.It occurs throuhout the world. In Indonesia it occurs at: Yogya, Solo, Madiun East Java."— Presentation transcript:







7 This organisms is the cause of Blackleg in ruminants.It occurs throuhout the world. In Indonesia it occurs at: Yogya, Solo, Madiun East Java (endemic area). In 1907 De Vletter found Anthrax disease at Subang  lame  death EPIZOOTIOLOGI

8 Castration, dehorning, injection tools, birth or calving help Spores contaminated Food & drink

9 Leg/thick muscle Increase blood viscocity cause heart failure Complication with another Clostridium cause clinical sign more complex Toxin affeted hemolysis of erythrocyte decrease supply of O 2 hypoksia or anoxia


11 * Fever, depression, inflamation, crepitant * Abortion in pregnant animal * Inflamation of labia In sheep : * Paralyse,frequent respiration,sudden death - Incision of infected organ secreting dark reddish brown fluid





16  Wound infection in animals are characterized by rapidly extending swellings  The extending swellings are soft and pit in palpasion  No crepitant  The diseased animals show fever, depression, pulsus ,dyspneu, diarrhea, mucous membrane and muscular tissue are dark red, contains little or no gas.  Abortion  Genital organ infection cause : swelling of labia, Vagina necrosis, subcutaneous edema  In sheep (Braxy) : die very suddenly without previously showing symptoms, paralysis, frequent respiration

17 PATHOLOGICAL CHANGES PATHOLOGICAL CHANGES Incision of infected o rgan show dark red fluid & bad smell DIAGNOSISAnamnesa Clinical sign Pathological changes Bacteriology examination : isolation & identification DIFFERENTIAL DIAGNOSIS DIFFERENTIAL DIAGNOSISBoutvuurAnthrax Streptococcosis in horse

18 PREVENTION & CONTROLLING THE DISEASE Prevention : Immunized by inactive vaccine & antitoxin Prevention : Immunized by inactive vaccine & antitoxin Sanitation Sanitation Controlling: Controlling: Do not slaughter the infected animals in slaughterhaouse. Discard the visceral & carcass totally Treatment : - Antiserum Treatment : - Antiserum - Chemoterapy: Sulfathiazol - Chemoterapy: Sulfathiazol - Antibiotic : Penicillin, Tetracycline - Antibiotic : Penicillin, Tetracycline - Combination of antiserum and antibiotic - Combination of antiserum and antibiotic

19 BIG HEAD Swelled head, Swollen head ETIOLOGY Clostridium novyi type A (Bacillus edematis maligni II, Clostridium edematiens)  Rods, Gram +(young culture), motile (peritrich flagella), spores are located subterminal & are oval This organism is more strictly anaerobic than others ANTIGENIC STRUCTURE -Somatic antigens -Flagellar antigens -Produce toxins (alpha,beta,gamma,epsilon)

20 EPIZOOTIOLOGY EPIZOOTIOLOGY The disease was found : Ind., Unite States, Erope, Australia, New Zealand PATHOGENESIS PATHOGENESIS Sensitive animals : cattle, sheep, goat,dog, horse Experimental animals : guinea pig, mice

21 Transmission: Infection of the head & neck area as a result from the trauma of fighting invasion of bacteria invasion of bacteria Wounds --------------  toxin production multiply (alpha toxin) Edema & gas gangrene of the head and neck area So the disease known as Big head, Swollen head So the disease known as Big head, Swollen head (E dema malignant) (E dema malignant) CLINICAL SIGN Swelling of the head and neck area Die very suddenly

22 PATHOLOGICAL CHANGES Hemorrhages in lung & red in color DIAGNOSIS * Clinical sign * Laboratory examination (Bacteriologic test) * Isolation & Identification organism * The demonstration of alpha toxin in the lesion and exudates is excellent diagnostic and exudates is excellent diagnostic proof proof * The fluorescents antibody test

23 PREVENTION, CONTROLLING THE DISEASE Prevent ion : Vaccination  A ttenuated toxin Alum-precipitated formalinized whole broth cultures In endemic are: antiserum/hyperimun serum Controlling the disease : Cl.novyi Type A  is found in the soil & intestinal tract herbivorous animals, so they were source of Cl.novyi infection

24 TREATMENT : Combination of Antibiotic (Penicillin) and Chemoterapy (Sulfadiazin) Combination of Antibiotic and Antisera

25 Sinonim : Enterotoxaemia, Over eating disease, Milk colic, Apoplexia Pendahuluan :  Pulpy Kidney -------- acute & fatal entoxication in sheep  Causa : absortion of epsilon toksin that resulted from Cl. welchii Type D (in the intestine)  Habitat : Cl. welchii is found in the soil & in the alimentary tract (warm blooded animals)  Toxicogenic varieties of the organism ---- fatal toxaemias in in sheep, calves, young pigs and man

26 Etiology : Cl. welchii, Cl. perfringens, Bacillus aerogenes capsulatus, B. phlegmonis empyssematousae, Welch bacillus, B.paludis, Cl.ovitoxicum, Gas bacillus. rods: singly or in pairs seldom in chains The spores are oval,central, subterminal. Spores do not form in highly acid media Capsules +, non motile, Gram positive in young culture Gram negative in old culture Resistancy & cultural features: see literature

27 Produce 4 toxins: alpha, beta, epsilon & iota Toxin is heat-labile Toxin + chemicals ----Toxoid : Antigenicity + Toxicity - Characteristic of the major toxins of Cl. welchii (see literature) Interpretation of serum neutralization test for Cl. perfringens toxin (see literature)

28 EpizootiologY : The disease in Indonesia ---- has not been found. The disease occurs in Australia, New Zealand England& United States Sensitive animals : depend on species & age of sheep, calves, goats, foals, man. Young animals more sensitive than the old ones Phatogenesis: Cl. welchii --------- Tr. Dig -----tissue-----produce toxin in small intestine------absorbtion---- mucous membrane

29 Clinical sign: Incubation period : 2 – 3 hours Incubation period : 2 – 3 hours Convulsion with agonal struggling, dyspneu and death Convulsion with agonal struggling, dyspneu and death Type of the disease (3 types) : a.Peracute neuro type : convulsion, dyspneu b.Subacute type : depression c.Digestitype : chronis, diarrhea, recovery after 1 week

30 In sheep Could be infected by Cl.welchii type A, type B, type C and type D Type A : Symptoms : anemia hemolitica Hb- Uria,icterus Tipe B : Symptoms : Dysentry (lamb dysentry) Tipe C : cause the disease of adult sheep called struck Symptoms : accumulation of fluid in the peritoneal and thoracic cavities dysentry or diarrhea are seldom present

31 P.A :enteritis,peritonitis, necrosis of the mucosa Abomasum and small intestine Cl.welchii type D Causes Pulpy Kidney & Enterotoxemia in adult sheep IN PIGS Could be infected by Cl. Welchii type C Piglets aged 1 to 3 days,this type causes an acute hemorrhagic enteritis with high mortality

32 IN CALVES Could be infected by Cl.welchii type A, Cl. Welchii type C Cl.welchii type D and E Enterotoxemic form Affected calves die in a few hours after showing clinical sign

33 IN POULTRY Could be infected by Cl. Welchii type C : Enteritis necroticans (E.ulcerative)

34 PHATOGENESIS Cl.welchii (anaerobic bacteria)----normal intestinal flora of healthy animals. Cl. Welchii type A : ---- causes a disease known as Yellow Lamb Disease in sheep Symptoms : depression, anaemia,icterus,Hb uria -- death Produce Alpha toksin --- absorb into the blood circulation--- causes massive intravascular hemolysis Capillary damage

35 In calves : -- inflamation of intestine --- death P.A : Pericardium --------- hydropericardium Lung ---------- edema,swelling ren -------------- dark swelling Hepar -------------- pale swelling Cl.welchii type B: ---------- causes LAMB DYSENTRI in lambs in the first days of life Infection bacteria p.o --- Intestine ------- Prod. Beta toksin Ulceration, irritation, hemorrhagic zones of the small intestine Diarrhea : dehidration, toxemia Death

36 P.A: Intestinal mucous : inflammation, congestion ulceration, hemorrhagic of the small intestine Caecum & colon : congestion & edematous Cl. Welchii type C : cause the disease of adult sheep called “STRUCK” (hemorrhagic entero – toxemia) --- symptom : convulsion, enteritis In calves, lambs, piglets: Hemorrhagic enteritis, necrotic enteritis, peritonitis Bacterial infection by p.o (food) --- intestine --- --- produce beta toxin --- hemorrhagic enteritis & necrosis on the mucosa of small intestine (je- junum)

37 P.A: Hemorrhagic enteritis with patches of necrosis on the mucosa & serosa----mainly the jejunum Accumulation of fluid in the peritoneal & thorac ic cavities Beta toksin may be demonstrated in the fluids Cl.welchii type D: This type causes Enteroxemia in sheep called Pulpy Kidney/overeating disease

38 Withlock & Fabricant (1947) ---devided into 3 diseases : 1. Pulpy Kidney suckling lambs 2. Braxy like enterotoxemia young sheep 3. Overeating disease Feeder lamb Intensive sheep-raising system, including feed lots, are particularly prone to outbreak of ente- rotoxemia

39 The organism is part of the normal intestinal flora-- --Highly proteinaceous diets ---- leads increase in multiplication of the organism in the gut ---- produces alpha & epsilon toxins Effect of toxins: loci of liquefactive necrosis, perivascular edema, hemorrhages especially in meningen, damage of vascular endotelium of the brain Clinical sign : Peracute – die without showing symp toms Acute ----- convulsion, diarrhea P.A : Intestinal tract : hemorrhages, congestion Endocard : ptechiae The kidney cortex : hyperemia & degenerative changes – become soft & friable (“pulpy kidney”) – autolysis --- this condition called Pulpy Kidney (patognomonis)

40 Cl.welchii type E : This type causes Enterotoxemia with hemor- rhagic & necrotic enteritis in lambs & calves P.A : abomasum mucous & small intestine --- hyperemia The intestinal contents : mucoid in concisten- cy & yellow to orange in color Pericardium : filled with fluid

41 DIAGNOSIS Anamnesa, Clinical sign,P.A changes Laboratory examination: - Isolation & identification of bacteria Identification toxin by serum-netralization test Differential diagnosis : Black disease Black leg Anthrax Hypomagnesia

42 CONTROL & TREATMENT : Administrative: deliver a report Prevention: by restriction of feed,prevention giving highly & suddenly of protinaceous diets. Carbohydrate diets ---give acid condition -----ulcera of abomasum --- as Port d’entre of bacteria Immunization : active --------- vaccination pasive --------- antiserum Treatment : Antibiotics --- Chlortetracycline,Penicil lin in the feed, Antiserum VET.PUBLIC HEALTH ASPECT Animals that suffer Pulpy kidney do not enter to salughterhouse Carcass and viscera must be discarded

43 Sinonim : Infectious icterohemoglobinuria, Haemorrhagic Disease INTRODUCTION: The disease attack -- cattle, sheep,pig The characteristic symptom -- the urine is a dark red or port-wine color, clear but foamy The disease has found in A.S, New Zealand, in alkaline area (pH > 8 ), in pastures that contain swampy areas which continually maintain a pH of 8.0 or higher ETIOLOGY: Clostridium hemolyticum ---- rods, singly, forming short chain The spora : oval & located subterminal Motile, Gram positive

44  Toxins :  1. Lecitinase toxins --- potent hemolytic & important in occuring the disease in occuring the disease  Toxin production >>> in 16 hours old culture  2. Toxin that cause necrose -- it produce in young cultureEPIZOOTIOLOGY:  The disease was found in United States & New Zealand. The disease occurs during the summer & early fall months  In Indonesia the disease has not been found  Sensitive animals : cattle, sheep & hog  Experimental animals: rabbit, guinea pig, mice

45 TRANSMISSION :  P.o (contaminated food with spore) ---- Tr. Dig ---germination of spore ---vegetative form --- portal vein --- liver ---toxin production : - nekrosis of liver & organ - subcutaneous & visceral haemorrha- - subcutaneous & visceral haemorrha-ge

46 Clinical sign:  Appetite, rumination, lactation and bowel movement suddenly cease suddenly cease  Mucous membrane icterus  Fever  The temperature become subnormal before death  Pulsus frequent  Feces become soft : dark red, deeply bile-stained or bloody  Urine : port-wine color or dark red & foamy  At the time when Hb uria appears : the red cell count de- creases and the leucocyte count increases  Death occurs 36 hours after the first symptoms appears

47 PATHOLOGICAL CHANGES :  Haemorrhage of nostril and anus  Conjunctiva : icterus & reddish  Neck and shoulder : hemorrhagic edema  Abdomen : filled with transudat  Liver: swelling, icterus  Kidney: red brownish, ptechiation in the kidney cortex, edema +, in incision red bloody fluid is present  Hemorrhagic enteritis

48 SAMPLE FOR LABORATORY TEST: SAMPLE FOR LABORATORY TEST:  Blood sample + anticoagulan ---- for blood examination  The abnormal of liver --- for bacteriology test

49 DIAGNOSIS:  Anamnesa  Clinical sign  Pathological changes  Bakteriology examination: Isolation & identifica- tion  Biologis test: in guinea pig  Blood examination : Erythrocyte 1.200.000 Hb 3,5 Hb 3,5 Leucocyte count: increase Leucocyte count: increase DIFFERENTIAL DIAGNOSIS :  Anthrax  SE  Black leg

50 CONTROL AND TREATMENT CONTROL AND TREATMENT  1.Administrative: deliver a report  2. Prevention:  Immunisation: Immun serum  Vaccination  Sanitation : Pasture in wet pastureland  Isolation & treatment of afflicted animals  3. Treatment:  Giving Antiserum every 2 weeks  Symptomatic therapy VET. PUBLIC HEALTH ASPECT: VET. PUBLIC HEALTH ASPECT:  Idem to Black leg

51 (Lock jaw)  The disease cause by entoxication of Cl. tetani  Characteristic symptom : tetanic spasm of the muscle  death  The disease affected in all animals & man ETIOLOGY  Clostridium tetani : Straight rods, motile Terminal spore (drum stick) Terminal spore (drum stick) Gram +, anaerobic condition Gram +, anaerobic condition  Cl.tetani produces 2 toxins: Tetanospasmin (neurotoxin) Hemolysin Hemolysin

52 EPIZOOTIOLOGY  The disease occurs throughout the world. In Indonesia  sporadic  The disease commonly attack : horse, cow, sheep, dog, pig, chicken, rats, guinea pig & monkey. PATHOGENESIS  Infections in all animals and man occur as a result of wound or umbilical contamination. Deep, penetrating wounds, the depth of which become necrotic with reduce oxygen  In horse : nail wounds in the foot  In sheep : wound after lambs are castrated or docked  In cattle : infection following calving,dehorning,castration

53 CLINICAL SIGN  Incubation period 1 – 3 weeks  Chronic or tetanic spasm of the muscles  irritation by : voice, light, touch  Characteristic symptom in horse: spasms of the nictitating membrane, facial and jaw muscle leading to Lock jaw  The nostril are dilated, the tail raise If the toxin destroy CNS  generally convulsion, convulsion become convulsion become  death  death

54 PREVENTION:  Discard the sharp materials  Wound treatment  Vaccination TREATMENT  Make new fresh wound  wash it with KMnO4, H2O2  Symptomatic treatment : sedative  Mephenesin tranquilizing drug  Chlorpromazine  Antibiotics : Aureomycin,Penicillin,Terramycin

55 DIAGNOSIS -Base on clinical sign -Bacteriology test DIFFERENTIAL DIAGNOSIS  Grass tetani  hypocalcemia  Entoxication of strichnin  Muscular rheumatism  chronis  Rabies  paralysis

56 ( LIMBERNECK, LAMZIEKTE )  Botulismus  food intoxication  paralysis of motoric nerve  death of motoric nerve  death  The disease commonly attack animals & man ETIOLOGY  Clostridium botulinum : large rods, form short chains, Gram +,motile, spore located centrally or subterminal, anaerobe.

57 EPIZOOTIOLOGY  Botulismus  was found througout the world & Indonesia  Sensitive animals : horse, cattle, sheep, chickens, ducks PATHOGENESIS  Incubation period in few hours  5 days  Occurence in animals  ingestion of food ma- terial contaminated with Clostridium botuli – num spore num spore

58 CLINICAL SIGN  Pharyngeal paralysis  the tongue often becomes paralyzed  Weakly, paralysis, respiratory paralysis  death  In cattle & sheep : hypersalivation, nasal discharge >>  In horse : difficult to eat & to drink (shorter in incubation period) The shorter the incubation period in tetanus, the worse the prognosis PATHOLOGICAL CHANGES  No specific pathological changes DIAGNOSIS  Clinical sign  Laboratory examination : demonstration of toxin in the serum

59 Prevention  Avoid rotten food  Administration of toksoid TREATMENT  Early intoxication  administration of polyvalent antitoksin  Symptomatic therapy

60  Sporadic outbreak of botulism type C  in broiler chicken  Age of 4 – 8 weeks old are sensitive  Mortality rate: 6 – 20 %  Causative agent:  Clostridium perfringens tipe C Colon and caecum Colon and caecum migration migration small intestine Produce toxin Produce toxin  Predisposition factor : Coccidiosis +  Change of diet * contain high fish meal * mycotoxin contamination * mycotoxin contamination

61 CLINICAL SIGN :  Diarrhea  bloody diarrhea resemble to Cocci- diosis  death  Depression  Delay of growth PATHOLOGICAL CHANGES  In Jejenum,ileum dan caecum  crumbly,disten tion (gas +)  The mucosa covered with hard necrotic membrane (yellow or green in color).  Necrotic lesion  at villi2 in intestinal canal  In liver  necrotic lesion  diffuse,bronze in color  Focal necrotic lesion

62 DiagnosIS : Base on: Clinical sign Anamnesa Anamnesa Change of pathology anatomic Change of pathology anatomic DIFFERENTIAL Diagnosis:  Enteritis ulcerative  Coccidiosis CONTROL & TREATMENT :  Treatment : antibiotic in drinking water  Prevention : Sanitation Disinfection Disinfection

63 = QUAIL DISEASE = QUAIL DISEASE  The disease in quail  morbidity & High mortality mortality  Young turkey,wild bird & young domestic chickens  Causative agent:Clostridium colinum  Predisposition factor : infection of Coccidiosis  disturbances of digestive tract.  Transmission :  Direct contact : with infected birds/chickens  Indirect contact : via the oral route (contaminated food & drinking water)

64 Clinical sign:  4 – 12 weeks of chickens more resistant  In quail  acute, high mortality rate  Affected birds may die without showing symptom  Acute form : general symptom(anorexia,inactive)  diarrhea  Chronic form : diarrhea, thinness PATHOLOGY FEATURES:  Lesion (tukak) is small and yellow in color and limited by area of hemorrhagic at cell of intestinal mucosa and ceccum  Diffuse liver necrosis  diffuse pinpoint necrosis or the necrosis is centrilobular, yellowish in color  Liver,spleen,kidney  inflammation

65 DiagnosIS :  Base on:Clinical sign Pathological changes Bacteriology test Differential diagnosis :  Coccidiosis  Salmonellosis  Necroticans enteritis: infection occur in 1/3 part of upper intestine, lesion occur on the superficial of mucous membrane  Ulcerative enteritis : infection occur in lower intestine & caecum, perforation of intestine wall

66 Controlling: Good management : good sanitation/desinfection avoid overcrowding avoid overcrowding good litter quality good litter quality Prevention : Bacitracin 0,005% - 0,01 % in diets / drinking water Therapy :  Bacitracin,Tetracyclines, Erythromycin, Doxicyklin,ampicillin,tylosin dan lincomycin.  Dosage of Bacitracin : 1g /1 kg diets


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