1. infectious diseases I I Departement of Vet.Mikrobiologyby
Drh. Ratih Ratnasari, S.U.
Departement of Vet.Mikrobiology
Faculty of Veterinary Medicine
Airlangga University, Surabaya

2. Genus Clostridium CLOSTRIDIOSIS CAUSED BY Rods shaped Spores forming
Gram +
Anaerobe
Rods shaped
Spores forming

3. On the basis of their dissease producing mechanisms
Infection
Entoxication
BACTERIA
BACTERIA
MULTIPLY
FORMING
POWERFUL
IN TISSUES
Absorption
TOXIN
PRODUCE TOXIN
LIVING TISSUES
TOXEMIA
Produce in
Local area
Produce in
Outside the body

4. Example Infection Entoxication Pulpy Kidney Boutvuur/ Black Leg
Cl.chauvoei
Tetanus
Cl.tetani
Paraboutvuur /
Malignant Edema
Cl.septicum
Botulismus
Cl.botulinum
Pulpy Kidney
Cl.perfringens

5. B L A C K L E G Clinical sign Boutvuur, rauch brand, quarter ill,
Gangraena emphysematosa, black quarter, charbon
Acute fever disease
attack
Cattle,sheep,goat,swine,deer
Clinical sign
Serohemorrhagic inflamation
Crepitant,spongy texture of the thick muscle

6. EPIZOOTIOLOGI ETIOLOGY Clostridium chauvoei
Rods,
Gram + (young culture),
Gram – (old culture),
Spores are located centrally / subterminally,
Proteolitic and Saccharolitic,
Antigens structure : O, H dan S antigen ,
etc
EPIZOOTIOLOGI
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

7. Cattle(6 months to 2 years old) ,
PATHOGENESIS
SENSITIVE ANIMAL
Cattle(6 months to 2 years old) ,
Buffalo,
Horse,
Goat ,
Sheep ,
Deer
and Swine
Transmission
Castration, dehorning, injection tools, birth or calving help
Wound
via
Per-oral
Spores contaminated Food & drink

8. Vegetative form & multiply in tissues Proteolitic Saccharolitic
Wound
spore
Tissues
Vegetative form
& multiply in tissues
Invade
Per oral
Produce
toxins
Predilection
Leg/thick muscle
spread
Proteolitic
Digest the muscle or collagen tissue
Black in color
Saccharolitic
Glycogen fermentation
Gas (+)
Toxin effect
Blood vessels permeability
Fluid excretion
Edema
Crepitant
cause
Spongy texture
Increase blood viscocity cause heart failure
Complication with another Clostridium cause clinical sign more complex
Toxin affeted hemolysis of erythrocyte decrease supply of O hypoksia or anoxia

9. Clinical sign & Pathological changes Bacteriology examination
DIAGNOSIS
Anamnesa
Isolation & identification
Clinical sign & Pathological changes
Biology test
Bacteriology examination
Serology test
DIFFERENTIAL DIAGNOSIS SE
PARABOUTVUUR
ANTHRAX
PREVENTION & CONTROLLING THE DISEASE
GIVING ANTISERUM (PASIVE IMUNISATION)
PREVENTION
VACCINATION & SANITATION
CONTROLLING THE DISEASE
DO NOT SLAUGHTER THE INFECTED ANIMAL
GIVING ANTIBIOTIC THERAPY & COMBINED WITH ANTISERUM

10. CLINICAL SIGN * 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

11. P A R A B O U T V U U R Disadventages Acute contagious disease
Gas Gangraena,Malignant oedema, Geburts Rausch Brand
Acute contagious disease
Cattle, Sheep, Horse, Goat, Swine and Human
Emphysematous Inflamation
Clinical sign
Malignant edema
Disadventages
Decrease Population

12. ETIOLOGY EPIZOOTIOLOGY Clostridium septicum Antigenic structure
Rods, spores forming, subterminal, Motile (peritrichous flagella), Gram +
Culture Features, resistancy. ( see literature )
Antigenic structure
O Antigen (somatic antigen), H Antigen (flagella antigen), S Antigen (spora antigen)
Produce 4 toxins
Alpha, Betha, Gamma dan Delta
Toxic subtance
Collagenase, Hyaluronidase
EPIZOOTIOLOGY
The disease occurs throughout the world but sporadic in Indonesia

13. PATHOGENESIS Spore Vegetative form Toxin production Multiply
Sensitive animal: horse, sheep, cattle, swine
Experimental animal : rabbit & guinea pig
Transmission : Wound
Spore
Vegetative form
Toxin production
Wound
Multiply

14. Predelection (liver & ren)
bloodstream
Toxin
Degeneration
Predelection (liver & ren)
bloodstream
Cardiac failure
Toxemia
Death
Lysis of Erythrocyte
O2 passage
Death
Anoxia
Hypoxia
Infection of Cl. Septicum in sheep is called BRADSOT/BRAXY

15. CLINICAL FEATURES
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

16. PATHOLOGICAL CHANGES
Incision of infected organ show dark red fluid & bad smell
DIAGNOSIS
Anamnesa
Clinical sign
Pathological changes
Bacteriology examination : isolation & identification
DIFFERENTIAL DIAGNOSIS
Boutvuur
Anthrax
Streptococcosis in horse

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

18. Swelled head, Swollen head
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)

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

20. Swelling of the head and neck area Die very suddenly
Transmission:
Infection of the head & neck area as a result from the trauma of fighting
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
(Edema malignant)
CLINICAL SIGN
Swelling of the head and neck area
Die very suddenly

21. 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
proof
* The fluorescents antibody test

22. PREVENTION, CONTROLLING THE DISEASE
Vaccination  Attenuated 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

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

24. PULPY KIDNEY
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

25. 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

26. Toxins 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)

27. EpizootiologY: Phatogenesis:
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

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

29. 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

30. 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

31. 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

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

33. Symptoms : depression, anaemia,icterus,Hb uria -- death
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

34. 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

35. 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)

36. 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

37. 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

38. 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)

39. 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

40. Differential 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

41. VET.PUBLIC HEALTH ASPECT
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

42. 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
Red Water Disease

43. Toxins :
1. Lecitinase toxins --- potent hemolytic & important
in occuring the disease
Toxin production >>> in 16 hours old culture
2. Toxin that cause necrose -- it produce in young
culture
EPIZOOTIOLOGY:
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

44. 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- ge

45. Clinical sign:
Appetite, rumination , lactation and bowel movement
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

46. 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

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

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

49. 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:
Idem to Black leg

50. TeTANuS (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)
Gram +, anaerobic condition
Cl.tetani produces 2 toxins:
Tetanospasmin (neurotoxin)
Hemolysin

51. EPIZOOTIOLOGY PATHOGENESIS
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

52. 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
 death

53. Discard the sharp materials Wound treatment Vaccination TREATMENT
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

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

55. (LIMBERNECK, LAMZIEKTE)
BOTULISMUS
(LIMBERNECK, LAMZIEKTE)
Botulismus  food intoxication  paralysis
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.

56. 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

57. CLINICAL SIGN DIAGNOSIS PATHOLOGICAL CHANGES
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

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

59. enteritis nekroticans
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
migration
small intestine
Produce toxin
Predisposition factor : Coccidiosis +
Change of diet * contain high fish meal
* mycotoxin contamination
enteritis nekroticans

60. 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

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

62. Ulcerative enteritis Transmission: = QUAIL DISEASE
The disease in quail  morbidity
& High
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)
Ulcerative enteritis

63. 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

64. 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

65. Prevention : Bacitracin 0,005% - 0,01 % in diets / drinking water
Controlling:
Good management : good sanitation/desinfection
avoid overcrowding
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

66. THANK YOU