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

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

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

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

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

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

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

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 O2 hypoksia or anoxia

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

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

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

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

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

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

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

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

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

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)

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

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

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

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

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

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

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

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)

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

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

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

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

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

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

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

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

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)

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

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

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)

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

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

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

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

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

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

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

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

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

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 Leucocyte count: increase DIFFERENTIAL DIAGNOSIS : Anthrax SE Black leg

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

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

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

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

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

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

(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.

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

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

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

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

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

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

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

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

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

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

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