Clostridium oedematiens
Also Known as Clostridium novyi
Distribution in Nature
• Normal inhabitant of soil.
• World-wide distribution.
• Cause of infectious necrotic hepatitis in sheep and catlle
known as black disease and gas gangrenous.
• Big head (Fighting)
• Cl. Oedematiens type D, also known as cl. haemolyticum
cause of bacillary haemoglobinurea (red water disease of cattle
and sheep.
Morphology & Staining
• Large rod 5-10um in length and 1-1.5um in
width.
• Spores are oval, either centrally or
subterminal.
• Non capsulated.
• Motile, peritrichous flagella
• Gram positive
Culture Characterisics
• Strict anaerobe
• Growth on ordinary laboratory media can be enhanced by the
addition glucose.
• Fresh brain infusion also encourage the growth.
• On fresh horse blood agar the colonies are flat with irregular
edges.
• On cooked meat broth colonies are pink.
• On egg yolk marked opalescence caused by alpha toxin
(lecithinase) referred to as Nagler reaction or lecithinase
reaction
Resistance to Physical & Chemical Agents
• Spores survives heating to 95c for 15 minutes but killed in
moist heat at temperature 120c for 5 minutes.
Antigens & Toxins
• Species are divided into four types labelled A, B, C and D, according to
antigens or toxins produced.
• Most important toxic in relation to aetiology of disease are alpha, beta and
gamma toxins.
• Type A (Cl. oedematiens (Alpha & Gamma Toxin) Gas gangrenous & Big
head in rams
• Type B (Cl. gigas alpha & Beta Toxin Black Disease (Chronic hepatitis)
• Type C Cl. bubalorum no toxin associated with cases of osteomyelitis not
of aetiological importance
• Type D Cl. haemolyticum beta toxin Bacillary hamoglobinuria
Epidemiology & Pathogenesis
• cause of gas gangrenous conditions in variety of animal species (Horses, catlle,
sheep, goats, pigs).
• Present in soil and intestine of animals and can be present on skin wound. Infected
surface wounds develop as localised gas gangrenous .
• A condition big head develop in sheep from wounds on the faces and heads or rams
which have been fighting. Laterly develop into gas gangrenous and swelling.
Severe cases may lead to death due to toxaemia.
• Black disease is the chronic hepatitis in sheep. Fluke migration provide suitable
environment for growth of Clostridium oedematiens. Animal dies from alpha toxin
(toxaemia).
• Bacillary haemoglobinurea by type D pathogenesis similar to black disease ie
spores germinate to vegatative form in liver and produce beta toxin.
Symptoms
• Big Head: swelling gas gangrenous around head and face. Followed by collapse and
death. Mortality rate 90 %.
• Black disease: acute toxeamia sudden death. Decreasing ability to move, unsteady
gait. Increase body temperature.
• Bacillary haemoglobinurea occur in summer, fever, abdominal pain, diarrhoea and
haemoglobinurea.
Diagnosis
• History
• Isolation of organisms
Clostridium septicum
• Distribution in Nature:
• Normal inhabitant of soil.
• Also present in faeces
• Associated with condition known as braxy in sheep.
Morphology & Staining
• Large rod shaped
• 2-10um length and .4-1um width.
• Sometimes short or long filaments
• Spore-forming (Centrally or subterminal.
• Motile (Pereitrichous flagella)
• Gram Positive
CULTURE CHARACTERISTICS
• Strict anaerobe.
• Optimum temperature for growth is 37c on ordinary lab media.
• Growth enhanced by addition of glucose into media.
• On solid media appear semi-transparent and rounded, greyish-white in colour.
• On horse blood agar produce haemolysis.
• Colonies on cooked meat broth turned pink (Sacchrolytic).
Antigens & Toxins
• divided into six groups on basis of two somatic and five flagellar antigens.
• Four toxic components labelled alpha, beta, gamma and delta.
• Most important is alpha toxin which is lethal, necrotizing .
• Beta toxin contains deoxyribonuclease and toxic to leucocytes.
• Gamma toxin is hyaluronidase.
• Delta toxin is haemolysin, antigenically realted to streptolysin O and is also
necrotizing.
Epidemiology & Pathogenesis
• Braxy in sheep is infection of abomasum.
• Organsim remain viable in faeces for as long as 1 year.
• Multiplication of Cl. septicum in mucosa and submucosa of abomasum .
Symptoms
• Loses appetite.
• Abdominal pain for few hours
• Sudden death.
Diagnosis
• Braxy suspected when sudden death occurs.
• Inflammation in wall of abomasum also indicate the disease.
• Stained smears prepared also indicate the presence of gram positive rods.
• Fluorescent antibody technique. Fluoroscent antibody bind to the bacteria on a
microscope slide, allowing ready detection of the bacteria using a fluorescence
microscope.
Clostridium Chauvoei (Black Quarter, black leg)
• Distribution in nature: occurs in sheep and cattle
• Name black quarter or black leg is descriptive for muscle which develop dark and
almost black coloured crepitant areas of infected tissue usually occur in the area of
hind quarter.
• Word-wide, soil, pasture.
• Morphology & Staining: rod shaped with rounded ends. 3-8um in length and .5um
width.
• Gram positive.
• Pleomorphic
• Motile (Peritrichous flagella)
• Spore forming centrally or subterminal.
CULTURAL CHARACTERISTICS
• Strict anaerobe
• Poor growth on ordinary lab media but enhanced by addition of liver extract or
glucose.
• Optimum temperature for growth is 37c.
• On blood agar whitish grey colony with irregular edges.
• Growth in cooked meat broth is slow with pink colour.
• Ferments glocose, lactose, sucrose and maltose with production of gas and acid.
• Resistance to Physical and chemical agents:
• Spores are killed by steam in 40-50 minutes and in 20 minutes when autoclaved at
120c. Spores are susceptible to 3 percent fomalin for 15 minutes.
• Antigens & Toxins: all strain have one common somatic antigen but organism
divided into two groups on basis of their flagellar antigens.
• The organism share a common spore antigen with Cl. septicum.
• Alpha, beta, gamma and delta toxin same effect as cl.septicum toxin.
Epidemiology & Pathogenesis
• Seasonal, highest during summer months, animals on pasture during spring and
summer the incidence is high.
• Wounds contamination with bacilli.
• Ingestion of organism.
• Spore develop into vegetative form under predisposing factors in a tissue and
multiplication in the particular areas of tissues.
• SYMPTOMS: younger animals 6months to 2 years of age.
• Obvious sign is crepitant swelling in the hind- or fore-quarter with gas production.
• Lame
• Affected muscle voilent twitching.
• Sudden death.
• Diagnosis: History and Symptoms
Clostridium welchii (Clostridium perfringens)
• Distribution in Nature: cause of gas gangrene in man and enterotoxaemia in sheep
and less frequently in other species.
• On the basis of toxin these organims are classified as types A, B, C, D, or E.
• Present in soil and intestines of healthy animals and man..
• Disease occurs when these intestinal organisms begin to multiply unusually rapidly
and produce toxin.
• Morphology and staining: rod shaped from 2-6um length and .8-1.5um width.
• Capsulated.
• Spores oval, central or subterminal.
• Gram positive.
CULTUR CHARACTERISTICS
• Anaerobe does not require strict anaerobic conditions for growth.
• Grow well on ordinary lab media in temperature range of 37-47c, the optimum
being 43-47c.
• Growth is enhanced by glucose or blood,
• Growth on solid surface colonies are round, smooth, evenly convex.
• On blood agar round colonies.
• On cooked meat medium the meat turned pink.
• On egg yolk marked opalescence caused by alpha toxin (lecithinase) referred to as
Nagler reaction or lecithinase reaction.
• Produce acid and gas in glucose, lactose, sucrose and maltose.
• Antigens and Toxins:
• Somatic antigens & Capsular polysaccharide antigens not major importance
Antigens and Toxins:
• Produce variety of toxic and enzymic substances important in relation to
identification of strains and patogenesis of disease.
• Alpha toxin: major lethal toxin is an enzyme, lecithinase produce by types of
clastridium welchii. Causes development of yellowish-green area of necrosis.
• In presense of Ca & Mg it can split lipoprotein complexes in serum or egg yolk
media causing opalescence (halo) (Nagler reaction)
• Beta Toxin: lethal and necrotizing toxin produced by Types B & C.
• Gamma Toxin: Minor lethal toxin produced by B & C.
• Delta Toxin: lethal toxin and haemolytic for RBCS produced by Type C.
• Epsilon toxin: major lethal & necrotizing produced by Type B & D.
• Eta Toxin: minor lethal toxin produced by Type A.
• Theta Toxin: haemolytic toxin produced by all types.
• Iota toxin: major lethal & Necrotizing produced by type E.
• Kappa toxin: a collagenase attacks on collagen.
Antigens and Toxins:
• Lambda toxin: a proteinase & gelatinase.
• Mu toxin: have properties of hyaluronidase produced by Type B. break down
polysaccharides cementing substance present in most tissues.
• Nu toxin: it is a deoxyribonuclease.
Epidemiology & Pathogenesis of Disease caused by clostridium
welchii type A (Less veterinary importance)
• Mainly human infections associated with gas gangrene and human food poisoning.
• Epidemiology & Pathogenesis of Disease caused by clostridium welchii type B
• Lamb Dysentary: acute disease of yuong lambs of 2-5days of age.
• Multiplication of organism in intestine and result into fatal toxaemia. Although
ingested by suckling but it is normal inhabitant of intestine.
• Predisposing factors which increases the rapid and unusual high rate of growth
include lambs which ingest large quantities of milk.
• Symptoms:
• Abdominal pain
• Bleat repeatedly.
• Cease to suck
• Collapse & die within few hours
• Diagnosis: age of lambs, symptoms, history
Epidemiology & Pathogenesis of Disease caused by clostridium
welchii type C
• Enterotoxaemia in sheep (struck)
• Affects adult sheep
• Acute & Fatal enterotoxamia
• Absorption of toxin from intestine.
• Toxaemia
• Symptoms:
• Sudden death
• Abdominal pain
• Seldom diarrhoea
Epidemiology & Pathogenesis of Disease caused by clostridium
welchii type D
• Enterotoxamia in Sheep (pulpy kidney disease, overeating disease)
• Multiplication of organism in abomasum and intestine.
• Occurs in different age groups.
• Normal inhabitant of soil and also intestine of sheep.
• Under particular circumstances (Overeating, concentrated diet) high toxin
production leads to toxaemia.
• The production of toxin may be due to feeding of feeding of concentrated protein
diets reduces acidity of stomach and favours rapid bacterial multiplication and
production of toxin.
• Also overfeeding result of undigested starch passes from stomach to intestine which
favour the multiplication of organism in intestine.
• Symptoms: deaths suddenly, animal become dull, weak.
• Diagnosis: sudden change in diet is suggestive of disease.

Clostridium oedematiens

  • 1.
  • 2.
    Distribution in Nature •Normal inhabitant of soil. • World-wide distribution. • Cause of infectious necrotic hepatitis in sheep and catlle known as black disease and gas gangrenous. • Big head (Fighting) • Cl. Oedematiens type D, also known as cl. haemolyticum cause of bacillary haemoglobinurea (red water disease of cattle and sheep.
  • 3.
    Morphology & Staining •Large rod 5-10um in length and 1-1.5um in width. • Spores are oval, either centrally or subterminal. • Non capsulated. • Motile, peritrichous flagella • Gram positive
  • 4.
    Culture Characterisics • Strictanaerobe • Growth on ordinary laboratory media can be enhanced by the addition glucose. • Fresh brain infusion also encourage the growth. • On fresh horse blood agar the colonies are flat with irregular edges. • On cooked meat broth colonies are pink. • On egg yolk marked opalescence caused by alpha toxin (lecithinase) referred to as Nagler reaction or lecithinase reaction
  • 5.
    Resistance to Physical& Chemical Agents • Spores survives heating to 95c for 15 minutes but killed in moist heat at temperature 120c for 5 minutes.
  • 6.
    Antigens & Toxins •Species are divided into four types labelled A, B, C and D, according to antigens or toxins produced. • Most important toxic in relation to aetiology of disease are alpha, beta and gamma toxins. • Type A (Cl. oedematiens (Alpha & Gamma Toxin) Gas gangrenous & Big head in rams • Type B (Cl. gigas alpha & Beta Toxin Black Disease (Chronic hepatitis) • Type C Cl. bubalorum no toxin associated with cases of osteomyelitis not of aetiological importance • Type D Cl. haemolyticum beta toxin Bacillary hamoglobinuria
  • 7.
    Epidemiology & Pathogenesis •cause of gas gangrenous conditions in variety of animal species (Horses, catlle, sheep, goats, pigs). • Present in soil and intestine of animals and can be present on skin wound. Infected surface wounds develop as localised gas gangrenous . • A condition big head develop in sheep from wounds on the faces and heads or rams which have been fighting. Laterly develop into gas gangrenous and swelling. Severe cases may lead to death due to toxaemia. • Black disease is the chronic hepatitis in sheep. Fluke migration provide suitable environment for growth of Clostridium oedematiens. Animal dies from alpha toxin (toxaemia). • Bacillary haemoglobinurea by type D pathogenesis similar to black disease ie spores germinate to vegatative form in liver and produce beta toxin.
  • 8.
    Symptoms • Big Head:swelling gas gangrenous around head and face. Followed by collapse and death. Mortality rate 90 %. • Black disease: acute toxeamia sudden death. Decreasing ability to move, unsteady gait. Increase body temperature. • Bacillary haemoglobinurea occur in summer, fever, abdominal pain, diarrhoea and haemoglobinurea.
  • 9.
  • 10.
    Clostridium septicum • Distributionin Nature: • Normal inhabitant of soil. • Also present in faeces • Associated with condition known as braxy in sheep.
  • 11.
    Morphology & Staining •Large rod shaped • 2-10um length and .4-1um width. • Sometimes short or long filaments • Spore-forming (Centrally or subterminal. • Motile (Pereitrichous flagella) • Gram Positive
  • 12.
    CULTURE CHARACTERISTICS • Strictanaerobe. • Optimum temperature for growth is 37c on ordinary lab media. • Growth enhanced by addition of glucose into media. • On solid media appear semi-transparent and rounded, greyish-white in colour. • On horse blood agar produce haemolysis. • Colonies on cooked meat broth turned pink (Sacchrolytic).
  • 13.
    Antigens & Toxins •divided into six groups on basis of two somatic and five flagellar antigens. • Four toxic components labelled alpha, beta, gamma and delta. • Most important is alpha toxin which is lethal, necrotizing . • Beta toxin contains deoxyribonuclease and toxic to leucocytes. • Gamma toxin is hyaluronidase. • Delta toxin is haemolysin, antigenically realted to streptolysin O and is also necrotizing.
  • 14.
    Epidemiology & Pathogenesis •Braxy in sheep is infection of abomasum. • Organsim remain viable in faeces for as long as 1 year. • Multiplication of Cl. septicum in mucosa and submucosa of abomasum .
  • 15.
    Symptoms • Loses appetite. •Abdominal pain for few hours • Sudden death.
  • 16.
    Diagnosis • Braxy suspectedwhen sudden death occurs. • Inflammation in wall of abomasum also indicate the disease. • Stained smears prepared also indicate the presence of gram positive rods. • Fluorescent antibody technique. Fluoroscent antibody bind to the bacteria on a microscope slide, allowing ready detection of the bacteria using a fluorescence microscope.
  • 17.
    Clostridium Chauvoei (BlackQuarter, black leg) • Distribution in nature: occurs in sheep and cattle • Name black quarter or black leg is descriptive for muscle which develop dark and almost black coloured crepitant areas of infected tissue usually occur in the area of hind quarter. • Word-wide, soil, pasture. • Morphology & Staining: rod shaped with rounded ends. 3-8um in length and .5um width. • Gram positive. • Pleomorphic • Motile (Peritrichous flagella) • Spore forming centrally or subterminal.
  • 18.
    CULTURAL CHARACTERISTICS • Strictanaerobe • Poor growth on ordinary lab media but enhanced by addition of liver extract or glucose. • Optimum temperature for growth is 37c. • On blood agar whitish grey colony with irregular edges. • Growth in cooked meat broth is slow with pink colour. • Ferments glocose, lactose, sucrose and maltose with production of gas and acid. • Resistance to Physical and chemical agents: • Spores are killed by steam in 40-50 minutes and in 20 minutes when autoclaved at 120c. Spores are susceptible to 3 percent fomalin for 15 minutes. • Antigens & Toxins: all strain have one common somatic antigen but organism divided into two groups on basis of their flagellar antigens. • The organism share a common spore antigen with Cl. septicum. • Alpha, beta, gamma and delta toxin same effect as cl.septicum toxin.
  • 19.
    Epidemiology & Pathogenesis •Seasonal, highest during summer months, animals on pasture during spring and summer the incidence is high. • Wounds contamination with bacilli. • Ingestion of organism. • Spore develop into vegetative form under predisposing factors in a tissue and multiplication in the particular areas of tissues. • SYMPTOMS: younger animals 6months to 2 years of age. • Obvious sign is crepitant swelling in the hind- or fore-quarter with gas production. • Lame • Affected muscle voilent twitching. • Sudden death. • Diagnosis: History and Symptoms
  • 20.
    Clostridium welchii (Clostridiumperfringens) • Distribution in Nature: cause of gas gangrene in man and enterotoxaemia in sheep and less frequently in other species. • On the basis of toxin these organims are classified as types A, B, C, D, or E. • Present in soil and intestines of healthy animals and man.. • Disease occurs when these intestinal organisms begin to multiply unusually rapidly and produce toxin. • Morphology and staining: rod shaped from 2-6um length and .8-1.5um width. • Capsulated. • Spores oval, central or subterminal. • Gram positive.
  • 21.
    CULTUR CHARACTERISTICS • Anaerobedoes not require strict anaerobic conditions for growth. • Grow well on ordinary lab media in temperature range of 37-47c, the optimum being 43-47c. • Growth is enhanced by glucose or blood, • Growth on solid surface colonies are round, smooth, evenly convex. • On blood agar round colonies. • On cooked meat medium the meat turned pink. • On egg yolk marked opalescence caused by alpha toxin (lecithinase) referred to as Nagler reaction or lecithinase reaction. • Produce acid and gas in glucose, lactose, sucrose and maltose. • Antigens and Toxins: • Somatic antigens & Capsular polysaccharide antigens not major importance
  • 22.
    Antigens and Toxins: •Produce variety of toxic and enzymic substances important in relation to identification of strains and patogenesis of disease. • Alpha toxin: major lethal toxin is an enzyme, lecithinase produce by types of clastridium welchii. Causes development of yellowish-green area of necrosis. • In presense of Ca & Mg it can split lipoprotein complexes in serum or egg yolk media causing opalescence (halo) (Nagler reaction) • Beta Toxin: lethal and necrotizing toxin produced by Types B & C. • Gamma Toxin: Minor lethal toxin produced by B & C. • Delta Toxin: lethal toxin and haemolytic for RBCS produced by Type C. • Epsilon toxin: major lethal & necrotizing produced by Type B & D. • Eta Toxin: minor lethal toxin produced by Type A. • Theta Toxin: haemolytic toxin produced by all types. • Iota toxin: major lethal & Necrotizing produced by type E. • Kappa toxin: a collagenase attacks on collagen.
  • 23.
    Antigens and Toxins: •Lambda toxin: a proteinase & gelatinase. • Mu toxin: have properties of hyaluronidase produced by Type B. break down polysaccharides cementing substance present in most tissues. • Nu toxin: it is a deoxyribonuclease.
  • 24.
    Epidemiology & Pathogenesisof Disease caused by clostridium welchii type A (Less veterinary importance) • Mainly human infections associated with gas gangrene and human food poisoning. • Epidemiology & Pathogenesis of Disease caused by clostridium welchii type B • Lamb Dysentary: acute disease of yuong lambs of 2-5days of age. • Multiplication of organism in intestine and result into fatal toxaemia. Although ingested by suckling but it is normal inhabitant of intestine. • Predisposing factors which increases the rapid and unusual high rate of growth include lambs which ingest large quantities of milk. • Symptoms: • Abdominal pain • Bleat repeatedly. • Cease to suck • Collapse & die within few hours • Diagnosis: age of lambs, symptoms, history
  • 25.
    Epidemiology & Pathogenesisof Disease caused by clostridium welchii type C • Enterotoxaemia in sheep (struck) • Affects adult sheep • Acute & Fatal enterotoxamia • Absorption of toxin from intestine. • Toxaemia • Symptoms: • Sudden death • Abdominal pain • Seldom diarrhoea
  • 26.
    Epidemiology & Pathogenesisof Disease caused by clostridium welchii type D • Enterotoxamia in Sheep (pulpy kidney disease, overeating disease) • Multiplication of organism in abomasum and intestine. • Occurs in different age groups. • Normal inhabitant of soil and also intestine of sheep. • Under particular circumstances (Overeating, concentrated diet) high toxin production leads to toxaemia. • The production of toxin may be due to feeding of feeding of concentrated protein diets reduces acidity of stomach and favours rapid bacterial multiplication and production of toxin. • Also overfeeding result of undigested starch passes from stomach to intestine which favour the multiplication of organism in intestine. • Symptoms: deaths suddenly, animal become dull, weak. • Diagnosis: sudden change in diet is suggestive of disease.