CLOSTRIDIAL DISEASES Introduction Clostridial
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CLOSTRIDIAL DISEASES Introduction Clostridial diseases are caused by bacteria of the genus Clostridium. (ANAEROBES) Clostridia are widespread in the environment and are normally found in soil and faeces. They are also present in the
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CLOSTRIDIAL DISEASES<br>
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Introduction Clostridial diseases are caused by bacteria of the genus Clostridium. (ANAEROBES)
Clostridia are widespread in the environment and are normally found in soil and faeces.
They are also present in the gastrointestinal tract and as spores in tissues of healthy animals.<br>
Clostridia are widespread in the environment and are normally found in soil and faeces.
They are also present in the gastrointestinal tract and as spores in tissues of healthy animals.<br>
03
CLASSIFIACTION The clostridia can be divided into four major groups according to the kind of disease they produce.<br>
04
The Histotoxic clostridia causes a variety of tissue (often muscle) infections frequently following wounds or other trauma (eg).<br>
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Hepatotoxic clostridia produces their toxins in the liver, thus resulting in the disease Bacillary haemoglobinuria and Black disease (Eg.)<br>
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The Enterotoxigenic clostridium produces mainly enterotoxaemia and food poisoning although they are occasionally histotoxic (Eg).<br>
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The Neurotoxic clostridia cause the disease by the production of the potent exotoxins (Neurotoxins) (eg.)<br>
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Tetanus Tetanus has been known from very early times, having been described by Hippocrates.
But the knowledge of the disease was achieved only in 1884.
Rosenbach –1886 - demonstrated a slender bacillus with round terminal spores in a case of tetanus.
Kitasato –1889 – isolated C.tetani in pure culture and reproduced the disease in animals by inoculation of pure culture.
The Greek term “tetanus” which means ‘contracture’ has been taken from the Latin medicine “rigor”.<br>
But the knowledge of the disease was achieved only in 1884.
Rosenbach –1886 - demonstrated a slender bacillus with round terminal spores in a case of tetanus.
Kitasato –1889 – isolated C.tetani in pure culture and reproduced the disease in animals by inoculation of pure culture.
The Greek term “tetanus” which means ‘contracture’ has been taken from the Latin medicine “rigor”.<br>
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HABITAT Soil, especially that contaminated by animal faeces, is the natural habitat as C.tetani is often transient in the intestines of horses and other animals.
It is ubiquitous and has been recovered from a wide variety of other sources, including street and hospital dust, cotton wool, bandages, catgut, plaster of paris, clothing etc.
It may occur as an apparently harmless contaminant in wounds.<br>
It is ubiquitous and has been recovered from a wide variety of other sources, including street and hospital dust, cotton wool, bandages, catgut, plaster of paris, clothing etc.
It may occur as an apparently harmless contaminant in wounds.<br>
10
tetnus Synonym : Lock jaw
Definition
Acute fatal infectious disease of man and animals characterized by involuntary contraction of voluntary muscles caused by toxins of Clostridium tetani
Horse is more susceptible and birds is resistant.<br>
Definition
Acute fatal infectious disease of man and animals characterized by involuntary contraction of voluntary muscles caused by toxins of Clostridium tetani
Horse is more susceptible and birds is resistant.<br>
11
Tetanus Aetiology
Clostridium tetani
Exotoxin - CI. Tetani - Gram positive sporulating, anaerobic, rod shaped anaerobe, Spores – “Drum Stick”
Incidence
Tetanus occurs in all parts of the world<br>
Clostridium tetani
Exotoxin - CI. Tetani - Gram positive sporulating, anaerobic, rod shaped anaerobe, Spores – “Drum Stick”
Incidence
Tetanus occurs in all parts of the world<br>
12
Tetnaus Susceptibility
Hores and mules are susceptible
Transmission
Wound infection<br>
Hores and mules are susceptible
Transmission
Wound infection<br>
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Pathogenesis The organisms enter the body through the nail prick, castration, docking, shearing, umbilical wound (tetanus neonatorum) or during parturition
Anaerobic condition allows germination of spores and release exotoxin
Reaches brain ether blood circulation or through nerve<br>
Anaerobic condition allows germination of spores and release exotoxin
Reaches brain ether blood circulation or through nerve<br>
14
Pathogenesis The tetanus toxin gets fixed to a substance called protagon ( made of cerebroside + oligosaccharides) in the nervous tissue.
It acts on the inhibitoty synapses interfering with the action of the inhibitory transmitter thus producing spastic action
The toxin causes hyperirritability responsible for the tetanic spasms.<br>
It acts on the inhibitoty synapses interfering with the action of the inhibitory transmitter thus producing spastic action
The toxin causes hyperirritability responsible for the tetanic spasms.<br>
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Tetnaus Three types of toxins
Haemolysin – Tetanolysin – Not important
tetanospasmin- Neurotoxin - responsible for the nervous symptoms
Fibrinolysin- not very potent<br>
Haemolysin – Tetanolysin – Not important
tetanospasmin- Neurotoxin - responsible for the nervous symptoms
Fibrinolysin- not very potent<br>
16
Tetnaus The toxin causing spasmodic contraction of muscles, stiffness and immobilization.<br>
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symptoms Contraction of muscles
Arched back
Twisting neck
Dropping of third eyelid
Convulsions
Sensitive to loud sound.<br>
Arched back
Twisting neck
Dropping of third eyelid
Convulsions
Sensitive to loud sound.<br>
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Tetanus Clinical signs
Involuntary, persistent, intense painful contraction of one or more group of muscles.
Horse- Stiffness and moves like 'wooden horse'.
Raised Tail, third eyelid Protrusion, and Stiffness of Jaw muscle -‘ Lock Jaw’
Ruminants – Symptoms are less severe<br>
Involuntary, persistent, intense painful contraction of one or more group of muscles.
Horse- Stiffness and moves like 'wooden horse'.
Raised Tail, third eyelid Protrusion, and Stiffness of Jaw muscle -‘ Lock Jaw’
Ruminants – Symptoms are less severe<br>
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Tetanus Gross lesion
No characteristic lesion
Death due to Toxaemia
Microscopic lesions
No specific microscopic lesions. Degeneration of the neurones in the brain and spinal cord (due to anoxaemia)<br>
No characteristic lesion
Death due to Toxaemia
Microscopic lesions
No specific microscopic lesions. Degeneration of the neurones in the brain and spinal cord (due to anoxaemia)<br>
20
Tetanus Diagnosis
Characteristic clinical signs.
Organisms are local but not septicaemic
Demonstration of toxin in the serum<br>
Characteristic clinical signs.
Organisms are local but not septicaemic
Demonstration of toxin in the serum<br>
21
BOTULISM Definition
Botulism is a rapidly and fatal motor paralytic condition caused by ingestion of CIostridium botulinum exotoxin.
Botulism is a food poisoning, the toxin being elaborated as an exotoxin by CIostridium botulinum .<br>
Botulism is a rapidly and fatal motor paralytic condition caused by ingestion of CIostridium botulinum exotoxin.
Botulism is a food poisoning, the toxin being elaborated as an exotoxin by CIostridium botulinum .<br>
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For the poisoning to occur, the toxin should be present in the food before ingestion, since the organism cannot generate the toxin in the alimentary tract
A, B, C, D, E, types
A – Limber neck – Poultry
D – Lamsiekte
C – Forage poisoning in horses
E – Fish and fish products<br>
A, B, C, D, E, types
A – Limber neck – Poultry
D – Lamsiekte
C – Forage poisoning in horses
E – Fish and fish products<br>
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Botolisum By clostridum botulinum
Disease which occur by ingestion of pre-formed toxin.
The toxin donot enter CNS but affect PNS.
The toxin block release of acetylcholine
The toxin through blood or nerves reach PNS and inhibit release of inhibtory neurotransmitters like GABA, glycine etc.
Due to this muscle remain in relaxed state.<br>
Disease which occur by ingestion of pre-formed toxin.
The toxin donot enter CNS but affect PNS.
The toxin block release of acetylcholine
The toxin through blood or nerves reach PNS and inhibit release of inhibtory neurotransmitters like GABA, glycine etc.
Due to this muscle remain in relaxed state.<br>
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Botolisum The disease is also known as Bulbar paralysis or loin disease.
The animal died of respiratory paralysis.
In birds disease is known as Limber neck and in hourse also known as Shakers foal syndrome.<br>
The animal died of respiratory paralysis.
In birds disease is known as Limber neck and in hourse also known as Shakers foal syndrome.<br>
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Clinical signs
Cattle -Pica-Chew bones (due to deficiency of phosphorus) which may contain toxin in the decaying meat and get poisoning.
Cattle and Horse: Forage Poisoning (Ingestion of hay contaminated with dead animals or poultry litter)
Wound botulism – Horses
Salivation, paralysis with difficulty of movement and impaired vision.
Tongue paralysed leads to swallowing is impossible.<br>
Cattle -Pica-Chew bones (due to deficiency of phosphorus) which may contain toxin in the decaying meat and get poisoning.
Cattle and Horse: Forage Poisoning (Ingestion of hay contaminated with dead animals or poultry litter)
Wound botulism – Horses
Salivation, paralysis with difficulty of movement and impaired vision.
Tongue paralysed leads to swallowing is impossible.<br>
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Swine are resistant since the toxin is poorly absorbed.
Botulism in birds is exhibited by torticollis – ‘Limber neck’ caused by eating infected blow fly maggots and vegetable matter
Head and neck droop
Death – Respiratory failure and asphyxia
No characteristic lesions<br>
Botulism in birds is exhibited by torticollis – ‘Limber neck’ caused by eating infected blow fly maggots and vegetable matter
Head and neck droop
Death – Respiratory failure and asphyxia
No characteristic lesions<br>
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Entertoxaemia There are 5 strains and there production of toxins
A – alpha – Gas gangrene, food poisoning in human.
B – alpha, beta, epsilon & iota - Lamb dysentery, Hemorrhagic enteritis in sheep & goat.
C – alpha, beta - Struck in sheep & enteritis in lambs, calves & piglet. Enteritis necroticans ( Human)
D – alpha& iota- Enterotoxaemia in sheep & Pulpy Kidney
E –alpha& iota- Enterotoxaemia in Calves and Lambs .<br>
A – alpha – Gas gangrene, food poisoning in human.
B – alpha, beta, epsilon & iota - Lamb dysentery, Hemorrhagic enteritis in sheep & goat.
C – alpha, beta - Struck in sheep & enteritis in lambs, calves & piglet. Enteritis necroticans ( Human)
D – alpha& iota- Enterotoxaemia in sheep & Pulpy Kidney
E –alpha& iota- Enterotoxaemia in Calves and Lambs .<br>
28
Cl. Perringens ( H, Co2 Gas formation in tissue)
Exotoxin
Alpha – Toxin
Phospholipase
Phosophlipids
Phospholipid lecithin
Which is in cell wall of RBC, WBC & Muscle cells
Produce characteristic hemolysis & myconecrosis
Myconecrosis with accompanying gas formation known as Gas gangrene.<br>
Exotoxin
Alpha – Toxin
Phospholipase
Phosophlipids
Phospholipid lecithin
Which is in cell wall of RBC, WBC & Muscle cells
Produce characteristic hemolysis & myconecrosis
Myconecrosis with accompanying gas formation known as Gas gangrene.<br>
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Cl. Per produce multiple other pathogenic toxin heat- labile entrotoxin which causes Cl. Food poisoning manifested abdominal pain & Diarrhea
The typical synerio involves meat i.e kept warm for long period of time alowing spore to germinate & produce bacteria in vegiate state that produce exotoxin.
Cl. Food poisoning rerarly fatal but gas gangrene can be rapidly lethal & lead to shock unless to death.<br>
The typical synerio involves meat i.e kept warm for long period of time alowing spore to germinate & produce bacteria in vegiate state that produce exotoxin.
Cl. Food poisoning rerarly fatal but gas gangrene can be rapidly lethal & lead to shock unless to death.<br>
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CI. perfringens type ‘A’
Enterotoxaemia occurs in lamb and calves
Haemolytic anaemia, Haemoglobinuria and Icterus - acute syndrome<br>
Enterotoxaemia occurs in lamb and calves
Haemolytic anaemia, Haemoglobinuria and Icterus - acute syndrome<br>
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Lamb dysentery CI. perfringens type ‘B’
Lamb – Less than 3 weeks
Also occurs in calves and foals
Haemorrhagic enteritis with ulceration
Beta toxin
Acute – Abdominal pain, depression and reluctance to suckle
Peracute -death without symptoms
Microscopic lesions : Haemorrhagic enteritis and ulceration.<br>
Lamb – Less than 3 weeks
Also occurs in calves and foals
Haemorrhagic enteritis with ulceration
Beta toxin
Acute – Abdominal pain, depression and reluctance to suckle
Peracute -death without symptoms
Microscopic lesions : Haemorrhagic enteritis and ulceration.<br>
32
‘Struck’ CI. Perfringens type 'C'
Adult Sheep – Haemorrhagic enteritis and ulceration of Jejunum and duodenum
Peritionitis with large volume of clear yellow fluid accumulation
Another form -CI. Perfringens type 'C' – Haemorrhagic enterotoxaemia
Affects lambs, calves and piglets within a few days of birth and fatal<br>
Adult Sheep – Haemorrhagic enteritis and ulceration of Jejunum and duodenum
Peritionitis with large volume of clear yellow fluid accumulation
Another form -CI. Perfringens type 'C' – Haemorrhagic enterotoxaemia
Affects lambs, calves and piglets within a few days of birth and fatal<br>
33
“Puply Kidney disease”, Synonym - “Over eating disease”
Definition
Acute toxaemia of fattening lambs and sheep which receive sample milk and high concentration of diet characterized by nervous symptoms and sudden death with development of pulpy kidney<br>
Definition
Acute toxaemia of fattening lambs and sheep which receive sample milk and high concentration of diet characterized by nervous symptoms and sudden death with development of pulpy kidney<br>
34
“Puply Kidney disease”, Incidence
It is occurs throughout the world including India
Susceptibility
It is an important disease of goats, sheep (fattening lambs) and less commonly in adult sheep
Enterotoxaemia has also been reported in calves<br>
It is occurs throughout the world including India
Susceptibility
It is an important disease of goats, sheep (fattening lambs) and less commonly in adult sheep
Enterotoxaemia has also been reported in calves<br>
35
Pathogenesis Organism is a normal inhabitant of alimentary tract and the toxin produced are removed by normal movement of ingesta
When excessive starch food is fed, the bacteria proliferate and liberate toxin.Hence the name “Over eating disease”
Atony of intestine & Stasis of ingests also favours growth of organisms
The epsilon toxin produced will be abosrbed immediately by intestinal mucosa resulting in toxaemia<br>
When excessive starch food is fed, the bacteria proliferate and liberate toxin.Hence the name “Over eating disease”
Atony of intestine & Stasis of ingests also favours growth of organisms
The epsilon toxin produced will be abosrbed immediately by intestinal mucosa resulting in toxaemia<br>
36
Smaller quantities of alpha and beta fractions
Toxins reaches the brain causing opisthotonus, convulsion and coma.
Toxaemia (Few hours - chronic convulsions)
Hyperglycaemia and glycos uria are also observed<br>
Toxins reaches the brain causing opisthotonus, convulsion and coma.
Toxaemia (Few hours - chronic convulsions)
Hyperglycaemia and glycos uria are also observed<br>
37
Gross lesions Petechial or ecchymotic haemorrhages of epicardium, endocardium, serous surface of intestine, abdominal muscles, diaphragm and hydropericardium
Catarrhal or haemorrhagic gastroenteritis
Kidneys – swollen and pulpy – “Puply Kidney disease”
Reaching the brain causing symmetrical encephalomalacia<br>
Catarrhal or haemorrhagic gastroenteritis
Kidneys – swollen and pulpy – “Puply Kidney disease”
Reaching the brain causing symmetrical encephalomalacia<br>
38
Microscopic lesions Kidney: Cloudy swelling and necrosis of epithelium of proximal convuluted tubules
Liver and spleen- Congested
Brain: Lysis and liquefaction of the white matter, while the grey matter is oedematous.
Hyperglycaemia due to increased glycogenolysis of liver glycogen<br>
Liver and spleen- Congested
Brain: Lysis and liquefaction of the white matter, while the grey matter is oedematous.
Hyperglycaemia due to increased glycogenolysis of liver glycogen<br>
39
BLACK QUARTER Synonym: Black leg, quarter ill, Symptomatic anthrax
Definition
Acute febrile disease of cattle (6 month to 2 years), less often of sheep, goat and swine characterized by emphysematous, sero haemorrhagic swelling in the heavy muscles, especially of the hind limbs.<br>
Definition
Acute febrile disease of cattle (6 month to 2 years), less often of sheep, goat and swine characterized by emphysematous, sero haemorrhagic swelling in the heavy muscles, especially of the hind limbs.<br>
40
BQ Etiology
Clostridium chauvoei - Gram + (positive), spore forming, rod shaped bacterium<br>
Clostridium chauvoei - Gram + (positive), spore forming, rod shaped bacterium<br>
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B Q This disease is spread generally in Rainey Season.<br>
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BQ Incubation period: 1- 5 days<br>
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Pathogenesis Infection is by ingestion of spore of Cl. Chauvoi
The organisms multiply in the intestinal mucosa.
Goes into the intestinal macrophase
Inters the lymph & blood
Precipitates' in the heavy muscle of thigh& limb & shoulder.<br>
The organisms multiply in the intestinal mucosa.
Goes into the intestinal macrophase
Inters the lymph & blood
Precipitates' in the heavy muscle of thigh& limb & shoulder.<br>
44
B Q During devitilization , when some injury to the muscles anaerobic condition sets up. ( due to wound or heave exercise anaerobic condition developed)
The bacteria vegetates in bacilli form.
start causing necrosis by release of toxins.
Causing emphysematous necrotizing myositis of the muscles.
Black gas gangrenous muscles with crepitating sound.<br>
The bacteria vegetates in bacilli form.
start causing necrosis by release of toxins.
Causing emphysematous necrotizing myositis of the muscles.
Black gas gangrenous muscles with crepitating sound.<br>
45
B Q Filled with serosaguinous fluid ( foul smelling)
FeS deposition
Toxemia
Death within 24 hrs to 60 hrs. Death may be due to toxaemia<br>
FeS deposition
Toxemia
Death within 24 hrs to 60 hrs. Death may be due to toxaemia<br>
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Different types of toxins are releases by Cl. Chauvoea
α – toxin is most imp toxin.
β
γ
δ
These toxins causes necrosis of muscles ( Gluteal)
Here breakdown of RBC
RBC lysis ---- Iron is release & due to necrosis of muscle H2S is release.<br>
α – toxin is most imp toxin.
β
γ
δ
These toxins causes necrosis of muscles ( Gluteal)
Here breakdown of RBC
RBC lysis ---- Iron is release & due to necrosis of muscle H2S is release.<br>
47
B Q H2S + Fe = Fe2S - which is black in colour of affected muscles.
Release of gas is due to fermentation of sugar in anaerobic medium.<br>
Release of gas is due to fermentation of sugar in anaerobic medium.<br>
48
B Q Clinical signs
Fever
lameness,
visible swelling of muscles- Tongue, diaphragm, myocardium and gluteal muscles
In early stages, the swelling is hot and painful to the touch but soon cold and painless and oedema and emphysema can be felt<br>
Fever
lameness,
visible swelling of muscles- Tongue, diaphragm, myocardium and gluteal muscles
In early stages, the swelling is hot and painful to the touch but soon cold and painless and oedema and emphysema can be felt<br>
49
Gross lesions Crepitating swelling of the muscle(extremities)
Rubber sponge and dark brown or black sero sanguineous fluid exudes with gas bubbles -Gas gangrene
Affected muscles appears black
Muscle – Centre area is dry and have odour of rancid butter
Regional lymph nodes – Swollen and oedematous
Large muscles – Diaphragm and tongue
Internal organs – Heart, lung, kidneys, liver, spleen and intestine showed acute congestion<br>
Rubber sponge and dark brown or black sero sanguineous fluid exudes with gas bubbles -Gas gangrene
Affected muscles appears black
Muscle – Centre area is dry and have odour of rancid butter
Regional lymph nodes – Swollen and oedematous
Large muscles – Diaphragm and tongue
Internal organs – Heart, lung, kidneys, liver, spleen and intestine showed acute congestion<br>
50
Microscopic lesions Muscle fibres separated and showed waxy degeneration and coagulation necrosis
Streaks of haemorrhages - Collection of neutrophils, lymphocytes and Gram positive organisms demonstrated in tissue sections<br>
Streaks of haemorrhages - Collection of neutrophils, lymphocytes and Gram positive organisms demonstrated in tissue sections<br>
51
Diseased muscle from a heifer that died suddenly from blackleg. The muscle tissue is dark red and has a dry appearance due to gas formation.<br>
52
Blackleg - generalised discoloration/gaseous
degeneration of carcass in Blackleg case.<br>
degeneration of carcass in Blackleg case.<br>
53
Blackleg – accurately located typically ‘dry’ lesion (area to right of label) from PM.<br>
54
Diagnosis
May be confirmed by gross lesions
Demonstration of organism – from the fluid incised swelling
Biological tests using guinea pigs
Fluorescent Antibody Technique (FAT)
Fatal course and found dead before signs of illness are seen<br>
May be confirmed by gross lesions
Demonstration of organism – from the fluid incised swelling
Biological tests using guinea pigs
Fluorescent Antibody Technique (FAT)
Fatal course and found dead before signs of illness are seen<br>