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Tuesday 19 May 2015

Clostridial diseases are caused by bacteria that occur widely in natural soil, sewage, water and in the gut of animals. They cause a wide range of signs and effects. They are most often to blame when an animal is taken suddenly sick and is found dead in a relatively short time afterwards.

Generally speaking, most livestock are affected by the same clostridial diseases; including cattle, sheep, pigs, goats and most fowl. There is little difference in geographiclal distribution globally. Some diseases have a higher prevalance in some areas of the UK. Diseases caused by the clostridia pathogen have been recognised in the UK for over 200 years, mostly due to their rapidly fatal nature of their pathogenic effect.

There are a range of clostridial diseases. Each different disease is caused by a specific type (species) of Clostridium bacteria.

There are certain factors which predispose some animals to contracting clostridial disease…
·         Change from poor to good food; when animals are changed from housing to lush pastures or are suddenly fed rich feeds such as maize.
   Lack of care taken when procedures such as castration, docking, wound cleaning and treatments during lambing take place.
·         Animals under new stress or placed in stressful housing during lambing.
·         Animals nibbling or grazing near carcasses of other dead animals.

Caused by...

Bacteria belonging to the Clostridium genus are the causal organism. There are many species of this type of bacteria but mostly all share the following common features… large, Gram-positive, rod-shaped, spore-bearing bacteria. Most are saprophytes (meaning they feed externally by secreting substances to digest their food outside of their cell body).
The bacteria commonly grow in soil, water, decomposing plant matter and rotting animal carcasses. Some are natural inhabitants of the gut of some animals, including chickens, sheep and cattle.

These bacteria can survive for very long periods in the environment; they produce spores (very resistant forms of bacteria) which spread easily and are fairly resistant to weather and climate.

Clostridial bacteria are ubiquitous (found everywhere) but when they produce spores in soil, can make some pastures particularly hazardous. 

Clostridial bacteria cause clinical disease by invading the body and producing toxins. Toxins are substances which are toxic (cause death or damage) to living cells/tissues.
The nature and disease causing effect of each specific bacterium has led to the classification of these clostridial bacteria into 3 different categories (Quinn et al 2000)…
   Neurotrophic clostridia
these bacteria produce powerful neurotoxins (toxins which affect the nervous system).

2.       Histotoxic clostridia
- these bacteria produce exotoxins which lead to local tissue necrosis (death) and toxaemia.

3.       Enterotoxin clostridia
these bacteria also produce toxins; these toxins tend to affect viscera and vital organs.

Clinical Disease

There a range of specific diseases in this bracket: Tetanus, Botulism, Blackleg, Malignant Oedema, Braxy (Abomasitis), Big Head, Black Disease (necrotic hepatitis), Bacillary haemoglobinuria, Gas Gangrene , Lamb Dysentery (Enterotoxemia type B), Pulpy Kidney (Enterotoxemia type D), bloody scours (Enterotoxemia type C).

Clostridial diseases are a constant threat to all cattle and can result in severe losses from sudden death.  The clostridial diseases of cattle include blackleg, malignant oedema, pulpy kidney, navel ill and tetanus.  Clostridial diseases usually occur suddenly and without warning.  Affected cattle are generally found dead due to blood poisoning or gangrene and treatment is rarely an option.
Disease is often linked to common farm management practices e.g. bruising from yarding and moving stock is thought to trigger blackleg; changes in diet can trigger pulpy kidney; tetanus can occur after castration, dehorning or docking of tails; malignant oedema is often associated with wounds or navel infections; and black disease can follow liver fluke infestations. 

Especially around lambing time, losses from clostridial disease can be huge. Much like cattle, the implications of farm procedures like castration, docking, feeding management and damages from falling/butting can be important triggers of the disease outbreaks.

The three types of clostridia can be broken down into which diseases they cause…

Neurotrophic Clostridia

> C. tetani this specific type of bacterium causes Tetanus; it can affect horses, sheep, goats, cattle and dogs. Tetanus occurs sporadically (randomly) in cattle and sheep of all ages. Tetanus endospores are present in the environment and may enter surgical wounds (e.g. like after castration or docking), or traumatised tissue such as damage to the genital tract during a difficult lambing procedure.
An idiopathic (cause unknown) version of tetanus also occurs, in which the organism multiplies in the intestinal tract following dietary imbalance or change.
Clinical presentation of tetanus includes early stiffness and reluctance to move, bloat, raised tail head and the third eyelid prolapses. The clinical signs are usually seen about 4 days to 3 weeks after infection is established in a wound. The animal may have a stiff gait (lockjaw). Death can occur within 1 – 3 days of clinical signs showing. In later stages of the disease the animal may become paralysed with head, neck and leg spasms. The main points of this disease are:
·         Stiffness in lambs in early cases – unwilling to rise or follow the dam, often lethargic or walking abnormally.
·         Paralysis and spasms of muscles in later stages - at this point it is fairly unhopeful that the lamb will survive. Most common in the back of the head and neck.
·         “Lock Jaw” – will become noticeable; stiff jaw and cannot open mouth normally.
·         Unsanitary surgical procedures – are the most important factor in causing this disease.
·         Anti-toxins – can be used if the disease is caught in the early stages to reduce severity.

> C. botulinum…this specific type of bacterium causes Botulism; it can affect cattle, sheep, goats, chickens, horses and donkeys. Typically this disease is associated with severe a progressive paralysis.
The animal can be partially or totally paralysed. The tongue often hangs out the mouth due to lack of muscle control. Affected animals may stop breathing due to the paralysis.
Botulism is a neuro-paralytic disease caused by the toxins produced by C. botulinum. These bacteria are commonly found in the environment and will grow in decaying carcasses and vegetable matter. There are 7 different types of botulinum toxin, (A-G) with Type C and D toxins causing most cases in cattle. As little as 10microgramms of these toxins is lethal to cows.
It can affect cattle and sheep of all ages. If large amounts of toxin have been ingested, the animal may be found dead without showing signs of illness. However, signs of illness usually show within 24 hours – 7 days of ingesting the toxin. The main clinical feature is lack of muscle tone, seen in the animal as progressive muscle weakness. In early stages the affected animal may stagger around, be stiff in the hind legs or be reluctant to move. They occasionally become aggressive. Muscle weakness is usually seen to affect the hind quarters first, before the forequarters, head and neck. Animals are sometimes found lying in a “milk fever” type position, flat out with the head bent round towards the hind. Muscle paralysis of the face may also occur, resulting in the inability to chew and swallow, drooling of saliva or protrusion of the tongue from the mouth. Main problems occur when breathing becomes impaired due to paralysis of the diaphragm muscles associated with inhalation/exhalation.
Botulism does not produce lesions so cannot be diagnosed as part of post-mortem examination. The standard diagnostic test for botulism is the mouse bioassay that is used to detect toxin in faeces or gastrointestinal contents of affected animals.
Outbreaks of the disease have been associated with the spreading of litter from fowl onto pastures and the ignorance of stock keepers to remove carcasses from their land. The presence of the litter and carcasses act as prime sources and breeding grounds for the bacteria which causes botulism.
The main points of this disease are:
·         Muscle tremors – showing as lack of co-ordination and hind limb stiffness; as well as a lack of desire to move.
·         Hind limb weakness – followed by weakness of the forequarters.
·         Breathing difficulties – due to paralysis of the diaphragm.
·         Inability to chew food or swallow – along with the drooling and protrusion of the tongue.
·         Suddenly found dead – as a result of a large amount of toxin ingested.
·         Carcasses of other animals – are an important source of infection that should be removed from pastures.

Histotoxic Clostridia

> C. chauvoei this specific type of bacterium causes Blackleg/Gangrenous myositis.
This disease is the most common clostridial disease seen in cattle carcases submitted for post-mortem. The disease occurs less commonly in sheep; however the same pathogen causes parturient metritis in sheep.
The most common predisposition to infection is trauma following shearing, docking, lambing, castration or any tissue trauma usually on the hind quarters. Soil contaminated wounds are responsible for vast majority of cases. Like all clostridial bacteria, C. chauvoei survives in the environment as a durable spore. The spores can survive in soil for many years. They are ingested from pasture by the animal, enter the bloodstream and lodge in the muscle. They can remain dormant without causing ill-effect. In cattle, the disease is thought to be caused by excessive bruising or excessive exercise. This causes the spores to germinate, multiply and cause the disease. Blackleg in sheep is frequently associated with wounding as a result of shearing, tail docking, and castration, injury to ewes at lambing or infection of the navel soon after birth.
Majority of cases of blackleg occur in young (3 months – 2 years) cattle at grass during the summer months. Most cases are found dead. Before death the cattle are usually found lame and depressed. Crepitation (crunching noise made) is present over affected muscle masses, which are initially warm and painful; later becoming cold and insensitive. When palpated the area may appear to feel swollen and spongey, as oedema collects under the skin. Death occurs within 12-24 hours; following signs of systemic toxaemia (dyspnoea, recumbency and coma).
At post-mortem, lesions are found in the large muscle masses of the fore- and hindquarters. Lesions are commonly found in other muscles such as intercostal, diaphragm, heart and tongue. There is a characteristic odour from the dissected muscles. As well as muscular lesions, visceral lesions are also seen commonly.
The presence of this bacterium can be identified by fluorescent anti-body technique.
Main points of the disease:
·         Tissue trauma of the muscles – are important triggers of the disease.
·         The bacteria spores in the muscle – cause local inflammation, eventually turning the muscle a black-red colour at post mortem and releasing toxins in the bloodstream.
·         Sudden depression - as well as fever and loss of appetite.
·         Lameness – quickly becomes apparent with the affected leg feeling hot, painful and swollen.
·         Crackling sensation – is noted when skin is pressed on the affected leg, due to gas bubbles in the muscles collecting under the skin.
·         Mostly young calves – are affected. Typical age is between 6 – 18 months old. All ages of sheep.
·         Treatment rarely effective – antibiotics and antitoxins can be used if the case is caught early. In severe cases death is quite sudden.

> C. septicum is the main cause of the disease known as Malignant Oedema; which affects cattle and sheep.
The affected animals show signs of subcutaneous accumulation of fluid, dullness and inappetance. The lesions may occur through a wound or intramuscular injection.
In sheep, blackleg and malignant oedema are indistinguishable.
Main points of this disease are:
·         Similar to blackleg – as the bacteria invades the body through wounds and releases toxins.
·         Clinical signs – occur generally within 24 hours of injury.
·         Fever, anorexia and swelling – is seen. When the swelling is pressed, the swelling spreads over a large area as if the fluid is spreading out under the skin.
·         Good hygiene and vaccination – can be used to prevent the disease.
·         Treatment – is generally unsuccessful but antibiotics and anti-inflammatory can be helpful.
 This bacterium also causes Braxy/Abomasitis in sheep. This disease is less common.
Generally speaking this disease is more common in colder climates. With the highest incidence seen in mountainous areas and among yearling sheep.
Affected animals usually show isolation from the flock, signs of abdominal pain and death occur suddenly. Characteristically there is haemorrhage and inflammation of the abomasal wall.

> C. novyi type D is the specific bacterium that causes Bacillary Haemoglobinuria; only affecting cattle. Also, C. novyi causes Black Disease/Infectious Hepatic Necrosis in sheep. This disease in sheep is reasonably rare and occurs mainly where liver fluke is a problem; the liver flukes infest the liver and create suitable conditions for the specific clostridia to multiply and cause infection.
Affected cattle are most commonly found to be dead.
Clinical disease is characterised by the presence of dark red urine and fresh blood in the rectal contents. When standing the animal will have an arched back and be reluctant to move, grunting when forced to do so. Breathing is distressed and the pulse is weak. When the animal becomes recumbent, death follows in 24 hours.
On post mortem examination, most cases have a mahogany-coloured liver in which there is at least one area of liver necrosis (death of tissue). Jaundice may be present from slight to pronounced severity. Widespread subcutaneous haemorrhages are seen mainly on the stomach and intestines.
To confirm the presence of C. novyi fluorescent anti-body test can be used. To differentiate between the type D and B of the bacterium serotypes, toxin-antitoxin tests are required.

> C. sordelli causes several diseases. Traditionally it is associated with gas gangrene; recently it has been connected with acute abomasitis in young lambs and cattle and even more recently metritis in ewes.
Gas Gangrene: also known as Clostridial myonecrosis. This disease is present in sheep, cattle, goats, pigs and horses.
Following injury there is an incubation period of the bacteria of 12-48 hours before symptoms occur. The bacteria invade the wound, multiply and cause the following changes in the animal: there is local oedema and pain, sometimes a thin bloodstained exudate. The pulse rate and temperature rise. Infected wounds which become gas gangrenous are swollen and oedematous, when the wound is palpated, the subcutaneous gas moves a produces a “crunching” sensation in touch. As the disease progresses, there are changes in the skin colour, turning black eventually. Remaining untreated, the wound will lead to toxaemia and extension of the infection; leading to death in the end.
Treating the disease is difficult due to rapid onset and progression of the disease. Penicillin can be used in very early stages of the disease.

In lambs 3 – 10 weeks old the abomasum is partially distended and displaced. The abomasal wall is thickened due to a combination of emphysema and oedema. Erosions and congestion are present in the abomasal mucosa.
In lambs 4 – 6 months old, abomasal congestion with some ulceration is the main feature. The carcasses appear toxaemic.
In older ewes the signs are much less pronounced and less specific. In some cases the infection spreads into a form of peritonitis with blood tinged fluid in the abdominal cavity and perforated abomasal ulcer.
Calves less than 3 weeks of age are the most affected. This disease is reasonably rare and with proper hygiene management and vaccination, can be easily avoided.

Enterotoxaemia (Enterotoxin releasing bacteria)

> C. perfringens Type B… causes Lamb Dysentery.
Lambs are usually affected with this disease at less than 2 weeks old and is characterised by haemorrhagic enteritis. Usually the strongest lambs under 14 days old are affected.
Bacteria invade the intestines, multiply and release toxins into the bloodstream. This causes fatal toxaemia. The bacteria are actually commonly found in healthy animals with no disease; the circumstances in which these bacteria start to cause disease are thought to be associated with a few factors: lambs which ingest high volumes of milk; lambs born later in the lambing season, due to higher presence of the organism in housing in later stages of lambing.
Affected lambs show signs of abdominal pain and have fluid in their abdomen as well as bloodstained faeces. The lamb may bleat repeatedly, refuse to suck collapse and suddenly die.
Generally, the symptoms include sudden death, listlessness, recumbency, abdominal pain and fetid diarrhoea that may be blood-tinged. Post mortem shows severe intestinal inflammation, ulcers and necrosis.

> C. perfringens Type C… causes haemorrhagic enteritis/bloody scours/struck. This is the  most rare type of enterotoxaemia.
Affects lambs during their first few weeks of life, causing a bloody infection of the small intestine. It is often related to indigestion and predisposed by a sudden change in feed such as beginning creep feeding or sudden increase in milk supply. Treatment is fairly unrewarding.

> C. perfringens Type D… causes Pulpy Kidney. This is the most common enterotoxeamic disease.
Mostly seen in sheep but is also seen in cattle. Reported in all ages of sheep but most commonly in lambs 1 – 3 months old and in finishing lambs over 6 months of age. The majority of cases are found dead.
On post-mortem examination the intestines are usually congested and the kidneys soft and friable in appearance. In severe cases nervous system signs develop, including ataxia, opisthotonus, convulsions and death. In these cases focal symmetrical encephalomalacia is seen on the brain.
Overeating disease (aka pulpy kidney) is one of the most common sheep diseases in the world. It is caused by Clostridium perfringens type D and most commonly strikes the largest, fastest growing lambs in the flock. It is caused by a sudden change in feed that causes the organism, which is already present in the lamb's gut, to proliferate causing a toxic reaction. Often it is the best and fittest group of animals that develop this disease.

It is most commonly observed in lambs that are consuming high concentrate rations, but it can also occur when lambs are nursing heavy milking dams. It usually affects lambs over one month of age. Treatment (antitoxin injected under the skin) is usually unrewarding
In cattle the disease is harder to diagnose. Sudden death is common, but diarrhoea/dysentery and profound depression occur in early stages of the disease. Bloat is usually present and the intestinal contents may be haemorrhagic. Further evidence of clostridial enterotoxaemia may be obtained by demonstration of the eplison toxin by ELISA test of the intestinal contents.
The main points of this disease are:
·         Lambs that are consuming high amounts of food – are at most risk. Or those being moved to a new pasture.
·         Usually found dead -  as the healthiest lambs are those that are not suspected of disease.
·         The bacteria cause toxaemia – as the bacteria multiply they produce substances which are converted to toxins by the action of trypsin (a protein). The toxin that is produced builds up in the blood to cause toxaemia and then death shortly follows.


In the UK vaccinations are readily available and highly efficacious against clostridial disease.

For sheep this vaccine is possibly the most important in order to maintain ewe health and to maintain a high number of lambs reaching weaning stage.
2 injections of the vaccine should be given 4 – 6 weeks apart. For breeding ewes they should be vaccinated 4 weeks before lambing to ensure that their colostrum contains a high level of antibodies which will be passed to the lamb. The passive immunity in these vaccines is not always guaranteed, so vaccinating the lambs at a later stage is also recommended.
Lambs which receive passive immunity from the dam will be protected for 6-8 weeks after birth. From 3 weeks old the lambs can be put onto primary course of the vaccine. Those being retained for breeding must be vaccinated, those being slaughter may only need protection against tetanus and pulp kidney.
Animals require a 12 month booster. In terms of scheduling, if sheep are vaccinated every year before lambing time then it is hard to miss-time.

>Heptavac-P Plus™ can be used which gives immunity to all the clostridial diseases 
affecting sheep in the UK. This vaccine also provides immunity against Pasteurellosis. This vaccine should be used to breeding ewes.

>Ovivac-P Plus™ can also be used which provides the same immunity as the Heptavac. This vaccine should be used for growing and store lambs.

Vaccinating ewes with Heptavac-P Plus initially helps protect their lambs via the colostrum. However, this passive immunity wanes, leaving lambs unprotected. To immunise growing and store lambs after this period, two 2ml doses of Ovivac-P Plus, 4 to 6 weeks apart, are required. The course can be started from as early as three weeks of age.

Only cattle that are at serious risk of these disease are vaccinated. In the UK, these vaccines are seldom used. In Australia, New Zealand and South Africa the vaccines are used as the diseases pose more of a risk to the cattle.


If vaccination is unsuccessful or animals are predisposed to a particular clostridial disease for some reason and clinical infection cannot be avoided then sometimes treatment can help. However, in most cases, the animal is found dead or is close to death so treatment is highly invariable depending on how ‘far gone’ the affected animal is.
General administration of an antibiotic such as penicillin can be helpful and reduce the severity of symptoms.

In cases of tetanus and botulism, antitoxin can be administered in the early stages of the disease to combat the effect of the paralysis. However this is only effective if the disease is caught early, therefore careful observation is essential.


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