Clostridial disease in cows Flashcards
BOTULISM is a?
neuroparalytic condition affecting birds, mammals and fish, and is caused by exposure to toxins produced by various biotypes of Clostridium botulinum.
However, since 2003, there has been an upsurge in the number of suspected cases reported, particularly in cattle and more recently sheep. The diagnosis of botulism is?
problematic and relies heavily on clinical signs. Confidence in the diagnosis is improved by identifying the risk factors and suspect sources, and by ruling out the more common differential diagnoses.
Worldwide, most cases of botulism in cattle are thought to be caused by toxins produced by?
Clostridium botulinum types C or D and are usually associated with carrion, as these biotypes proliferate in decomposing carcases.
Intoxication with botulism toxin appears as?
A progressive, symmetrical, flaccid, cranial and peripheral nerve paralysis, beginning with the hindlimbs and progressing cranially. The speed of progression is variable (probably dose related), resulting in peracute, acute and chronic forms of the disease. Some cases may present as sudden deaths. Otherwise, clinical signs may be first observed from about 24 hours up to 17 days after exposure to the toxin.
What is the prognosis of intoxication with botulism?
The fatality rate is very high (often around 90 per cent). Many animals require euthanasia on welfare grounds and mortality would probably be significantly lower if affected animals could be provided with supportive therapy.
List the other clinical signs which may be associated with botulism intoxication?
Some or all of the following clinical signs may be observed:
- Anorexia and adipsia
- Lack of muscle tone, resulting in progressive weakness, starting with shifting of weight on to the hindlimbs at rest, knuckling of the fetlocks and an unsteady gait
- Dilated pupils, with poor response to light
- Flaccidity of the tail, eyelids, jaw and/or tongue. In some cases, the tongue may be withdrawn easily, or may protrude from the mouth at rest due to lack of muscle tone
- Difficulty chewing and swallowing, with drooling of saliva
- Sternal recumbency, often with the head swept round to one side (as typically seen in cases of milk fever), followed (terminally) by lateral recumbency
- Respiratory depression with abdominal breathing, ultimately developing into respiratory paralysis
- Dry mucous membranes
- Occasionally, initial diarrhoea but usually sluggish rumen and intestinal movements and later constipation
Animals do not experience pyrexia or a loss of sensibility. Note that nervousness, apprehension and unilateral neurological signs are not typical features of botulism.
What are the epidemiological and risk factors associated with botulism in the UK?
Group morbidity in outbreaks of botulism in livestock is variable and can be very high. Low morbidity outbreaks suggest either patchy, unevenly distributed sources of toxin, or spore ingestion/toxicoinfection. Outbreaks with high morbidity suggest more homogeneous contamination of a common feedstuff (eg, complete diet/total mixed ration) or the water supply with toxin. A point source is suggested if many animals are affected in a short period of time.
How is botulism intoxication definitively diagnosed?
Diagnosis is confirmed by demonstrating toxin in serum or viscera such as the liver in animals that have not undergone autolysis.
What are the differentials for botulism intoxication?
METABOLIC DISEASE. Hypocalcaemia, hypophosphataemia, downer cow syndrome, postparturient paresis, ketosis, hypokalaemia
INFECTIONS. Bacterial, viral or chlamydial encephalitides, such as Histophilus somni (thromboembolic meningoencephalitis), listeriosis, paralytic/dumb rabies, and other encephalopathies (eg, bovine spongiform encephalopathy), brain abscess
INTOXICATIONS. Hepatoencephalopathies (terminal changes), lead poisoning (subacute/chronic), organophosphate (OP) poisoning, especially delayed axonopathy, which presents as an ascending flaccid paralysis and not as typical acute OP poisoning
MISCELLANEOUS CONDITIONS. Peripheral neuropathies, myopathies, acidosis
OTHER CONDITIONS CAUSING FLACCID PARALYSIS. Other conditions, such as Phalaris species poisoning, tick paralysis and snakebite, are not likely to occur in the UK. Some conditions, such as lead poisoning, can cause hyperaesthetic changes that are not typical of botulism, but may sometimes present with a flaccid paralysis
What are the major risk factors for ruminant livestock intoxication with botulism?
- Access to broiler litter
- Access to decaying carcase material in feeds
- Access to water contaminated by decaying carcase material
- Access to spoiled decaying plant crops/vegetable material
What is clostridial myositis?
A group of per acute to acute disorders characterised by myonecrosis and rapid death. Usually associated with anaerobic conditions in the musclc tissues anywhere in thc body (e.g. injury, bruising. intramuscular injections). Most affected young cattle less than 2 years old in a good body condition. May occur as sporadic cases or as an outbreak. Risk factor is tissue bruising. Outbreaks often after some farm protocol (c.g. yarding). low grazing or flooding.
What are common names for clostridial myositis?
blackleg
malignant oedema
false blackleg
Gas gangrene
What are the clinical findings of clostridial myositis?
Clinical findings
- Sudden death
- In acute cases severe depression, (fever, anorexia, tachypnoea, lameness, recumbency, coma, death within 12—24 hours. Sometimes subcutaneous emphysema, cold area over the affected muscle and crepitus.
Post- mortem findings:
- Rapid autolysis. darkened, dry emphysematous muscle, sometimes with smell of rancid butter.
How is clostridial myositis diagnosed?
Diagnosis
- history,
- signs
- post-mortem findings, detection at causativc pathogens or exotoxins
What are the differential diagnosis for clostridial myositis?
Principal differential diagnosis
- Acute poisoning
- black disease
- anthrax
- snakebite
What is the treatment for clostridial myositis?
Treatment Rarely successful due to the rapid course:
- Antimicrobials (drug of choice procaine penicillin) around affected tissues
- Aggressive surgical
How can clostridial myositis be controlled?
Control
Vaccination. In face of outbreak simultaneous vaccination and administration of procaine penicillin. Carcasses should be destroyed by deep burial or burning to minimise soil contamination.
What is tetanus?
Tetanus has long been recognized as a highly fatal disease of all species of farm livestock. The disease is produced by the toxin of CIostridium tetani and is characterized by hyperaesthesia. tetany and convulsions.
Where is clostridium tetani mainly found?
Soil
GI tract
What is the usual portal of entry for clostridium tetani?
Deep puncture wound
Genital tract at partuition
What are the clinical signs of clostridium tetani?
As the incubation period may vary quite considerably it is not always possible to relate the onset of clinical disease to specific incidents of injury or surgical interference.
The first signs are those of:
- apparent stiffness and reluctance to move, accompanied by muscle tremors that become more pronounced
- prolapse of the third eyelid, which becomes more prominent with handling of the head.
These signs are progressively followed by the appearance of;
- slight but persistent ruminal tympany
- elevation of the tail
- unsteady gait of the hindlimhs
- especially when turning
- trismus with saliva drooling from the mouth
- Because of inability to adopt the normal urinating posture urine is retained
Further progression leads to:
- generalised muscular tetany with the adoption of a ‘rocking horse—like posture
- Attempts at walking lead to lateral recumbency and an inability to rise
- Tetanic convulsions and opisthotonus soon develop. initially, the convulsions are triggered by external stimuli, but later these occur spontaneously
What is the diagnosis of clostridium tetani?
Diagnosis:
Because of the distinctive clinical signs, classical tetanus is seldom confused with other diseases. Clinical hypo magnesaemia in calves and cattle is accompanied by tetany and convulsions, but there is no prolapse of the third eyelid or ruminai tympany
What are some differential diagnosis of clostridium tetany intoxication?
Hypomagnesaemia
Cerebrocortical necrosis
Lead poisoning
What is the treatment and prevention of clostridium tetani?
It is unlikely that fully developed tetanus will respond and therefore under such circumstances euthanasia should he considered
When treatment is undertaken it should have three objectives:
- Elimination of tetani, neutralisation of unfixed neurotoxin and the induction and maintenance of muscle relaxation until all the neurotoxin has been destroyed or eliminated.
- Large doses penicillin.
- Irrigation and topical treatment of infected site
- Antitoxin
- Animals that are treated should be kept in dark quiet surroundings with ample bedding and sufficient space to avoid injuring themselves if convulsions occur.
What can be done to prevent tetanus?
Vaccination
