Clostridium diseases in animals
1. Black quarter :- Click here
2. Tetanus:- Click here
3. Enterotoxaemia :- Click here
4. Bacillary haemoglobinuria:- Click here
5. Botulism
6. Braxy
7. Infectious Necrotic hepatitis
8. Malignant oedema
Organism | Disease |
Cl. chauvoei | Black quarter/ black leg |
Cl. tetani | Tetanus |
Cl. perfringens | Enterotoxaemia |
Cl. septicum | Braxy, malignant edema (gas agangrene) |
Cl. haemolyticum | Bovine bacillary haemoglobinuria / red water disease |
Cl. novyi | Black disease |
Cl. botulinum | Botulism |
Introduction
- Tetanus is caused by Clostridium tetani, which is gram positive, spore-forming obligate anaerobe bacillus.
- Tetanus occurs in all parts of the world.
- It is most common in closely settled areas under intensive cultivation.
- It occurs in all animals and occasionally observed in young cattle, young pigs, and lambs during wound management.
- Horse are most susceptible than the cattle.
- Causative
agent: Clostridium tetani.
- Gram positive, spore-forming obligate anaerobe bacillus.
- Ubiquitous
(present, appearing and found everywhere)
organism and a commensal of the gastrointestinal tract of domestic animals and
humans.
- Highly resistant spores that can persist in soil for many years.
- Destroyed heating at 115°C (239°F) for 20 minutes.
- After a period of anaerobic incubation spores germinate to their vegetative form and starts replicating and producing a complex of exotoxins.
- This exotoxins are responsible for clinic signs.
- The toxins produced are …
1.Tetanolysin,
2.Tetanospasmin
3. Neurotoxin or nonspasmolytic toxin.
Source of Infection
- It is commonly
present in the faeces of animals, especially horses, and in the soil which is
contaminated by faeces.
Transmission
- Puncture wounds: The
hooves are common sites of entry in horses.
- Genital tract at the time of parturition is the portal of entry in cattle.
- A high incidence of tetanus may occur in young pigs following by castration, shearing, docking, vaccinations, or injections of pharmaceuticals like anthelmintics.
- Neonatal tetanus observed during the Umbilical infection, thermic,dehorning and ear tagging.
- Idiopathic tetanus observed
in young Cattle without wound, which is associated with grazing of rough and
fibrous feeding so toxin is produce in mouth and GI tract and also proliferation
in rumen and produce toxins.
The
tetanus spores remain localized at their site of introduction and do not
invade surrounding tissues.
⇩
Spores germinate to their vegetative form to proliferate and produce tetanolysin, tetanospasmin, and neurotoxin.
⇩
only if certain environmental conditions are attained, particularly a lowering of the local tissue oxygen tension.
⇩
Toxin production may occur immediately after introduction if the accompanying trauma has been sufficiently severe, or if foreign material has also been introduced to the wound, or may be delayed for several months until subsequent trauma to the site causes tissue damage.
⇩
The original
injury may be in apparent by then. Of the three mentioned exotoxins.
tetanospasmin
is the most relevant for the pathophysiology of the
condition. Although tetanolysin was found to promote local tissue
necrosis, its role in the pathogenesis of tetanus remains doubtful.
The role
of the more recently identified neurotoxin, or nonspasmogenic toxin, which is a
peripherally active for the pathophysiology of tetanus, is currently unknown.
Tetanospasmin diffuses
to the systemic circulation and it is bound to motor end plates, and travels up
peripheral nerve trunks via retrograde intraaxonal transport to the CNS.
The
exact mechanisms by which the toxin exerts its effects on nervous tissue are
not known, but it blocks the release of neurotransmitters such as GABA and
glycine, which are essential for the synaptic inhibition of gamma motor neurons
in the spinal cord.
There it
leads to an unmodulated spread of neural impulses produced by normally
innocuous stimuli, causing exaggerated responses and a state of constant muscular
spasticity.
No
structural lesions are produced.
Death
occurs by asphyxiation caused by fixation of the muscles of respiration.
Clinical Signs
- Clinical sign are same in almost all animals.
- Temperature - 42°C (107°F).
- Initially increase muscles stiffness and after accompanied by muscles tremor
- Trismus with restriction of jaw movement (The animal may continue to eat and drink in the early stages but mastication is soon prevented by tetany of the masseter muscles and saliva may drool from the mouth. If food or water is taken, attempts at swallowing are followed by regurgitation from the nose.)
- Prolapse of 3rd eyelid
- Stiffness of the hind limbs causing an unsteady, straddling gait.
- The tail is held out stiffly when animal is backing or turning.
- Dilation of the nostrils, and hyperesthesia
- Constipation is usual and the urine is retained, partly as a result of the inability to assume the normal position for urination.
- The rectal temperature and pulse rate are normal in early stage but raise after increase muscles tone
- As the
disease progresses, muscular tetany increases and the animal adopts a sawhorse
posture
- Uneven muscular contractions may cause the development of a curve in the spine and deviation of the tail to one side.
- Opisthotonus
(spasm of the muscles causing backward arching of the head, neck, and
spine, as in severe tetanus and also seen meningitis, and strychnine poisoning).
- The hind limbs are stuck out stiffly behind and the forelegs forward.
- Fatal cases there is often a transient period of improvement for several hours before a final, severe tetanic spasm during which respiration is arrested.
- The duration of a fatal illness in horses and cattle is usually 5 to 10 days
- sheep usually die on about the 3rd or 4th day.
- A long incubation period is usually associated with a mild syndrome, a long course and a favorable prognosis.
- Mild
cases that recover usually do so slowly, with the stiffness disappearing
gradually over a period of weeks or even months.
Prognosis
- The prognosis is poor when signs rapidly progress.
- Animals vaccinated in the past year have a better prognosis, as do horses that have received parenteral penicillin and tetanus antitoxin and in which the wound was aggressively cleaned when fresh
Pathological
lesions
- Minimal autolysis has occurred by the time of necropsy, the identification of large gram-positive rods with terminal spores in smears prepared from the wound site or spleen is supportive of a diagnosis of tetanus.
Diagnosis
- Clinical sign and symptoms.
- Bacteriology: air-dried impression smears from spleen, wound site (cyto, Gram stain), culture swab from wound site in anaerobic transport media.
- Spleen in sterile, leak-proof container (anaerobic, bioassay).
- Culture wit PCR
Treatment
Eliminate
the causative bacteria: Penicillin and oxytetracycline
Neutralize residual toxin
Control muscle spasms until the toxin is eliminated or destroyed :
- Chlorpromazine (0.4–0.8 mg/kg BW intravenously, or 1.0 mg/kg BW intramuscularly, three or four times daily)
- Acepromazine (0.05 mg/kg BW three to four times daily) administered until severe signs subside, are widely used in horses.
- A combination of diazepam (0.1– 0.4 mg/kg) and xylazine (0.5–1.0 mg/kg intravenously or intramuscularly) may be effective in horses refractory to phenothiazine tranquilizers.
Maintain
hydration and nutrition
- Intravenous or stomach-tube feeding during the critical stages when the animal cannot eat or drink.
Provide
supportive treatment
Control
- Tetanus Antitoxin: Tetanus antitoxin should be given to any horse with a penetrating wound or deep laceration, and the wound should also be cleaned aggressively
- Tetanus antitoxin is often routinely given to mares following foaling and to newborn foals.
- Many cases of tetanus could be avoided by proper skin and instrument disinfection at castrating, docking, and shearing time.
- These operations should be performed in clean surroundings in the case of lambs docked in the field, temporary pens are preferred over permanent yards for catching and penning.
- Tetanus toxoid provides active immunization to those with known complete tetanus immunization histories as well as those with unknown or incomplete histories.
- Human tetanus immune globulin (antitoxin) provides passive immunity by neutralizing circulating tetano spasmin and unbound toxin in a wound.
- Inject one 1-ml dose intramuscularly using aseptic technique
- Administer a second 1-ml dose four to eight weeks after the first dose.
- A 1-mL booster dose should be given annually.
- If injury during the initial vaccination or if annual boosters have not been given, a prophylactic dose of at least 1,500 units of tetanus antitoxin should be given.
- For therapeutic purpose large doses 100,000 - 200,000 IU of antitoxin should be given very slowly by intravenous route followed by smaller weekly doses intramuscularly as required.
1. Neutralization of circulating free toxin
2. Destruction of Cl.tetani
3. Relaxation of muscles to prevent asphyxiation
4. Supportive therapy.
1).Neutralization of
Toxin :
Antitoxin therapy is
indicated. Antitoxin ranging from 3000-7000 I.U. can be used depending on size
of organism @12 hours interval.
TAT (tetanus anti toxin)
helps to neutralize free toxin but has no effect on bound toxin.
2) Destruction of Cl.tetani
Antibiotic therapy :
penicillin G is doc
3)Relaxation of muscles
In large animals
·
Chlorpromazine
(0.4-0.1mg/kg bw)
·
Promazine
(0.5-1.0 mg/kg bw)
·
Acetyl
promazine ( 0.03/lb bw)
·
5%
sodium pento barbital (2-4 ml/50kg bw)
·
Diazepam
(0.01-0.4mg/kg bw)
REFERENCES
1. Valgaeren B, et al. Vlaams Tiergeneesk Tijdschr. 2011;80:351.
2. Kay G, Knottenbelt DC. Equine Vet Educ. 2007;19:107.
3. Reichmann P, et al. J Equine Vet Sci. 2008;28:518.
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