Tetanus




 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.

 Etiology

  • 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.  

 Pathogenesis

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

  •  The incubation period varies between 3 days and 4 weeks as long as several months after the infection is introduced.
  •  In sheep and lambs cases appear 3 to 10 days after shearing, docking or castration.
  • 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

  •  There are no gross or histologic findings by which a diagnosis can be confirmed.
  • 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.

Difference B/W Tetanus toxoid and Tetanus antitoxin 

  • 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.

 Tetanus toxoid

  • 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.

 ·         4 Step treatment

       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 Tijdschr2011;80:351.

2. Kay G, Knottenbelt DC. Equine Vet Educ2007;19:107.

3. Reichmann P, et al. J Equine Vet Sci. 2008;28:518.


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