Botulism
Etiology:-
Caused by Clostridium Botulinum. There are 7 distinct forms of botulinum
toxin, types A-G. These 7 types contain 4 groups.
- Group 1 (G1) contain proteolytic form A, B, F.
- Group 2 contain non-proteolytic form B, F, E.
- Group 3 contain C&D.
- Group 4 contains only G.
Four of these (A, B, E&F) cause human botulism, type C, D&E
cause illness in other mammals, birds, and fish. Very dangerous zoonotic
disease, used as bioweapons because of potent toxins. It can survive for a longer
period in the environment due to its spore-forming, rod-shaped and anaerobic nature.
Produces neurotoxins called BOTN. It is found in the USA, South Africa, and Australia. Toxins are heat stable. B, C, D are important from an animal point
of view. Its host includes cattle, sheep, horses, and pigs. It depends on the pH of the soil, feeding of animal& processed food in the animal in poor quality. Silage
and big bales are the major sources. Also in grazing animals in which dead carcass
present.
Source of infection:-
1. Mainly ingestion through silage
2. Through the wound.
Based on the source of infection, forage botulism occurred
through performed toxins which are present in big bales of silage and no proper
silage. Fodder used for silage has a low level of soluble carbohydrates & no
proper lactic acid production, so pH not normal but rises & there will be
anaerobic environment.
3. Carrier associated: by
dead carcasses of animals, due to putrefaction & moisture favor production
of toxins. They infect pasture & grazing animals can take it. The most common
cause of botulism is type C&D. toxins stable for 1 year. Poultry manure
that is used as a fertilizer when put on pasture, it will become a source of
botulism which is most common in carrier associated. Migratory birds carry Wild
bird carcasses, cases are sporadic. Mouse death also causes it. One mouse can
contaminate 22 lac bales. In P-deficient animals, starvation occurs, pica
develops, bones ingested and infection occur due to mineral deficiency.
4. Wound associated: Injury
contaminated with spores. Most common in horses. The wound has an anaerobic
environment, toxins grow on the wound and cause toxicosis, but also infection
because bacteria enter named Toxicon-infectious botulism.
5. Shake foal’s syndrome/toxic infection:- Bacteria ingested, reaches alimentary canal, and produces toxins.
Over there, more common occur by type B.
Pathogenesis:-
It blocks the release of Ach, entry of pathogen occur through ingestion, and then there will be toxin production due to which functional paralysis of
muscles occur without any lesion. Toxins enter via blood reaches cholinergic
nerve endings at NMJ & bock release of Ach from nerve terminals. So, no
contraction occurs and the muscle becomes flaccid and paralysis occurs. There will be
no tone in muscles.
Clinical findings:-
Per acute death occurs without signs.
In Acute type, inability to
take water &feed (prehension stops), paralysis occur and there will be
engulfing problem. There will be progressive muscle weakness, firstly paralysis
of limb, jaw, muscles, tongue, throat& hind limbs, and then there will be
forelimb followed by head and neck muscles. In horses, initially muscle tremors
and colic signs as well.
In sub-acute type,
there will be restlessness, incoordination in movement, stumbling and knuckling
in ataxia, inability to raise the head. There is mydriasis & ptosis but skin
sensation remains normal. The animal will be in sterna recumbency just like milk
fever but with a slight difference. The Head is down to the ground or turns to one
side. Tongue hangout from the mouth with the drooling of saliva. There are
depression and cessation of ruminal movement, constipation may occur,
difficulty in respiration due to paralysis of chest muscles (intercostal
muscles) death of animal occur.
In mild type, self-recovery
within 3-4 weeks. There will be mild signs like anuria.
In chronic type,
there will be adipsia, roaring with each respiration (persist for 3 months). In
shaker‘s foal syndrome, for up to 8 months (mostly 3-8 weeks), nervous signs
are more pronounced. For example, muscle tremors, stiffness of gait initially,
dragging of toes, drooling of milk from the mouth( if dry hay gave) then
regurgitation of feed through nostrils, constipation, prostration & anima
falls down but remains conscious till the end and peristaltic movement steps.
In the case of sheep, called limber neck disease in which neck shivers
and only abnormalities of gait. There will be no muscle tremor. Upper and
downward movement of the head continues that’s why called the limber neck. There will
be the nasal discharge of serous consistency. Not common in goat, because of
browsing nature while more common in cattle & sheep due to grazing nature.
Diagnosis:-
1. based on bacterial isolation and culturing.
2. ELISA.
3. Pain sensation of the animal remains ever except during paralysis.
Treatment:-
Case fatality is high but the recovery rate is 96% when there is proper
treatment.
Antitoxin available @ 30,000 IU/foal while in adult horses @ 70,000
IU. Both of these are singes doses enough for survival. In suppurative therapy,
fluid and electrolyte therapy can be done parenterally. Foals have to apply
muzzles so that when they suckle, it may lead to drenching pneumonia.
Urinary catheterization should be done to facilitate urination.
Administration of mineral ions to relieve constipation.
Indirectly acting cholinergic drugs like Neostigmine and
Physostigmine will not work because they inhibit acetylcholinesterase which is normal, only release of Ach is affected.
The antibiotics which cause muscle weakness just like penicillin
L.A, tetracycline, and aminoglycosides are not recommended
Control:-
Vaccines are not available in our country. Disposal of poultry
manure and carcass should be done properly. Mineral deficiency should be
avoided.
