Can a dog get botulism? Botulism. Veterinary. Diagnosis and differential diagnosis
4.1.5. Botulism
(Botulismus)
Botulism fur-bearing carnivores is an acute non-contagious foodborne disease caused by the consumption of feed containing botulinum toxin. It is manifested by paresis and paralysis of muscles due to blockade of acetylcholine toxin in nerve synapses.
Botulism type C in animals is a classic example of alimentary toxicosis (intoxication, poisoning) of infectious origin, not transmitted from animal to animal by contact. Like mycotoxicoses, in animals, as well as in susceptible animals and birds, it develops without reproduction of the pathogen in the body, while type E botulism can also occur as a toxic infection.
Etiology. The causative agent of the disease is a spore-forming anaerobe Clostridium botulinum. There are 7 types of pathogen: A, B, C, D, E, F and G, each of which produces its own specific exotoxin. In the vast majority of cases, the death of minks and ferrets is caused by type C toxin, to which they are highly sensitive even when administered orally. Animals are less sensitive to toxins C.I. botulinum types A, B, D and E, possibly because these toxins are rapidly degraded in the feed mixture by microbial proteinases.
The toxicity for minks of toxin type E (from fish feed) is 25 times less than type C, and type A, dangerous to humans, is 400 times less.
Toxin formation occurs most actively at a temperature of +27...37°C without air access, at +11...20°C - more slowly, at +10°C and below - stops.
History reference. Under the names allantiazis (from the Greek. allantiksa- sausage), ichthyoism (from the Greek. ichtis- fish) from the 18th century. cases of people being poisoned by black pudding and fish are known. The term "botulism" (from lat. botulus- sausage) was introduced by the Belgian scientist E. Van Ermengem in 1896, having isolated the pathogen.
In s.-x. animals and animals, botulism was established at the beginning of the 20th century. The first outbreak of type A botulism? in minks, in which 96% of the livestock died, Hall J.C. and Stiles G.W. in 1938, type C - Quortrup E.R., Gorham J.R. (1940). Botulism in silver-black foxes and minks was registered by Pile, Brown (1939), Skulberg (1961).
Botulism in minks occurs after eating food containing a toxin Clostridium botulinum type C. Other types of toxin (A, E and B) also cause the death of not only minks, but foxes and arctic foxes.
In 1956–59 Matveev K.I., Bulatov T.I. and Sergeeva T.I. developed a method for the specific prevention of botulism with toxoid type C, and Buzinov I.A. and Novikova L.S. (1959) proposed a type C formol alum vaccine, which was put into production.
Susceptibility. Minks and ferrets are most susceptible to botulism, although there are reports in the literature about the defeat of arctic foxes and foxes. In arctic foxes, out of 10 outbreaks of botulism, four cases were identified as the pathogen type E, in one case of type C, and in two cases of type A; Of the three outbreaks of botulism in foxes, two were isolated toxin type C and one was type E.
The sensitivity of minks and arctic foxes to toxin A is the same, while foxes show high resistance. It is characteristic that repeated feeding to minks, arctic foxes and foxes of sublethal doses of botulinum toxins and cultures of pathogen types C and E leads to their disease from total doses of toxin 2.5...10 times less than the minimum oral dose. lethal dose(Behring phenomenon). In general, the resistance of arctic foxes and foxes to type C toxin is 800 and 5000 times (respectively) greater than that of minks. From this it becomes clear why foxes and arctic foxes, differing from minks in high resistance, can get botulism of one type or another - this requires a long supply of toxin with food.
Sables are highly resistant to botulism. In practice, they never died from this disease.
When making an assessment of the sensitivity of different animals, it must be borne in mind that it depends not only on the type of toxin and the frequency of its intake, but also on the method of administration. The sensitivity of minks to the oral intake of toxin C is 500 times less than to the intramuscular one.
In addition to animals, horses and birds are susceptible to botulinum toxin and most often get sick, less often cattle and pigs. Domestic carnivores are much more stable.
Humans are also susceptible to botulism. It is usually caused by toxins of types A, B and E, found in mushrooms, dried and smoked fish, canned vegetables.
Spreading. Botulism, despite the availability of an immunogenic toxoid vaccine, still continues to infect many farms in different countries. In the Netherlands, 2-3 outbreaks of botulism occurred annually among grafted minks, in 1986-1989. botulism was diagnosed in 0.7...5.1% of dead minks, and in 1976–1979. there was a massive loss (from 5.0 to 19.4% of the population) of blue foxes on 12 farms. In Norway in 1967, 23,000 minks died on 250 farms. In 1974 on the fur farm "Belarussky" and on the collective farm "Iskra" (Belarus) in 1976, respectively, 8907 and 5000 minks fell, and even earlier (in 1963) 18000 minks died on this state farm. In Lithuania in the 1980s, in one fur farm, 40% of the main herd fell in April, in a farm near Moscow in April a year later, more than 1,000 adult animals. In the USA, 50% of minks died on one of the farms, in Russia in 2001 - more than 10,000 mink puppies. In Finland, about 60,000 blue foxes died in 2002 on about 60 farms. The farms used feed from the central feed kitchen. Adult mink on some farms were also affected, but puppies vaccinated in 2002 were not affected. Based on the PCR results, type C and D botulism was established. The damage amounted to 5 million euros.
Source and routes of infection. The microbe is widely distributed in nature - it can be isolated from the soil, marine and river sediments, sometimes from the feces of people, animals and birds. Spores from the external environment enter the feed, where, when favorable conditions germinate into a vegetative form. During the growing season, toxin accumulates in the breeding grounds of the microbe.
The disease occurs after eating raw food containing botulinum toxin - the most powerful of all microbial poisons! It is formed in meat, fish and vegetable products in the absence of oxygen, high humidity, neutral or slightly alkaline reaction. The most favorable conditions for reproduction C.I. botulinum occur in the intestines of dead animals and fish, in canned food, as well as in the thickness of vegetable feed that has undergone self-heating. From here, the toxin gradually enters adjacent areas. Usually, botulism occurs after feeding minks raw meat and offal from forcedly killed or fallen farm animals in cases where the intestines were removed later than 2 hours after the death of the animal. Often the cause of botulism can also be feeding meat products from marine animals, poor-quality fish, chicken corpses and offal, horse or deer meat containing a toxin. C.I. botulinum types E and C.
Pathogenesis. The toxin is absorbed into small intestine and enters various organs. It acts on nerve tissue by blocking the release of acetylcholine and disrupts neuromuscular connections. This leads to relaxation of muscle tone, loss of mobility, paralysis of the respiratory and cardiac muscles, asphyxia and death. Botulism type E in minks, arctic foxes, foxes and type C in the last two species of animals proceeds according to the type food poisoning with a long incubation period and detection of the pathogen in the gastrointestinal tract, in contrast to type C botulism in minks, which usually develops according to the type of intoxication. For the occurrence of type E toxic infection, a necessary condition is a long-term intake of toxin with food (fish, beluga meat, etc.).
Symptoms. Incubation period the disease lasts from 6 to 24 hours, less often - up to 2 ... 4 days, in ferrets - 12 ... 96 hours. 97% of botulism cases occur in May-September with a peak in August. In sick minks and ferrets, paresis and paralysis of the fore and hind limbs occur, the pupils dilate, salivation is sometimes observed. Taken in the hands of a sick animal, it hangs helplessly and does not respond to irritation. The hind limbs are affected first, which is typical of botulism.
The disease lasts from several hours to a day, in rare cases up to 5-6 days. Lethality depends on the dose of toxin that enters the body, and is 20...100%. It should be noted that in minks, arctic foxes and foxes, when fed with low-quality fish, horse or deer meat (causative agents of types E, C and A, respectively), botulism proceeded as a toxic infection with a long incubation period. The death of the animals occurred in 15...30 days, of the diseased animals, only a part of the animals died, from the internal organs of which the causative agent of botulism was isolated.
Arctic foxes have paralysis of the posterior girdle, impaired coordination of movements, weakness of the limbs, abdominal breathing, vomiting, severe depression, swaying gait, tail paralysis, complete paralysis and death. Animals, even those with mild signs of the disease, die two days after the onset of its symptoms.
Pathological changes. Fallen animals of normal fatness. Rigor mortis is usually not expressed, the stomach is empty. The mucous membranes of the stomach and intestines are hyperemic, the spleen is somewhat swollen, light cherry in color; in the lungs, dark red areas of focal hemorrhages are found; the liver is filled with blood, loose, dark cherry color.
Diagnostics. The basis for suspicion of botulism is the sudden onset of the disease, high mortality and characteristic clinical signs. Of great diagnostic value are typical pathological changes: the absence of rigor mortis, an empty stomach, and focal hemorrhages in the lungs. The fact of feeding suspicious for the presence of toxin feed can serve as a help.
Samples of food fed to animals are sent to the laboratory (food samples should be stored in the refrigerator for 7 days), the remains of uneaten food, scrapings from the mucous membrane of the stomach and intestines, whole corpses. The diagnosis is considered established if it is possible to isolate botulinum toxin.
Differential Diagnosis. The sudden death of a large number of animals can be mistakenly regarded as poisoning with dimethylnitrosamine or some pesticides. With botulism, paralysis of the limbs, the absence of rigor mortis, and the absence of contents in the stomach of animals are typical, although the food was eaten by them the day before (this indicates a time gap between the start of absorption of food and the disease, i.e., the presence of an incubation period that is characteristic only for biological poisons; on the contrary, in case of chemical poisoning, the disease develops immediately after the absorption of food and therefore the stomach in most animals does not have time to empty).
In the event of the death of minks and ferrets vaccinated against botulism, an important diagnostic value should be given to the fact of the death of animals of one of the two age groups - one-year-olds or adults. This is because the previous or last vaccination was made with a non-immunogenic vaccine.
The final conclusion is made on the basis of the indication of the toxin. At the same time, it must be remembered that it is not always possible to detect a toxin in the study of single randomly selected corpses or food residues, since the toxin quickly decomposes. Therefore, for research it is necessary to send 10 ... 20 undeniably fresh corpses of animals (and if there are sick, then sick), from which it is advisable to take a combined sample in the laboratory (scrapings from the mucous membrane of the stomach and intestines). Simultaneously with the corpses, feed samples taken from storage are sent for the day preceding the death.
The prognosis for minks is unfavorable. Lethality depends on the dose of toxin that enters the body, and can be 100%.
Treatment. Specific therapy for mink has not been developed. An effective remedy is epinephrine(1 ml/head subcutaneously). Treatment of PZ with vitamins of the group AT, by various means ended unsuccessfully.
Preventionandmeasures to eradicate the disease. When a disease occurs, suspicious (usually conditionally suitable) foods are excluded from the diet or they are fed boiled. Carry to suspicious forages: badly exsanguinated carcasses of page - x. animals, meat by-products of low quality in terms of freshness and fish feed, meat of marine animals even of good quality in terms of organoleptic data, feed of unknown origin, self-heated vegetable and animal feed.
The meat of forcedly slaughtered animals is allowed to feed only after heat treatment. Carcasses of dead animals are not used for feeding animals. Carcasses of animals killed by lightning or electric current, if cut in time, can be fed to animals only after thorough boiling. When slaughtering animals intended for feeding animals directly on farms, the carcasses are cut up no later than 2 hours after slaughter. Meat and by-products of marine animals are included in the feed for minks only 3 weeks after their vaccination against botulism. They can often be contaminated with botulinum toxin, as well as various pathogenic microbes - strepto- and staphylococci, salmonella, pseudomonas, Escherichia, Proteus, Klebsiella, Pasteurella, etc. Vegetable feed that has undergone self-heating, as well as moldy, can be fed to animals only after heat treatment.
With preventive purpose and in forced cases Animals are required to be given a monovaccine against mink botulism (alum precipitate of anatoxin-vaccine) or a polyvaccine against botulism, parvovirus enteritis, plague and mink pseudomonosis (BIONOR). Puppies are immunized according to the instructions for the use of the vaccine, starting from 45 or 60 days of age (June-July), the main herd - after the restoration of normal body condition (July-August). Immunity occurs 2-3 weeks after immunization and persists for at least 12-18 months. If a 4-component vaccine is used, then these vaccination periods are unacceptable due to the blocking effect of colostral antibodies on the formation of immunity against plague and parvovirus enteritis.
Colostral immunity is not formed in botulism. 3...5 days prior to the start of mass vaccination, it is recommended to do a trial vaccination of 50...100 animals, which makes it possible to make sure that the vaccine is harmless and that there is no anaphylactic shock after its administration. Anaphylactic shock usually develops 1-30 minutes after injection. Severe anemia (hemoglobin levels are reduced by 1/3 or 1/2) and poor development of puppies contribute to the development of shock.
Compliance with the proper temperature regime in refrigerators (not higher than -18 ° C) is a good help in the prevention of botulism in all types of fur-bearing animals.
4.1.6. Pseudomonosis
(Pseudomonosis)
Pseudomonosis (hemorrhagic pneumonia or Pseudomonas infection) - this is a very dangerous disease, first of all, of minks, starting as an alimentary infection and extremely quickly acquiring the features of an acute highly contagious disease with symptoms of hemorrhagic pneumonia and sepsis.
In arctic foxes and foxes, it usually manifests itself as an organ (local) or secondary infection, in which the most serious damage occurs due to abortions in females and the death of young animals.
Diseases are also susceptible to plants, animals, birds and humans.
Etiology.Pathogen - microbe Pseudomonas aeruginosa from the genus Pseudomonas families Pseudomonadaceae, better known as Pseudomonas aeruginosa ( bacillus pyocyaneum). This is a short, movable rod with one polar flagellum, does not form a spore, stains negatively according to Gram. Grows on conventional nutrient media, forming R- and S-form colonies and 4 types of pigment: pyocyanin, fluorescein, pyorubin and black pigment. According to its biochemical activity, it belongs to the number of weakly active bacteria; in relation to individual carbohydrates, the activity of various strains is not the same. Referring to the group of psychrophilic (cold-loving) microbes, Pseudomonas aeruginosa is able to grow at a temperature not lower than 5°C. For this reason, the microbe is widely distributed in external environment, is often found in the feces of animals and humans, on the surface of the body, in the external genitalia, feces, as well as in feed, bedding and water, even in animal farms that are free from pseudomonosis, and the same serotypes that cause this dangerous infection. The microbe is involved in putrefactive spoilage of meat, fish, dairy and vegetable products (when they are contaminated), oxidizes ammonia to nitrites, and can also multiply in an environment poor in organic and mineral substances, in particular, in water. It is weakly resistant to physical and chemical factors, however, in plant-protein substrates it remains viable for at least 6 months, in a lyophilized state - for at least 3 years. A special distinguishing property of the causative agent of pseudomonosis is its high resistance to many antibiotics. The pathogenicity of Pseudomonas strains varies, which is associated with the activity of bacterial elastase.
P. aeruginosa has a complex antigenic structure - different antigens are contained in flagella, mucous capsule, cell wall, as well as in metabolic products. The serological variability of the microbe includes more than 20 serotypes, but sera prepared from the thermostable O-antigen received the greatest recognition for serotyping. In a typical disease, serovars (according to Habs) 05, 06, 08, 011 in minks, 06, 03, 02 and 05 are especially often distinguished, and less often 01, 04, 09, 011 and 016 in arctic foxes and foxes. Immunization of minks with one of these four serotypes does not prevent infection with the rest.
, Diseases ,
Botulism is food poisoning. Accompanied by damage to the central nervous system, paralysis of the pharynx, tongue and mandible, a sharp weakening of the tone skeletal muscles and gastrointestinal upset. Dogs and cats are rarely affected by botulism.
The causative agent is a spore-forming anaerobe that looks like a stick. Botulinum toxin is formed in meat and vegetable feed, in conditions of high humidity and a neutral or slightly alkaline environment. Optimum temperature for toxin formation 25-38 °C.
Botulinum toxin in liquid media when boiled is destroyed after 15-20 minutes, in dense media (meat, fish, etc.) - after 2 hours. Gastric juice and the digestive enzymes of the stomach do not destroy the toxin. The spores of the pathogen are especially resistant. When boiled, they are destroyed only after 6 hours.
The disease is most often observed when eating poor-quality meat and fish feed, especially canned food. White mice and guinea pigs are very sensitive to this toxin.
The toxin in feed is distributed unevenly. This explains the disease and death of not all animals that ate the same food. The disease is more common in the summer, when conditions are created for food spoilage. By appearance and the smell of food containing botulinum toxin does not differ from the usual. The disease occurs as a result of eating a toxin, and not due to the development of microbes in the body.
Course of the disease.
Toxin, having got into the feed digestive tract absorbed into the blood and has an irritating effect on the nerve endings of many organs and tissues. Continuous and strong irritation of receptors with botulinum toxin causes a disorder in the activity of the brain. Paralysis of the pharynx, tongue and other organs develops. The toxin inhibits the release of acetylcholine, which leads to a gradual shutdown and relaxation of the muscles. The incubation period lasts from several hours to 10-12 days. The severity of the disease depends on the amount of toxin that has entered the body. When over acute course the death of the animal occurs within a few hours.
In dogs, there is a refusal to feed, lethargy, increased thirst, frequent defecation, semi-liquid, fetid feces, with blood mucus and undigested food particles. Sometimes observed frequent vomiting. On palpation, there is pain in the abdominal wall, the animal may moan. Signs of damage to the central nervous system are excitation, periods of anxiety are replaced by a coma, paralysis of the hind limbs can develop, relaxation of the muscles of the body is observed, the animal moves with difficulty wobbly gait.
Cats have dilated pupils, prolapse of the third eyelid and tongue, discharge of thick mucus from the nasal and oral cavities, coughing, urinary and fecal retention. Body temperature rises.
Treatment and prevention.
The diagnosis is made on the basis of epizoological and clinical data, the relationship of the disease with the consumption of a particular feed is established. Conduct laboratory tests to determine the toxin in the feed, stomach contents or blood.
Prevention lies in the proper storage of feed. They must not be allowed to mold, rot and become soiled. Bowls must be washed from food residues and disinfected.
Botulism (Botulismus) is a severe food intoxication (rarely toxic infection) characterized by damage to the central nervous system and manifested by paralysis of the pharynx, tongue, lower jaw and a sharp weakening of the tone of skeletal muscles. Humans are also susceptible to botulinum toxin.
History reference. Before the discovery of the causative agent, the term botulism was synonymous with sausage poisoning (from the Latin word botulus - sausage) and canned meat. The German researcher Justinus Kerner in 1820 studied and described the clinic of a human disease, calling it botulism. Yu. Kerner considered the cause of the disease to be “sausage poison”. In 1895, Van Ermengem, studying the flash food poisoning, isolated a bacillus from the corpse of a deceased person, the elucidation of the properties of which revealed the essence of the disease. The microbe was named B. Botulinus. As a human disease, botulism has been known for a long time (the first outbreak was described in 1753), information about the disease of botulism in domestic animals dates back to the beginning of the 20th century. In Russia, poisoning of horses with signs of botulism was noted in 1900 and 1912. In the USSR, botulism in horses was described by R.V. Konyshev, S.Kh. Gamaleya and I.A. Dukalov (1932-38). Botulism various kinds animals are registered in almost all countries of the world.
Economic damage. The disease is rare. But it is characterized by high mortality (90-95%) and therefore causes great damage to farms in case of occurrence.
Etiology. The causative agent of the disease Clostridium botulinum is a polymorphic with rounded edges, anaerobic, spore-forming, weakly mobile bacillus, 3.4-8.6µ long and 0.3-1.3µ wide, stained with all aniline dyes and Gram. The optimum cultivation temperature is 30-35°C, the optimum pH is 7.4-7.7. Spores are oval, usually located at the ends of the stick, which because of this takes the form of a tennis racket. Six types of Cl are known. Botulinum: A, B, C, D, E, F. Type Cα and Cβ. Types Cl. Botulinum differ immunologically: each type produces its own specific toxin, which is neutralized only by the serum obtained from hyperimmunization of animals with a toxin of this type.
Toxin Cl. Botulinum is formed in vegetable and meat feeds under conditions of anaerobiosis, high humidity and a neutral or slightly alkaline reaction of the environment. The optimum temperature for toxin formation is 25-38°C. The microbe does not multiply in feed with an acidic reaction (pH 3-4) and at a concentration table salt above 10%.
Microorganisms develop well in liquid nutrient media prepared on the basis of meat, casein, fish and other protein substrates.
The strength of the toxin is characterized by the following data. Broth culture filtrate of some strains, especially type A, when subcutaneous application at a dose of 1/10,000,000 ml causes the death of a guinea pig, 1 g of this toxin can destroy 60 billion mice, weighing 1200 thousand tons. According to American authors, 28.3 g of the toxin (one ounce) kills 24,000 cows. For humans, a lethal dose of the toxin is 3500 mouse lethal doses.
The vegetative forms of the pathogen and its toxin are relatively easily killed and inactivated by boiling. The toxin in the grain can persist for months, in the mud after cleaning the corpses of dead waterfowl - up to 17 days.
The spores of the pathogen are especially resistant. Spores of some strains do not die even when boiled for 6 hours. Reliable decontamination requires moist heat (120°C) for 10 minutes.
epidemiological data. Botulism affects many species of animals and birds. AT vivo animal botulism outbreaks certain types are caused by toxins of certain types of Cl.botulinum. In horses, botulism is most often caused by toxin type B, less commonly A and C. cattle caused by toxins types D and C. Sheep, like fur animals(mink), as well as birds, are sensitive to type C toxin. Of the small experimental animals, the most susceptible to botulinum toxin various types white mice, guinea pigs, rabbits.
Differences in susceptibility to the toxin of animals depending on age were not noted.
Relatively high resistance to natural infection is shown by gray rats, dogs, wolves and foxes.
Botulism germs are widely distributed in nature. They can be found in the soil, on various plants, fruits, vegetables, animal and bird feces, in rotting animal corpses. Spores of Cl. Botulinum is also found in the body of earthworms and in decaying plant matter in the coastal silt of lakes and ponds. The pathogen enters the feed different ways: with earth particles, faeces, etc. Under conditions of anaerobiosis, at a certain temperature, humidity, reaction of the environment, in soaked, musty, spoiled (silo, steamed feed, bran, chaff, cut, etc.), self-heating feed (oats, barley, wheat), microbes multiply and the formation botulinum toxins. For omnivores and carnivores, spoiled meat and fish products, as well as animal corpses, are dangerous.
In contaminated feed, the toxin is usually found in separate sections, which in smell and appearance are not much different from the rest of the food. The nest location of the toxin in the feed is the reason that when eating such feed, not all animals that consumed this species feed, get sick. Animal botulism usually occurs as a result of ingestion of the toxin, and not due to the development of microbes in the body. Botulism microbes in the gastrointestinal intestinal tract animals are almost incapable of producing the toxin. At the same time, in birds, in some cases, botulism has the character of a toxic infection. In the goiter of birds, the pathogen forms a toxin, multiplying, for example, in the larvae of flies eaten by birds.
Under natural conditions, animal poisoning with botulinum toxin occurs most often through the gastrointestinal tract.
Pathogenesis. The main pathogenetic factor of the disease is the toxin. The toxin that has entered the animal's body with food is found in the blood, in the small and large intestines, in the bile and liver, in the urine, and sometimes in the brain.
Toxin after penetration begins to irritate the nerve endings in many organs and tissues. Continuous and severe irritation Receptors with botulinum toxin causes a disruption in the activity of the cerebral cortex, which sends signals to coordinate the organs and systems of the animal's body. Disruption of coordination occurs due to the fact that the cells of some nerve centers are exhausted and die as a result of overexcitation. Due to the gradual disruption of the centers in medulla oblongata paralysis of the pharynx, tongue, heart and other organs develops. Botulinum toxin also acts directly on the peripheral nerves, disrupting the transmission of impulses from the nerve centers along the motor nerve fibers. It is known that the transmission of impulses from the nerve to the muscle is carried out with the help of the mediator (intermediary) acetylcholine, which is formed in the endings motor nerve. Botulinum toxin, like curare poison, inhibits the release of acetylcholine. This leads to a gradual shutdown and relaxation of the muscles. In large animals sharp drop muscle tone disrupts movement, there is a general relaxation of the body and asphyxia gradually increases.
Clinical signs. The incubation period, depending on the amount of toxin that has entered the animal's body, ranges from several hours to 18-20 days. Most often, the disease occurs 1-3 days after the animal has received toxic feed. The severity and duration of the disease depends on the amount and strength of the toxin that has entered the body. The duration of an outbreak of botulism is usually 8-12 days, and the maximum release of patients is in the first three days. The disease develops with normal or even low temperature body. The acute course of the disease in all animal species lasts from one to 3-4, less often 6-10 days. With a hyperacute course of the disease, death occurs within a few hours.
The clinical signs are better understood in horses, which are more likely to develop botulism than other large animal species. With a relatively slow development of the disease, the signs of botulism appear in the following sequence. Horses have lethargic chewing, salivation, and frequent yawning. Sometimes you have to observe short-lived mild colic. During this period of illness, the tongue of the horse, taken out of the mouth, is slowly retracted. After some time (10-20 hours), the horse develops paralysis of the pharynx. The horse retains its full appetite, the thirst even intensifies. The food offered to the horse is chewed continuously, but it falls out of the mouth. As the disease progresses, the horse's chewing becomes increasingly difficult and tongue paralysis occurs. At first, the tip of the tongue sticks out of the oral cavity, then the tongue falls out, is infringed between the teeth and undergoes ulceration. Further development disease causes paralysis of the lower jaw in the horse and upper eyelids. The process of chewing for the horse becomes almost impossible. The lower jaw droops. This usually occurs shortly before the death of the animal.
In sick horses, skeletal muscle relaxation gradually occurs. Horses move reluctantly and with difficulty, their gait becomes shaky. By the end of the illness, the horse can no longer stand and lies down. Sick horses also gradually lose their voice (neighing is quiet, hoarse). On clinical examination, the mucous membranes of the eyes, nose and mouth are most often hyperemic, sometimes icteric, and cyanotic towards the end of the disease. Breathing in sick animals is rapid and superficial, the nostrils are funnel-shaped. With a prolonged course of the disease (7-8 days), some horses develop pneumonia or gangrene of the lungs as a complication due to aspiration of food masses. The pulse in sick horses at the height of the disease reaches 80-100 beats per minute. In the activity of the heart, we note arrhythmia and the development of cardiac weakness. From the very beginning of the disease, botulism is characterized by a weakening of intestinal motility, turning into persistent intestinal atony, constipation, as a result of which the feces are discharged in small portions, the scoobies are hard, covered with mucus. In sick horses, urination slows down. Not fever body before the death of the horse falls below normal. Sensitivity to external stimuli is preserved. Corneal, palpebral, ear, tail and other reflexes are preserved. AT serious condition, as well as before the death of the animal, skin sensitivity to a needle prick is lowered.
In the study of blood, we note a slowdown in ESR and a slight increase in the number of erythrocytes, which is associated with dehydration of the body. The number of leukocytes is within the normal range.
In large and small cattle clinical picture botulism is almost the same as that of a horse. Celebrating fatigue, difficulty in movement, violation of the act of swallowing, constipation, weakening of cardiac activity, depression. In cows and oxen, botulism can sometimes be chronic and last up to 33 or even 60 days. An animal suffering from botulism develops persistent accumulation and progressive emaciation.
Botulism is very rare in pigs. On clinical examination, we note the loss of voice, profuse salivation, impaired coordination of movements, partial and complete blindness. Due to paralysis of the chewing muscles and pharynx, food intake becomes impossible. The death of pigs occurs within a few hours or 2-3 days.
In birds (chickens, ducks, geese) with botulism, lethargy is observed, they are reluctant to take food and water, move with difficulty and sit more ruffled. There are digestive disorders (diarrhea, constipation), as well as paralysis of the nictitating membrane. Paralysis of the wings gradually sets in, then the neck and legs. The bird sits, it cannot hold its head and lowers it down, resting its beak on the ground. This posture in birds is characteristic of birds with botulism.
From fur-bearing animals, under natural conditions, only minks suffer from botulism. Botulism in minks is manifested by oppression, relaxation of all muscles, loss of mobility, a sharp expansion palpebral fissures and pupils. Animals develop a coma and die. Recovery is rare.
Pathological changes. Postmortem changes are not typical. Jaundice is sometimes found at autopsy. subcutaneous tissue and muscle aponeuroses. When the vessels are cut, thick dark red blood flows out. The stomach usually contains a small amount of food masses, the intestinal mucosa is catarrhal, slightly hyperemic, in some places small hemorrhages are found. Colon moderately filled with fodder masses, in the rectum dense, mucus-covered feces. More intense hemorrhages are expressed in the pharynx and epiglottis. The parenchyma of the kidneys, liver, spleen is usually without visible changes. The lungs are edematous, in complicated cases there is a picture characteristic of pneumonia and gangrene of the lungs. in the head and spinal cord- congestion. At histological examination the most severe lesions are found in the brainstem (medulla oblongata, pons). In the medulla oblongata, ganglion cell degeneration is observed, as well as changes in the nerve pathways, up to the breakdown of myelin. In other neurocerebrovascular diseases in horses, similar lesions of the conduction neural pathways are not observed.
Diagnosis. When making a diagnosis, epidemiological and clinical data are taken into account (loss of motor muscle tone, paralysis of the tongue and lower jaw, swallowing disorder, normal temperature, preservation of reflexes and consciousness). Establish a relationship between the disease and the consumption of certain feed by animals. With botulism, the maximum release of sick animals is observed in the first three days of the outbreak, it lasts no more than 8-12 days. Lifetime diagnosis can be confirmed laboratory research food residues, stomach contents, urine and blood of sick animals for the presence of toxin in them. Urine and blood are administered subcutaneously guinea pigs or mice at a dose of 1 to 5 ml. To determine the type of pathogen, a toxin neutralization reaction is used with type-specific antitoxic sera.
Differential Diagnosis. It is necessary to exclude, in horses, additional infectious encephalomyelitis, atypical forms of stachybotryotoxicosis, wormwood poisoning, in cattle - and acetonemia, and in birds - and.
Treatment. Treatment of sick animals usually begins with gastric lavage with a solution of bicarbonate of soda (30 g of soda per 15 liters of water). Strong laxatives are used. Horses are given arecoline at a dose of 0.03-0.06 g. At the same time, warm enemas are used to empty the rectum. After the arecoline has worked, the horse needs to inject 12-15 liters of water through the nasopharyngeal probe. If this is not possible, physiological saline solution of sodium chloride is administered intravenously (2 liters several times a day). Arecoline can be used only at the very beginning of the disease and how prophylactic for animals that have eaten suspicious food, but have not yet become ill.
Of the symptomatic remedies, to maintain the nutrition of the body, especially in protracted cases of the disease, it is necessary to apply intravenous administration 40% glucose solution. Cardiac activity is supported by the introduction of caffeine. The oral cavity is washed with a solution of potassium permanganate.
To cleanse the gastrointestinal tract, a bird that has become ill with botulism and is suspected of poisoning should be periodically given bitter salt. It is mixed with flour feed at a dose of 200-500g per 100 chickens.
Specific therapy of animals with botulism is carried out using anti-botulinum serum. Serum is effective only if it is administered at the very beginning of the disease in large doses. For a horse, the therapeutic dose should be at least 600 thousand. AE per intravenous injection. If the serum used is bivalent (against types A and B), increase the dosage to 900 thousand AU or more.
Immunity and immunization. Immunity in botulism is antitoxic. Animals can be actively immunized against botulism with toxoid. This was first installed in 1925. Mason and Stern. In 1935, Bennett and Hall immunized tens of thousands of sheep in Australia with Type C toxoid.
In our country, vaccination against mink botulism is widely used, which is used annually to immunize caged animals aged 45 days and older. In vaccinated animals, 12-15 days after vaccination, antitoxic immunity is formed, which lasts for more than one year.
Prevention and control measures. During the preparation and storage of feed, contamination with particles of earth, rodent corpses, and bird droppings is not allowed. Wet, spoiled, moldy food should not be fed even after drying. When harvesting silage, agrotechnical rules should be carefully observed. Moistened feed (bran, chopped, compound feed) must be fed immediately after preparation. Feed of animal origin (corpses, spoiled canned food) can only be given to animals after thorough boiling for 2 hours. Special attention should be given to the prevention of botulism in waterfowl during the hot season. It is necessary to clean the small muddy places of reservoirs from rotting plant masses.
In outbreaks of botulism, antibotulinum serum can be used not only for therapeutic, but also for prophylactic purposes.
Food poisoning in medicine is well known, since every year (especially during the summer and during the holidays) thousands of people who have eaten "something wrong" end up in hospitals. Many of the forms of such disorders can end very sadly. Pets are poisoned by low-quality food much less often. This is partly due to their physiology (dogs, like their wild ancestors, are not averse to eating slightly “spirited” meat - this is a completely physiological phenomenon), but it is largely due to this phenomenon the legibility of our pets. They simply will not eat frankly spoiled food.
The exception is botulism in dogs. The toxins released by the harmful microorganism are tasteless and odorless, but deadly to all mammals. Botulism is a rare but potentially fatal form of poisoning that occurs when eating foods contaminated with Clostridium botulinum. Oddly enough, this microorganism is not considered pathogenic in nature. This Clostridium is a Gram-positive, rod-shaped, anaerobic, spore-forming, motile bacterium that lives in soil. Unfortunately, the toxin it synthesizes is specific to the mammalian organism, and if it enters the body, the consequences are extremely severe.
Important! The causative agent is very stable in the external environment. So, boiling kills spore forms only after six hours, and even in an autoclave Clostridium spores can withstand at least 20 minutes. A solution of 50% formalin is able to destroy them only after a daily exposure.
We note right away that the food preferences of the ancestors of dogs favorably affected the sensitivity of these animals to Clostridium botulinum neurotoxins: cases of botulism in dogs are relatively rare, and even if a very decent dose of the toxin is taken, the animal, as a rule, remains alive. In cats, by the way, the likelihood of developing botulism is generally minimal.
Read also: We diagnose and treat a furuncle in a dog
After the toxin has entered the body, clinical signs of poisoning do not appear immediately: it takes from several hours to a couple of days. Bacterial neurotoxin causes weakness, first affecting hind legs, gradually covering the back, neck and front legs, ending in complete paralysis of all the limbs of the animal. Other symptoms of botulism in dogs include: difficulty chewing and swallowing food, constant and profuse pain, abdominal pain, and marked drying of the conjunctival membranes of the animal's eye.
Sick animals are completely refuse food, they become very lethargic, but at the same time their overall body remains within the normal range. This often misleads breeders. A sick dog starts constantly , and stool take the form of a semi-liquid greenish mucus with a disgusting odor. In the secretions, you can often see streaks of blood and undigested food residues.
Shortly after the onset of the first symptoms, the pet begins vomit, and the vomit also often contains blood and even Over time, the animal shows signs severe pain in the abdomen, the dog whines and groans. At the same time, periods can be observed worries that soon change complete apathy to everything that's going on. After that, the clinical signs of paralysis develop, which we already wrote about above.
An unfavorable outcome is “hinted”: quickening and breathing, stop or severely slow bowel movements and urination. It is believed that the probability lethal outcome, depending on the physiological state and age of the animal, varies from 25 to 57%.
If any of these signs appear in your pet, call your veterinarian immediately. The specialist will need to know what and in what quantities your pet has been eating over the past couple of days. Keep in mind that initial symptoms botulism is in many ways similar to poisoning by some, so the more information you give the specialist, the faster he will be able to make the correct diagnosis. In addition, you need to conduct urine and feces as soon as possible, including toxicology. Of course, if there are such opportunities.
Read also: Why the dog tucks its tail: we correctly interpret our pet
In addition, to facilitate the diagnosis, the owner himself (if the dog has vomiting) can take a sample of vomit, immediately passing it to the veterinarian. Oddly enough, radiography and ultrasound examination of the chest cavity are also important. This is due to the fact that neurotoxin has an unpleasant habit of blocking the transmission of neuromuscular impulses, and this is especially pronounced in the case of expirators and inspirators (muscles that act on exhalation and inhalation, respectively). The sooner signs of disturbing changes in muscle tissue are detected, the sooner action can be taken.
Therapy and prevention
How is botulism treated in dogs? To neutralize the effect of the poison and stop the development of the disease, type C antitoxin is used. Additional Treatment will depend on the severity of the case in each individual animal. In particular, the American homeopathic remedy Botulinum, which facilitates the course of pathology.
Need to remember! In severe cases, the dog needs mandatory hospitalization, since it has to be fed exclusively intravenously. In addition, in these situations, breathing problems are often observed, so the trachea of sick animals is intubated, maintaining breathing until the condition of the pet stabilizes.
When the animal begins to feel somewhat better, with parenteral nutrition it can be switched to feeding liquid food, which is forcibly fed into the gastrointestinal tract using a gastric tube. Full recovery (on average) takes one to three weeks.
Botulism (botulismus) - the disease refers to toxic infections and is characterized by damage to the central nervous system, paralysis of the muscles of the pharynx, tongue, lower jaw and skeletal muscles.
The disease is registered in all countries of the world, including the Republic of Belarus. The economic damage consists of a high (up to 95%) mortality of animals.
Etiology. The causative agent - Clastridium botulinum - anaerobe, is a gram-positive rod-shaped form of a microbe with a size of 4-9 × 0.5-1.2 microns, mobile, toxic and spore-forming. With a lack nutrients for its reproduction pH above 6, the access of oxygen, it forms gram-positive, subterminally large spores. The causative agent of botulism produces 7 types of toxins. The most powerful of the toxins is neurotoxin, which is formed under conditions of anaerobiosis. The microbe does not multiply in feed and food products at pH below 3-4 and above 8, NaCl concentration above 5-10%, in the presence of nitrates. Spores of Cl. Botulinum is stored in the soil for over 10 years. At +100 ?С, they are destroyed only after 5 hours, at +120 ?С - after 10 minutes. The causative agent is particularly resistant to disinfectants (Group 4). The toxin is destroyed by boiling in liquid media after 15-20 minutes, in dense media - after 2 hours.
epidemiological data. Animals of many species are susceptible to the disease, regardless of age. Horses and minks are most commonly affected. Wild carnivores are resistant to the disease.
The source of the infectious agent is soil, manure, water, corpses contaminated with Cl. Botulinum, from which the spores of the pathogen enter the feed and, under favorable conditions, germinate, releasing the toxin. Infection of animals occurs when botulinum toxin enters the digestive tract. Mass disease of animals usually occurs in the warm season, which occurs sporadically, less often in the form of enzootics. Mortality - 70-95%.
Pathogenesis. The toxin that enters with food is absorbed through the mucous membranes of the gastrointestinal tract and accumulates in large quantities in the tissues of the lungs, liver and heart, in bile, urine and brain. Botulinum toxin is a neurotoxin. As a result of a disorder under its influence, the activity of the cerebral cortex develops paralysis of the muscles of the pharynx, tongue, lower jaw, movement disorders, paralysis of the respiratory muscles, asphyxia and death of the animal.
The course and symptoms of the disease. The incubation period is from several hours to two weeks. The disease can proceed at lightning speed, acutely, subacutely and less often - chronically.
In horses and cattle, the fulminant course is characterized by the sudden death of animals without any signs of illness. The acute course (lasts from 1 to 4 days) is manifested by anxiety, decreased reflex sensitivity, impaired coordination of movements, hyperemia or icterus of visible mucous membranes. There is salivation, paralysis of the lower jaw and tongue, which falls out of the mouth. Lethality 90-95%. In subacute (up to 7 days) and chronic (up to 3-4 weeks) course of the disease, clinical signs are less pronounced.
In sheep, impaired coordination of movements, bending of the neck, paralysis of the tongue and salivation (in acute course) are noted. Pigs rarely get sick. They note profuse salivation, impaired coordination of movements, blindness, paralysis of the masticatory muscles and pharynx.
pathological changes. Not typical, but often there is jaundice of the subcutaneous tissue, catarrhal-hemorrhagic inflammation of the intestinal mucosa, hemorrhages in the pharynx and epiglottis, on the heart and serous integument, pulmonary edema. The brain is swollen, often with hemorrhages. Spleen, liver, kidneys without visible changes.
Diagnostics carried out on the basis of epidemiological data, clinical signs, the results of a post-mortem examination and the detection of botulinum toxin or the isolation of a culture of the causative agent of the disease.
Differential diagnosis. Anthrax, rabies, Aujeszky's disease, listeriosis, stachybotryotoxicosis, poisoning should be excluded in animals. poisonous plants and lead salts. Horses also have infectious encephalomyelitis.
Treatment. washed oral cavity a solution of potassium permanganate, the stomach - a solution of bicarbonate of soda. Apply laxatives, warm enemas. Anti-botulinum antitoxic mono- or polyvalent sera are administered intravenously.
Immunity. There is no specific prophylaxis for botulism in animals other than minks and dogs.
Prevention and control measures. During harvesting and storage of feed, soil, carcasses of small animals, bird droppings are not allowed to enter them. It is forbidden to feed moldy and spoiled food to animals. If botulism occurs, sick animals are isolated and treated. Slaughtering them for meat is prohibited. Corpses (carcasses) with internal organs and destroy the skin.