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BOTULISM. TOXIC FOOD-BORNE DISEASES. CAMPYLOBACTERIOSIS BOTULISM

Botulism is a life-threatening infectious disease, produced by neurotoxins elaborated by Clostridium botulinum. Botulism is characterized with intoxication of the organism with the principal damage of the central and vegetative nervous system.

Historic reference

Because early accounts of botulism frequently incriminated sausages, the name of the disease was derided from the Latin word for sausage - "botulus". Outbreaks of "sausage poisoning" were common in Germany during the nineteenth century, and Justinius Kerner, poet and physician, published several monographs on the subject. For a time, botulism was known as "Kerner's disease". Investigating an outbreaks in 1895, the Belgian bacteriologits Van Ermengem performed classic experiments in which he isolated the causative anaerobic spore-forming bacillus from the incriminated ham and demonstrated that both the ham and a toxin produced by the organism could induce a paralytic illness in cats.

Etiology

Clostridium botulinum is a gram-positive, anaerobic and forming spores bacillus. Eight immunologically distinct toxin types have been described (types A, B, C, D, E, F, G. Types À, Â and E most commonly cause disease in man; types F and G have only rarely caused human illness. Types C and D are associated with animal botulism, especially in cattle, ducks and chickens.

One of the peculiarities of the agent is mobility. It is connected with presence of flagellars. The spores of C.botulinum are heat resistant; they can withstand 100 Ñ for hours. Fortunately, the toxins are rather heat labile; boiling for 10 minutes or heating at 80C for 30 minutes destroy them.

All serotypes of Clostridium botulinum produce neurotoxin. Neurotoxin is protein, it consists of 19 aminoacids. Neurotoxin of Clostridium botulinum is one of the most strong natural poisons.

Epidemiology

Botulism is saprozoonosis. The spores of C.botulinum are ubiquitous in soil; the distribution of type A and  spores is worldwide. The principal reservoirs of the agent of botulism are grass feeding animals, and rarely fish, mollusks and crayfishes which absorbing the spores of C.botulinum with water and food.

 

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The human is infected by botulism due to use of the contaminated food by spores. The greatest part of the cases of botulism is connected with use home-canned food, for example mushrooms, vegetables, fish, meat and other.

The disease occurs under three circumstances: 1) botulism food poisoning results from eating food that contains preformed toxin; 2) wound botulism occurs when toxin is produced by C.botulinum organisms contaminating traumatic wounds; 3) infant botulism is due to toxin production by C.botulinum within the gastrointestinal tract of infants.

Pathogenesis

The vegetative forms of the agent and botulotoxin enter into the human organism due to use contaminated food-stuffs. The action of the toxin is intensified in the stomach under influence of proteolytic enzymes. The people are more sensitive to serotypes of toxin À, Â, Å.



The toxin are absorbed primarily from the stomach and small bowel. The digestive enzymes do not destroy the toxin molecules. The toxins interfere with neurotransmission at peripheral cholinergic synapses by binding tightly to the presynaptic membrane and presenting the release of the neurotransmitter acetylcholine. Adrenergic fibers are spared. The effect of botulinus toxin on cholinergic pathways in the central nervous system remains in dispute. The motoneurones of spinal cord and oblong brain have special sensitiveness to botulism. The bulbaric and paralytic syndromes develop as a result.

Hypoxia plays the leading role in the pathogenesis of botulism. The development of progressive respiratory insufficiency is connected with depression of the activity of the large motoneurones, innerving the respiratory muscles.

Anatomic pathology

The pathologoanalomic alterations in botulism have nonspecific character. They are connected with deep hypoxia. There are hyperemia of the internal organs, edeijia of the cerebrum, small hemorrhages into mucous membrane of the gastrointestinal tract.

Clinical manifestations

The incubation period ranges from 2-12 hours till 10 days (in average 6-24 hours). There are the next leading syndromes in botulism: paralytic, gastrointestinal and intoxicative syndromes. The onset of the disease is, as a rule, an acute. In patients pain in the epigastric area, nausea, vomiting, diarrhea occur. The vomiting and diarrhea are not prolonged. The temperature is normal or subfebrile. The rapid fatigue, progressive'muscle's weakness are marked. The symptoms of the defeat of the muscles, of cranial nerves and paralytic violations of innervation of the internal organs develop through 3-4 hours after the onset of the disease. These violations are characterized by symmetrical defeat.

 

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The first typical signs of botulism are usually dryness in the mouth (Fig. 4) and ophthalmoplegic symptoms. The patients complain of vision disorders, "net" or "fog" in front of the eyes. The patients cannot read, because the paresis of the accommodation and diplopia develop. Medriasis (Fig. 5), decreased reaction on the light, the limitation of the eyes motion, sometimes full inmotility, ptosis (Fig. 6), squint, horizontal nystagmus are observed.

The violations of the swallow and speech are early observed. These violations is connected with damage of IX and XII nucleuses of cranial nerves pairs. In patients dysphonia, dysarthria, nose shade of the voice are marked. The paresis of the throat muscles develops. In the patients dysphagia appears as a result. The liquid is poured out through the nose.

Botulism is accompanied with functional disorders of cardiovascular system. The widening of the heart's borders and muffed heart sounds are observed.

The violations of the functions of the gastrointestinal tract are accompanied with dryness of the mucous membranes of the mouth, thirst, distention of the abdomen, retention of stool, and intestine paresis.

The large motoneurones of the neck's and chest's portions of the spinal cord are involved into the process. This process leads to development of paresis and paralysis of the muscles. The patient may breathe with difficulty. The patient must accept special position. The cough's reflex disappears. The disorder and break of breath is one of the leading causes of the death at botulism.

In terminal period the appearances of myoneuralgia are observed: myasthenia and adynamia. The muscles have like-dough consistence. The recovery comes slowly, during 1-1.5 months.

In peripheral blood moderate leukocytosis, neutrophylosis are marked with shift of the formula to the left. In botulism the prognosis is always serious. When adequate therapy is not applied the lethal outcomes compose near 25 %.

Diagnosis

The diagnosis is made on the basis of clinical manifestations of the disease, epidemiological data and results of the laboratory researches. The toxin and the agent may be revealed in the materials, collected from the patient (blood, vomitory masses, water after irrigation of the stomach, stool) and also at the suspicious food-stuffs. The reaction of neutralization may be used for revelation of toxin.

 

Differential diagnosis

Botulism may be confused with the Guillant-Barre syndrome, poliomyelitis, stroke, myastenia gravis, tick paralysis, and poisoning due to curare or belladonna alkaloids.

Treatment

The first aid (independently of term, that pasted from the beginning of disease) consists of careful lavage of stomach and intestine with 2-5 % solution of a Sodii carbonate. It is necessary to remember, that at muscles paralysis of

 

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pharynx, larynx and tongue, the probe may penetrate into a trachea, therefore before lavaging it is necessary to be convinced that the probe is in stomach. After lavaging prescribe enterosorbent-SKN, enterodes, sillard P.

Medical antibotulism serums are injected at first hours of the disease. Before determination of species of the infection inject mixture of serums types A and E 10,000 IU and type  on 5,000 IU. After definition of specie of infection monovalent serum is used. In serious cases during 1st day 4-6 medical doses of serum are prescribed, 2 of them - intravenous by drops in isotonic solution of Sodii chloride or 5 % solution of glucose. Before injection of serum intracutaneous test is made. Serum is injected according the method of fractional deallergization depending on degree of disease gravity during 2 4 days. Etiotropic agent is specific treatment with homological plasma 250 mL, 1-2 times per day.

Nonspecific desintoxication therapy consists of injection of glucose solution, polyionic solutions (lactasault,threesault,quartasault) and simultaneously diuretics - furosemid (lasix).

For suppression of infection in a digestive tract ampicillin, oxacillin, levomycetin or tetracyclin are indicated. A course of antibiotic therapy lasts for 5-7 days.

In serious cases and for prophylaxy of serum disease prednisolone on 40 mg per day or its analogues is indicated. At disorders of respiration of the patient he is required to hospitalize to reanimation departament and transfer on controlled artificial respiration immediately.

At failure of cardiovascular system there are prescribed cordiamin, sulfocamphocain, cardiac glicosides, at disorders of nervous system - vitamin

I

preparations of group B, cocarboxylase, riboxin. At allergic reactions, development of a serum disease there are used prednisolone, antihistaminics - suprastin and also calcy gluconate, phencarole, terfenadin.

Prophylaxis

The observance of the sanitary and hygienic rules at processing, transportion, keeping and preparing of the food-stuffs experts possibility of accumulation of botulotoxin. It is necessary to perform the strict control under sterilization and keeping preserved food-stuffs.

The explanation to the people of the rules of the procurement and preservation of food-stuffs in home conditions has important value especially such food-stuffs as meat, mushrooms, vegetables.

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Date: 2014-12-21; view: 925


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