Botulism

Overview

Botulism, recognized at least since the eighteenth century, is a neuroparalytic disease cause by botulinum toxin, one of the most toxic substances known. While initially thought to cause only by the ingestion of botulinum toxin in contaminated food (food-borne botulism), three additional forms cause by in situ toxin production after germination of spores in either a wound or the intestine are now recognized worldwide: wound botulism, infant botulism, and adult intestinal colonization botulism.

In addition to occurring in these recognized natural forms of the disease, botulism symptoms have report in patients receiving injections of botulinum toxin for cosmetic or therapeutic purposes (iatrogenic botulism). Moreover, botulism was reported after inhalation of botulinum toxin in a laboratory setting.

Spread of Botulism

All forms of botulism manifest as a relatively distinct clinical syndrome of symmetric cranial-nerve palsies followed by descending bilateral flaccid paralysis of voluntary muscles, which may progress to respiratory compromise and death. The mainstays of therapy are meticulous intensive care and treatment with antitoxin as soon as botulism is suspected and before other illnesses have been ruled out.[1]

Botulism occurs worldwide, but the number of cases reported varies among countries and regions.

The variation may be due not only to actual differences in incidence but also to

(1) availability of resources to identify botulism, a rare disease

(2) differences in reporting requirements

(3) limited external access to data collections

There is no universal surveillance system to capture worldwide botulism incidence. However, 30 countries currently participate in voluntary reporting of botulism cases to the European Union through an established surveillance system that includes standardized case definitions similar to those used in the United States and Canada. Other countries (e.g., Argentina, China, Thailand, Japan) maintain independent botulism surveillance. [1]

Indian epidemiology then other

Causes

Seven serologically distinct confirmed serotypes of botulinum toxin (A through G) have confirm. Botulinum toxin produce by four recognized species of clostridia: Clostridium botulinum, Clostridium argentinense, Clostridium baratii, and Clostridium butyricum. Certain strains may produce more than one serotype.

All are anaerobic gram positive organisms that form subterminal spores; C. botulinum and C. argentinense spores have recover from the environment. The spores survive environmental conditions and ordinary cooking procedures. Toxin production, however, requires a rare confluence of product storage conditions: an anaerobic environment, a pH of >4.6, low salt and sugar concentrations, and temperatures of >4°C. Although commonly ingested, spores do not normally germinate and produce toxin in the adult human intestine.[1]

Food-borne botulism

Food-borne botulism cause by consumption of foods contaminated with botulinum toxin; no confirmed host-specific factors involved in the disease. Wound botulism cause by contamination of wounds with C. botulinum spores, subsequent spore germination, and toxin production in the anaerobic milieu of an abscess or a wound.

Infant botulism

Infant botulism results from absorption of toxin produced in situ by toxigenic clostridia colonizing the intestine of children ≤1 year of age. Colonization thought to occur because the normal bowel microbiota not yet fully establish; this theory support by studies in animals. Adult intestinal colonization botulism, a very rare form that poorly understood, has a pathology similar to that of infant botulism but occurs in adults; typically, patients have some anatomic or functional bowel abnormality or have recently used antibiotics that may help toxigenic clostridia compete more successfully against the normal bowel microbiota.

Antitoxin treatment

Despite antitoxin treatment, relapse due to intermittent intraluminal production of toxin may observe in patients with adult intestinal colonization botulism.[1] Regardless of how exposure occurs, botulinum neurotoxin enters the vascular system and transport to peripheral cholinergic nerve terminals, including neuromuscular junctions, postganglionic parasympathetic nerve endings, and peripheral ganglia.

Botulinum toxin is a zinc-endopeptidase protein of ~150 kDa, consisting of a 100-kDa heavy chain and a 50-kDa light chain.

Steps in neurotoxin activity include

(1) Heavy-chain binding to nerve terminals

(2) Internalization in endocytic vesicles

(3) Translocation of the light chain to cytosol

(4) Light chain serotype-specific cleavage of one of several proteins involved in the release of the neurotransmitter acetylcholine.

Inhibition of acetylcholine release by any of the seven toxin serotypes results in characteristic flaccid paralysis. Recovery follows sprouting of new nerve terminals.

Botulinum toxin serotypes

All botulinum toxin serotypes have demonstrated to cause botulism in nonhuman primates. Human cases associated with serotypes A, B, E, and F are reported each year. Serotype A produces the most severe syndrome, with the greatest proportion of patients requiring mechanical ventilation. Serotype B appears to cause milder disease than type A in both food-borne and infant botulism.

Other serotype

Besides this, Serotype E, most often associated with foods of aquatic origin, produces a syndrome of variable severity. The rare cases of illness caused by toxin serotype F, whether in infants or adults, characterize by rapid progression to quadriplegia and respiratory failure but also by relatively rapid recovery.

Recent studies have shown that at least some serotypes can be differentiated into subtypes through neurotoxin gene sequencing; however, the impact of these subtype differences on clinical illness is not yet known. [1]

Food borne botulism: –

From 1899 to 2011, 1225 food-borne botulism events (single cases or outbreaks) reported in the United States; from 1990 to 2000, a median of 23 cases were reported annually. Most such events (~80%) involve vegetables or fish/ aquatic animals, usually home-preserved (canned, jarred). Native communities in both the United States (Alaska) and Canada have a high incidence of food-borne botulism due to traditional food preparation practices; 85% of all cases in Canada occur in Native communities. Outbreaks typically involve two or three cases; however, one restaurant-associated outbreak in 1977 affected 59 persons.

Wound botulism: –

This form of disease first recognized in 1951 as a result of a review of the clinical records on an accidental injury in 1943. Between 1943 and 2011, 491 cases of wound botulism were reported in the United States; 97% of cases reported after 1990 were associated with injection drug use. The typical patient a 30- to 50-year-old resident of the western United States with a long history of black-tar heroin injection. In the early 2000s, wound botulism associated with drug use emerged in Europe, and at least two case clusters have reported.[1]

Infant botulism: –

More than 3900 infant botulism cases have reported worldwide (84% in the United States alone) since this form of the disease first recognized in 1976; ~80–100 cases (commonly caused by serotypes A and B) reported annually in the United States.[1]

Adult intestinal colonization botulism.: –

This form of botulism difficult to confirm because it is poorly understand and because no clear guidelines are available to help differentiate it from other adult botulism cases. Often these cases cause by C. baratii type F, but the involvement of both C. botulinum type A and C. butyricum type E has report.[1]

Iatrogenic botulism: –

Paralysis of variable severity has followed injection of licensed botulinum toxin products for treatment of conditions involving hypertonicity of large muscle groups. The U.S. Food and Drug Administration received 658 reports of adverse events related to botulinum toxin use—some very serious—between 1997 and 2006. Although some patients had symptoms consistent with botulism, no cases laboratory confirmed. Injection of approved doses of licensed products for cosmetic purposes has not associated with botulism. However, four cases of laboratory-confirmed botulism resulted from illegal injection of research-grade toxin for cosmetic purposes in a U.S. medical facility in 2004[1]

Inhalational botulism: –

Inhalational botulism does not occur naturally. One report from Germany has described botulism resulting from possible inhalational exposure to botulinum toxin in a laboratory incident.[1]

Intentional botulism: –

Botulinum toxin has been “weaponized” by governments and terrorist organizations. An attack might use aerosolization of toxin or contamination of foods or beverages ranging in scope from small-scale tampering to contamination of a widely distributed food item. An unnatural event may be suggested by unusual relationships between patients (e.g., a visit to the same building), atypical exposure vehicles, or atypical toxin serotypes.[1]

Risk factors of Botulism

Botulism risk factors can be characterized based on each type of botulism as follows:

Infant botulism

Infants are especially vulnerable to botulism. Risk factors for infant botulism include:

• Living in rural areas
• Consuming corn or corn-containing products
• Penetrating trauma
• Being in contact with soil
• Honey intake
• Slow intestinal movement

Foodborne botulism

Using home canning methods increase risk for contracting botulism.

• Canned food such as:
  • Fish
  • Vegetables
    • Beets
    • Corn
    • Spinach
    • String beans
    • Chili peppers
    • Asparagus
    • Honey
    • Processed cheese
  • Ingestion of foods that are not freshly prepared

Canned foods provide an environment with optimal pH for clostridium botulinum to survive. Additionally, the anaerobic environment in canned products allows the bacteria to thrive.

Wound botulism

Wound botulism is a rare type of the disease yet, it is important to know the risk factors in order to completely prevent it. Wound botulism risk factors include the following:

• Intravenous drug abuse
• Penetrating trauma with an infected object. (4)

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Pathophysiology of Botulism

• Botulism is most commonly caused by neurotoxins produced by C. botulinum, but C. baratii produces similar neurotoxins (5, 6). These toxins have been designated by letters, and human botulism has been caused by toxins A, B, E, and F.
• The neurotoxins which cause botulism are the most potent toxins currently known and cause paralysis through the inhibition of acetylcholine release in human nerve endings.
• Symptoms may begin as a headache and vomiting and progress to proximal and then distal paralysis (6).
• Eventually respiratory failure may occur due to paralysis and the morality rate for botulism is currently only 3 to 5 percent, in part due to mechanical respiration technology
• The video presented here is of Botulinum toxin B and provides a general overview of the cause of Botulism. It describes the mechanism of action that the toxin takes within the nerve cells.
• Clostridium botulinum is an obligate anaerobe that forms spores. The natural habitat for the Clostridium botulinum spores is the soil. The species of Clostridium botulinum is made up of 4 genetically diverse groups that do not have much in common other than the fact that they all produce the botulinum toxin.
• The botulinum toxin itself exists as 7 different antigenic types and these 7 antigenic types have been assigned a series of letters: A, B, C, D, E, F, G.
• These toxins have a specific definition, and they are defined by their inability to cross neutralize the other types.
• The botulinum molecule itself is composed of a heavy chain as well as a light chain polypeptide. It is referred to as a dichain polypeptide.
• The light chain of the toxin contains an endopeptidase that blocks acetylcholine-containing vesicles from being able to fuse with the membrane at the end of the motor neuron.
• If acetylcholine is not present, it will result in flaccid muscle paralysis.
• Many people may not realize it, but the commercial therapeutic procedure termed "Botox" actually contains the botulinum toxin.
• However, there is a very small amount of it present, otherwise it would present an extensive danger.
• A vial of type A preparation, which is currently licensed in the US, contains only about 0.005% of the lethal oral dose and 0.3% of the lethal inhalation
• Clostridium botulinum is divided into 4 groups:
• Group I – can produce toxins specifically A, B, or F proteolytic
• Group II – can produce toxins specifically B, E, or F, nonproteolytic
• Group III – can produce toxins C or D
• Group IV – can produce toxin G but toxin G has not been shown to cause neuroparalytic illness.
• Honey, corn syrup, and other sweeteners are potentially dangerous for infants. This is partly because the digestive juices of an infant are less acidic than older children and adults, and may be less likely to destroy ingested spores.
• In addition, young infants do not yet have sufficient numbers of resident microbiota in their intestines to competitively exclude C. botulinum. Unopposed in the small intestine, the warm body temperature combined with an anaerobic environment creates a medium for botulinum spores to germinate, divide and produce toxin.
• Thus, C. botulinum is able to colonize the gut of an infant with relative ease, whereas older children and adults are not typically susceptible to ingested spores. C. botulinum spores are widely present in the environment, including honey.
• For this reason, it is advised that neither honey, nor any other sweetener, be given to children until after 12 months. Nevertheless, the majority of infants with botulism have no history of ingestion of honey, and the exact source of the offending spores is unclear about 85% of the time.
• Spores present in the soil are a leading candidate for most cases, and often a history of construction near the home of an affected infant may be obtained.(4)

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No matter how you get botulism, the symptoms are usually the same. The most defining symptom is weakness that starts on both sides of your face, goes down to your neck, and then to the rest of your body.

Other early symptoms e.g.:

• Either Double or blurred vision
• Drooping eyelids
• Difficulty swallowing
• Slurred speech
• Shortness of breath

Other symptoms that can follow include vomiting, belly pain, and diarrhea. Later, you may have a very hard time urinating and have severe constipation. Symptoms do not include a fever.[1]

If you don’t get treatment, your symptoms could progress to paralysis of your arms and legs and the muscles used for breathing.[1]

Infants with botulism have symptoms that i.e.:

• Lethargy
• Poor muscle tone starting in the head and neck and moving down
• Poor feeding
• Drooling
• Weak cry

Symptoms of wound botulism

Symptoms of wound botulism are similar to general botulism but may take about 2 weeks to appear. They also can i.e.:

• Fever
• Skin redness, swelling, also other signs of infection

Symptoms of inhalation botulism

Symptoms of inhalation botulism are the same as those for general botulism but usually happen more quickly. Respiratory failure can occur.

Symptoms of adult intestinal toxemia

Symptoms of adult intestinal toxemiaare similar to infant botulism. They are the same as general botulism but may also include i.e.:

1. Firstly, Constipation
2. Secondly, Poor feeding
3. Lastly, Lack of energy (lethargy)

Symptoms of iatrogenic botulism

Symptoms of iatrogenic botulism are the same as those seen in general botulism. Along with muscle weakness, you could have i.e.:

• Eye muscle weakness
• A hard time speaking
• A paralyzed face
• A thick, weak tongue
• Reduced gag reflex [1]

Cranial nerve deficits i.e.

• Diplopia, Dysarthria
• Dysphonia, Ptosis
• Ophthalmoplegia
• Facial paralysis
• Impaired gag reflex
• Pupillary reflexes may be depressed, also fixed or dilated pupils
• Autonomic symptoms such as dizziness, dry mouth, and very dry, occasionally sore throat are common.
• Constipation
• Respiratory failure may occur due to either paralysis of the diaphragm and accessory breathing muscles or pharyngeal collapse secondary to cranial nerve paralysis.
• Weakness descends, often rapidly, from the head to involve the neck, arms, thorax, and legs; occasionally, weakness is asymmetric.
• Deep tendon reflexes may be normal or may progressively disappear.

Other symptoms

• Paresthesias, while rare, have been reported and may represent secondary nerve compression from immobility due to paralysis.
• Absence of cranial nerve palsies or their onset after the appearance of other true neurologic symptoms makes botulism highly unlikely.
• Nausea, vomiting, and abdominal pain may precede or follow the onset of paralysis in food-borne botulism.
• Infants with botulism typically present with reduced ability to suck and swallow, constipation, weakened voice, ptosis, sluggish pupils, hypotonia, and floppy neck; as in adults, illness can progress to generalized flaccidity and respiratory compromise.[1]

Clinical examination of Botulism

Appearance of the patient– Patients of botulism may appear lethargic and dizzy, Infants appear pale with less crying and unable to eat

Vital signs- Botulism patients have normal vital signs., Unstable blood pressure and heart rate

Skin-In wound botulism, the following may be observed:

• Wounds
• Bruises
• Subcutaneous abscesses
• Pale skin with bruises and signs of penetrating trauma in infant.

HEENT-Absent or decreased gag reflex

• Tongue hypotonia
• Weakness of the eye muscles
• Nystagmus
• Ptosis

Abdomen: Paralytic ileus: Decreased or absent bowel sounds (Foodborne botulism)

Lungs: Bradypnea due to respiratory muscle paralysis

CVS-Normal heart sounds, No murmurs, gallops or rubs

Neuromscular:

• Absent or decreased deep tendon reflexes
• Motor deficit
• Facial nerve impairment
• Speech impairment

Extremities: Weakness of lower and upper extremities (4)

Diagnosis

Botulism is diagnosed primarily on clinical grounds, with laboratory confirmation by specific tests that identify botulinum toxin in clinical and food samples. In the setting of an outbreak with multiple patients presenting to the same treatment facility, the diagnosis is apparent as long as physicians recognize that cases within a cluster may have varied signs and symptoms.

The temporal occurrence of two or more cases with symptoms compatible with botulism is essentially pathognomonic because other illnesses that resemble botulism do not usually occur in clusters. In lone (sporadic) cases, the diagnosis is often missed. The rarity of this disease prevents many physicians from gaining experience with its clinical diagnosis, and some patients present with signs and symptoms that do not fit the classic pattern. Assessing clinical characteristics of other paralytic illnesses in single cases is sometimes critical to rule in or rule out the diagnosis of botulism. [1]

In adults

a food history and the names of contacts who may have shared foods should be obtained before illness progresses to respiratory failure; specific questions should include information about the consumption of home-preserved and/or foreign foods and of products requiring refrigeration that have been left at room temperature in sealed plastic containers or bags. A history of recent consumption of home-canned food substantially enhances the probability of food-borne botulism.

Ascertainment of the patient’s behavioral history related to injection drug use is critical to the diagnosis of wound botulism unless an accidental wound is evident. A history of recent abdominal surgery or antibiotic use may 989 be important in the diagnosis of adult intestinal colonization botulism. [1]

Differential Diagnosis

The illnesses most commonly considered in the differential diagnosis of adult botulism cases include Guillain Barré syndrome (GBS), myasthenia gravis, stroke syndromes, Eaton Lambert syndrome, and tick paralysis. Less likely possibilities are poisoning by tetrodotoxin, shellfish, or a host of rarer agents and antimicrobial drug–associated paralysis. A thorough history and a meticulous physical examination can effectively eliminate most alternative diagnoses, but a workup for other diagnoses should not delay treatment with botulinum antitoxin. [1]

GBS

GBS, a rare autoimmune demyelinating polyneuropathy that often follows an acute infection, presents most often as an ascending paralysis. Case clusters are rare. Occasional GBS cases present as the Miller Fisher variant, whose characteristic triad of ophthalmoplegia, ataxia, and areflexia easily mistake for the early descending paralysis of botulism.

Pathogenesis

Protein levels in cerebrospinal fluid (CSF) elevate in GBS; because this increase may delay until several days after symptom onset, an early lumbar puncture with a negative result may need to repeat. In contrast, CSF findings generally normal in botulism, although marginally elevate CSF protein concentrations have reported. In experienced hands, electromyography may differentiate GBS from botulism.

edrophonium (Tensilon) test

The edrophonium (Tensilon) test is sometimes of value in distinguishing botulism from myasthenia gravis. In most cerebrovascular accidents, physical examination reveals asymmetry of paralysis and upper motor neuron signs. Brain imaging can reveal the rare basilar stroke that produces symmetric bulbar palsies. Eaton-Lambert syndrome usually manifests as proximal limb weakness in a patient already debilitated by cancer.

Tick paralysis

Tick paralysis is a rare flaccid condition closely resembling botulism and caused by neurotoxins of certain ticks. [1]

Complications are what happen after you have a disease. They are the negative consequences of the disease process.

Investigation

Botulism is confirmed in the laboratory by demonstration of toxin in clinical specimens (e.g., serum, stool, gastric aspirate, and sterile-water enema samples) or in samples of ingested foods.

Isolation of toxigenic clostridia from stool also provides evidence of botulism.

Wound cultures yielding the organism are highly suggestive in symptomatic cases.

mouse bioassay

The universally accepted method for confirmation of botulism is the mouse bioassay, which is available only in specialized laboratories.

Specific guidance about what specimens to collect should be obtained from the testing laboratory because the requirements vary with the form of botulism suspected.

Hospitalization

Clinical specimens collected early in the hospital admission process should be submitted for testing; toxin results may be negative if specimens are collected >7 days after symptom onset. Because of the extreme potency of botulinum toxin, a test may yield a negative result even when a patient has botulism; thus, a negative result does not exclude this diagnosis.

Nerve conduction studies

Nerve conduction studies showing reduced amplitude of motor potentials—with or without potentiation by rapid repetitive stimulation in weak muscles—and needle electromyography showing small-motor-unit action potentials are consistent with botulism; these results and those that make alternative diagnoses more likely may be useful. Standard blood work and radiologic studies are not useful in diagnosing botulism.[1]

Treatment

The cornerstones of treatment for botulism are meticulous intensive care and immediate administration of botulinum antitoxin. Because antitoxin most beneficial early in the course of clinical illness. It should administer as soon as botulism suspect and before the time-consuming workup for other illnesses is complete.

Hosptalization

Persons of all ages in whom botulism suspect should hospitalize immediately so that respiratory failure—the usual cause of death—can detect and managed promptly.

Vital capacity should monitor frequently and mechanical ventilation provided as needed.

Botulinum antitoxin can limit the progression of illness because it neutralizes toxin molecules in the circulation that have not yet bound to nerve endings.

However, antitoxin does not reverse existing paralysis, which may take weeks to improve.

Vaccination

In the United States, there two license antitoxin products: Botulism Antitoxin Heptavalent an equine-derived heptavalent product enzymatically de-speciated for treatment of all forms of adult botulism and infant cases not involving serotypes A and B; and Botulism Immune Globulin Intravenous, a human derived product for treating infant botulism caused by serotype A and/or B only.

Antitoxin is also available in some other countries. Aminoglycosides and other medications that block the neuromuscular junction may potentiate botulism and should avoid. [1]

In wound botulism, suspect wounds and abscesses should cleaned, debrided, and drained promptly.

Medications

The role of penicillin and metronidazole in treatment and decolonization is unclear.

It has hypothesize that antimicrobial agents may increase circulating botulinum toxin from lysis of bacterial cells. Person-to-person transmission of botulism does not occur.

Universal precautions the only infection-control measures require during inpatient care. [1]

Prevention

No prophylaxis or licensed vaccine is available against botulism. Home canning instructions and equipment have changed over the years. Up-to-date canning instructions from reliable sources should follow to ensure food safety. Processed food should store properly and heated thoroughly prior to consumption.

Because of the possible presence of spores, honey should not give to infants (≤12 months of age). Injection of illicit drugs should avoid. All wounds should be meticulously cleaned to eliminate possible contamination with bacterial spores.

Role of clinician

Clinicians should educate individuals or family members of at-risk individuals, including infants, illegal drug users, and preparers of home-preserved foods.[1]

Homeopathic Treatment of Botulism

Homeopathy treats the person as a whole. It means that homeopathic treatment focuses on the patient as a person, as well as his pathological condition. The homeopathic medicines selected after a full individualizing examination and case-analysis.

Which includes

• The medical history of the patient,
• Physical and mental constitution,
• Family history,
• Presenting symptoms,
• Underlying pathology,
• Possible causative factors etc.

A miasmatic tendency (predisposition/susceptibility) also often taken into account for the treatment of chronic conditions.

What Homoeopathic doctors do?

A homeopathy doctor tries to treat more than just the presenting symptoms. The focus is usually on what caused the disease condition? Why ‘this patient’ is sick ‘this way’?

The disease diagnosis is important but in homeopathy, the cause of disease not just probed to the level of bacteria and viruses. Other factors like mental, emotional and physical stress that could predispose a person to illness also looked for. Now a days, even modern medicine also considers a large number of diseases as psychosomatic. The correct homeopathy remedy tries to correct this disease predisposition.

The focus is not on curing the disease but to cure the person who is sick, to restore the health. If a disease pathology not very advanced, homeopathy remedies do give a hope for cure but even in incurable cases, the quality of life can greatly improve with homeopathic medicines.

Homeopathic Medicines for Botulism:

The homeopathic remedies (medicines) given below indicate the therapeutic affinity but this is not a complete and definite guide to the homeopathy treatment of this condition. The symptoms listed against each homeopathic remedy may not be directly related to this disease because in homeopathy general symptoms and constitutional indications also taken into account for selecting a remedy, potency and repetition of dose by Homeopathic doctor.

So, here we describe homeopathic medicine only for reference and education purpose. Do not take medicines without consulting registered homeopathic doctor (BHMS or M.D. Homeopath).

Medicines:

Arsenicum album:

With nausea and vomiting. Burning in the stomach. Additionally, Restlessness. Despairing. Intense thirst – drinks little but often. Craves ice water which vomit (Phos.). Violent abdominal pains. Rolls about in anguish. Worse after (1) spoiled food, especially meat and watery fruit.

Carbo veg:

Patient is lifeless. Cold body and breath (but hot head). Weak pulse, quick breathing -needs air (to be fanned). Skin blue. Flatulent. Loud belching. Burning in stomach. Vomiting of blood.

Apis:

Confluent eruption, with pronounced oedema of the skin; oedematous swelling of the throat; cerebral complications.

Bryonia:

Cases calling for Bryonia characterize by a predominance of catarrhal symptoms from the very beginning with tendency to extend the finer bronchial tubes. Additionally, involve the pulmonary parenchyma. The rash slow in coming out, but, when once establish, it is usually abundant and characteristic. The accompanying symptoms are dry, painful cough. Furthermore, great lassitude and irritability anorexia, with thirst for large quantities of water; constipation, etc. Bryonia look upon somewhat as a specific to bring out the rash. On the other hand, any well-selected remedy will accomplish the same result.

Euphrasia:

Profuse corroding discharge from the eyes, with profuse, bland, nasal discharge.

Trifolium repens:

This remedy, the white clover, in the 3rd potency, is a remedy for the slobbering, drooling, or slavering of infants, or others- so they say.

Silicea:

In brief, Blindness-Momentary attacks of sudden blindness.

Must avoid this type of food:

• The botulism toxin has found in a variety of foods, including low-acid preserved vegetables. For example; green beans, spinach, mushrooms and beets; fish, including canned tuna, fermented, salted and smoked fish. Besides this; meat products, such as ham and sausage [2]

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Reference

[1]Harrison-s_Principles_of_Internal_Medicine-_19th_Edition-_2_Volume_Set

[2]https://www.webmd.com/food-recipes/food-poisoning/what-is-botulism

[3] A Complete Repertory of The Tissue Remedies of Schussler by S. F. Shannon

[4], clinical examination

Frequently Asked Questions

What is Botulism?

Botulism a paralytic disease caused by potent protein neurotoxins elaborated by clostridium botulinum.

Homeopathic Medicines used by Homeopathic Doctors in treatment of Botulism?

• Arsenicum album
• Carbo veg
• Apis
• Bryonia
• Euphrasia
• Trifolium Repens

What are the symptoms of Botulism?

• Double or blurred vision
• Drooping eyelids
• Difficulty swallowing
• Slurred speech
• Shortness of breath
• Vomiting, belly pain, diarrhea

What are the causes of Botulism?

• Clostridium botulinum
• Clostridium argentinense
• Clostridium baratii
• Clostridium butyricum