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Bacterial growth

Bacterial growth is proliferation of bacterium into two daughter cells, in a process called binary fission. Providing no mutation event occurs, the resulting daughter cells are genetically identical to the original cell. Hence, bacterial growth occurs. Both daughter cells from the division do not necessarily survive. However, if the surviving number exceeds unity on average, the bacterial population undergoes exponential growth. The measurement of an exponential bacterial growth curve in batch culture was traditionally a part of the training of all microbiologists; the basic means requires bacterial enumeration (cell counting) by direct and individual (microscopic, flow cytometry ), direct and bulk (biomass), indirect and individual (colony counting), or indirect and bulk (most probable number, turbidity, nutrient uptake) methods. Models reconcile theory with the measurements.

Phases
In autecological studies, the growth of bacteria (or other microorganisms, as protozoa, microalgae or yeasts) in batch culture can be modeled with four different phases: lag phase (A), log phase or exponential phase (B), stationary phase (C), and death phase (D). This basic batch culture growth model draws out and emphasizes aspects of bacterial growth which may differ from the growth of macrofauna. It emphasizes clonality, asexual binary division, the short development time relative to replication itself, the seemingly low death rate, the need to move from a dormant state to a reproductive state or to condition the media, and finally, the tendency of lab adapted strains to exhaust their nutrients. In reality, even in batch culture, the four phases are not well defined. The cells do not reproduce in synchrony without explicit and continual prompting (as in experiments with stalked bacteria ) and their exponential phase growth is often not ever a constant rate, but instead a slowly decaying rate, a constant stochastic response to pressures both to reproduce and to go dormant in the face of declining nutrient concentrations and increasing waste concentrations.
 * 1) During lag phase, bacteria adapt themselves to growth conditions. It is the period where the individual bacteria are maturing and not yet able to divide. During the lag phase of the bacterial growth cycle, synthesis of RNA, enzymes and other molecules occurs.  During the lag phase cells change very little because the cells do not immediately reproduce in a new medium. This period of little to no cell division is called the lag phase and can last for 1 hour to several days. During this phase cells are not dormant.
 * 2) The log phase (sometimes called the logarithmic phase or the exponential phase) is a period characterized by cell doubling. The number of new bacteria appearing per unit time is proportional to the present population.  If growth is not limited, doubling will continue at a constant rate so both the number of cells and the rate of population increase doubles with each consecutive time period. For this type of exponential growth, plotting the natural logarithm of cell number against time produces a straight line. The slope of this line is the specific growth rate of the organism, which is a measure of the number of divisions per cell per unit time. The actual rate of this growth (i.e. the slope of the line in the figure) depends upon the growth conditions, which affect the frequency of cell division events and the probability of both daughter cells surviving. Under controlled conditions, cyanobacteria can double their population four times a day and then they can triple their population. Exponential growth cannot continue indefinitely, however, because the medium is soon depleted of nutrients and enriched with wastes.
 * 3) The stationary phase is often due to a growth-limiting factor such as the depletion of an essential nutrient, and/or the formation of an inhibitory product such as an organic acid. Stationary phase results from a situation in which growth rate and death rate are equal. The number of new cells created is limited by the growth factor and as a result the rate of cell growth matches the rate of cell death. The result is a “smooth,” horizontal linear part of the curve during the stationary phase. Mutations can occur during stationary phase. Bridges et al. (2001) presented evidence that DNA damage is responsible for many of the mutations arising in the genomes of stationary phase or starving bacteria.  Endogenously generated reactive oxygen species appear to be a major source of such damages. Bacteria in this phase sometimes enter dormancy, using  hibernation factors to slow their metabolism.
 * 4) At death phase (decline phase), bacteria die. This could be caused by lack of nutrients, environmental temperature above or below the tolerance band for the species, or other injurious conditions.

The decrease in number of bacteria may even become logarithmic. Hence, this phase of growth may also be called as negative logarithmic or negative exponential growth phase.

Near the end of the logarithmic phase of a batch culture, competence for natural genetic transformation may be induced, as in Bacillus subtilis and in other bacteria. Natural genetic transformation is a form of DNA transfer that appears to be an adaptation for repairing DNA damages.

Batch culture is the most common laboratory growth method in which bacterial growth is studied, but it is only one of many. It is ideally spatially unstructured and temporally structured. The bacterial culture is incubated in a closed vessel with a single batch of medium. In some experimental regimes, some of the bacterial culture is periodically removed and added to fresh sterile medium. In the extreme case, this leads to the continual renewal of the nutrients. This is a chemostat, also known as continuous culture. It is ideally spatially unstructured and temporally unstructured, in a steady state defined by the rates of nutrient supply and bacterial growth. In comparison to batch culture, bacteria are maintained in exponential growth phase, and the growth rate of the bacteria is known. Related devices include turbidostats and auxostats. When Escherichia coli is growing very slowly with a doubling time of 16 hours in a chemostat most cells have a single chromosome.

Bacterial growth can be suppressed with bacteriostats, without necessarily killing the bacteria. Certain toxins can be used to suppress bacterial growth or kill bacteria. Antibiotics (or, more properly, antibacterial drugs) are drugs used to kill bacteria; they can have side effects or even cause adverse reactions in people, however they are not classified as toxins. In a synecological, true-to-nature situation in which more than one bacterial species is present, the growth of microbes is more dynamic and continual.

Liquid is not the only laboratory environment for bacterial growth. Spatially structured environments such as biofilms or agar surfaces present additional complex growth models.

The 5th phase: Long-term stationary phase
Long-term stationary phase, unlike early stationary phase (in which there is little cell division), is a highly dynamic period in which the birth and death rates are balanced. It's been proven that after death phase E. coli can be maintained in batch culture for long periods without adding nutrients. By providing sterile distilled water to maintain volume and osmolarity, aerobically grown cultures can be maintained at densities of ~106 colony-forming units (CFUs) per ml for more than 5 years without the addition of nutrients in batch culture.

Environmental conditions
Environmental factors influence rate of bacterial growth such as acidity (pH), temperature, water activity, macro and micro nutrients, oxygen levels, and toxins. Conditions tend to be relatively consistent between bacteria with the exception of extremophiles. Bacterium have optimal growth conditions under which they thrive, but once outside of those conditions the stress can result in either reduced or stalled growth, dormancy (such as formation spores), or death. Maintaining sub-optimal growth conditions is a key principle to food preservation.

Temperature
Low temperatures tend to reduce growth rates which has led to refrigeration being instrumental in food preservation. Depending on temperature, bacteria can be classified as:

Psychrophiles are extremophilic cold-loving bacteria or archaea with an optimal temperature for growth at about 15 °C or lower (maximal temperature for growth at 20 °C, minimal temperature for growth at 0 °C or lower). Psychrophiles are typically found in Earth's extremely cold ecosystems, such as polar ice-cap regions, permafrost, polar surface, and deep oceans. Mesophiles are bacteria that thrive at moderate temperatures, growing best between 20° and 45 °C. These temperatures align with the natural body temperatures of humans, which is why many human pathogens are mesophiles. Survive under temperatures of 45–80 °C.
 * Psychrophiles
 * Mesophiles
 * Thermophiles

Acidity
Optimal acidity for bacteria tends to be around pH 6.5 to 7.0 with the exception of acidophiles. Some bacteria can change the pH such as by excreting acid resulting in sub-optimal conditions.

Oxygen
Bacteria can be aerobes or anaerobes. Depending on the degree of oxygen required bacteria can fall into the following classes:

 * 1) facultative-anaerobes-ie aerotolerant absence or minimal oxygen required for their growth
 * 2) obligate-anaerobes grow only in complete absence of oxygen
 * 3) facultative aerobes-can grow either in presence or minimal oxygen
 * 4) obligate aerobes-grow only in the presence of oxygen

Micronutrients
Ample nutrients

Toxic compounds
Toxic compounds such as ethanol can hinder growth or kill bacteria. This is used beneficially for disinfection and in food preservation.

title: Bacterial growth


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Bdellovibrio

Bdellovibrio is a genus of Gram-negative, obligate aerobic bacteria. One of the more notable characteristics of this genus is that members can prey upon other Gram-negative bacteria and feed on the biopolymers, e.g. proteins and nucleic acids, of their hosts. They have two lifestyles: a host-dependent, highly mobile phase, the "attack phase", in which they form "bdelloplasts" in their host bacteria; and a slow-growing, irregularly shaped, host-independent form.

Bdellovibrio bacteriovorus
The most well studied of these is Bdellovibrio bacteriovorus, which is found almost exclusively in host dependent growth in nature. In this free swimming attack form after searching for prey using its pili, it burrows through the host outer membrane/ peptidoglycan cell wall and enters the periplasmic space. The Bdellovibrio bacterium then forms a structure called a bdelloplast. This bdelloplast is created as the host cell is modified to become spherical in shape. Inside the bdelloplast, the singular large flagellum of the predatory Bdellovibrio is lost. The host cell is then rapidly killed allowing the passage of molecules from the interior of the host cytoplasm through to the periplasm freely, and the periplasm dwelling Bdellovibrio to feed. Using some of these molecules the Bdellovibrio creates a protective environment by reinforcing the peptidoglycan cell wall of the host in which it now dwells using amidases and transpeptidases. After around 4hrs, depending on ambient temperature, the Bdellovibrio has increased in size dramatically through this nourishment. It divides to replicate and then leaves via a final lysis of the host's cell wall and membranes. The newly emerging Bdellovibrio use their newly grown powerful flagella to swim away and find the next suitable host. Because of this intermittent bdelloplast stage, and momentary parasitic phase (15-20 mins), Bdellovibrio could be considered bacterial predators or parasites.

Bdellovibrio bacteriovorus was first described by Stolp and Petzold in 1962. In 2012 another member of the Bdellovibrio species was identified "Bdellovibrio tiberius" of the River tiber. This species is more capable of host-independent growth.

Little is known of Bdellovibrio exovorus, an extra-parasitic bdellovibrio, which cannot enter its prey, and does not form Bdelloplasts.

Appearance
Under a light microscope, host-dependent Bdellovibrio appears to be a comma-shaped motile rod that is about 0.3–0.5 by 0.5–1.4 μm in size with a barely discernible flagellum. Bdellovibrio show up as a growing clear plaque in an E. coli "lawn". Notably, Bdellovibrio has a sheath that covers its flagellum – a rare feature for bacteria. Flagellar motion stops once Bdellovibrio has penetrated its prey, and the flagella is then shed.

Host-independent Bdellovibrio appear amorphous, and larger than the predatory phase.

Culture conditions
B. bacteriovorus appears to be ubiquitous in nature and manmade habitats. They have been found in soil samples, rhizosphere of plant roots, rivers, oceans, sewage, intestines and feces of birds and mammals, and even in oyster shells and the gills of crabs. B. bacteriovorus are able to thrive in almost any habitat, the general requirements are that there needs to be oxygen and some other Gram-negative bacteria present in its environment. Its optimal temperature is between 28-30 °C, making B. bacteriovorus a mesophile. Bdellovibrio is grown in the laboratory in its stationary HI (host-independent) phase at 29 °C on yeast peptone broth agar. Host-dependent (predatory) cultures are grown with a population of E. coli S-17 at 29 °C for 16 hrs. They may also be cultured using YPSC (yeast extract, peptone, sodium acetate, calcium chloride) overlays or prey lysates.

Life cycle and parasitism

Bdellovibrio cells can swim as fast as 160 μm/s, or over 100 times their body-length per second. It swims using a single sheathed polar flagellum with a characteristic dampened filament waveform. Bdellovibrio attacks other Gram-negative bacteria by attaching itself to the prey cell's outer membrane and peptidoglycan layer, after which it creates a small hole in the outer membrane. The Bdellovibrio cell then enters the host periplasmic space. It remains reversibly attached to it for a short "recognition" period.

After the recognition period, it becomes irreversibly attached via the pole opposite the flagellum. Once inside the periplasm, the Bdellovibrio cell seals the membrane hole and converts the host cell to a spherical morphology, this is due to secretion of L,D transpeptidases which breaks the peptidoglycan apart, and therefore causes the cell to become amorphous. The two-cell complex formed is called a bdelloplast. The Bdellovibrio cell uses hydrolytic enzymes to break down the host cell molecules, which it uses to grow filamentously. When the host cell nutrients are exhausted, the filament septates to form progeny Bdellovibrios. The progeny become motile before they lyse the host cell and are released into the environment. The entire life cycle takes three to four hours, and produces an average of 3–6 progeny cells from a single E. coli, or up to 90 from larger prey such as filamentous E. coli.

Targets of Bdellovibrio species, including Vibrio vulnificus, may undergo co-infection by Bdellovibrio and bacteriophage. Although the Bdellovibrio rounding of prey is thought to be evolved to reduce co-infection of multiple Bdellovibrio, larger prey that do not round may be infected by multiple Bdello's.

Genomics
The genome of Bdellovibrio bacteriovorus HD100 was sequenced in 2004. The HD100 genome is 3 782  950 nucleotides long, larger than expected given its small size.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

title: Bdellovibrio


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Talk:Bdellovibrio

''Text from a flashcard I wrote. Article already updated with info. maveric149''

Bdellovibrio

1) Inoculum source, lifestyle

2) Enrichment strategy

3) Microscopic appearance

4) Gram reaction, catabolic pathway

5) Colony appearance

6) Other special properties

1) river water or soil, intraperiplasmic

2) NB/500 (nutrient broth 1:500 dil.), hot soft agar w/ E. coli, 30ªC/week

3) comma motile rods 0.3×1.5µ, flag.

4) -, obligate aerobic O2 respiration

5) as a growing plaque in E. coli lawn

6) attack gram - bacteria, enter into periplasmic space, host dies, becomes bdelloplast,invader elongates,divides -

More Images
It would be nice to show more images on the predator-effect of Bdellovibrio.

I have found a link here but I don't own the copyright to it so I can not link it into the article - it would be nice if someone else could find a kind soul to provide such images to Wikipedia. I find it a very interesting image of how Bdellovibrio attacks another bacteria:

http://i.imgur.com/joexlad.png

2A02:8388:1601:E000:BE5F:F4FF:FECD:7CB2 (talk) 16:11, 28 November 2014 (UTC)

- The sentence starting with "They have two lifestyles" is hardly readable. Not sure what the two styles are as there are so many enumerated items. — Preceding unsigned comment added by 84.10.108.210 (talk) 08:51, 28 September 2020 (UTC)

title: Talk:Bdellovibrio


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Botulism

Botulism is a rare and potentially fatal illness caused by a toxin produced by the bacterium Clostridium botulinum. The disease begins with weakness, blurred vision, feeling tired, and trouble speaking. This may then be followed by weakness of the arms, chest muscles, and legs. Vomiting, swelling of the abdomen, and diarrhea may also occur. The disease does not usually affect consciousness or cause a fever.

Botulism can occur in several ways. The bacterial spores which cause it are common in both soil and water and are very resistant. They produce the botulinum toxin when exposed to low oxygen levels and certain temperatures. Foodborne botulism happens when food containing the toxin is eaten. Infant botulism instead happens when the bacterium develops in the intestines and releases the toxin. This typically only occurs in children less than one year old, as protective mechanisms against development of the bacterium develop after that age. Wound botulism is found most often among those who inject street drugs. In this situation, spores enter a wound, and in the absence of oxygen, release the toxin. The disease is not passed directly between people. Its diagnosis is confirmed by finding the toxin or bacteria in the person in question.

Prevention is primarily by proper food preparation. The toxin, though not the spores, is destroyed by heating it to more than 85 °C for longer than five minutes. The clostridial spores can be destroyed in the autoclave with moist heat (120°C/ 250°F for at least 15 minutes) or dry heat (160°C for 2 hours) or by irradiation. The spores of group I strains are inactivated by heating at 121°C (250°F) for 3 minutes during commercial canning. Spores of group II strains are less heat-resistant, and they are often damaged by 90°C (194°F) for 10 minutes, 85°C for 52 minutes, or 80°C for 270 minutes; however, these treatments may not be sufficient in some foods. Honey can contain the organism, and for this reason, honey should not be fed to children under 12 months. Treatment is with an antitoxin. In those who lose their ability to breathe on their own, mechanical ventilation may be necessary for months. Antibiotics may be used for wound botulism. Death occurs in 5 to 10% of people. Botulism also affects many other animals. The word is from Latin botulus, meaning 'sausage'.

Signs and symptoms
The muscle weakness of botulism characteristically starts in the muscles supplied by the cranial nerves—a group of twelve nerves that control eye movements, the facial muscles and the muscles controlling chewing and swallowing. Double vision, drooping of both eyelids, loss of facial expression and swallowing problems may therefore occur. In addition to affecting the voluntary muscles, it can also cause disruptions in the autonomic nervous system. This is experienced as a dry mouth and throat (due to decreased production of saliva), postural hypotension (decreased blood pressure on standing, with resultant lightheadedness and risk of blackouts), and eventually constipation (due to decreased forward movement of intestinal contents). Some of the toxins (B and E) also precipitate nausea, vomiting, and difficulty with talking. The weakness then spreads to the arms (starting in the shoulders and proceeding to the forearms) and legs (again from the thighs down to the feet).

Severe botulism leads to reduced movement of the muscles of respiration, and hence problems with gas exchange. This may be experienced as dyspnea (difficulty breathing), but when severe can lead to respiratory failure, due to the buildup of unexhaled carbon dioxide and its resultant depressant effect on the brain. This may lead to respiratory compromise and death if untreated.

Clinicians frequently think of the symptoms of botulism in terms of a classic triad: bulbar palsy and descending paralysis, lack of fever, and clear senses and mental status ("clear sensorium").

Infant botulism

Infant botulism (also referred to as floppy baby syndrome) was first recognized in 1976, and is the most common form of botulism in the United States. Infants are susceptible to infant botulism in the first year of life, with more than 90% of cases occurring in infants younger than six months. Infant botulism results from the ingestion of the C. botulinum spores, and subsequent colonization of the small intestine. The infant gut may be colonized when the composition of the intestinal microflora (normal flora) is insufficient to competitively inhibit the growth of C. botulinum and levels of bile acids (which normally inhibit clostridial growth) are lower than later in life.

The growth of the spores releases botulinum toxin, which is then absorbed into the bloodstream and taken throughout the body, causing paralysis by blocking the release of acetylcholine at the neuromuscular junction. Typical symptoms of infant botulism include constipation, lethargy, weakness, difficulty feeding, and an altered cry, often progressing to a complete descending flaccid paralysis. Although constipation is usually the first symptom of infant botulism, it is commonly overlooked.

Honey is a known dietary reservoir of C. botulinum spores and has been linked to infant botulism. For this reason, honey is not recommended for infants less than one year of age. Most cases of infant botulism, however, are thought to be caused by acquiring the spores from the natural environment. Clostridium botulinum is a ubiquitous soil-dwelling bacterium. Many infant botulism patients have been demonstrated to live near a construction site or an area of soil disturbance.

Infant botulism has been reported in 49 of 50 US states (all save for Rhode Island), and cases have been recognized in 26 countries on five continents.

Complications
Infant botulism has no long-term side effects.

Botulism can result in death due to respiratory failure. However, in the past 50 years, the proportion of patients with botulism who die has fallen from about 50% to 7% due to improved supportive care. A patient with severe botulism may require mechanical ventilation (breathing support through a ventilator) as well as intensive medical and nursing care, sometimes for several months. The person may require rehabilitation therapy after leaving the hospital.

Cause

Clostridium botulinum is an anaerobic, Gram-positive, spore-forming rod. Botulinum toxin is one of the most powerful known toxins: about one microgram is lethal to humans when inhaled. It acts by blocking nerve function (neuromuscular blockade) through inhibition of the excitatory neurotransmitter acetylcholine's release from the presynaptic membrane of neuromuscular junctions in the somatic nervous system. This causes paralysis. Advanced botulism can cause respiratory failure by paralysing the muscles of the chest; this can progress to respiratory arrest. Furthermore, acetylcholine release from the presynaptic membranes of muscarinic nerve synapses is blocked. This can lead to a variety of autonomic signs and symptoms described above.

In all cases, illness is caused by the botulinum toxin which the bacterium C. botulinum produces in anaerobic conditions and not by the bacterium itself. The pattern of damage occurs because the toxin affects nerves that fire (depolarize) at a higher frequency first.

Mechanisms of entry into the human body for botulinum toxin are described below.

Colonization of the gut
The most common form in Western countries is infant botulism. This occurs in infants who are colonized with the bacterium in the small intestine during the early stages of their lives. The bacterium then produces the toxin, which is absorbed into the bloodstream. The consumption of honey during the first year of life has been identified as a risk factor for infant botulism; it is a factor in a fifth of all cases. The adult form of infant botulism is termed adult intestinal toxemia, and is exceedingly rare.

Food
Toxin that is produced by the bacterium in containers of food that have been improperly preserved is the most common cause of food-borne botulism. Fish that has been pickled without the salinity or acidity of brine that contains acetic acid and high sodium levels, as well as smoked fish stored at too high a temperature, presents a risk, as does improperly canned food.

Food-borne botulism results from contaminated food in which C. botulinum spores have been allowed to germinate in low-oxygen conditions. This typically occurs in improperly prepared home-canned food substances and fermented dishes without adequate salt or acidity. Given that multiple people often consume food from the same source, it is common for more than a single person to be affected simultaneously. Symptoms usually appear 12–36 hours after eating, but can also appear within 6 hours to 10 days.

No withdrawal periods have been established for cows affected by Botulism. Lactating cows injected with various doses of Botulinum toxin C have not resulted in detectable Botulinum neurotoxin in milk produced. Using mouse bioassays and immunostick ELISA tests, botulinum toxin was detected in whole blood and serum but not in milk samples, suggesting that botulinum type C toxin does not enter milk in detectable concentrations. Cooking and pasteurization denatures botulinum toxin but does not necessarily eliminate spores. Botulinum spores or toxins can find their way into the dairy production chain from the environment. Despite the low risk of milk and meat contamination, the protocol for fatal bovine botulism cases appears to be incineration of carcasses and withholding any potentially contaminated milk from human consumption. It is also advised that raw milk from affected cows should not be consumed by humans or fed to calves.

Wound
Wound botulism results from the contamination of a wound with the bacteria, which then secrete the toxin into the bloodstream. This has become more common in intravenous drug users since the 1990s, especially people using black tar heroin and those injecting heroin into the skin rather than the veins. Wound botulism accounts for 29% of cases.

Inhalation
Isolated cases of botulism have been described after inhalation by laboratory workers.

Injection
Symptoms of botulism may occur away from the injection site of botulinum toxin. This may include loss of strength, blurred vision, change of voice, or trouble breathing which can result in death. Onset can be hours to weeks after an injection. This generally only occurs with inappropriate strengths of botulinum toxin for cosmetic use or due to the larger doses used to treat movement disorders. Following a 2008 review the FDA added these concerns as a boxed warning.

Mechanism
The toxin is the protein botulinum toxin produced under anaerobic conditions (where there is no oxygen) by the bacterium Clostridium botulinum.

Clostridium botulinum is a large anaerobic Gram-positive bacillus that forms subterminal endospores.

There are eight serological varieties of the bacterium denoted by the letters A to H. The toxin from all of these acts in the same way and produces similar symptoms: the motor nerve endings are prevented from releasing acetylcholine, causing flaccid paralysis and symptoms of blurred vision, ptosis, nausea, vomiting, diarrhea or constipation, cramps, and respiratory difficulty.

Botulinum toxin is broken into eight neurotoxins (labeled as types A, B, C [C1, C2], D, E, F, and G), which are antigenically and serologically distinct but structurally similar. Human botulism is caused mainly by types A, B, E, and (rarely) F. Types C and D cause toxicity only in other animals.

In October 2013, scientists released news of the discovery of type H, the first new botulism neurotoxin found in forty years. However, further studies showed type H to be a chimeric toxin composed of parts of types F and A (FA).

Some types produce a characteristic putrefactive smell and digest meat (types A and some of B and F); these are said to be proteolytic; type E and some types of B, C, D and F are nonproteolytic and can go undetected because there is no strong odor associated with them.

When the bacteria are under stress, they develop spores, which are inert. Their natural habitats are in the soil, in the silt that comprises the bottom sediment of streams, lakes, and coastal waters and ocean, while some types are natural inhabitants of the intestinal tracts of mammals (e.g., horses, cattle, humans), and are present in their excreta. The spores can survive in their inert form for many years.

Toxin is produced by the bacteria when environmental conditions are favourable for the spores to replicate and grow, but the gene that encodes for the toxin protein is actually carried by a virus or phage that infects the bacteria. Little is known about the natural factors that control phage infection and replication within the bacteria.

The spores require warm temperatures, a protein source, an anaerobic environment, and moisture in order to become active and produce toxin. In the wild, decomposing vegetation and invertebrates combined with warm temperatures can provide ideal conditions for the botulism bacteria to activate and produce toxin that may affect feeding birds and other animals. Spores are not killed by boiling, but botulism is uncommon because special, rarely obtained conditions are necessary for botulinum toxin production from C. botulinum spores, including an anaerobic, low-salt, low-acid, low-sugar environment at ambient temperatures.

Botulinum inhibits the release within the nervous system of acetylcholine, a neurotransmitter, responsible for communication between motor neurons and muscle cells. All forms of botulism lead to paralysis that typically starts with the muscles of the face and then spreads towards the limbs. In severe forms, botulism leads to paralysis of the breathing muscles and causes respiratory failure. In light of this life-threatening complication, all suspected cases of botulism are treated as medical emergencies, and public health officials are usually involved to identify the source and take steps to prevent further cases from occurring.

Botulinum toxin A, C, and E cleave the SNAP-25, ultimately leading to paralysis.

Diagnosis
For botulism in babies, diagnosis should be made on signs and symptoms. Confirmation of the diagnosis is made by testing of a stool or enema specimen with the mouse bioassay.

In people whose history and physical examination suggest botulism, these clues are often not enough to allow a diagnosis. Other diseases such as Guillain–Barré syndrome, stroke, and myasthenia gravis can appear similar to botulism, and special tests may be needed to exclude these other conditions. These tests may include a brain scan, cerebrospinal fluid examination, nerve conduction test (electromyography, or EMG), and an edrophonium chloride (Tensilon) test for myasthenia gravis. A definite diagnosis can be made if botulinum toxin is identified in the food, stomach or intestinal contents, vomit or feces. The toxin is occasionally found in the blood in peracute cases. Botulinum toxin can be detected by a variety of techniques, including enzyme-linked immunosorbent assays (ELISAs), electrochemiluminescent (ECL) tests and mouse inoculation or feeding trials. The toxins can be typed with neutralization tests in mice. In toxicoinfectious botulism, the organism can be cultured from tissues. On egg yolk medium, toxin-producing colonies usually display surface iridescence that extends beyond the colony.

Prevention
Although the vegetative form of the bacteria is destroyed by boiling, the spore itself is not killed by the temperatures reached with normal sea-level-pressure boiling, leaving it free to grow and again produce the toxin when conditions are right.

A recommended prevention measure for infant botulism is to avoid giving honey to infants less than 12 months of age, as botulinum spores are often present. In older children and adults the normal intestinal bacteria suppress development of C. botulinum.

While commercially canned goods are required to undergo a "botulinum cook" in a pressure cooker at 121 °C for 3 minutes, and thus rarely cause botulism, there have been notable exceptions. Two were the 1978 Alaskan salmon outbreak and the 2007 Castleberry's Food Company outbreak. Foodborne botulism is the rarest form, accounting for only around 15% of cases (US) and has more frequently resulted from home-canned foods with low acid content, such as carrot juice, asparagus, green beans, beets, and corn. However, outbreaks of botulism have resulted from more unusual sources. In July 2002, fourteen Alaskans ate muktuk (whale meat) from a beached whale, and eight of them developed symptoms of botulism, two of them requiring mechanical ventilation.

Other, much rarer sources of infection (about every decade in the US ) include garlic or herbs stored covered in oil without acidification, chili peppers, improperly handled baked potatoes wrapped in aluminum foil, tomatoes, and home-canned or fermented fish.

When canning or preserving food at home, attention should be paid to hygiene, pressure, temperature, refrigeration and storage. When making home preserves, only acidic fruit such as apples, pears, stone fruits and berries should be used. Tropical fruit and tomatoes are low in acidity and must have some acidity added before they are canned.

Low-acid foods have pH values higher than 4.6. They include red meats, seafood, poultry, milk, and all fresh vegetables except for most tomatoes. Most mixtures of low-acid and acid foods also have pH values above 4.6 unless their recipes include enough lemon juice, citric acid, or vinegar to make them acidic. Acid foods have a pH of 4.6 or lower. They include fruits, pickles, sauerkraut, jams, jellies, marmalades, and fruit butters.

Although tomatoes usually are considered an acid food, some are now known to have pH values slightly above 4.6. Figs also have pH values slightly above 4.6. Therefore, if they are to be canned as acid foods, these products must be acidified to a pH of 4.6 or lower with lemon juice or citric acid. Properly acidified tomatoes and figs are acid foods and can be safely processed in a boiling-water canner.

Oils infused with fresh garlic or herbs should be acidified and refrigerated. Potatoes which have been baked while wrapped in aluminum foil should be kept hot until served or refrigerated. Because the botulism toxin is destroyed by high temperatures, home-canned foods are best boiled for 10 minutes before eating. Metal cans containing food in which bacteria are growing may bulge outwards due to gas production from bacterial growth or the food inside may be foamy or have a bad odor; cans with any of these signs should be discarded.

Any container of food which has been heat-treated and then assumed to be airtight which shows signs of not being so, e.g., metal cans with pinprick holes from rust or mechanical damage, should be discarded. Contamination of a canned food solely with C. botulinum may not cause any visual defects to the container, such as bulging. Only assurance of sufficient thermal processing during production, and absence of a route for subsequent contamination, should be used as indicators of food safety.

The addition of nitrites and nitrates to processed meats such as ham, bacon, and sausages reduces growth and toxin production of C. botulinum.

Vaccine
Vaccines are under development, but they have disadvantages. As of 2017 work to develop a better vaccine was being carried out, but the US FDA had not approved any vaccine against botulism.

Treatment
Botulism is generally treated with botulism antitoxin and supportive care.

Supportive care for botulism includes monitoring of respiratory function. Respiratory failure due to paralysis may require mechanical ventilation for 2 to 8 weeks, plus intensive medical and nursing care. After this time, paralysis generally improves as new neuromuscular connections are formed.

In some abdominal cases, physicians may try to remove contaminated food still in the digestive tract by inducing vomiting or using enemas. Wounds should be treated, usually surgically, to remove the source of the toxin-producing bacteria.

Antitoxin
Botulinum antitoxin consists of antibodies that neutralize botulinum toxin in the circulatory system by passive immunization. This prevents additional toxin from binding to the neuromuscular junction, but does not reverse any already inflicted paralysis.

In adults, a trivalent antitoxin containing antibodies raised against botulinum toxin types A, B, and E is used most commonly; however, a heptavalent botulism antitoxin has also been developed and was approved by the U.S. FDA in 2013. In infants, horse-derived antitoxin is sometimes avoided for fear of infants developing serum sickness or lasting hypersensitivity to horse-derived proteins. To avoid this, a human-derived antitoxin has been developed and approved by the U.S. FDA in 2003 for the treatment of infant botulism. This human-derived antitoxin has been shown to be both safe and effective for the treatment of infant botulism. However, the danger of equine-derived antitoxin to infants has not been clearly established, and one study showed the equine-derived antitoxin to be both safe and effective for the treatment of infant botulism.

Trivalent (A,B,E) botulinum antitoxin is derived from equine sources utilizing whole antibodies (Fab and Fc portions). In the United States, this antitoxin is available from the local health department via the CDC. The second antitoxin, heptavalent (A,B,C,D,E,F,G) botulinum antitoxin, is derived from "despeciated" equine IgG antibodies which have had the Fc portion cleaved off leaving the F(ab')2 portions. This less immunogenic antitoxin is effective against all known strains of botulism where not contraindicated.

Prognosis
The paralysis caused by botulism can persist for two to eight weeks, during which supportive care and ventilation may be necessary to keep the patient alive. Botulism can be fatal in five to ten percent of people who are affected. However, if left untreated, botulism is fatal in 40 to 50 percent of cases.

Infant botulism typically has no long-term side effects but can be complicated by treatment-associated adverse events. The case fatality rate is less than two percent for hospitalized babies.

Epidemiology
Globally, botulism is fairly rare, with approximately 1,000 identified cases yearly.

United States
In the United States an average of 145 cases are reported each year. Of these, roughly 65% are infant botulism, 20% are wound botulism, and 15% are foodborne. Infant botulism is predominantly sporadic and not associated with epidemics, but great geographic variability exists. From 1974 to 1996, for example, 47% of all infant botulism cases reported in the U.S. occurred in California.

Between 1990 and 2000, the Centers for Disease Control and Prevention reported 263 individual foodborne cases from 160 botulism events in the United States with a case-fatality rate of 4%. Thirty-nine percent (103 cases and 58 events) occurred in Alaska, all of which were attributable to traditional Alaskan aboriginal foods. In the lower 49 states, home-canned food was implicated in 70 events (~69%) with canned asparagus being the most frequent cause. Two restaurant-associated outbreaks affected 25 people. The median number of cases per year was 23 (range 17–43), the median number of events per year was 14 (range 9–24). The highest incidence rates occurred in Alaska, Idaho, Washington, and Oregon. All other states had an incidence rate of 1 case per ten million people or less.

The number of cases of food borne and infant botulism has changed little in recent years, but wound botulism has increased because of the use of black tar heroin, especially in California.

All data regarding botulism antitoxin releases and laboratory confirmation of cases in the US are recorded annually by the Centers for Disease Control and Prevention and published on their website.
 * On 2 July 1971, the U.S. Food and Drug Administration (FDA) released a public warning after learning that a New York man had died and his wife had become seriously ill due to botulism after eating a can of Bon Vivant vichyssoise soup.
 * Between 31 March and 6 April 1977, 59 individuals developed type B botulism. All who fell ill had eaten at the same Mexican restaurant in Pontiac, Michigan, and had consumed a hot sauce made with improperly home-canned jalapeño peppers, either by adding it to their food, or by eating nachos that had been prepared with the hot sauce. The full clinical spectrum (mild symptomatology with neurologic findings through life-threatening ventilatory paralysis) of type B botulism was documented.
 * In April 1994, the largest outbreak of botulism in the United States since 1978 occurred in El Paso, Texas. Thirty people were affected; 4 required mechanical ventilation. All ate food from a Greek restaurant. The attack rate among people who ate a potato-based dip was 86% (19/22) compared with 6% (11/176) among people who did not eat the dip (relative risk [RR] = 13.8; 95% confidence interval [CI], 7.6–25.1). The attack rate among people who ate an eggplant-based dip was 67% (6/9) compared with 13% (24/189) among people who did not (RR = 5.2; 95% CI, 2.9–9.5). Botulism toxin type A was detected in patients and in both dips. Toxin formation resulted from holding aluminum foil-wrapped baked potatoes at room temperature, apparently for several days, before they were used in the dips. Food handlers should be informed of the potential hazards caused by holding foil-wrapped potatoes at ambient temperatures after cooking.
 * In 2002, fourteen Alaskans ate muktuk (whale blubber) from a beached whale, resulting in eight of them developing botulism, with two of the affected requiring mechanical ventilation.
 * Beginning in late June 2007, 8 people contracted botulism poisoning by eating canned food products produced by Castleberry's Food Company in its Augusta, Georgia plant. It was later identified that the Castleberry's plant had serious production problems on a specific line of retorts that had under-processed the cans of food. These issues included broken cooking alarms, leaking water valves and inaccurate temperature devices, all the result of poor management of the company. All of the victims were hospitalized and placed on mechanical ventilation. The Castleberry's Food Company outbreak was the first instance of botulism in commercial canned foods in the United States in over 30 years.
 * One person died, 21 cases were confirmed, and 10 more were suspected in Lancaster, Ohio when a botulism outbreak occurred after a church potluck in April 2015. The suspected source was a salad made from home-canned potatoes.
 * A botulism outbreak occurred in Northern California in May 2017 after 10 people consumed nacho cheese dip served at a gas station in Sacramento County. One man died as a result of the outbreak.

United Kingdom
The largest recorded outbreak of foodborne botulism in the United Kingdom occurred in June 1989. A total of 27 patients were affected; one patient died. Twenty-five of the patients had eaten one brand of hazelnut yogurt in the week before the onset of symptoms. Control measures included the cessation of all yogurt production by the implicated producer, the withdrawal of the firm's yogurts from sale, the recall of cans of the hazelnut conserve, and advice to the general public to avoid the consumption of all hazelnut yogurts.

China
From 1958 to 1983 there were 986 outbreaks of botulism in China involving 4,377 people with 548 deaths.

Qapqal disease
After the Chinese Communist Revolution in 1949, a mysterious plague (named Qapqal disease) was noticed to be affecting several Sibe villages in Qapqal Xibe Autonomous County. It was endemic with distinctive epidemic patterns, yet the underlying cause remained unknown for a long period of time. It caused a number of deaths and forced some people to leave the place.

In 1958, a team of experts were sent to the area by the Ministry of Health to investigate the cases. The epidemic survey conducted proved that the disease was primarily type A botulism, with several cases of type B. The team also discovered that the source of the botulinum was local fermented grain and beans, as well as a raw meat food called mi song hu hu. They promoted the improvement of fermentation techniques among local residents, and thus eliminated the disease.

Canada
From 1985 to 2005 there were outbreaks causing 91 confirmed cases of foodborne botulism in Canada, 85% of which were in Inuit communities, especially Nunavik, as well as First Nations of the coast of British Columbia, following consumption of traditionally prepared marine mammal and fish products.

Ukraine
In 2017, there were 70 cases of botulism with 8 deaths in Ukraine. The previous year there were 115 cases with 12 deaths. Most cases were the result of dried fish, a common local drinking snack.

Vietnam
In 2020, several cases of botulism were reported in Vietnam. All of them were related to a product containing contaminated vegetarian pâté. Some patients were put on life support.

Other susceptible species
Botulism can occur in many vertebrates and invertebrates. Botulism has been reported in such species as rats, mice, chicken, frogs, toads, goldfish, aplysia, squid, crayfish, drosophila and leeches.

Death from botulism is common in waterfowl; an estimated 10,000 to 100,000 birds die of botulism annually. The disease is commonly called "limberneck". In some large outbreaks, a million or more birds may die. Ducks appear to be affected most often. An enzootic form of duck botulism in the Western US and Canada is known as "western duck sickness". Botulism also affects commercially raised poultry. In chickens, the mortality rate varies from a few birds to 40% of the flock.

Botulism seems to be relatively uncommon in domestic mammals; however, in some parts of the world, epidemics with up to 65% mortality are seen in cattle. The prognosis is poor in large animals that are recumbent.

In cattle, the symptoms may include drooling, restlessness, incoordination, urine retention, dysphagia, and sternal recumbency. Laterally recumbent animals are usually very close to death. In sheep, the symptoms may include drooling, a serous nasal discharge, stiffness, and incoordination. Abdominal respiration may be observed and the tail may switch on the side. As the disease progresses, the limbs may become paralyzed and death may occur. Phosphorus-deficient cattle, especially in southern Africa, are inclined to ingest bones and carrion containing clostridial toxins and consequently develop lame sickness or lamsiekte.

The clinical signs in horses are similar to cattle. The muscle paralysis is progressive; it usually begins at the hindquarters and gradually moves to the front limbs, neck, and head. Death generally occurs 24 to 72 hours after initial symptoms and results from respiratory paralysis. Some foals are found dead without other clinical signs.

Clostridium botulinum type C toxin has been incriminated as the cause of grass sickness, a condition in horses which occurs in rainy and hot summers in Northern Europe. The main symptom is pharynx paralysis.

Domestic dogs may develop systemic toxemia after consuming C. botulinum type C exotoxin or spores within bird carcasses or other infected meat but are generally resistant to the more severe effects of C. botulinum type C. Symptoms include flaccid muscle paralysis, which can lead to death due to cardiac and respiratory arrest.

Pigs are relatively resistant to botulism. Reported symptoms include anorexia, refusal to drink, vomiting, pupillary dilation, and muscle paralysis.

In poultry and wild birds, flaccid paralysis is usually seen in the legs, wings, neck and eyelids. Broiler chickens with the toxicoinfectious form may also have diarrhea with excess urates.

Prevention in non-human species
One of the main routes of exposure for botulism is through the consumption of food contaminated with C. botulinum. Food-borne botulism can be prevented in domestic animals through careful inspection of the feed, purchasing high quality feed from reliable sources, and ensuring proper storage. Poultry litter and animal carcasses are places in which C. botulinum spores are able to germinate so it is advised to avoid spreading poultry litter or any carcass containing materials on fields producing feed materials due to their potential for supporting C. botulinum growth. Additionally, water sources should be checked for dead or dying animals, and fields should be checked for animal remains prior to mowing for hay or silage. Correcting any dietary deficiencies can also prevent animals from consuming contaminated materials such as bones or carcasses. Raw materials used for silage or feed mixed on site should be checked for any sign of mold or rotten appearance. Acidification of animal feed can reduce, but will not eliminate, the risk of toxin formation, especially in carcasses that remain whole.

Vaccines in animals
Vaccines have been developed for use in animals to prevent botulism. The availability and approval of these vaccines varies depending on the location, with places experiencing more cases generally having more vaccines available and routine vaccination is more common.

A variety of vaccines have been developed for the prevention of botulism in livestock. Most initial vaccinations require multiple doses at intervals from 2–6 weeks, however, some newer vaccines require only one shot. This mainly depends on the type of vaccine and manufacturers recommendations. All vaccines require annual boosters to maintain immunity. Many of these vaccines can be used on multiple species including cattle, sheep, and goats with some labeled for use in horses and mules as well as separate vaccines for mink. Additionally, vaccination during an outbreak is as beneficial as therapeutic treatment in cattle, and this method is also used in horses and pheasants.

The use of region specific toxoids to immunize animals has been shown to be effective. Toxoid types C and D used to immunize cattle is a useful vaccination method in South Africa and Australia. Toxoid has also been shown to be an appropriate method of immunizing minks and pheasants. In endemic areas, for example Kentucky, vaccination with type B toxoid appears to be effective.

United States
Based on CIA research in Fort Detrick on biological warfare, anthrax and botulism were widely regarded as the two most effective options. During the 1950s, a highly lethal strain was discovered during the biological warfare program. The CIA continued to hold 5 grams of Clostridium botulinum, even after Nixon's ban on biological warfare in 1969. During the Gulf War, when the United States were concerned with a potential biowarfare attack, the efforts around botulism turned to prevention. However, the only way to make antitoxin in America until the 1990s was by drawing antibodies from a single horse named First Flight, raising much concern from Pentagon health officials.

Iraq
Iraq has historically possessed many types of germs, including botulism. The American Type Culture Collection sold 5 variants of botulinum to the University of Baghdad in May 1986. 1991 CIA reports also show Iraqis filled shells, warheads, and bombs with biological agents like botulinum (though none have been deployed). The Iraqi air force used the code name "tea" to refer to botulinum, and it was also referred to as bioweapon "A."

Japan
A Japanese cult called Aum Shinrikyo created laboratories that produced biological weapons, specifically botulinum, anthrax, and Q fever. From 1990 to 1995, the cult staged numerous unsuccessful bioterrorism attacks on civilians. They sprayed botulinum toxin from a truck in downtown Tokyo and in the Narita airport, but there are no reported cases of botulism as a result.

title: Botulism


text:
Talk:Botulism

Talk:Botulism/Archive

History
Historical note about 1919-25 prominent outbreaks: 10.7326/M17-2853 JFW | T@lk  08:28, 17 April 2018 (UTC)

Infant botulism
I think somewhere in the infant botulism section we should add something about C. Botulinum spores can only affect infants because their immune systems aren’t strong enough where as older kids and adults immune systems are strong enough to kill the C. Botulinum spores Pakrs123 (talk) 00:02, 20 November 2018 (UTC)

Botulism in prehistory?
Should this article mention about botulism occurring in prehistoric times as well? Episode 6 of Planet Dinosaur showed a group of 'Zunityrannus' had died from eating a carcass of one of their own that had been contaminated by botulism. And is it mentioned here for that matter that the botulism bacteria thrives in rotting flesh? Visokor (talk) 11:30, 17 May 2019 (UTC)

 * There should definitely be a history section. I came here expecting to find one and was surprised not to find it. 68.50.42.62 (talk) 01:24, 23 October 2023 (UTC)

Prescribing information
This is dictated in part by the FDA so yes of course they are all the same. We paraphrase rather than quote. We do not need to list the page number in the text. They can go in the reference. You own search of fis is not a source. Doc James (talk · contribs · email) 06:53, 6 December 2019 (UTC)

Thoughts on this text?
"The public can research botulism and adverse events related to botulinum toxin injectables that were reported to the FDA (Food and Drug Administration) at no charge by accessing the FAERS database. As of October 2019, the query executed as "botulinum toxin" in the FDA Adverse Event Reporting System (FAERS) database generated 50,000 adverse reports; some included botulism and death."

Added 4 times now? Doc James (talk · contribs · email) 20:12, 6 December 2019 (UTC)
 * have reverted, agree with above editor --Ozzie10aaaa (talk) 22:12, 6 December 2019 (UTC)

Why would you want to deprive wiki users to access of the records of reported iatrogenic botulism cases? Please explain who is helped by withholding this knowledge? Skye Bravo (talk) 02:51, 8 December 2019 (UTC)Skye Bravo
 * We do not generally link to searches. Doc James  (talk · contribs · email) 01:24, 9 December 2019 (UTC)

Where/how do you suggest the existence of the FDA searchable database be placed in the botulism article so that curious people who want to researh botulism through the FDA FAERS system can at least know it exists. They can run their own search results. Skye Bravo (talk) 02:30, 29 December 2019 (UTC)

Iatrogenic botulism
Source says

"Iatrogenic botulism. Iatrogenic botulism is caused by injection of botulinum toxin for cosmetic or therapeutic purposes. Doses recommended for cosmetic treatment are too low to cause systemic disease. Higher doses injected for treatment of muscle movement disorders have caused anecdotal cases of systemic botulism-like symptoms [34]. Injection of unlicensed, highly concentrated botulinum toxin caused severe botulism in 4 patients who received it for cosmetic purposes (unpublished data)"

as for the (unpublished data) sentence, we can cite that with these two papers: Daniel S. Chertow, MD was the lead author on the paper covering the Florida tragedy. It is available as a free PDF, which is nice access for wikipedia users who want to research the citations. Chertow is from the NIH. Chertow, D. S., Tan, E. T., Maslanka, S. E., Schulte, J., Bresnitz, E. A., Weisman, R. S., ... & Sobel, J. (2006). Botulism in 4 adults following cosmetic injections with an unlicensed, highly concentrated botulinum preparation. Jama, 296(20), 2476-2479. https://scholar.google.com/scholar?hl=en&as_sdt=0%2C5&q=Botulism+in+4+adults+following+cosmetic+injections+with+an+unlicensed%2C+highly+concentrated+botulinum+preparation&btnG=

Here is another paper on one of the four patients in Florida who got botulism from lab grade botulinum toxin. A horrific narrative, but very creative and effective...because the writing format alternates between the physician and the patient. Marcus, Steven M. "Screams from a Glass Coffin." In Medical Toxicology: Antidotes and Anecdotes, pp. 57-69. Springer, Cham, 2017. Skye Bravo (talk) 04:26, 9 December 2019 (UTC) Skye Bravo (talk) 04:26, 9 December 2019 (UTC)

Doc James (talk · contribs · email) 01:06, 8 December 2019 (UTC)

This is NOT an accurate assumption: "Doses recommended for cosmetic treatment are too low to cause systemic disease" 13 Neurologists at the NIH, including Dr. Mark Hallett, diagnosed a 50 units dose of Botox Cosmetic as the source of iatrogenic botulism, based on a patient interview in person and a chart review. Unpublished data, but documented on NIH letterhead. Skye Bravo (talk) 02:49, 8 December 2019 (UTC)Skye Bravo
 * We generally go by what sources says. Doc James  (talk · contribs · email) 01:25, 9 December 2019 (UTC)

Please review this article: Bai, Lili, Xiaobo Peng, Yanqing Liu, Yawei Sun, Xin Wang, Xingwang Wang, Guodong Lin et al. "Clinical analysis of 269 botulism cases caused by cosmetic injection of botulinum neurotoxin." Toxicon 158 (2019): S15. Skye Bravo (talk) 04:15, 9 December 2019 (UTC)

Also, the prescribing information specifically mentions "botulism" on page 47.
 * //media.allergan.com/actavis/actavis/media/allergan-pdf-documents/product-prescribing/20190620-BOTOX-100-and-200-Units-v3-0USPI1145-v2-0MG1145.pdf

Skye Bravo (talk) 02:49, 8 December 2019 (UTC)Skye Bravo

the terminology "anecdotal cases" sounds as if it is folklore, yet there are many cases documented in the literature. One that comes to mind is Dr. You's case in New Jersey in 2016. The patient was injected with 80 Units of Botox to aid in swallowing, she experienced severe botulism THE SAME DAY, which is shocking. The CDC provided antitoxin to her yet she remained in ICU for months and later died. Her lab tests later confirmed she had botulism, mouse or mass spec they did not indicate which one. This was an off-label use, but it does show how low doses can cause systemic botulism. Article: "Rapidly Progressive Muscle Paralysis and Acute Respiratory Failure Following Endoscopic Botulinum Toxin Injection" Geoffrey You,MD. Skye Bravo (talk) 02:49, 8 December 2019 (UTC)Skye Bravo
 * Since it seems from what you write that there are lots of reported cases, aren't there any review that covers a significant set of these cases? Even if they are not clinical trials (which is difficult for adverse effects), a review would at least provide a "bigger picture" view on the matter. --Signimu (talk) 23:20, 8 December 2019 (UTC)
 * See WP:MEDRS
 * This case report is NOT about cosmetic use Doc James  (talk · contribs · email) 01:26, 9 December 2019 (UTC)

A dose under 100 units is generally considered a "low dose" and a cosmetic dose, though the FDA approval is for 20 units. Skye Bravo (talk) 04:05, 9 December 2019 (UTC)

 * We simple go by what high quality references say. Doc James  (talk · contribs · email) 21:43, 9 December 2019 (UTC)

Would the FDA communication be considered a high quality reference? To quote: "FDA has received reports of systemic adverse reactions including respiratory compromise and death following the use of botulinum toxins types A and B for both FDA-approved and unapproved uses. The reactions reported are suggestive of botulism, which occurs when botulinum toxin spreads in the body beyond the site where it was injected. The most serious cases had outcomes that included hospitalization and death,..... These serious systemic adverse reactions occurred following treatment of a variety of conditions using a wide range of botulinum toxin doses." Skye Bravo (talk) 02:22, 29 December 2019 (UTC)

Other countries are more open about COSMETIC BoNT injections causing iatrogenic botulism, so perhaps it would be useful to the global audience to include those perspectives? Skye Bravo (talk) 02:25, 29 December 2019 (UTC) Example below:

Toxicon Journal: ••••••••••••••••••••••• CLINICAL ANALYSIS OF 269 BOTULISM CASES CAUSED BY COSMETIC INJECTION OF BOTULINUM NEUROTOXIN Lili Bai, Xiaobo Peng, Yanqing Liu, Yawei Sun, Xin Wang, Xingwang Wang, Guodong Lin, Shufang Feng, Peng Zhang, Kun Wan, Zewu Qiu*. Department of Poisoning Treatment, Afliated Hospital, Academy of Military Medical Science, Poisoning Treatment Center of the Army, Beijing, China *

Abstract Objective: This study was conducted to analyze the clinical characteristics and treatment methods of botulism among patients receiving cosmetic injection of BoNT. Methods: A total of 269 botulism patients due to cosmetic injection of BoNT were enrolled in our study. Botulism diagnosis was according to cosmetic BoNT use history, clinical symptoms, and auxiliary examinations. All the patients received comprehensive and antitoxin treatments. Chisquare test was applied to estimate the association between injection dose of BoNT and severity of botulism.

Results: The clinical symptoms of botulism occurred within 0-36 days after BoNT injection, especially on the 2nd to 6th days. 78 cases (29%) presented mild botulism, 110 patients (41%) presented moderate botulism, and the remaining 81 cases (30%) developed severe botulism.

Furthermore, the injection dose of BoNT was positively correlated with severity of botulism (P ¼ 0.001). Patients with more than 200 U BoNT injection were more likely to undergo severe botulism. The botulism symptoms of the cases relieved or disappeared when discharged. Conclusion: The injection dosage of BoNT should be strictly controlled to minimize the occurrence of botulism. Once botulism occurs, timely and appropriate treatments are critical to improve the outcomes of the cases.Skye Bravo (talk) 02:25, 29 December 2019 (UTC)

Veterinary
I consulted this article to find out about botulism in animals, but it contains no information as yet.Ttocserp 14:59, 29 October 2022 (UTC)

Another "famous" incident
In the book "Uboat Far from Home", which is the story of U862, the WWII Uboat that travelled all the way to Australia, he reports in great detail that the crew got very sick after leaving Singapore (I think it was Singapore). Where they had taken on food. It turned out that the mushrooms and the meat had not been properly canned. From the description of the crew sickness, it was almost certainly botulism and not salmonella. 2001:8003:E40F:9601:25B8:DB70:9795:ACE0 (talk) 09:36, 2 December 2023 (UTC)

Why do they call it Botulism.
It said it come from botulus which means sausage. How did it get its name? Is it how the sympstoms tend to look like a sausage? 174.135.36.220 (talk) 05:45, 17 April 2024 (UTC)

title: Talk:Botulism


text:
Talk:Ain't I a Woman? (book)

Naming Conventions
On the bell hooks discussion page, it has been argued that despite her wish for her name to remain in all lowercase letters, when either part of her name is used at the beginning of a sentence it should be capitalised as per standard written english conventions.

Are people happy for her name to be capitalised on this page as well (in these specific instances), so that both are in accordance with one-another?

Leftblank 16:31, 26 April 2007 (UTC)

Source?
Could we have a source for this text? --Robert Merkel

 * I Googled for the first sentence; one web source cites it as
 * (a speech recorded by Frances D. Gage, Chair Presiding of the woman's convention at Akron, Ohio, 1851)

The above comment and response deal with the speech "Ain't I a Woman" by Sojourner Truth. That article is found here. If someone knows how to shift it to that article's Talk page, I'm sure that would be preferrable. -Acjelen 22:06, 25 May 2005 (UTC)

Misogynist
User:170.140.231.224 ("Mysoginist?!? Are you kidding? It irks me how quick Wikipedia writers are to make up crap and write it as fact. And please differentiate between bell hooks' beliefs and objective reality."), I'm surprise you're complaining about a long term trend in wikipedia that you've noticed, concidering you're an anonymous user. If you're going to stay a while, create a username, sign in, its fun. I am the one who supposedly made "up crap" and "wrote it as fact." hooks believes that black nationalism was largely misogynist, there is no reason to remove that from the article (also, I'm not sure if that conflicts with "objective reality" at all). While I'm assuming you haven't read hooks' book, you still could have added, "Since, [hook argues], black nationalism..." and otherwise modified the article to specify hooks beliefs. Hyacinth 19:00, 8 Apr 2004 (UTC) ---

Clarify
User:MrJones, could you clarify what you wish clarified?
 * "bell hooks argued that black nationalism was largely a patriarchical and misogynist movement and thus that it sought to overcome racial divisions by strengthening sexist ones, that it readily latched onto the idea of the emasculating black matriarch proposed by Daniel Patrick Moynihan which is repeatedly criticised by hooks. "

It did say:

 * "bell hooks argued that because black nationalism was largely a patriarchical and misogynist movement that sought to overcome racial divisions by strengthening sexist ones, it readily latched onto the idea of the emasculating black matriarch proposed by Daniel Patrick Moynihan and repeatedly criticised by hooks

What was criticised repeatedly? The "patriarchical and misogynist movement" or the "emasculating black matriarch"? Mr. Jones 18:03, 12 Aug 2004 (UTC)

Actually, it is the fiction of the emasculating black matriarch that hooks repeatedly criticizes. I changed to: "bell hooks argued that black nationalism was largely a patriarchical and misogynist movement and thus that it sought to overcome racial divisions by strengthening sexist ones, that it readily latched onto the idea of the emasculating black matriarch proposed by Daniel Patrick Moynihan whose theories are repeatedly criticised by hooks." Hows that? Hyacinth 18:21, 12 Aug 2004 (UTC)
 * Much better. Thanks :-) Mr. Jones 05:13, 13 Aug 2004 (UTC)

Regarding WP:NBOOK
Mikeblas has questioned the notability of this page's topic. Hoping to satisfy #4 of WP:NBOOK, here are examples of online syllabi that require or recommend Ain't I a Woman? using a very lazy google search: Cheers, EvergreenFir (talk) 03:39, 26 March 2014 (UTC)
 * http://www.umass.edu/wost/syllabi/spring03/wost394h.htm
 * http://www.umass.edu/wost/syllabi/fall2012/301-gust.pdf
 * http://faculty.virginia.edu/alexy/courses/summer2012/gender/syllabus/index.html
 * http://blog.lib.umn.edu/puot0002/gwss4402/HistoryWesternFeminismssyllabus.doc
 * http://webbox.lafayette.edu/~alexya/courses/2011/spring/gender/syllabus/index.html
 * www.kennesaw.edu/upcc/year_06_07/proposals/feb_2.22.07/GWST 3020 syllabus.doc
 * http://nmu.ac.in/Portals/56/Syllabi/II%20Semester.pdf
 * http://www.ethnicstudies.ucsd.edu/_files/syllabi/FA09-ETHN-289-Mendes.pdf
 * https://www.msu.edu/~aaas/aaas300/dox/AAAS%20300%20Syllabus.pdf
 * http://www2.ivcc.edu/jbeyer/PHL%201001/course%20info%20PHL%201001.htm
 * http://ssms.socialsciences.uottawa.ca/vfs/.horde/offre_cours/syllabus/00068714715_MDG5196A.pdf
 * https://www.kcl.ac.uk/artshums/depts/philosophy/modules/syllabus2013/6AANB039modulesyllabus2013-14.pdf
 * https://www.amherst.edu/media/view/225455/original/Syllabus+-+WAGS+11+Cross-Cultural+Construction+of+Gender.pdf
 * www.csus.edu/indiv/m/mosupyoeb/files/COURSE SYLLABUS INTRODUCTION TO WOMEN.doc
 * Great! now all you have to do is integrate them into the article. -- Mikeblas (talk) 07:15, 26 March 2014 (UTC)
 * Lol how am I supposed to do that? All I can think of is say "This book is often used college courses, especially in women's studies, Black studies, and philosophy" and put all of these in the reference... That sound acceptable Mikeblas? EvergreenFir (talk) 18:42, 26 March 2014 (UTC)

Original research
I've added the original research tag to the article. Wikpedia's policies state: "All analyses and interpretive or synthetic claims about primary sources must be referenced to a secondary or tertiary source, and must not be an original analysis of the primary-source material by Wikipedia editors. (WP:PRIMARY)" Any help finding reliable, secondary sources that comment on this book would be appreciated. —Sangdeboeuf (talk) 18:15, 13 May 2017 (UTC)

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title: Talk:Ain't I a Woman? (book)


text:
Witan

The witan (lit. 'wise men') was the king's council in the Anglo-Saxon government of England from before the 7th century until the 11th century. It comprised important noblemen, including ealdormen, thegns, and bishops. Meetings of the witan were sometimes called the witenagemot.

Its primary function was to advise the king on legislation, judicial cases, land transfers, and other matters of national importance. The witan may have elected new kings from among members of the ruling dynasty. After the Norman Conquest in 1066, these roles were performed by a similar council known as the curia regis.

The witan is considered an ancestor of the Parliament of England. Before the 20th century, historians thought it had been a proto-parliament, an institution that was both democratic and representative. In the 20th century, historians shifted to emphasise the witan's ad hoc and essentially royal nature.

Etymology
The Old English word witan (lit. 'wise men') described the counsellors of Anglo-Saxon kings. At the same time, the word could also refer to other kinds of counsellors, such as the witan of a shire court. Wulfstan II, Archbishop of York (1002–1023), wrote in his Institutes of Polity that "it is incumbent on bishops, that venerable 'witan' always travel with them, and dwell with them, at least of the priesthood; that they may consult with them... and who may be their counsellors at every time." A contemporary account of a dispute over an estate in Middlesex in the 950s refers to a decision of the Myrcna witan (Mercian witan).

The most common Old English term for a meeting of the witan is gemot, sometimes expanded as micel gemot (great assembly). Writers of Latin texts used conventus or magnum sapientium conventus (lit. 'great assembly of wise men'). Modern scholars use witenagemot (assembly of counsellors) as a technical term, but historian John Maddicott noted its rarity in the 11th century with only nine pre-Conquest examples, mainly in the crisis of 1051–1052. Patrick Wormald was also cautious, describing it as "a word always rare and unattested before 1035".

Origins
The origins of the witan lie in the practice of Germanic kings seeking the advice of their great men. This practice survived within the many Anglo-Saxon kingdoms established after the end of Roman rule in Britain. Maddicott writes that these early "royal assemblies lacked the institutional qualities of regularity, formality of structure, and a distinctive agenda" seen in later assemblies. They were also distinctly local. The first recorded act of a witenagemot was the law code of King Æthelberht of Kent c. 600, the earliest document which survives in sustained Old English prose.

Before the 9th century, only church councils, such as the Council of Hertford in 672, transcended the boundaries of individual kingdoms. With the unification of England in the 10th century, the witan acquired a national scope for the first time.

Attendance and locations
According to historian Bryce Lyon, the witan "was an amoebic sort of organization with no definite composition or function". It does appear, however, that an indispensable requirement was the presence of leading secular and ecclesiastical magnates. Kings issued royal charters at meetings of the witan, and the witness lists to these charters also served as attendance lists. About 2,000 charters and 40 law codes attest to the workings of around 300 recorded witan meetings. Typically, scribes listed witnesses in hierarchical order, with the king listed first, followed by:
 * the queen
 * æthelings (princes)
 * bishops
 * abbots
 * ealdormen (later earls)
 * thegns

When English kings claimed overlordship over their Welsh neighbors, the Welsh kings might also be in attendance.

Anglo-Saxon England lacked a fixed capital, and the royal court was itinerant. The witan convened at various locations, including royal palaces, towns, and hunting lodges. Between 900 and 1066, over 50 locations were recorded. London and Winchester were popular meeting places, and other locations included: Abingdon, Amesbury, Andover, Aylesford, Cookham, Dorchester, Faversham, King's Enham, Southampton, Wantage, Oxford, Kirtlington, and Woodstock. In the West Country, meetings were held at Gloucester, Axminster, Bath, Calne, Cheddar, Chippenham, Cirencester, Edington, Malmesbury, Winchcombe, and Exeter. While meetings in the North were rare, the witan did convene at Nottingham in 934 and at Lincoln in 1045. The witan could meet at any time, but it often gathered during Christmas, Lent, and Easter when many nobles were present at court.

Role
The witan played a significant role in legislation. The king and his advisers would draft laws and then seek the witan's consultation and consent. As Lyon points out, this process was a testament to the king's belief in gathering opinions from all parts of the kingdom, which "produced a wider sampling of opinion and gave the law more solid support". The witan took part in both secular and ecclesiastical legislation. Church law, however, was drafted by the clergy, with lay nobles merely giving consent.

The witan's influence was not limited to legislation. The king sought its advice and consent for extraordinary taxation that would burden the nobility, such as the Danegeld.The witan deliberated on matters of war, peace, and treaties. The declaration of royal wills occurred at witan meetings.

Kings issued charters granting bookland at witan meetings. The witness lists attached to these charters proved that the witan consented to the grants. This practice originated from the late Roman law, which required witnesses for private transactions. Historian Levi Roach explains that the "adoption of this method of authentication for early English diplomas is understandable: in the absence of direct bureaucratic continuity with the late Roman Empire, which effectively precluded sealing or notarial subscription, as practised elsewhere, the use of witnesses, mirroring the methods of authentication used for private transactions on the continent, was an elegant solution."

Electing and deposing kings
The witan was noted by contemporary sources as having the singular power to ceosan to cynige, to choose the king from amongst the extended royal family. Nevertheless, at least until the 11th century, royal succession generally followed the "ordinary system of primogeniture". The historian Chadwick interpreted these facts as proof that the so-called election of the king by the witan merely amounted to formal recognition of the deceased king's natural successor. But Liebermann was generally less willing than Chadwick to see the witan's significance as buried under the weight of the royal prerogative:

"The influence of the king, or at least of kingship, on the constitution of the assembly seems, therefore, to have been immense. But on the other hand he (the king) was elected by the witan... He could not depose the prelates or ealdormen, who held their office for life, nor indeed the hereditary thanes... At any rate, the king had to get on with the highest statesmen appointed by his predecessor, though possibly disliked by him, until death made a post vacant that he could fill with a relation or a favourite, not, however, without having a certain regard to the wishes of the aristocracy."

Liebermann's more subtle position seems to be vindicated by testimony from abbot Ælfric of Eynsham, the leading homilist of the late tenth century, who wrote:

"No man can make himself king, but the people has the choice to choose as king whom they please; but after he is consecrated as king, he then has dominion over the people, and they cannot shake his yoke off their necks."

In addition to having a role in the election of kings, it is often held that the witenagemots had the power to depose an unpopular king. However, there are only two occasions when this probably happened, in 757 and 774 with the depositions of kings Sigeberht of Wessex and Alhred of Northumbria respectively.

The witan's powers are illustrated by the following event. In the year 1013 King Æthelred II (Æthelred the Unready) fled the country from Sweyn Forkbeard, who then had the witan proclaim him king. Within a few weeks, however, Sweyn died and Æthelred was called back to England by the witan. According to the Anglo-Saxon Chronicle, the witan would only receive him back under the condition that he promise to rule better than he had. Æthelred did so, and was reinstated as King of England. His nickname of the 'Unræd' or 'Unready' means ill-advised, indicating that contemporaries regarded those who sat in the witan as part responsible for the failure of his reign.

Norman Conquest
After the Norman Conquest in 1066, William I replaced the witan with the curia regis (Latin for king's court). In a sign of the witan's enduring legacy, the curia regis continued to be dubbed a witan by chroniclers until as late as the 12th century. Maddicott writes that the witan (what he terms "royal assemblies") were "the direct forebears of the councils of post-Conquest England and the parliaments which were the councils' descendants".

Historiography
The "Saxon myth" claimed that the old Saxon witan was the representative assembly of English landholders until disbanded by the Norman invaders and that it reemerged as the Parliament of England. This idea was held across the Thirteen Colonies in North America in the years prior to the American Revolution (1776–1783). Among the believers were Thomas Jefferson and Jonathan Mayhew. The Whig historians of the 19th century were concerned with explaining the evolution of the English constitution, and they found in the witan a proto-parliament or in the words of Felix Liebermann, "one of the lineal ancestors of the British Parliament".

After World War I, historians such as Frank Stenton and Dorothy Whitelock shifted their focus to understanding the Anglo-Saxon period on its on terms. In his 1943 Anglo-Saxon England, Stenton chose to use the term "King's Council" in place of witan and witenagemot. This change in terminology signaled an important change in the way Anglo-Saxon political assemblies were perceived. Instead of proto-parliaments, the assemblies were essentially royal institutions. Other historians followed Stenton's lead.

Scholars such as Stenton have noted that the witenagemot was in many ways different from the future institution of the Parliament of England; it had substantially different powers and some major limitations, such as a lack of a fixed procedure, schedule, or meeting place. In his 1995 biography of Alfred the Great, historian David Sturdy argues that the witan did not embody modern notions of a "national institution" or a "democratic" body. He writes, "Victorian notions of a national 'witan' are crazy dreams without foundation, myths of a 'democratic parliament' that never was."

While many modern historians avoid the terms witan and witenagemot, few would go as far as Geoffrey Hindley, who described witenagemot as an "essentially Victorian" coinage. The Blackwell Encyclopaedia of Anglo-Saxon England prefers "king's council" but adds that it was known in Old English as the witan. Maddicott regarded the word witan with suspicion, even though it is used in sources such as the Anglo-Saxon Chronicle. In his study of the origins of the English parliament, he generally preferred the more neutral word "assembly":

"But the word carries with it, however unjustifiably, a fustian air of decayed scholarship, and, in addition, its use may seem to prejudge the answer to an important question: do we have here an institution, a capitalized 'Witan', as it were, or merely a lower-case ad hoc gathering of the wise men who were the king's councillors?"

Henrietta Leyser commented in 2017 that for decades historians avoided using the word witan for assemblies in case they were interpreted as proto-parliaments, and she went on: "Recent historiography, however, has reintroduced the term since it is clear that it was generally accepted that certain kinds of business could only be transacted with a substantial number of the king's wise men, in other words, in the company of his 'witan. She does not mention the term witenagemot.

title: Witan