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

The paralysis caused by botulism can persist for 2 to 8 weeks, during which supportive care and ventilation may be necessary to keep the person alive. Botulism is fatal in 5% to 10% of people who are affected. However, if left untreated, botulism is fatal in 40% to 50% 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 1% for hospitalized babies.

The presence of avian botulism is extremely hard to detect before an outbreak. Frequent surveillance of sites at risk is needed for early detection of the disease in order to take action and remove carcasses. Vaccines are also developed, but they are expected to have limited effectiveness in stemming outbreaks in wild waterbird populations. However may be effective in reducing mortality for endangered island waterfowl and small non-migratory wild populations. Field tests are needed.

Avian Botulism is a strain of botulism that affects wild and captive bird populations, most notably waterfowl. This is a paralytic disease brought on by the Botulinum neurotoxin (BoNt) of the bacterium "Clostridium botulinum". "C. botulinum" can fall into one of 7 different types which are strains A through G. Type C BoNt is most frequently associated with waterfowl mortality. The Type E strain is also commonly associated with avian outbreaks and is frequently found in fish species which is why most outbreaks occur in piscivorous birds.

Avian Botulism occurs all over the world and its understanding is important for wildlife managers, hunters, bird watchers, and anyone who owns wetland property as this disease can account for over 1,000,000 waterbird deaths in a year.

Bacteria are a common cause of foodborne illness. In the United Kingdom during 2000, the individual bacteria involved were the following: "Campylobacter jejuni" 77.3%, "Salmonella" 20.9%, 1.4%, and all others less than 0.56%. In the past, bacterial infections were thought to be more prevalent because few places had the capability to test for norovirus and no active surveillance was being done for this particular agent. Toxins from bacterial infections are delayed because the bacteria need time to multiply. As a result, symptoms associated with intoxication are usually not seen until 12–72 hours or more after eating contaminated food. However, in some cases, such as Staphylococcal food poisoning, the onset of illness can be as soon as 30 minutes after ingesting contaminated food.

Most common bacterial foodborne pathogens are:

- "Campylobacter jejuni" which can lead to secondary Guillain–Barré syndrome and periodontitis

- "Clostridium perfringens", the "cafeteria germ"

- "Salmonella" spp. – its "S. typhimurium" infection is caused by consumption of eggs or poultry that are not adequately cooked or by other interactive human-animal pathogens

- "" enterohemorrhagic (EHEC) which can cause hemolytic-uremic syndrome

Other common bacterial foodborne pathogens are:

- "Bacillus cereus"

- "Escherichia coli", other virulence properties, such as enteroinvasive (EIEC), enteropathogenic (EPEC), enterotoxigenic (ETEC), enteroaggregative (EAEC or EAgEC)

- "Listeria monocytogenes"

- "Shigella" spp.

- "Staphylococcus aureus"

- "Staphylococcal enteritis"

- "Streptococcus"

- "Vibrio cholerae", including O1 and non-O1

- "Vibrio parahaemolyticus"

- "Vibrio vulnificus"

- "Yersinia enterocolitica" and "Yersinia pseudotuberculosis"

Less common bacterial agents:

- "Brucella" spp.

- "Corynebacterium ulcerans"

- "Coxiella burnetii" or Q fever

- "Plesiomonas shigelloides"

Globally, infants are a population that are especially vulnerable to foodborne disease. The World Health Organization has issued recommendations for the preparation, use and storage of prepared formulas. Breastfeeding remains the best preventative measure for protection of foodborne infections in infants.

Breastfeeding is associated with a lower risk of SIDS. It is not clear if co-sleeping among mothers who breastfeed without any other risk factors increased SIDS risk.

SIDS rates decrease with increasing maternal age, with teenage mothers at greatest risk. Delayed or inadequate prenatal care also increases risk. Low birth weight is a significant risk factor. In the United States from 1995 to 1998, the SIDS death rate for infants weighing 1000–1499 g was 2.89/1000, while for a birth weight of 3500–3999 g, it was only 0.51/1000. Premature birth increases the risk of SIDS death roughly fourfold. From 1995 to 1998, the U.S. SIDS rate for births at 37–39 weeks of gestation was 0.73/1000, while the SIDS rate for births at 28–31 weeks of gestation was 2.39/1000.

Anemia has also been linked to SIDS (note, however, that per item 6 in the list of epidemiologic characteristics below, extent of anemia cannot be evaluated at autopsy because an infant's total hemoglobin can only be measured during life.). SIDS incidence rises from zero at birth, is highest from two to four months of age, and declines toward zero after the infant's first year. Baby boys have a ~50% higher risk of SIDS than girls.

Transmission may occur via consumption of contaminated water, or when people share personal objects. In places with wet and dry seasons, water quality typically worsens during the wet season, and this correlates with the time of outbreaks. In areas of the world with four seasons, infections are more common in the winter. Bottle-feeding of babies with improperly sanitized bottles is a significant cause on a global scale. Transmission rates are also related to poor hygiene, especially among children, in crowded households, and in those with pre-existing poor nutritional status. After developing tolerance, adults may carry certain organisms without exhibiting signs or symptoms, and thus act as natural reservoirs of contagion. While some agents (such as "Shigella") only occur in primates, others may occur in a wide variety of animals (such as "Giardia").

In the developed world "Campylobacter jejuni" is the primary cause of bacterial gastroenteritis, with half of these cases associated with exposure to poultry. In children, bacteria are the cause in about 15% of cases, with the most common types being "Escherichia coli", "Salmonella", "Shigella", and "Campylobacter" species. If food becomes contaminated with bacteria and remains at room temperature for a period of several hours, the bacteria multiply and increase the risk of infection in those who consume the food. Some foods commonly associated with illness include raw or undercooked meat, poultry, seafood, and eggs; raw sprouts; unpasteurized milk and soft cheeses; and fruit and vegetable juices. In the developing world, especially sub-Saharan Africa and Asia, cholera is a common cause of gastroenteritis. This infection is usually transmitted by contaminated water or food.

Toxigenic "Clostridium difficile" is an important cause of diarrhea that occurs more often in the elderly. Infants can carry these bacteria without developing symptoms. It is a common cause of diarrhea in those who are hospitalized and is frequently associated with antibiotic use. "Staphylococcus aureus" infectious diarrhea may also occur in those who have used antibiotics. Acute "traveler's diarrhea" is usually a type of bacterial gastroenteritis, while the persistent form is usually parasitic. Acid-suppressing medication appears to increase the risk of significant infection after exposure to a number of organisms, including "Clostridium difficile", "Salmonella", and "Campylobacter" species. The risk is greater in those taking proton pump inhibitors than with H2 antagonists.

Intestinal infectious diseases include a large number of infections of the bowels including: cholera, typhoid fever, paratyphoid fever, other types of salmonella infections, shigellosis, botulism, gastroenteritis, and amoebiasis among others.

Typhoid and paratyphoid resulted in 221,000 deaths in 2013 down from 259,000 deaths in 1990. Other diseases which result in diarrhea caused another 1.3 million additional deaths in 2013 down from 2.6 million deaths in 1990.

For infecting organisms to survive and repeat the infection cycle in other hosts, they (or their progeny) must leave an existing reservoir and cause infection elsewhere. Infection transmission can take place via many potential routes:

- Droplet contact, also known as the "respiratory route", and the resultant infection can be termed airborne disease. If an infected person coughs or sneezes on another person the microorganisms, suspended in warm, moist droplets, may enter the body through the nose, mouth or eye surfaces.

- Fecal-oral transmission, wherein foodstuffs or water become contaminated (by people not washing their hands before preparing food, or untreated sewage being released into a drinking water supply) and the people who eat and drink them become infected. Common fecal-oral transmitted pathogens include "Vibrio cholerae", "Giardia" species, rotaviruses, "Entameba histolytica", "Escherichia coli", and tape worms. Most of these pathogens cause gastroenteritis.

- Sexual transmission, with the resulting disease being called sexually transmitted disease

- Oral transmission, Diseases that are transmitted primarily by oral means may be caught through direct oral contact such as kissing, or by indirect contact such as by sharing a drinking glass or a cigarette.

- Transmission by direct contact, Some diseases that are transmissible by direct contact include athlete's foot, impetigo and warts

- Vehicle Transmission, transmission by an inanimate reservoir (food, water, soil).

- Vertical transmission, directly from the mother to an embryo, fetus or baby during pregnancy or childbirth. It can occur when the mother gets an infection as an intercurrent disease in pregnancy.

- Iatrogenic transmission, due to medical procedures such as injection or transplantation of infected material.

- Vector-borne transmission, transmitted by a vector, which is an organism that does not cause disease itself but that transmits infection by conveying pathogens from one host to another.

The relationship between "virulence versus transmissibility" is complex; if a disease is rapidly fatal, the host may die before the microbe can be passed along to another host.

Disease can arise if the host's protective immune mechanisms are compromised and the organism inflicts damage on the host. Microorganisms can cause tissue damage by releasing a variety of toxins or destructive enzymes. For example, Clostridium tetani releases a toxin that paralyzes muscles, and staphylococcus releases toxins that produce shock and sepsis. Not all infectious agents cause disease in all hosts. For example, less than 5% of individuals infected with polio develop disease. On the other hand, some infectious agents are highly virulent. The prion causing mad cow disease and Creutzfeldt–Jakob disease invariably kills all animals and people that are infected.

Persistent infections occur because the body is unable to clear the organism after the initial infection. Persistent infections are characterized by the continual presence of the infectious organism, often as latent infection with occasional recurrent relapses of active infection. There are some viruses that can maintain a persistent infection by infecting different cells of the body. Some viruses once acquired never leave the body. A typical example is the herpes virus, which tends to hide in nerves and become reactivated when specific circumstances arise.

Persistent infections cause millions of deaths globally each year. Chronic infections by parasites account for a high morbidity and mortality in many underdeveloped countries.

The newborn`s exposure to the maternal vaginal bacterial flora which contains aerobic and anaerobic bacterial flora can lead to the development of anaerobic bacterial infection. These infections include cellulitis of the site of fetal monitoring (caused by "Bacterodes" spp.), bacteremia, aspiration pneumonia (caused by "Bacterodes" spp.), conjunctivitis (caused by clostridia,) omphalitis (caused by mixed flora), and infant botulism. Clostridial species may play a role in necrotizing enterocolitis. Management of these infection necessitates treating of the underlying condition(s) when present, and administration of proper antimicrobial therapy

Condition predisposing to anaerobic infections include: exposure of a sterile body location to a high inoculum of indigenous bacteria of mucous membrane flora origin, inadequate blood supply and tissue necrosis which lower the oxidation and reduction potential which support the growth of anaerobes. Conditions which can lower the blood supply and can predispose to anaerobic infection are: trauma, foreign body, malignancy, surgery, edema, shock, colitis and vascular disease. Other predisposing conditions include splenectomy, neutropenia, immunosuppression, hypogammaglobinemia, leukemia, collagen vascular disease and cytotoxic drugs and diabetes mellitus. A preexisting infection caused by aerobic or facultative organisms can alter the local tissue conditions and make them more favorable for the growth of anaerobes. Impairment in defense mechanisms due to anaerobic conditions can also favor anaerobic infection. These include production of leukotoxins (by "Fusobacterium" spp.), phagocytosis intracellular killing impairments (often caused by encapsulated anaerobes and by succinic acid ( produced by "Bacteroides" spp.), chemotaxis inhibition (by "Fusobacterium, Prevotella" and "Porphyromonas" spp.), and proteases degradation of serum proteins (by Bacteroides spp.) and production of leukotoxins (by "Fusobacterium" spp.).

The hallmarks of anaerobic infection include suppuration, establishment of an abscess, thrombophlebitis and gangrenous destruction of tissue with gas generation. Anaerobic bacteria are very commonly recovered in chronic infections, and are often found following the failure of therapy with antimicrobials that are ineffective against them, such as trimethoprim–sulfamethoxazole (co-trimoxazole), aminoglycosides, and the earlier quinolones.

Some infections are more likely to be caused by anaerobic bacteria, and they should be suspected in most instances. These infections include brain abscess, oral or dental infections, human or animal bites, aspiration pneumonia and lung abscesses, amnionitis, endometritis, septic abortions, tubo-ovarian abscess, peritonitis and abdominal abscesses following viscus perforation, abscesses in and around the oral and rectal areas, pus-forming necrotizing infections of soft tissue or muscle and postsurgical infections that emerge following procedures on the oral or gastrointestinal tract or female pelvic area. Some solid malignant tumors, ( colonic, uterine and bronchogenic, and head and neck necrotic tumors, are more likely to become secondarily infected with anaerobes. The lack of oxygen within the tumor that are proximal to the endogenous adjacent mucosal flora can predispose such infections.

Myasthenia gravis is the most common neuromuscular disease affecting function of the end plate in patients. It is present in 100 people out of 1,000,000 in the population, and its onset is usually in either younger or older individuals.(reference 14)

Acquired myasthenia gravis is the most common neuromuscular junction disease.(reference 7) Important observations were made by Patrick and Lindstrom in 1973 when they found that antibodies attacking the acetylcholine receptors were present in around 85% of cases of myasthenia gravis.(reference renamed form 13)(reference 36) The remaining diseases were also a result of antibody attacks on vital proteins, but instead of the acetylcholine receptor, the culprits were MuSK, a muscle-specific serum kinase, and lipoprotein receptor-related protein.(reference 36) So these mechanisms describe myasthenia gravis that is acquired, and not congenital, affecting these vital proteins by an immunological response against self-antigens. The cases not caused by antibodies against the acetylcholine receptors became by convention called seronegative myasthenia gravis.(reference 37) The term seronegative came about because scientists would be testing for acetylcholine receptor antibodies in patients that had myasthenia gravis resulting in negative tests in the serum. This does not imply that there are no antibodies present, but this terminology only became present because scientists were testing for the wrong antigen.(reference 36)(reference 38)

Neonatal myasthenia gravis is a very rare condition in which a mother with myasthenia gravis passes down her antibodies to her infant through the placenta, causing the it to be born with antibodies that will attach self-antigens.(reference 12)

Drug-induced myasthenia gravis is also a very rare condition in which pharmacological drugs cause a blockade or disruption of the NMJ machinery.(reference 12) Robert W. Barrons summarizes the possible causes of drug-induced myasthenia gravis: "Prednisone was most commonly implicated as aggravating myasthenia gravis, and D-penicillamine was most commonly associated with myasthenic syndrome. The greatest frequency of drug-induced neuromuscular blockade was seen with aminoglycoside-induced postoperative respiratory depression. However, drugs most likely to impact myasthenic patients negatively are those used in the treatment of the disease. These include overuse of anticholinesterase drugs, high-dose prednisone, and anesthesia and neuromuscular blockers for thymectomy."(reference 39)

Neurotoxin may act on the neuromuscular junction either post synaptically or presynaptically as there are several different forms of toxins that the NMJ is sensitive to.(reference 14) Common mechanisms of action include blockage of acetylcholine release at the synapse thus causing the NMJ to become abnormal in function.(reference 12)