Dumping syndrome occurs when food, especially sugar, moves too fast from the stomach to the duodenum—the first part of the small intestine—in the upper gastrointestinal (GI) tract. This condition is also called rapid gastric emptying. It is mostly associated with conditions following gastric or esophageal surgery, though it can also arise secondary to diabetes or to the use of certain medications; it is caused by an absent or insufficiently functioning pyloric sphincter, the valve between the stomach and the duodenum.

Dumping syndrome has two forms, based on when symptoms occur. Early dumping syndrome occurs 10 to 30 minutes after a meal. It results from rapid movement of fluid into the intestine following a sudden addition of a large amount of food from the stomach. The small intestine expands rapidly due to the presence of hypertonic/hyperosmolar contents from the stomach, especially sweet foods. This causes symptoms due to the shift of fluid into the intestinal lumen, with plasma volume contraction and acute intestinal distention. Osmotic diarrhea, distension of the small bowel leading to crampy abdominal pain, and reduced blood volume can result.

Late dumping syndrome occurs 2 to 3 hours after a meal. It results from excessive movement of sugar into the intestine, which raises the body's blood glucose level and causes the pancreas to increase its release of the hormone insulin. The increased release of insulin causes a rapid drop in blood glucose levels, a condition known as alimentary hypoglycemia, or low blood sugar.

The first step to minimizing symptoms of dumping syndrome involves changes in eating, diet, and nutrition, and may include

- eating five or six small meals a day instead of three larger meals

- delaying liquid intake until at least 30 minutes after a meal

- increasing intake of protein, fiber, and complex carbohydrates—found in starchy foods such as oatmeal and rice

- avoiding simple sugars such as table sugar, which can be found in candy, syrup, sodas, and juice beverages

- increasing the thickness of food by adding pectin or guar gum—plant extracts used as thickening agents

Some people find that lying down for 30 minutes after meals also helps reduce symptoms, though some health care providers advise against this.

Sores or ulcerations can become infected by virus, bacteria or fungus. Pain and loss of taste perception makes it more difficult to eat, which leads to weight loss. Ulcers may act as a site for local infection and a portal of entry for oral flora that, in some instances, may cause septicaemia (especially in immunosuppressed patients). Therefore, oral mucositis can be a dose-limiting condition, disrupting a patient’s optimal cancer treatment plan and consequentially decreasing their chances of survival.

Mucositis is the painful inflammation and ulceration of the mucous membranes lining the digestive tract, usually as an adverse effect of chemotherapy and radiotherapy treatment for cancer. Mucositis can occur anywhere along the gastrointestinal (GI) tract, but oral mucositis refers to the particular inflammation and ulceration that occurs in the mouth. Oral mucositis is a common and often debilitating complication of cancer treatment.

Oral and gastrointestinal (GI) mucositis affects almost all patients undergoing high-dose chemotherapy and hematopoietic stem cell transplantation (HSCT), 80% of patients with malignancies of the head and neck receiving radiotherapy, and a wide range of patients receiving chemotherapy. Alimentary tract mucositis increases mortality and morbidity and contributes to rising health care costs.

For most cancer treatment, about 5–15% of patients get mucositis. However, with 5-fluorouracil (5-FU), up to 40% get mucositis, and 10–15% get grade 3–4 oral mucositis. Irinotecan is associated with severe GI mucositis in over 20% of patients. Seventy-five to eighty percent of bone marrow transplantation recipients experience mucositis, of which oral mucositis is the most common and most debilitating, especially when melphalan is used. In grade 3 oral mucositis, the patient is unable to eat solid food, and in grade 4, the patient is unable to consume liquids as well.

Radiotherapy to the head and neck or to the pelvis or abdomen is associated with Grade 3 and Grade 4 oral or GI mucositis, respectively, often exceeding 50% of patients. Among patients undergoing head and neck radiotherapy, pain and decreased oral function may persist long after the conclusion of therapy. Fractionated radiation dosage increases the risk of mucositis to > 70% of patients in most trials. Oral mucositis is particularly profound and prolonged among HSCT recipients who receive total-body irradiation.

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.

The term alimentary mycotoxicoses refers to the effect of poisoning by Mycotoxins (The term 'mycotoxin' is usually reserved for the toxic chemical products produced by fungi that readily colonize crops) through food consumption. Mycotoxins sometimes have important effects on human and animal health. For example, an outbreak which occurred in the UK in 1960 caused the death of 100,000 turkeys which had consumed aflatoxin-contaminated peanut meal. In the USSR in World War II, 5,000 people died due to Alimentary Toxic Aleukia (ALA). The common foodborne Mycotoxins include:

- Aflatoxins – originated from Aspergillus parasiticus and Aspergillus flavus. They are frequently found in tree nuts, peanuts, maize, sorghum and other oilseeds, including corn and cottonseeds. The pronounced forms of Aflatoxins are those of B1, B2, G1, and G2, amongst which Aflatoxin B1 predominantly targets the liver, which will result in necrosis, cirrhosis, and carcinoma. In the US, the acceptable level of total aflatoxins in foods is less than 20 μg/kg, except for Aflatoxin M1 in milk, which should be less than 0.5 μg/kg. The official document can be found at FDA's website.

- Altertoxins – are those of Alternariol (AOH), Alternariol methyl ether (AME), Altenuene (ALT), Altertoxin-1 (ATX-1), Tenuazonic acid (TeA) and Radicinin (RAD), originated from Alternaria spp. Some of the toxins can be present in sorghum, ragi, wheat and tomatoes. Some research has shown that the toxins can be easily cross-contaminated between grain commodities, suggesting that manufacturing and storage of grain commodities is a critical practice.

- Citrinin

- Citreoviridin

- Cyclopiazonic acid

- Cytochalasins

- Ergot alkaloids / Ergopeptine alkaloids – Ergotamine

- Fumonisins – Crop corn can be easily contaminated by the fungi Fusarium moniliforme, and its Fumonisin B1 will cause Leukoencephalomalacia (LEM) in horses, Pulmonary edema syndrome (PES) in pigs, liver cancer in rats and Esophageal cancer in humans. For human and animal health, both the FDA and the EC have regulated the content levels of toxins in food and animal feed.

- Fusaric acid

- Fusarochromanone

- Kojic acid

- Lolitrem alkaloids

- Moniliformin

- 3-Nitropropionic acid

- Nivalenol

- Ochratoxins – In Australia, The Limit of Reporting (LOR) level for Ochratoxin A (OTA) analyses in 20th Australian Total Diet Survey was 1 µg/kg, whereas the EC restricts the content of OTA to 5 µg/kg in cereal commodities, 3 µg/kg in processed products and 10 µg/kg in dried vine fruits.

- Oosporeine

- Patulin – Currently, this toxin has been advisably regulated on fruit products. The EC and the FDA have limited it to under 50 µg/kg for fruit juice and fruit nectar, while limits of 25 µg/kg for solid-contained fruit products and 10 µg/kg for baby foods were specified by the EC.

- Phomopsins

- Sporidesmin A

- Sterigmatocystin

- Tremorgenic mycotoxins – Five of them have been reported to be associated with molds found in fermented meats. These are Fumitremorgen B, Paxilline, Penitrem A, Verrucosidin, and Verruculogen.

- Trichothecenes – sourced from Cephalosporium, Fusarium, Myrothecium, Stachybotrys and Trichoderma. The toxins are usually found in molded maize, wheat, corn, peanuts and rice, or animal feed of hay and straw. Four trichothecenes, T-2 toxin, HT-2 toxin, diacetoxyscirpenol (DAS) and deoxynivalenol (DON) have been most commonly encountered by humans and animals. The consequences of oral intake of, or dermal exposure to, the toxins will result in Alimentary toxic aleukia, neutropenia, aplastic anemia, thrombocytopenia and/or skin irritation. In 1993, the FDA issued a document for the content limits of DON in food and animal feed at an advisory level. In 2003, US published a patent that is very promising for farmers to produce a trichothecene-resistant crop.

- Zearalenone

- Zearalenols

A person's sex also seems to have some role in the development of autoimmunity; that is, most autoimmune diseases are "sex-related". Nearly 75% of the more than 23.5 million Americans who suffer from autoimmune disease are women, although it is less-frequently acknowledged that millions of men also suffer from these diseases. According to the American Autoimmune Related Diseases Association (AARDA), autoimmune diseases that develop in men tend to be more severe. A few autoimmune diseases that men are just as or more likely to develop as women include: ankylosing spondylitis, type 1 diabetes mellitus, granulomatosis with polyangiitis, Crohn's disease, Primary sclerosing cholangitis and psoriasis.

The reasons for the sex role in autoimmunity vary. Women appear to generally mount larger inflammatory responses than men when their immune systems are triggered, increasing the risk of autoimmunity. Involvement of sex steroids is indicated by that many autoimmune diseases tend to fluctuate in accordance with hormonal changes, for example: during pregnancy, in the menstrual cycle, or when using oral contraception. A history of pregnancy also appears to leave a persistent increased risk for autoimmune disease. It has been suggested that the slight, direct exchange of cells between mothers and their children during pregnancy may induce autoimmunity. This would tip the gender balance in the direction of the female.

Another theory suggests the female high tendency to get autoimmunity is due to an imbalanced X chromosome inactivation. The X-inactivation skew theory, proposed by Princeton University's Jeff Stewart, has recently been confirmed experimentally in scleroderma and autoimmune thyroiditis. Other complex X-linked genetic susceptibility mechanisms are proposed and under investigation.

Alimentary toxic aleukia, or Aleukia, is a mycotoxin-induced condition characterized by nausea, vomiting, diarrhea, leukopenia (aleukia), hemorrhaging, skin inflammation, and sometimes death. Alimentary Toxic Alekia almost always refers to the human condition associated with presence of T2 Toxin.

Immunodeficiency or immunosuppression can be caused by:

- Malnutrition

- Fatigue

- Recurrent infections

- Immunosuppressing agents for organ transplant recipients

- Advanced HIV infection

- Chemotherapy for cancer

- Genetic predisposition

- Skin damage

- Antibiotic treatment leading to disruption of the physiological microbiome, thus allowing some microorganisms to outcompete others and become pathogenic (e.g. disruption of intestinal flora may lead to "Clostridium difficile" infection

- Medical procedures

- Pregnancy

- Ageing

- Leukopenia (i.e. neutropenia and lymphocytopenia)

The lack of or the disruption of normal vaginal flora allows the proliferation of opportunistic microorganisms and will cause the opportunistic infection - bacterial vaginosis.

According to the hygiene hypothesis, high levels of cleanliness expose children to fewer antigens than in the past, causing their immune systems to become overactive and more likely to misidentify own tissues as foreign, resulting in autoimmune conditions such as asthma.

Amphistomiasis or paramphistomiasis (alternatively spelled amphistomosis or paramphistomosis) is a parasitic disease of livestock animals, more commonly of cattle and sheep, and humans caused by immature helminthic flatworms belonging to the order Echinostomida. The term amphistomiasis is used for broader connotation implying the disease inflicted by members of Echinostomida including the family Paramphistomidae/Gastrodiscidae (to be precise, the species "Gastrodiscoides hominis"); whereas paramphistomiasis is restricted to that of the members of the family Paramphistomatidae only. "G. discoides" and "Watsonius watsoni" are responsible for the disease in humans, while most paramphistomes are responsible in livestock animals, and some wild mammals. In livestock industry the disease causes heavy economic backlashes due to poor production of milk, meat and wool.

DES (diethylstilbestrol) is a drug that mimics estrogen, a female hormone. From 1938 until 1971 doctors prescribed this drug to help some pregnant women who had had miscarriages or premature deliveries on the theory that miscarriages and premature births occurred because some pregnant women did not produce enough estrogen naturally to sustain the pregnancy for full term . An estimated 5-10 million pregnant women and the children born during this period were exposed to DES. Currently, DES is known to increase the risk of breast cancer, and cause a variety of birth-related adverse outcomes exposed female offsprings such as spontaneous abortion, second-trimester pregnancy loss, preterm delivery, stillbirth, neonatal death, sub/infertility and cancer of reproductive tissues . DES is an important developmental toxicant which links the fetal basis of adult disease.

Alimentary Toxic Aleukia was first characterized in the early 19th century after affecting a large population in the Orenburg district of the former U.S.S.R. during World War II. The sick people had eaten overwintered grain colonized with Fusarium sporotrichioides and Fusarium poae

An interesting inverse relationship exists between infectious diseases and autoimmune diseases. In areas where multiple infectious diseases are endemic, autoimmune diseases are quite rarely seen. The reverse, to some extent, seems to hold true. The hygiene hypothesis attributes these correlations to the immune manipulating strategies of pathogens. While such an observation has been variously termed as spurious and ineffective, according to some studies, parasite infection is associated with reduced activity of autoimmune disease.

The putative mechanism is that the parasite attenuates the host immune response in order to protect itself. This may provide a serendipitous benefit to a host that also suffers from autoimmune disease. The details of parasite immune modulation are not yet known, but may include secretion of anti-inflammatory agents or interference with the host immune signaling.

A paradoxical observation has been the strong association of certain microbial organisms with autoimmune diseases.

For example, "Klebsiella pneumoniae" and coxsackievirus B have been strongly correlated with ankylosing spondylitis and diabetes mellitus type 1, respectively. This has been explained by the tendency of the infecting organism to produce super-antigens that are capable of polyclonal activation of B-lymphocytes, and production of large amounts of antibodies of varying specificities, some of which may be self-reactive (see below).

Certain chemical agents and drugs can also be associated with the genesis of autoimmune conditions, or conditions that simulate autoimmune diseases. The most striking of these is the drug-induced lupus erythematosus. Usually, withdrawal of the offending drug cures the symptoms in a patient.

Cigarette smoking is now established as a major risk factor for both incidence and severity of rheumatoid arthritis. This may relate to abnormal citrullination of proteins, since the effects of smoking correlate with the presence of antibodies to citrullinated peptides.

Methylmercury and inorganic mercury is excreted in human breast milk and infants are particularly susceptible to toxicity due to this compound. The fetus and infant are especially vulnerable to mercury exposures with special interest in the development of the CNS since it can easily cross across the placental barrier, accumulate within the placenta and fetus as the fetus cannot eliminate mercury and have a negative effect on the fetus even if the mother does not show symptoms. Mercury causes damage to the nervous system resulting from prenatal or early postnatal exposure and is very likely to be permanent.

Pneumonia is a form of acute respiratory infection that affects the lung parenchyma and oxygenation. When a patient with pneumonia is an alcoholic, the mortality rate exceeds by 50% if they are placed into intensive care (ICU). According to Kershaw, C 2008 page 1, "[a]s of 2001, pneumonia was the sixth most common cause of death in the United States". Alcoholics are at an increased risk for infection with tissue-damaging gram-negative pathogens or for the spread of bacteria in the blood.

The mechanisms of alcoholic lung disease are:

- Metabolism of alcohol reduces glutathione anti-oxidant levels in the lungs.

- Oxidation damage to the cells impairs the ability of the lungs to remove fluid.

- Oxidative damage to cells reduces immune response.

- Oxidative damage to cells results in a reduced ability to recover from injury.

These chemical changes compound the negative mechanical and microbiological effects of alcoholism on the respiratory system. These include impaired gag reflex and cilia function and greater likelihood of colonies of pneumococcal bacteria in the upper respiratory system.

Although lung damage from concurrent smoking and drug use is often indistinguishable from alcoholic lung disease, there is support for considering alcoholic lung disease as an independent syndrome. Over the last decade, evidence from epistemological studies show that alcohol abuse alone can increase by as much as fourfold the risk for acute respiratory distress syndrome.

Amphistomiasis in farm and wild mammals is due to infection of paramphistomes, such as the species of "Paramphistomum", "Calicophoron", "Cotylophoron", "Pseudophisthodiscus", etc. These are essentially rumen flukes, of which "Paramphistomum cervi" is the most notorious in terms of prevalence and pathogenicity. Infection occurs through ingestion of contaminated vegetables and raw meat, in which the viable infective metacercaria are deposited from snails, which are the intermediate hosts. The immature flukes are responsible for destroying the mucosal walls of the alimentary tract on their way to growing into adults. It is by this fervent tissue obliteration that the clinical symptoms are manifested. The adult flukes, on the other hand, are quite harmless, as they merely prepare for reproduction.

The zoonotic infection in human is caused by "G. discoides" and "W. watsoni" which are essentially intestinal flukes. The disease due to "G. discoides" is more specifically termed gastrodiscoidiasis. In their natural hosts such as pigs and monkeys, their infection in asymptomatic, but human infection is prevalent, by which they cause serious health problems, characterised by diarrhoea, fever, abdominal pain, colic, and an increased mucous production. In extreme situations such as in Assam, India, a number of mortality among children is attributed to this disease.

Opportunistic infections caused by Feline Leukemia Virus and Feline immunodeficiency virus retroviral infections can be treated with Lymphocyte T-Cell Immune Modulator.

The first estimate of US prevalence for autoimmune diseases as a group was published in 1997 by Jacobson, et al. They reported US prevalence to be around 9 million, applying prevalence estimates for 24 diseases to a US population of 279 million. Jacobson's work was updated by Hayter & Cook in 2012. This study used Witebsky's postulates, as revised by Rose & Bona, to extend the list to 81 diseases and estimated overall cumulative US prevalence for the 81 autoimmune diseases at 5.0%, with 3.0% for males and 7.1% for females. The estimated community

prevalence, which takes into account the observation that many people have more than one autoimmune disease, was 4.5% overall, with 2.7% for males and 6.4% for females.

Neutropenia is usually detected shortly after birth, affecting 6% to 8% of all newborns in neonatal intensive care units (NICUs). Out of the approximately 600,000 neonates annually treated in NICUs in the United States, 48,000 may be diagnosed as neutropenic. The incidence of neutropenia is greater in premature infants. Six to fifty-eight percent of preterm neonates are diagnosed with this auto-immune disease. The incidence of neutropenia correlates with decreasing birth weight. The disorder is seen up to 38% in infants that weigh less than 1000g, 13% in infants weighing less than 2500g, and 3% of term infants weighing more than 2500 g. Neutropenia is often temporary, affecting most newborns in only first few days after birth. In others, it becomes more severe and chronic indicating a deficiency in innate immunity.

A method for repairing long-gap esophageal atresia using magnets has been developed, that does not require replacing the missing section with grafts of the intestine or other body parts. Using electromagnetic force to attract the upper and lower ends of the esophagus together was first tried in the 1970s by using steel pellets attracted to each other by applying external electromagnets to the patient. In the 2000s a further refinement was developed by Mario Zaritzky's group and others. The newer method uses permanent magnets and a balloon.

1. The magnets are inserted into the upper pouch via the baby's mouth or nose, and the lower via the gastrotomy feeding tube hole (which would have had to be made anyway to feed the baby, therefore not requiring any additional surgery).

2. The distance between the magnets is controlled by a balloon in the upper pouch, between the end of the pouch and the magnet. This also controls the force between the magnets so it is not strong enough to cause damage.

3. After the ends of the esophagus have stretched enough to touch, the upper magnet is replaced by one without a balloon and the stronger magnetic attraction causes the ends to fuse (anastomosis).

In April 2015 Annalise Dapo became the first patient in the United States to have their esophageal atresia corrected using magnets.

The cause of immunodeficiency varies depending on the nature of the disorder. The cause can be either genetic or acquired by malnutrition and poor sanitary conditions. Only for some genetic causes, the exact genes are known. Although there is no true discrimination to who this disease affects, the genes are passed from mother to child, and on occasion from father to child. Women tend not to show symptoms due to their second X chromosome not having the mutation while man are symptomatic, due to having one X chromosome.

It occurs in approximately 1 in 2500 live births.

Congenital esophageal atresia (EA) represents a failure of the esophagus to develop as a continuous passage. Instead, it ends as a blind pouch. Tracheoesophageal fistula (TEF) represents an abnormal opening between the trachea and esophagus. EA and TEF can occur separately or together. EA and TEF are diagnosed in the ICU at birth and treated immediately.

The presence of EA is suspected in an infant with excessive salivation (drooling) and in a newborn with drooling that is frequently accompanied by choking, coughing and sneezing. When fed, these infants swallow normally but begin to cough and struggle as the fluid returns through the nose and mouth. The infant may become cyanotic (turn bluish due to lack of oxygen) and may stop breathing as the overflow of fluid from the blind pouch is aspirated (sucked into) the trachea. The cyanosis is a result of laryngospasm (a protective mechanism that the body has to prevent aspiration into the trachea). Over time respiratory distress will develop.

If any of the above signs/symptoms are noticed, a catheter is gently passed into the esophagus to check for resistance. If resistance is noted, other studies will be done to confirm the diagnosis. A catheter can be inserted and will show up as white on a regular x-ray film to demonstrate the blind pouch ending. Sometimes a small amount of barium (chalk-like liquid) is placed through the mouth to diagnose the problems.

Treatment of EA and TEF is surgery to repair the defect. If EA or TEF is suspected, all oral feedings are stopped and intravenous fluids are started. The infant will be positioned to help drain secretions and decrease the likelihood of aspiration. Babies with EA may sometimes have other problems. Studies will be done to look at the heart, spine and kidneys.

Surgery to repair EA is essential as the baby will not be able to feed and is highly likely to develop pneumonia. Once the baby is in condition for surgery, an incision is made on the side of the chest. The esophagus can usually be sewn together. Following surgery, the baby may be hospitalized for a variable length of time. Care for each infant is individualized.

Its very commonly seen in a newborn with imperforate anus.

A localized disease is an infectious or neoplastic process that originates in and is confined to one organ system or general area in the body, such as a sprained ankle, a boil on the hand, an abscess of finger.

A localized cancer that has not extended beyond the margins of the organ involved can also be described as localized disease, while cancers that extend into other tissues are described as invasive. Tumors that are non-hematologic in origin but extend into the bloodstream or lymphatic system are known as metastatic.

Localized diseases are contrasted with disseminated diseases and systemic diseases.

Some diseases are capable of changing from local to disseminated diseases. Pneumonia, for example, is generally confined to one or both lungs but can become disseminated through sepsis, in which the microbe responsible for the pneumonia "seeds" the bloodstream or lymphatic system and is transported to distant sites in the body. When that occurs, the process is no longer described as a localized disease, but rather as a disseminated disease.