Areas with the highest prevalence of helminthiasis are tropical and subtropical areas including sub-Saharan Africa, central and east Asia, and the Americas.

Some types of helminthiases are classified as neglected tropical diseases. They include:

- Soil-transmitted helminthiases

- Roundworm infections such as lymphatic filariasis, dracunculiasis, and onchocerciasis

- Trematode infections, such as schistosomiasis, and food-borne trematodiases, including fascioliasis, clonorchiasis, opisthorchiasis, and paragonimiasis

- Tapeworm infections such as cysticercosis, taeniasis, and echinococcosis

Anthelmintics such as mebendazole and albendazole have been reported to eliminate infestation of humans more effectively than thiabendazole.

Prevention is as simple as avoiding eating small, whole, uncooked fish. However, in "C. philippinensis" endemic areas, such dietary habits are common and have been practiced for many generations.

Good hygiene is necessary to avoid reinfection. The Rockefeller Foundation's hookworm campaign in Mexico in the 1920s was extremely effective at eliminating hookworm from humans with the use of anthelmintics. However, preventative measures were not adequately introduced to the people that were treated. Therefore, the rate of reinfection was extremely high and the project evaluated through any sort of scientific method was a marked failure. More education was needed to inform the people of the importance of wearing shoes, using latrines (better access to sanitation), and good hygiene.

Intestinal parasite prevention methods are not isolated to specific geographical areas; however, many of the research-based interventions have primarily taken place in underdeveloped countries and regions, where sanitation is a large concern for spreading disease.Current best practice behaviors that prevent intestinal parasites include: using proper hand washing practices, using correctly-built latrines with ample ventilation, having a piped water source, and wearing shoes. Currently, in some parts of Ethiopia where disease prevalence is high, up to 80% of people in a population lack access to washing facilities. While is this high, 93% did have access to a latrine, but only 29.2% of those latrines had proper construction to decrease parasitic infections.Behavioral interventions have focused on promoting washing, sometimes with soap, in context of education at schools and child care facilities. In recent studies, the best interventions follow a multidisciplinary approach by:

- Increasing environmental sanitation to promote hand washing and shoe wearing habits

- Educating children at young ages at school and at home

Specific evidence-based interventions that may lower disease prevalence include:

- Interventions at schools, focusing on the construction of pit latrines (ventilated and improved), providing clean drinking water and educating the students about hygiene

- The SAFE (surgery, antibiotics, facial cleanliness, environmental sanitation) strategy to address trachoma, primarily the facial cleanliness and the environmental sanitation components

- Hand-washing with soap at critical times and nail clipping to decrease reinfection rates, although further research is needed to develop and implement similar interventions at scale

- Programs combining anthelmintic drug administration with interventions to increase environmental sanitation (such as decreasing fecal contamination)

The prevalence of intestinal parasites is the highest among children that are living in the poorest communities in developing nations. The most common causes of intestinal parasites are through consumption of contaminated water, infected soil, inadequate sanitation and hygiene, and improper hygiene. Specifically, lack of access to facilities for safe disposal of human waste can result in intestinal parasites and disease. Poor hygiene habits or lacking available hygiene resources, such as hand washing facilities, also negatively impact rates of disease. Parasitic contamination can also occur from eating raw vegetables and fruits, soil-eating behavior, and lack of available safe water.

Parasites can get into the intestine by going through the mouth from uncooked or unwashed food, contaminated water or hands, or by skin contact with larva infected soil; they can also be transferred by the sexual act of anilingus in some cases.

When the organisms are swallowed, they move into the intestine, where they can reproduce and cause symptoms. Children are particularly susceptible if they are not thoroughly cleaned after coming into contact with infected soil that is present in environments that they may frequently visit such as sandboxes and school playgrounds. People in developing countries are also at particular risk due to drinking water from sources that may be contaminated with parasites that colonize the gastrointestinal tract.

Some intestinal parasitic infections may play a role in irritable bowel syndrome and other long-term sequelae.

Symptoms in infested humans include watery diarrhea, abdominal pain, edema, weight loss, borborygmus (stomach growling), and depressed levels of potassium and albumin in the blood. In humans, the parasites damage the cells of the intestinal wall. This damage interferes with the absorption of nutrients and the maintenance of a proper electrolyte balance. Untreated "C. philippinensis" infestations are often fatal.

In cats, giardiasis responds to metronidazole, although this should not be administered to pregnant cats as it can cause developmental malformations. An alternative and effective drug is febendazole.

The coccidian parasite "Isospora belli" infects the epithelial cells of the small intestine, and is the least common of the three intestinal coccidia that infect humans ("Toxoplasma", "Cryptosporidium", and "Isospora").

Avoiding food or water that may be contaminated with stool can help prevent the infection of "Cystoisospora" (Isosporiasis). Good hand-washing, and personal-hygiene practices should be used as well. One should wash their hands with soap and warm water after using the toilet, changing diapers, and before handling food (CDC.gov). It is also important to teach children the importance of washing their hands, and how to properly wash their hands.

Parasitic worms have been used as a medical treatment for various diseases, particularly those involving an overactive immune response. As humans have evolved with parasitic worms, proponents argue they are needed for a healthy immune system. Scientists are looking for a connection between the prevention and control of parasitic worms and the increase in allergies such as hay-fever in developed countries. Parasitic worms may be able to damp down the immune system of their host, making it easier for them to live in the intestine without coming under attack. This may be one mechanism for their proposed medicinal effect.

One study suggests a link between the rising rates of metabolic syndrome in the developed worlds and the largely successful efforts of Westerners to eliminate intestinal parasites. The work suggests eosinophils (a type of white blood cell) in fat tissue play an important role in preventing insulin resistance by secreting interleukin 4, which in turn switches macrophages into "alternative activation". Alternatively-activated macrophages are important to maintaining glucose homeostasis (i.e., blood sugar regulation). Helminth infection causes an increase in eosinophils. In the study, the authors fed rodents a high-fat diet to induce metabolic syndrome, and then injected them with helminths. Helminth infestation improved the rodents' metabolism. The authors concluded:

Although sparse in blood of persons in developed countries, eosinophils are often elevated in individuals in rural developing countries where intestinal parasitism is prevalent and metabolic syndrome rare. We speculate that eosinophils may have evolved to optimize metabolic homeostasis during chronic infections by ubiquitous intestinal parasites….

Helminths (), also commonly known as parasitic worms, are large multicellular organisms, which can generally be seen with the naked eye when they are mature. They are often referred to as intestinal worms even though not all helminths reside in the intestines. For example, schistosomes are not intestinal worms, but rather reside in blood vessels. The word helminth comes from Greek "hélmins", a kind of worm.

There is no consensus on the taxonomy of helminths. It is simply a commonly used term to describe certain worms with some similarities. These are flatworms (platyhelminthes), namely cestodes (tapeworms) and trematodes (flukes), and roundworms or nemathelminths (nematodes) – both of these are parasitic worm types – and the annelida, which are not parasitic or at the most ectoparasites like the leeches.

Helminths are worm-like organisms living in and feeding on living hosts. They receive nourishment and protection while disrupting their hosts' nutrient absorption. This can cause weakness and disease of the host. Those helminths that live inside the digestive tract are called intestinal parasites. They can live inside humans and other animals. In their adult form, helminths cannot multiply in humans. Helminths are able to survive in their mammalian hosts for many years due to their ability to manipulate the immune response by secreting immunomodulatory products. All helminths produce eggs (also called ova) for reproduction. These eggs have a strong shell that protects them against a range of environmental conditions. The eggs can therefore survive in the environment, outside their hosts, for many months or years.

Many, but not all, of the worms referred to as helminths belong to the group of intestinal parasites. An infection by a helminth is known as helminthiasis, helminth infection or intestinal worm infection. There is a naming convention which applies to all helminths: the ending "-asis" (or in veterinary science: "-osis") is added at the end of the name of the worm to denote the infection with that particular worm. For example, "Ascaris" is the name of a type of helminth, and ascariasis is the name of the infectious disease caused by that helminth.

Preventive measures for visitors to tropical areas where the condition exists include steps to reduce the likelihood of gastroenteritis. These may comprise using only bottled water for drinking, brushing teeth, and washing food, and avoiding fruits washed with tap water (or consuming only peeled fruits, such as bananas and oranges). Basic sanitation is necessary to reduce fecal-oral contamination and the impact of environmental enteropathy in the developing world.

The prognosis for tropical sprue may be excellent after treatment. It usually does not recur in people who get it during travel to affected regions. The recurrence rate for natives is about 20%, but another study showed changes can persist for several years.

Capillariasis is a disease caused by nematodes in the "Capillaria" genus. The two principal forms of the disease are:

- Intestinal capillariasis, caused by "Capillaria philippinensis"

- Hepatic capillariasis, caused by "Capillaria hepatica"

human intestinal spirochetosis, also intestinal spirochetes, colonic spirochetosis and colonic spirochetes, is an infection of the colonic-type mucosa with spirochete microorganisms.

Insufficient data exists, but "Shigella" is estimated to have caused the death of 34,000 children under the age of five in 2013, and 40,000 deaths in people over five years of age. "Amebiasis" infects over 50 million people each year, of whom 50,000 die.

Dysentery caused by amoebiasis, an infection by the amoeba "Entamoeba histolytica", which is found mainly in tropical areas, is known as amoebic dysentery. Proper treatment of the underlying infection of amoebic dysentery is important; insufficiently treated amoebiasis can lie dormant for years and subsequently lead to severe, potentially fatal, complications.

When amoebae inside the bowel of an infected person are ready to leave the body, they group together and form a shell that surrounds and protects them. This group of amoebae is known as a cyst, which is then passed out of the person's body in the feces and can survive outside the body. If hygiene standards are poor — for example, if the person does not dispose of the feces hygienically — then it can contaminate the surroundings, such as nearby food and water.

If another person then eats or drinks food or water that has been contaminated with feces containing the cyst, that person will also become infected with the amoebae. Amoebic dysentery is particularly common in parts of the world where human feces are used as fertilizer.

After entering the person's body through the mouth, the cyst travels down into the stomach. The amoebae inside the cyst are protected from the stomach's digestive acid. From the stomach, the cyst travels to the intestines, where it breaks open and releases the amoebae, causing the infection. The amoebae can burrow into the walls of the intestines and cause small abscesses and ulcers to form. The cycle then begins again.

In Germany, 90% of cases of infectious enteritis are caused by four pathogens, Norovirus, Rotavirus, "Campylobacter" and "Salmonella". Other common causes of infectious enteritis include bacteria such as "Shigella" and "E. coli," as well as viruses such as adenovirus, astrovirus and calicivirus. Other less common pathogens include "Bacillus cereus, Clostridium perfringens, Clostridium difficile" and "Staphylococcus aureus".

"Campylobacter jejuni" is one of the most common sources of infectious enteritis, and the most common bacterial pathogen found in 2 year old and smaller children with diarrhoea. It has been linked to consumption of contaminated water and food, most commonly poultry and milk. The disease tends to be less severe in developing countries, due to the constant exposure which people have with the antigen in the environment, leading to early development of antibodies.

Rotavirus is responsible for infecting 140 million people and causing 1 million deaths each year, mostly in children younger than 5 years. This makes it the most common cause of severe childhood diarrhoea and diarrhea-related deaths in the world. It selectively targets mature enterocytes in the small intestine, causing malabsorption, as well as inducing secretion of water. It has also been observed to cause villus ischemia, and increase intestinal motility. The net result of these changes is induced diarrhoea.

Enteritis necroticans is an often fatal illness, caused by β-toxin of "Clostridium perfringens". This causes inflammation and segments of necrosis throughout the gastrointestinal tract. It is most common in developing countries, however has also been documented in post-World War II Germany. Risk factors for enteritis necroticans include decreased trypsin activity, which prevent intestinal degradation of the toxin, and reduced intestinal motility, which increases likelihood of toxin accumulation.

Human intestinal spirochetosis is caused by "Brachyspira pilosicoli" and "Brachyspira aalborgi". Porcine and avian intestinal spirochetosis are caused by "Brachyspira pilosicoli".

Due to the difficulty of exploring host and amebic factors involved in the pathogenesis of amebic liver abscess in humans, most studies have been conducted with animal models (e.g., mice, gerbils, and hamsters). Histopathological findings revealed that the chronic phase of amebic liver abscess in humans corresponds to lytic or liquefactive necrosis, whereas in rodent models there is granulomatous inflammation. However, the use of animal models has provided important information on molecules and mechanisms of the host/parasite interaction in amebic liver abscess.

Until 1964, all available amoebicides were selective in their sites of action. The development of newer nitro-imidazole derivatives led to Niridazole. It was given in a daily dose of 25–30 mgm. per kg to 50 patients for seven days. The cure rate was found to be 84% with serious side effects in one patient. An Indian study of 30 patients on this drug revealed that it acted as a contact amoebicide and also against the invasive forms.23 The therapeutic action of Ambilhar was found to be significantly better than that produced by a combination of dehydroemetine and chloroquine.

Ischemic enteritis is uncommon compared to ischemic colitis due to the highly vascularised nature of the small intestine, allowing for sufficient blood flow in most situations. It develops due to circulatory shock of mesenteric vessels in the absence of major vessel occlusion, often associated with an underlying condition such as hypertension, arrhythmia or diabetes. Thus it has been considered to be associated with atherosclerosis. Surgical treatment is usually required due to the likelihood of stenosis or complete occlusion of the small intestine. Ischemic damage can range from mucosal infarction, which is limited only to the mucosa; mural infarction of the mucosa and underlying submucosa; to transmural infarction of the full thickness of the gastrointestinal wall. Mucosal and mural infarcts in and of themselves may not be fatal, however may progress further to a transmural infarct. This has the potential for perforation of the wall, leading to peritonitis.

Horses may develop pharyngitis, laryngitis, or esophagitis secondary to indwelling nasogastric tube. Other complications include thrombophlebitis, laminitis (which subsequently reduces survival rate), and weight loss. Horses are also at increased risk of hepatic injury.

Survival rates for DPJ are 25–94%. Horses that survive the incident rarely have reoccurrence.

Blind loop syndrome is a complication of surgical operations of the abdomen, as well as inflammatory bowel disease or scleroderma. Another cause is jejunoileal diverticula.