Megaesophagus, also known as esophageal dilatation, is a disorder of the esophagus in humans and other mammals, whereby the esophagus becomes abnormally enlarged. Megaesophagus may be caused by any disease which causes the muscles of the esophagus to fail to properly propel food and liquid from the mouth into the stomach (that is, a failure of peristalsis). Food can become lodged in the flaccid esophagus, where it may decay, be regurgitated, or may be inhaled into the lungs (leading to aspiration pneumonia).

Megaesophagus may occur secondary to diseases such as achalasia or Chagas disease. Achalasia is caused by a loss of ganglion cells in the myenteric plexus. There is a marked lack of contraction within the muscles involved in peristalsis with a constant contraction of the lower esophageal sphincter. Dilation of the esophagus results in difficulty swallowing. Retention of food bolus is also noted.

External signs and symptoms are constipation of very long duration, abdominal bloating, abdominal tenderness and tympany, abdominal pain, palpation of hard fecal masses and, in toxic megacolon, fever, low blood potassium, tachycardia and shock. Stercoral ulcers are sometimes observed in chronic megacolon, which may lead to perforation of the intestinal wall in approximately 3% of the cases, leading to sepsis and risk of death.

Megacolon is an abnormal dilation of the colon (also called the large intestine). The dilation is often accompanied by a paralysis of the peristaltic movements of the bowel. In more extreme cases, the feces consolidate into hard masses inside the colon, called fecalomas (literally, "fecal tumor"), which can require surgery to be removed.

A human colon is considered abnormally enlarged if it has a diameter greater than 12 cm in the cecum (it is usually less than 9 cm), greater than 6.5 cm in the rectosigmoid region and greater than 8 cm for the ascending colon. The transverse colon is usually less than 6 cm in diameter.

A megacolon can be either acute or chronic. It can also be classified according to cause.

Signs of laryngeal paralysis include voice change (the dog's bark becomes hoarse-sounding), gagging or coughing (often during or after eating or drinking), exercise intolerance, inspiratory stridor (noisy breathing on inspiration), difficulty breathing, and in severe cases cyanosis or syncope (fainting). Secondary problems may also occur, including aspiration or edema in the lungs, though often the problem remains an upper respiratory problem. Affected dogs are vulnerable to heat stroke and heat exhaustion due to their limited ability to cool themselves down by panting, but the disorder itself can be mistaken for heat stroke.

Signs may occur at any time, but initially owners may only notice that their dog's bark sounds different, that their dog can't run as much as before, or that the dog has trouble in hot weather in unilateral cases because the unaffected side can compensate for the paralysed side. However most unilateral cases will eventually progress to include both sides of the larynx, a more serious problem with symptoms appearing more often.

Signs are usually worse in hot and humid weather, during exercise, during times of stress or excitement, and in obese pets. Acute or late-stage symptoms are usually unmistakable and require immediate emergency treatment.

This condition is usually diagnosed by direct examination of the larynx under light sedation, which also allows checking for benign or malignant tumors. Tests, such as thoracic radiographs, CT-scans, or echocardiography, are sometimes needed to rule out heart, lung, or mediastinal diseases or other possible causes of the symptoms often seen with LP. Some vets may also recommend running a thyroid profile since LP can be a symptom or complication of hypothyroidism.

The human disease occurs in two stages: an acute stage, which occurs shortly after an initial infection, and a chronic stage that develops over many years.

The acute phase lasts for the first few weeks or months of infection. It usually occurs unnoticed because it is symptom-free or exhibits only mild symptoms that are not unique to Chagas disease. These can include fever, fatigue, body aches, muscle pain, headache, rash, loss of appetite, diarrhea, nausea, and vomiting. The signs on physical examination can include mild enlargement of the liver or spleen, swollen glands, and local swelling (a chagoma) where the parasite entered the body.

The most recognized marker of acute Chagas disease is called Romaña's sign, which includes swelling of the eyelids on the side of the face near the bite wound or where the bug feces were deposited or accidentally rubbed into the eye. Rarely, young children, or adults may die from the acute disease due to severe inflammation/infection of the heart muscle (myocarditis) or brain (meningoencephalitis). The acute phase also can be severe in people with weakened immune systems.

If symptoms develop during the acute phase, they usually resolve spontaneously within three to eight weeks in approximately 90% of individuals. Although the symptoms resolve, even with treatment the infection persists and enters a chronic phase. Of individuals with chronic Chagas disease, 60–80% will never develop symptoms (called "indeterminate" chronic Chagas disease), while the remaining 20–40% will develop life-threatening heart and/or digestive disorders during their lifetime (called "determinate" chronic Chagas disease). In 10% of individuals, the disease progresses directly from the acute form to a symptomatic clinical form of chronic Chagas disease.

The symptomatic (determinate) chronic stage affects the nervous system, digestive system and heart. About two-thirds of people with chronic symptoms have cardiac damage, including dilated cardiomyopathy, which causes heart rhythm abnormalities and may result in sudden death. About one-third of patients go on to develop digestive system damage, resulting in dilation of the digestive tract (megacolon and megaesophagus), accompanied by severe weight loss. Swallowing difficulties (secondary achalasia) may be the first symptom of digestive disturbances and may lead to malnutrition.

20% to 50% of individuals with intestinal involvement also exhibit cardiac involvement. Up to 10% of chronically infected individuals develop neuritis that results in altered tendon reflexes and sensory impairment. Isolated cases exhibit central nervous system involvement, including dementia, confusion, chronic encephalopathy and sensory and motor deficits.

The clinical manifestations of Chagas disease are due to cell death in the target tissues that occurs during the infective cycle, by sequentially inducing an inflammatory response, cellular lesions, and fibrosis. For example, intracellular amastigotes destroy the intramural neurons of the autonomic nervous system in the intestine and heart, leading to megaintestine and heart aneurysms, respectively. If left untreated, Chagas disease can be fatal, in most cases due to heart muscle damage.

Chagas disease, also known as American trypanosomiasis, is a tropical parasitic disease caused by the protist "Trypanosoma cruzi". It is spread mostly by insects known as Triatominae, or "kissing bugs". The symptoms change over the course of the infection. In the early stage, symptoms are typically either not present or mild, and may include fever, swollen lymph nodes, headaches, or local swelling at the site of the bite. After 8–12 weeks, individuals enter the chronic phase of disease and in 60–70% it never produces further symptoms. The other 30 to 40% of people develop further symptoms 10 to 30 years after the initial infection, including enlargement of the ventricles of the heart in 20 to 30%, leading to heart failure. An enlarged esophagus or an enlarged colon may also occur in 10% of people.

"T. cruzi" is commonly spread to humans and other mammals by the blood-sucking "kissing bugs" of the subfamily Triatominae. These insects are known by a number of local names, including: "vinchuca" in Argentina, Bolivia, Chile and Paraguay, "barbeiro" (the barber) in Brazil, "pito" in Colombia, "chinche" in Central America, and "chipo" in Venezuela. The disease may also be spread through blood transfusion, organ transplantation, eating food contaminated with the parasites, and by vertical transmission (from a mother to her fetus). Diagnosis of early disease is by finding the parasite in the blood using a microscope. Chronic disease is diagnosed by finding antibodies for "T. cruzi" in the blood.

Prevention mostly involves eliminating kissing bugs and avoiding their bites. Other preventive efforts include screening blood used for transfusions. A vaccine has not been developed as of 2017. Early infections are treatable with the medication benznidazole or nifurtimox. Medication nearly always results in a cure if given early, but becomes less effective the longer a person has had Chagas disease. When used in chronic disease, medication may delay or prevent the development of end–stage symptoms. Benznidazole and nifurtimox cause temporary side effects in up to 40% of people including skin disorders, brain toxicity, and digestive system irritation.

It is estimated that 6.6 million people, mostly in Mexico, Central America and South America, have Chagas disease as of 2015. In 2015, Chagas was estimated to result in 8,000 deaths. Most people with the disease are poor, and most do not realize they are infected. Large-scale population movements have increased the areas where Chagas disease is found and these include many European countries and the United States. These areas have also seen an increase in the years up to 2014. The disease was first described in 1909 by the Brazilian physician Carlos Chagas, after whom it is named. Chagas disease is classified as a neglected tropical disease. It affects more than 150 other animals.

The most common clinical manifestations are related to mental status and gastrointestinal function; they include lethargy, anorexia, vomiting, weight loss, and weakness. Additional findings may include dehydration, bradycardia, weak femoral pulses, and abdominal pain. Polyuria and polydipsia, diarrhea, and shivering are occasionally reported.

Symptoms of hypoadrenocorticism can include vomiting, diarrhea, lethargy, lack of appetite, tremors or shaking, muscle weakness, low body temperature, collapse, low heart rate, and pain in the hind quarters. Hypoglycemia can also be present, and initially may be confused with seizure disorders, insulin-secreting pancreatic tumor (insulinoma), food poisoning, parvovirus enteritis, gastric volvulus, spinal or joint problems, earning hypoadrenocorticism the nicknames of "the Great Mimic" and "the Great Imitator". It is possible not to see any signs of the disease until 90% of the adrenal cortex is no longer functioning.

If hyponatremia (low sodium) and hyperkalemia (high potassium) are severe, the resulting hypovolemia, prerenal azotemia, and cardiac arrhythmias may result in an Addisonian crisis. In severe cases, the patient may be presented in shock and moribund. Addisonian crisis must be differentiated from other life-threatening disorders such as diabetic ketoacidosis, necrotizing pancreatitis, and septic peritonitis.