Signs and symptoms may range from mild abdominal discomfort to full-blown dysentery characterized by cramps, diarrhea, with slimy-consistent stools, fever, blood, pus, or mucus in stools or tenesmus. Onset time is 12 to 96 hours, and recovery takes 5 to 7 days.

Infections are associated with mucosal ulceration, rectal bleeding, and drastic dehydration. Reactive arthritis and hemolytic uremic syndrome are possible sequelae that have been reported in the aftermath of shigellosis.

"Shigella" can be transmitted through food, including salads (potato, tuna, shrimp, macaroni, and chicken), raw vegetables, milk and dairy products, and meat. Contamination of these foods is usually through the fecal-oral route. Fecally contaminated water and unsanitary handling by food handlers are the most common causes of contamination. Apart from hand-to-mouth infection, shigellosis is transmitted through fomites, water and mechanical vectors like houseflies.

The most common neurological symptom includes seizures.

Shigellosis is a type of diarrhea caused by a bacterial infection with "Shigella". Symptoms generally start one to two days after exposure and include diarrhea, fever, abdominal pain, and pain with passing stool. Blood may be present in the stool. Symptoms typically last five to seven days. Complications can include post infectious arthritis, sepsis, seizures, and hemolytic uremic syndrome.

Shigellosis is caused by four specific types of "Shigella". These are typically spread by exposure to infected feces. This can occur via contaminated food, water, or hands. Contamination may be spread by flies or when changing diapers. Diagnosis is by stool culture.

Prevention is by properly washing the hands. There is no vaccine. Shigellosis usually resolves without specific treatment. Sufficient fluids by mouth and rest is recommended. Bismuth subsalicylate may help with the symptoms; however, medications that slow the bowels such as loperamide are not recommended. In severe cases antibiotics may be used but resistance is common. Commonly used antibiotics include ciprofloxacin or azithromycin.

Globally shigellosis occurs in at least 80 million people and results in about 700,000 deaths a year. Most cases occur in the developing world. Young children are most commonly affected. Outbreaks of disease may occur in childcare settings and schools. It is also relatively common among travelers. In the United States about half a million cases occur a year.

The prodromal symptoms are fever, headache, and myalgia, which can be severe, lasting as long as 24 hours. After 1–5 days, typically, these are followed by diarrhea (as many as 10 watery, frequently bloody, bowel movements per day) or dysentery, cramps, abdominal pain, and fever as high as 40 °C (104 °F). In most people, the illness lasts for 2–10 days. It is classified as invasive/inflammatory diarrhea, also described as bloody diarrhea or dysentery.

There are other diseases showing similar symptoms. For instance, abdominal pain and tenderness may be very localized, mimicking acute appendicitis. Furthermore, "Helicobacter pylori" is closely related to Campylobacter and causes peptic ulcer disease.

Bacillary dysentery is a type of dysentery, and is a severe form of shigellosis.

Bacillary dysentery is associated with species of bacteria from the Enterobacteriaceae family. The term is usually restricted to "Shigella" infections.

Shigellosis is caused by one of several types of "Shigella" bacteria. Three species are associated with bacillary dysentery: "Shigella sonnei, Shigella flexneri" and "Shigella dysenteriae". A study in China indicated that "Shigella flexneri" 2a was the most common serotype.

Salmonellosis caused by "Salmonella enterica" (serovar "Typhimurium") has also been described as a cause of bacillary dysentery, though this definition is less common. It is sometimes listed as an explicit differential diagnosis of bacillary dysentery, as opposed to a cause.

Bacillary dysentery should not be confused with diarrhea caused by other bacterial infections. One characteristic of bacillary dysentery is blood in stool, which is the result of invasion of the mucosa by the pathogen.

Complications include toxic megacolon, dehydration and sepsis. Such complications generally occur in young children (< 1 year of age) and immunocompromised people. A chronic course of the disease is possible; this disease process is likely to develop without a distinct acute phase. Chronic campylobacteriosis features a long period of sub-febrile temperature and asthenia; eye damage, arthritis, endocarditis may develop if infection is untreated.

Occasional deaths occur in young, previously healthy individuals because of blood volume depletion (due to dehydration), and in persons who are elderly or immunocompromised.

Some individuals (1–2 in 100,000 cases) develop Guillain–Barré syndrome, in which the nerves that join the spinal cord and brain to the rest of the body are damaged, sometimes permanently. This occurs only with infection of "C. jejuni" and "C. upsaliensis".

The onset of TD usually occurs within the first week of travel, but may occur at any time while traveling, and even after returning home, depending on the incubation period of the infectious agent. Bacterial TD typically begins abruptly, but "Cryptosporidium" may incubate for seven days, and "Giardia" for 14 days or more, before symptoms develop. Typically, a traveler experiences four to five loose or watery bowel movements each day. Other commonly associated symptoms are abdominal cramping, bloating, fever, and malaise. Appetite may decrease significantly. Though unpleasant, most cases of TD are mild, and resolve in a few days without medical intervention.

Blood or mucus in the diarrhea, significant abdominal pain, or high fever suggests a more serious cause, such as cholera, characterized by a rapid onset of weakness and torrents of watery diarrhea with flecks of mucus (described as "rice water" stools). Medical care should be sought in such cases; dehydration is a serious consequence of cholera, and may trigger serious sequelae—including, in rare instances, death—as rapidly as 24 hours after onset if not addressed promptly.

Transmission is fecal-oral and is remarkable for the small number of organisms that may cause disease (10 ingested organisms cause illness in 10% of volunteers, and 500 organisms cause disease in 50% of volunteers). "Shigella" bacteria invade the intestinal mucosal cells but do not usually go beyond the lamina propria. Dysentery is caused when the bacteria escape the epithelial cell phagolysosome, multiply within the cytoplasm, and destroy host cells. Shiga toxin causes hemorrhagic colitis and hemolytic-uremic syndrome by damaging endothelial cells in the microvasculature of the colon and the glomeruli, respectively. In addition, chronic arthritis secondary to "S. flexneri" infection, called reactive arthritis, may be caused by a bacterial antigen; the occurrence of this syndrome is strongly linked to HLA-B27 genotype, but the immunologic basis of this reaction is not understood.

The most common form of dysentery is bacillary dysentery, which is typically a mild illness, causing symptoms normally consisting of mild stomach pains and frequent passage of stool or diarrhea. Symptoms normally present themselves after one to three days, and are usually no longer present after a week. The frequency of urges to defecate, the large volume of liquid feces passed, and the presence of mucus, pus, and blood depends on the pathogen causing the disease. Temporary lactose intolerance can occur, as well. In some caustic occasions severe abdominal pain, fever, shock, and delirium can all be symptoms.

In extreme cases, dysentery patients may pass more than one litre of fluid per hour. More often, individuals will complain of nausea, abdominal pain, and frequent watery and usually foul-smelling diarrhea, accompanied by mucus, blood, rectal pain, and fever. Vomiting, rapid weight-loss, and generalized muscle aches sometimes also accompany dysentery. On rare occasions, the amoebic parasite will invade the body through the bloodstream and spread beyond the intestines. In such cases, it may more seriously infect other organs such as the brain, lungs, and most commonly the liver.

Dysentery is a type of gastroenteritis that results in diarrhea with blood. Other symptoms may include fever, abdominal pain, and a feeling of incomplete defecation.

It is caused by several types of infections such as bacteria, viruses, parasitic worms, or protozoa. The mechanism is an inflammatory disorder of the intestine, especially of the colon.

Amoebiasis, also known amoebic dysentery, is an infection caused by any of the amoebas of the "Entamoeba" group. Symptoms are most common during infection by "Entamoeba histolytica". Amoebiasis can be present with no, mild, or severe symptoms. Symptoms may include abdominal pain, diarrhea, or bloody diarrhea. Complications can include inflammation of the colon with tissue death or perforation, which may result in peritonitis. People affected may develop anemia due to loss of blood.

Cysts of "Entamoeba" can survive for up to a month in soil or for up to 45 minutes under fingernails. Invasion of the intestinal lining can cause bloody diarrhea. If the parasite reaches the bloodstream it can spread through the body, most frequently ending up in the liver where it can cause amoebic liver abscesses. Liver abscesses can occur without previous diarrhea. Diagnosis is typical by stool examination using a microscope, but may not reliably exclude infection or separate between specific types. An increased white blood cell count may be present in severe cases. The most accurate test is finding specific antibodies in the blood, but it may remain positive following treatment. Bacterial colitis can result in similar symptoms.

Prevention of amoebiasis is by improved sanitation, including separating food and water from faeces. There is no vaccine. There are two treatment options depending on the location of the infection. Amoebiasis in tissues is treated with either metronidazole, tinidazole, nitazoxanide, dehydroemetine or chloroquine, while luminal infection is treated with diloxanide furoate or iodoquinoline. Effective treatment against all stages of the disease may require a combination of medications. Infections without symptoms do not require treatment but infected individuals can spread the parasite to others and treatment can be considered. Treatment of other "Entamoeba" infections apart from "E. histolytica" is not needed.

Amoebiasis is present all over the world. About 480 million people are infected with amoebiasis and this results in the death of between 40,000–110,000 people a year. Most infections are now believed due to "E. dispar". "E. dispar" is more common in certain areas and symptomatic cases may be less common than previously reported. The first case of amoebiasis was documented in 1875 and in 1891 the disease was described in detail, resulting in the terms "amoebic dysentery" and "amoebic liver abscess". Further evidence from the Philippines in 1913 found that upon swallowing cysts of "E. histolytica" volunteers developed the disease.

Traveler's diarrhea (TD) is a stomach and intestinal infection. TD is defined as the passage of unformed stool (one or more by some definitions, three or more by others) while traveling. It may be accompanied by abdominal cramps, nausea, fever, and bloating. Occasionally bloody diarrhea may occur. Most travelers recover within four days with little or no treatment. About 10% of people may have symptoms for a week.

Bacteria are responsible for more than half of cases. The bacteria enterotoxigenic "Escherichia coli" (ETEC) are typically the most common except in Southeast Asia, where "Campylobacter" is more prominent. About 10% to 20% of cases are due to norovirus. Protozoa such as "Giardia" may cause longer term disease. The risk is greatest in the first two weeks of travel and among young adults. People affected are more often from the developed world.

Recommendations for prevention include eating only properly cleaned and cooked food, drinking bottled water, and frequent hand washing. The oral cholera vaccine, while effective for cholera, is of questionable use for traveler's diarrhea. Preventative antibiotics are generally discouraged. Primary treatment includes drinking lots of fluids and replacing lost salts (oral rehydration therapy). Antibiotics are recommended for significant or persistent symptoms, and can be taken with loperamide to decrease diarrhea. Hospitalization is required in less than 3% of cases.

Estimates of the percentage of people affected range from 20 to 50% among travelers to the developing world. TD is particularly common among people travelling to Asia (except Japan), the Middle East, Africa, Mexico, and Central and South America. The risk is moderate in Southern Europe, Russia, and China. TD has been linked to later irritable bowel syndrome and Guillain–Barré syndrome. It has colloquially been known by a number of names, including "Montezuma's revenge" and "Delhi belly".

Enteroinvasive "Escherichia coli" (EIEC) is a type of pathogenic bacteria whose infection causes a syndrome that is identical to shigellosis, with profuse diarrhea and high fever. EIEC are highly invasive, and they use adhesin proteins to bind to and enter intestinal cells. They produce no toxins, but severely damage the intestinal wall through mechanical cell destruction.

It is closely related to "Shigella".

After the "E. coli" strain penetrates through the epithelial wall, the endocytosis vacuole gets lysed, the strain multiplies using the host cell machinery, and extends to the adjacent epithelial cell. In addition, the plasmid of the strain carries genes for a type III secretion system that is used as the virulent factor. Although it is an invasive disease, the invasion usually does not pass the submucosal layer. The similar pathology to shigellosis may be because both strains of bacteria share some virulent factors. The invasion of the cells can trigger a mild form of diarrhea or dysentery, often mistaken for dysentery caused by "Shigella" species. The illness is characterized by the appearance of blood and mucus in the stools of infected individuals or a condition called colitis.

Dysentery caused by EIEC usually occurs within 12 to 72 hours following the ingestion of contaminated food. The illness is characterized by abdominal cramps, diarrhea, vomiting, fever, chills, and a generalized malaise. Dysentery caused by this organism is generally self-limiting with no known complications.

Enterovirulent classes of "E. coli" are referred to as the EEC group (enterovirulent "E. coli"):

1. Enteroinvasive "E. coli" (EIEC) invades (passes into) the intestinal wall to produce severe diarrhea.

2. Enterohemorrhagic "E. coli" (EHEC): A type of EHEC, "E. coli" 0157:H7, can cause bloody diarrhea and hemolytic uremic syndrome (anemia and kidney failure).

3. Enterotoxigenic "E. coli" (ETEC) produces a toxin that acts on the intestinal lining, and is the most common cause of traveler's diarrhea.

4. Enteropathogenic "E. coli" (EPEC) can cause diarrhea outbreaks in newborn nurseries.

5. Enteroaggregative "E. coli" (EAggEC) can cause acute and chronic (long-lasting) diarrhea in children.

It is currently unknown what foods may harbor EIEC, but any food contaminated with human feces from an ill individual, either directly or via contaminated water, could cause disease in others. Outbreaks have been associated with hamburger meat and unpasteurized milk.

Classically, the course of untreated typhoid fever is divided into four distinct stages, each lasting about a week. Over the course of these stages, the patient becomes exhausted and emaciated.

- In the first week, the body temperature rises slowly, and fever fluctuations are seen with relative bradycardia (Faget sign), malaise, headache, and cough. A bloody nose (epistaxis) is seen in a quarter of cases, and abdominal pain is also possible. A decrease in the number of circulating white blood cells (leukopenia) occurs with eosinopenia and relative lymphocytosis; blood cultures are positive for "Salmonella" Typhi or "S. paratyphi". The Widal test is usually negative in the first week.

- In the second week, the person is often too tired to get up, with high fever in plateau around and bradycardia (sphygmothermic dissociation or Faget sign), classically with a dicrotic pulse wave. Delirium is frequent, often calm, but sometimes agitated. This delirium gives to typhoid the nickname of "nervous fever". Rose spots appear on the lower chest and abdomen in around a third of patients. Rhonchi are heard in lung bases.

- The abdomen is distended and painful in the right lower quadrant, where borborygmi can be heard. Diarrhea can occur in this stage: six to eight stools in a day, green, comparable to pea soup, with a characteristic smell. However, constipation is also frequent. The spleen and liver are enlarged (hepatosplenomegaly) and tender, and liver transaminases are elevated. The Widal test is strongly positive, with antiO and antiH antibodies. Blood cultures are sometimes still positive at this stage.

- (The major symptom of this fever is that the fever usually rises in the afternoon up to the first and second week.)

- In the third week of typhoid fever, a number of complications can occur:

- Intestinal haemorrhage due to bleeding in congested Peyer's patches; this can be very serious, but is usually not fatal.

- Intestinal perforation in the distal ileum: this is a very serious complication and is frequently fatal. It may occur without alarming symptoms until septicaemia or diffuse peritonitis sets in.

- Encephalitis

- Respiratory diseases such as pneumonia and acute bronchitis

- Neuropsychiatric symptoms (described as "muttering delirium" or "coma vigil"), with picking at bedclothes or imaginary objects.

- Metastatic abscesses, cholecystitis, endocarditis, and osteitis

- The fever is still very high and oscillates very little over 24 hours. Dehydration ensues, and the patient is delirious (typhoid state). One-third of affected individuals develop a macular rash on the trunk.

- Platelet count goes down slowly and risk of bleeding rises.

- By the end of third week, the fever starts subsiding

Most infected people, about 90%, are asymptomatic, but this disease has the potential to make the sufferer dangerously ill. It is estimated that about 40,000 to 100,000 people worldwide die annually due to amoebiasis.

Infections can sometimes last for years. Symptoms take from a few days to a few weeks to develop and manifest themselves, but usually it is about two to four weeks. Symptoms can range from mild diarrhea to severe dysentery with blood and mucus. The blood comes from lesions formed by the amoebae invading the lining of the large intestine. In about 10% of invasive cases the amoebae enter the bloodstream and may travel to other organs in the body. Most commonly this means the liver, as this is where blood from the intestine reaches first, but they can end up almost anywhere in the body.

Onset time is highly variable and the average asymptomatic infection persists for over a year. It is theorized that the absence of symptoms or their intensity may vary with such factors as strain of amoeba, immune response of the host, and perhaps associated bacteria and viruses.

In asymptomatic infections the amoeba lives by eating and digesting bacteria and food particles in the gut, a part of the gastrointestinal tract. It does not usually come in contact with the intestine itself due to the protective layer of mucus that lines the gut. Disease occurs when amoeba comes in contact with the cells lining the intestine. It then secretes the same substances it uses to digest bacteria, which include enzymes that destroy cell membranes and proteins. This process can lead to penetration and digestion of human tissues, resulting first in flask-shaped ulcers in the intestine. "Entamoeba histolytica" ingests the destroyed cells by phagocytosis and is often seen with red blood cells (a process known as erythrophagocytosis) inside when viewed in stool samples. Especially in Latin America, a granulomatous mass (known as an amoeboma) may form in the wall of the ascending colon or rectum due to long-lasting immunological cellular response, and is sometimes confused with cancer.

"Theoretically, the ingestion of one viable cyst can cause an infection."

The signs and symptoms of malaria typically begin 8–25 days following infection; however, symptoms may occur later in those who have taken antimalarial medications as prevention. Initial manifestations of the disease—common to all malaria species—are similar to flu-like symptoms, and can resemble other conditions such as sepsis, gastroenteritis, and viral diseases. The presentation may include headache, fever, shivering, joint pain, vomiting, hemolytic anemia, jaundice, hemoglobin in the urine, retinal damage, and convulsions.

The classic symptom of malaria is paroxysm—a cyclical occurrence of sudden coldness followed by shivering and then fever and sweating, occurring every two days (tertian fever) in "P. vivax" and "P. ovale" infections, and every three days (quartan fever) for "P. malariae". "P. falciparum" infection can cause recurrent fever every 36–48 hours, or a less pronounced and almost continuous fever.

Severe malaria is usually caused by "P. falciparum" (often referred to as falciparum malaria). Symptoms of falciparum malaria arise 9–30 days after infection. Individuals with cerebral malaria frequently exhibit neurological symptoms, including abnormal posturing, nystagmus, conjugate gaze palsy (failure of the eyes to turn together in the same direction), opisthotonus, seizures, or coma.

The most commonly reported symptoms in conjunction with infection with "D. fragilis" include abdominal pain (69%) and diarrhea (61%). Diarrhea may be intermittent and may not be present in all cases. It is often chronic, lasting over two weeks. The degree of symptoms may vary from asymptomatic to severe, and can include weight loss, vomiting, fever, and involvement of other digestive organs.

Symptoms may be more severe in children. Additional symptoms reported have included:

1. Weight loss

2. Fatigue

3. Nausea and vomiting

4. Fever

5. Urticaria (skin rash)

6. Pruritus (itchiness)

7. Biliary infection

Malaria has several serious complications. Among these is the development of respiratory distress, which occurs in up to 25% of adults and 40% of children with severe "P. falciparum" malaria. Possible causes include respiratory compensation of metabolic acidosis, noncardiogenic pulmonary oedema, concomitant pneumonia, and severe anaemia. Although rare in young children with severe malaria, acute respiratory distress syndrome occurs in 5–25% of adults and up to 29% of pregnant women. Coinfection of HIV with malaria increases mortality. Renal failure is a feature of blackwater fever, where hemoglobin from lysed red blood cells leaks into the urine.

Infection with "P. falciparum" may result in cerebral malaria, a form of severe malaria that involves encephalopathy. It is associated with retinal whitening, which may be a useful clinical sign in distinguishing malaria from other causes of fever. Enlarged spleen, enlarged liver or both of these, severe headache, low blood sugar, and hemoglobin in the urine with renal failure may occur. Complications may include spontaneous bleeding, coagulopathy, and shock.

Malaria in pregnant women is an important cause of stillbirths, infant mortality, abortion and low birth weight, particularly in "P. falciparum" infection, but also with "P. vivax".

Typhoid fever, also known simply as typhoid, is a bacterial infection due to "Salmonella" typhi that causes symptoms. Symptoms may vary from mild to severe and usually begin six to thirty days after exposure. Often there is a gradual onset of a high fever over several days. Weakness, abdominal pain, constipation, and headaches also commonly occur. Diarrhea is uncommon and vomiting is not usually severe. Some people develop a skin rash with rose colored spots. In severe cases there may be confusion. Without treatment, symptoms may last weeks or months. Other people may carry the bacterium without being affected; however, they are still able to spread the disease to others. Typhoid fever is a type of enteric fever along with paratyphoid fever.

The cause is the bacterium "Salmonella" typhi, also known as "Salmonella enterica" serotype Typhi, growing in the intestines and blood. Typhoid is spread by eating or drinking food or water contaminated with the feces of an infected person. Risk factors include poor sanitation and poor hygiene. Those who travel to the developing world are also at risk and only humans can be infected. Diagnosis is by either culturing the bacteria or detecting the bacterium's DNA in the blood, stool, or bone marrow. Culturing the bacterium can be difficult. Bone marrow testing is the most accurate. Symptoms are similar to that of many other infectious diseases. Typhus is a different disease.

A typhoid vaccine can prevent about 30% to 70% of cases during the first two years. The vaccine may have some effect for up to seven years. It is recommended for those at high risk or people traveling to areas where the disease is common. Other efforts to prevent the disease include providing clean drinking water, better sanitation, and better handwashing. Until it has been confirmed that an individual's infection is cleared, the individual should not prepare food for others. Treatment of disease is with antibiotics such as azithromycin, fluoroquinolones or third generation cephalosporins. Resistance to these antibiotics has been developing, which has made treatment of the disease more difficult.

In 2015, there were 12.5 million new cases worldwide. The disease is most common in India. Children are most commonly affected. Rates of disease decreased in the developed world in the 1940s as a result of improved sanitation and use of antibiotics to treat the disease. Each year in the United States, about 400 cases are reported and it is estimated that the disease occurs in about 6,000 people. In 2015, it resulted in about 149,000 deaths worldwide – down from 181,000 in 1990 (about 0.3% of the global total). The risk of death may be as high as 20% without treatment. With treatment, it is between 1 and 4%. The name typhoid means "resembling typhus" due to the similarity in symptoms.

Trench fever, also known as five-day fever or quintan fever, is the initial manifestation of "B. quintana" infection. Clinical manifestations range from asymptomatic infection to severe illness. Classical presentations include a febrile illness of acute onset, headache, dizziness, and shin pain. Chronic infection manifestations include attacks of fever and aching in some cases and persistent bacteremia in soldiers and homeless people.

"B. henselae" is the etiologic agent for peliosis hepatis, which is defined as a vascular proliferation of sinusoid hepatic capillaries resulting in blood-filled spaces in the liver in HIV patients and organ transplant recipients. Peliosis hepatis can be associated with peliosis of the spleen, as well as bacillary angiomatosis of the skin in HIV patients.

"Bartonella quintana" is transmitted by contamination of a skin abrasion or louse-bite wound with the faeces of an infected body louse ("Pediculus humanus corporis"). There have also been reports of an infected louse bite passing on the infection.

Dientamoebiasis is a medical condition caused by infection with "Dientamoeba fragilis", a single-cell parasite that infects the lower gastrointestinal tract of humans. It is an important cause of traveler's diarrhea, chronic abdominal pain, chronic fatigue, and failure to thrive in children.

The disease is classically a five-day fever of the relapsing type, rarely exhibiting a continuous course. The incubation period is relatively long, at about two weeks. The onset of symptoms is usually sudden, with high fever, severe headache, pain on moving the eyeballs, soreness of the muscles of the legs and back, and frequently hyperaesthesia of the shins. The initial fever is usually followed in a few days by a single, short rise but there may be many relapses between periods without fever. The most constant symptom is pain in the legs. Recovery takes a month or more. Lethal cases are rare, but in a few cases "the persistent fever might lead to heart failure". Aftereffects may include neurasthenia, cardiac disturbances and myalgia.

Response to infection by "Leishmania donovani" varies a great deal, not only by the strength but also by the type of the patient's immune reaction. People with a history of infection by strains of leishmania that cause visceral leishmaniasis show a continuum of immune responses from protective to non-protective. Those who acquired protective immunity (skin test positive) without ever having visceral leishmaniasis have a strong type 1 CD4+ response to leishmania antigens. Antigen specific interferon-gamma and proliferation, as well as the ability to kill intracellular leishmania, are hallmarks of protective immunity. Because visceral leishmaniasis patients lack these responses to leishmania and other antigens, they usually die of secondary infections if left untreated. In addition, increased interleukin-10 secretion is characteristic of the disease. Addition of interleukin-12, anti-interleukin-10, or anti-interleukin-4 to peripheral blood mononuclear cells from acute patients sometimes increases interferon-gamma secretion and proliferation. Acute patient peripheral blood mononuclear cells include CD8+ T regulatory cells that decrease interferon-gamma secretion and proliferation responses to leishmania and other antigens and increase interleukin-10 secretion when added to autologous peripheral blood mononuclear cells harvested after successful treatment. Thus, the CD8+ T regulatory cells reproduce the immune response characteristic of visceral leishmaniasis. CD8+ T regulatory cells are also associated with post kala azar dermal leishmaniasis. Addition of interleukin-12 or interferon-gamma does not prevent CD8+ T regulatory activity. The dominance of type 1 CD4+ T cells in skin test positive adults maybe explained by their secretion of factors that inhibit and kill CD8+ T regulatory cells. Successfully treated patients rarely develop visceral leishmaniasis a second time. Their peripheral blood mononuclear cells show a mixed T1/T2 CD4+ and CD8+ T suppressor response but do have the ability to kill intracellular leishmania.

When people develop visceral leishmaniasis, the most typical symptoms are fever and the enlargement of the spleen, with enlargement of the liver sometimes being seen as well. The blackening of the skin that gave the disease its common name in India does not appear in most strains of the disease, and the other symptoms are very easy to mistake for those of malaria. Misdiagnosis is dangerous, as without proper treatment the mortality rate for kala-azar is close to 100%. "L. donovani" itself is not usually the direct cause of death in kala-azar sufferers, however. Pneumonia, tuberculosis, and dysentery are omnipresent in the depressed regions where leishmaniasis thrives, and, as with AIDS, it is these opportunistic infections that are more likely to kill, flaring up in a host whose immune system has been weakened by the "L. donovani" infection. Progress of the disease is extremely variable, taking anywhere from one to twenty weeks, but a typical duration for the Sudanese strain of the disease is narrower, between twelve and sixteen weeks.

Even with recovery, kala-azar does not always leave its hosts unmarked. Some time after successful treatment—generally a few months with African kala-azar, or as much as several years with the Indian strain—a secondary form of the disease may set in, called post kala-azar dermal leishmaniasis, or PKDL. This condition manifests first as small, measle-like skin lesions on the face, which gradually increase in size and spread over the body. Eventually the lesions may coalesce to form disfiguring, swollen structures resembling leprosy, and occasionally causing blindness if they spread to the eyes. (This disease is not the same as cutaneous leishmaniasis, a milder disease caused by another protozoan of the Leishmania genus which also causes skin lesions.)

Enterocolitis or coloenteritis is an inflammation of the digestive tract, involving enteritis of the small intestine and colitis of the colon. It may be caused by various infections, with bacteria, viruses, fungi, parasites, or other causes. Common clinical manifestations of enterocolitis are frequent diarrheal defecations, with or without nausea, vomiting, abdominal pain, fever, chills, alteration of general condition. General manifestations are given by the dissemination of the infectious agent or its toxins throughout the body, or – most frequently – by significant losses of water and minerals, the consequence of diarrhea and vomiting.

Among the causal agents of acute enterocolitis are:

- bacteria: "Salmonella", "Shigella", "Escherichia coli", "Campylobacter" etc.;

- viruses: enteroviruses, rotaviruses, Norwalk virus, adenoviruses;

- fungi: candidiasis, especially in immunosuppressed patients or who have previously received prolonged antibiotic treatment;

- parasites: "Giardia lamblia" (with high frequency of infestation in the population, but not always with clinical manifestations), "Balantidium coli", "Blastocystis homnis", "Cryptosporidium" (diarrhea in people with immunosuppression), "Entamoeba histolytica" (produces the amebian dysentery, common in tropical areas).