Dysentery is initially managed by maintaining fluid intake using oral rehydration therapy. If this treatment cannot be adequately maintained due to vomiting or the profuseness of diarrhea, hospital admission may be required for intravenous fluid replacement. Ideally, no antimicrobial therapy should be administered until microbiological microscopy and culture studies have established the specific infection involved. When laboratory services are not available, it may be necessary to administer a combination of drugs, including an amoebicidal drug to kill the parasite and an antibiotic to treat any associated bacterial infection.

Anyone with bloody diarrhea needs immediate medical help. Treatment often starts with an oral rehydrating solution—water mixed with salt and carbohydrates—to prevent dehydration. (Emergency relief services often distribute inexpensive packets of sugars and mineral salts that can be mixed with clean water and used to restore lifesaving fluids in dehydrated children gravely ill from dysentery.)

If "Shigella" is suspected and it is not too severe, the doctor may recommend letting it run its course—usually less than a week. The patient will be advised to replace fluids lost through diarrhea. If the infection is severe, the doctor may prescribe antibiotics, such as ciprofloxacin or TMP-SMX (Bactrim). Unfortunately, many strains of "Shigella" are becoming resistant to common antibiotics, and effective medications are often in short supply in developing countries. If necessary, a doctor may have to reserve antibiotics for those at highest risk for death, including young children, people over 50, and anyone suffering from dehydration or malnutrition.

No vaccine is available. There are several "Shigella" vaccine candidates in various stages of development that could reduce the incidence of dysentery in endemic countries, as well as in travelers suffering from traveler's diarrhea.

Treatment consists mainly of replacing fluids and salts lost because of diarrhea. Replacement by mouth is satisfactory for most people, but some may need to receive fluids intravenously. Antidiarrheal drugs (such as diphenoxylate or loperamide) may prolong the infection and should not be used.

Dysentery is managed by maintaining fluids by using oral rehydration therapy. If this treatment cannot be adequately maintained due to vomiting or the profuseness of diarrhea, hospital admission may be required for intravenous fluid replacement. In ideal situations, no antimicrobial therapy should be administered until microbiological microscopy and culture studies have established the specific infection involved. When laboratory services are not available, it may be necessary to administer a combination of drugs, including an amoebicidal drug to kill the parasite, and an antibiotic to treat any associated bacterial infection.

If shigellosis is suspected and it is not too severe, letting it run its course may be reasonable — usually less than a week. If the case is severe, antibiotics such as ciprofloxacin or TMP-SMX may be useful. However, many strains of "Shigella" are becoming resistant to common antibiotics, and effective medications are often in short supply in developing countries. If necessary, a doctor may have to reserve antibiotics for those at highest risk for death, including young children, people over 50, and anyone suffering from dehydration or malnutrition.

Amoebic dysentery is often treated with two antimicrobial drug such as metronidazole and paromomycin or iodoquinol.

Antibiotics should only be used in severe cases or for certain populations with mild symptoms (elderly, immunocompromised, food service industry workers, child care workers). For "Shigella"-associated diarrhea, antibiotics shorten the length of infection, but they are usually avoided in mild cases because many "Shigella" strains are becoming resistant to common antibiotics. Furthermore, effective medications are often in short supply in developing countries, which carry the majority of the disease burden from "Shigella". Antidiarrheal agents may worsen the sickness, and should be avoided.

In most cases, the disease resolves within four to eight days without antibiotics. Severe infections may last three to six weeks. Antibiotics, such as trimethoprim-sulfamethoxazole, ciprofloxacin may be given when the person is very young or very old, when the disease is severe, or when the risk of the infection spreading to other people is high. Additionally, ampicillin (but not amoxicillin) was effective in treating this disease previously, but now the first choice of drug is pivmecillinam.

With correct treatment, most cases of amoebic and bacterial dysentery subside within 10 days, and most individuals achieve a full recovery within two to four weeks after beginning proper treatment. If the disease is left untreated, the prognosis varies with the immune status of the individual patient and the severity of disease. Extreme dehydration can delay recovery and significantly raises the risk for serious complications.

"E. histolytica" infections occur in both the intestine and (in people with symptoms) in tissue of the intestine and/or liver. As a result, two different classes of drugs are needed to treat the infection, one for each location. Such anti-amoebic drugs are known as amoebicides.

If diarrhea becomes severe (typically defined as three or more loose stools in an eight-hour period), especially if associated with nausea, vomiting, abdominal cramps, fever, or blood in stools, medical treatment should be sought. Such patients may benefit from antimicrobial therapy. A 2000 literature review found that antibiotic treatment shortens the duration and severity of TD; most reported side effects were minor, or resolved on stopping the antibiotic.

Fluoroquinolone antibiotics are the drugs of choice. Trimethoprim–sulfamethoxazole and doxycycline are no longer recommended because of high levels of resistance to these agents. Antibiotics are typically given for three to five days, but single doses of azithromycin or levofloxacin have been used. Rifaximin is approved in the U.S. for treatment of TD caused by ETEC. If diarrhea persists despite therapy, travelers should be evaluated for bacterial strains resistant to the prescribed antibiotic, possible viral or parasitic infections, bacterial or amoebic dysentery, "Giardia", helminths, or cholera.

Most cases of TD are mild and resolve in a few days without treatment, but severe or protracted cases may result in significant fluid loss and dangerous electrolytic imbalance. Dehydration due to diarrhea can also alter the effectiveness of medicinal and contraceptive drugs. Adequate fluid intake (oral rehydration therapy) is therefore a high priority. Commercial rehydration drinks are widely available; alternatively, purified water or other clear liquids are recommended, along with salty crackers or oral rehydration salts (available in stores and pharmacies in most countries) to replenish lost electrolytes. Carbonated water or soda, left open to allow dissipation of the carbonation, is useful when nothing else is available. In severe or protracted cases, the oversight of a medical professional is advised.

Antibiotic treatment only has a marginal effect on the duration of symptoms, and its use is not recommended except in high-risk patients with clinical complications.

Erythromycin can be used in children, and tetracycline in adults. Some studies show, however, that erythromycin rapidly eliminates "Campylobacter" from the stool without affecting the duration of illness. Nevertheless, children with dysentery due to "C. jejuni" benefit from early treatment with erythromycin. Treatment with antibiotics, therefore, depends on the severity of symptoms. Quinolones are effective if the organism is sensitive, but high rates of quinolone use in livestock means that quinolones are now largely ineffective.

Antimotility agents, such as loperamide, can lead to prolonged illness or intestinal perforation in any invasive diarrhea, and should be avoided. Trimethoprim/sulfamethoxazole and ampicillin are ineffective against "Campylobacter".

The infection is usually self-limiting, and in most cases, symptomatic treatment by liquid and electrolyte replacement is enough in human infections.

This nitroimidazole compound, like metronidazole, has shown a marked therapeutic response in amoebic liver abscess. Occasional side effects include nausea and dizziness. Tinidazole is not widely available though it is more effective than metronidazole. Zuberi and Ibrahim found tinidazole to be effective in 86.7% cases of intestinal amoebiasis and in 100% cases of amoebic liver abscess.

Luminal amoebicides like halogenated oxyquinolines, e.g. diiodohydroxyquinoline in a dose of 0.6 G. thrice daily for 3 weeks, diloxanide furoate 0.5 G. three times a day for 10 days and sometimes tetracyclines 1–2 G./day for 5 days should be used concurrently with any of the above drugs as adjuncts to eliminate intestinal infection.

Surgery is usually indicated in cases of intestinal perforation. Most surgeons prefer simple closure of the perforation with drainage of the peritoneum. Small-bowel resection is indicated for patients with multiple perforations.

If antibiotic treatment fails to eradicate the hepatobiliary carriage, the gallbladder should be resected. Cholecystectomy is not always successful in eradicating the carrier state because of persisting hepatic infection.

The introduction of cinchona into therapeutics was due to the discovery of its efficacy in malaria. In 1921, John used quinine hydrochloride, an alkaloid of cinchona in the treatment of amoebic liver abscess.

Later when synthetic derivatives of quinine were introduced, chloroquine phosphate, a 4-aminoquinoline was found to be less toxic than the parent drug. The drug was first quoted in the treatment of this condition in very early reports by Conan (1948)15, Murgatroyd and Kent (1948).

It is absorbed rapidly and completely from the gastrointestinal tract. It is found to be very effective in invasive amoebiasis although the drug is a weaker amoebicide when compared to emetine. It is only feebly amoebicidal in the intestinal lumen.

The high concentration in the liver parenchyma and the lung allows the drug to act upon E. Histolytica in cases of amoebic liver abscess and pleuropulmonary amoebiasis.

It is usually well tolerated, but in some individuals it may cause mild headache, itching, nausea, vomiting or blurred vision. Rarely incoordination, convulsions, peripheral neuritis and bleaching of hair can occur. Diminution of T waves has been noticed on routine electrocardiographic recordings. Retinopathy does not occur with the usual dosage for amoebic liver abscess. Psychic disturbances though rare may interfere with the safe operation of machines and vehicles. The drug may be toxic to children in large doses18 and causes deafness in the foetus.

Each 0.5 G. tablet contains chloroquine diphosphate equivalent to 0.3 G. of the base. For the treatment of amoebic liver abscess, it is administered in doses of 0.6 G. base per day in 2 to 3 divided doses orally for 2 days followed by 0.15 G. base twice daily for 2 to 3 weeks. However, Plorde recommends that it be given as 0.6 G. base initially, 0.3 G. base six hours later and then 0.3 G. base twice daily for fourteen to twenty eight days.19 Chloroquine is also available in an injectable form. Since it is quite toxic by this route, it should not be used for more than 24–48 hours after which oral therapy should be continued. Rarely, when patients of amoebic liver abscess are vomiting, injection chloroquine can be used in a dose of 0.3–0.6 G. base in 24 hours not exceeding 0.9 G.).

Chloroquine given alone is a safer drug than emetine in amoebic liver abscess, but unfortunately the relapse rate is almost 25%. Rarely repetition of the course may induce a dramatic response.

The rediscovery of oral rehydration therapy in the 1960s provided a simple way to prevent many of the deaths of diarrheal diseases in general.

Where resistance is uncommon, the treatment of choice is a fluoroquinolone such as ciprofloxacin. Otherwise, a third-generation cephalosporin such as ceftriaxone or cefotaxime is the first choice. Cefixime is a suitable oral alternative.

Typhoid fever, when properly treated, is not fatal in most cases. Antibiotics, such as ampicillin, chloramphenicol, trimethoprim-sulfamethoxazole, amoxicillin, and ciprofloxacin, have been commonly used to treat typhoid fever in microbiology. Treatment of the disease with antibiotics reduces the case-fatality rate to about 1%.

Without treatment, some patients develop sustained fever, bradycardia, hepatosplenomegaly, abdominal symptoms and, occasionally, pneumonia. In white-skinned patients, pink spots, which fade on pressure, appear on the skin of the trunk in up to 20% of cases. In the third week, untreated cases may develop gastrointestinal and cerebral complications, which may prove fatal in up to 10–20% of cases. The highest case fatality rates are reported in children under 4 years. Around 2–5% of those who contract typhoid fever become chronic carriers, as bacteria persist in the biliary tract after symptoms have resolved.

Concomitant pinworm infection should also be excluded, although the association has not been proven. Successful treatment of the infection with iodoquinol, doxycycline, metronidazole, paromomycin, and secnidazole has been reported. Resistance requires the use of combination therapy to eradicate the organism. All persons living in the same residence should be screened for "D. fragilis", as asymptomatic carriers may provide a source of repeated infection. Paromomycin is an effective prophylactic for travellers who will encounter poor sanitation and unsafe drinking water.

To help prevent the spread of amoebiasis around the home :

- Wash hands thoroughly with soap and hot running water for at least 10 seconds after using the toilet or changing a baby's diaper, and before handling food.

- Clean bathrooms and toilets often; pay particular attention to toilet seats and taps.

- Avoid sharing towels or face washers.

To help prevent infection:

- Avoid raw vegetables when in endemic areas, as they may have been fertilized using human feces.

- Boil water or treat with iodine tablets.

- Avoid eating street foods especially in public places where others are sharing sauces in one container

Good sanitary practice, as well as responsible sewage disposal or treatment, are necessary for the prevention of "E. histolytica" infection on an endemic level. "E.histolytica" cysts are usually resistant to chlorination, therefore sedimentation and filtration of water supplies are necessary to reduce the incidence of infection.

"E. histolytica" cysts may be recovered from contaminated food by methods similar to those used for recovering "Giardia lamblia" cysts from feces. Filtration is probably the most practical method for recovery from drinking water and liquid foods. "E. histolytica" cysts must be distinguished from cysts of other parasitic (but nonpathogenic) protozoa and from cysts of free-living protozoa as discussed above. Recovery procedures are not very accurate; cysts are easily lost or damaged beyond recognition, which leads to many falsely negative results in recovery tests.

In many cases of diarrhea, replacing lost fluid and salts is the only treatment needed. This is usually by mouth – oral rehydration therapy – or, in severe cases, intravenously. Diet restrictions such as the BRAT diet are no longer recommended. Research does not support the limiting of milk to children as doing so has no effect on duration of diarrhea. To the contrary, WHO recommends that children with diarrhea continue to eat as sufficient nutrients are usually still absorbed to support continued growth and weight gain, and that continuing to eat also speeds up recovery of normal intestinal functioning. CDC recommends that children and adults with cholera also continue to eat.

Medications such as loperamide (Imodium) and bismuth subsalicylate may be beneficial; however they may be contraindicated in certain situations.

While antibiotics are beneficial in certain types of acute diarrhea, they are usually not used except in specific situations. There are concerns that antibiotics may increase the risk of hemolytic uremic syndrome in people infected with . In resource-poor countries, treatment with antibiotics may be beneficial. However, some bacteria are developing antibiotic resistance, particularly "Shigella". Antibiotics can also cause diarrhea, and antibiotic-associated diarrhea is the most common adverse effect of treatment with general antibiotics.

While bismuth compounds (Pepto-Bismol) decreased the number of bowel movements in those with travelers' diarrhea, they do not decrease the length of illness. Anti-motility agents like loperamide are also effective at reducing the number of stools but not the duration of disease. These agents should only be used if bloody diarrhea is not present.

Bile acid sequestrants such as cholestyramine can be effective in chronic diarrhea due to bile acid malabsorption. Therapeutic trials of these drugs are indicated in chronic diarrhea if bile acid malabsorption cannot be diagnosed with a specific test, such as SeHCAT retention.

Malaria is treated with antimalarial medications; the ones used depends on the type and severity of the disease. While medications against fever are commonly used, their effects on outcomes are not clear.

Simple or uncomplicated malaria may be treated with oral medications. The most effective treatment for "P. falciparum" infection is the use of artemisinins in combination with other antimalarials (known as artemisinin-combination therapy, or ACT), which decreases resistance to any single drug component. These additional antimalarials include: amodiaquine, lumefantrine, mefloquine or sulfadoxine/pyrimethamine. Another recommended combination is dihydroartemisinin and piperaquine. ACT is about 90% effective when used to treat uncomplicated malaria. To treat malaria during pregnancy, the WHO recommends the use of quinine plus clindamycin early in the pregnancy (1st trimester), and ACT in later stages (2nd and 3rd trimesters). In the 2000s (decade), malaria with partial resistance to artemisins emerged in Southeast Asia. Infection with "P. vivax", "P. ovale" or "P. malariae" usually do not require hospitalization. Treatment of "P. vivax" requires both treatment of blood stages (with chloroquine or ACT) and clearance of liver forms with primaquine. Treatment with tafenoquine prevents relapses after confirmed "P. vivax" malaria.

Severe and complicated malaria are almost always caused by infection with "P. falciparum". The other species usually cause only febrile disease. Severe and complicated malaria are medical emergencies since mortality rates are high (10% to 50%). Cerebral malaria is the form of severe and complicated malaria with the worst neurological symptoms.

Recommended treatment for severe malaria is the intravenous use of antimalarial drugs. For severe malaria, parenteral artesunate was superior to quinine in both children and adults. In another systematic review, artemisinin derivatives (artemether and arteether) were as efficacious as quinine in the treatment of cerebral malaria in children. Treatment of severe malaria involves supportive measures that are best done in a critical care unit. This includes the management of high fevers and the seizures that may result from it. It also includes monitoring for poor breathing effort, low blood sugar, and low blood potassium.

Drug resistance poses a growing problem in 21st-century malaria treatment. Resistance is now common against all classes of antimalarial drugs apart from artemisinins. Treatment of resistant strains became increasingly dependent on this class of drugs. The cost of artemisinins limits their use in the developing world. Malaria strains found on the Cambodia–Thailand border are resistant to combination therapies that include artemisinins, and may, therefore, be untreatable. Exposure of the parasite population to artemisinin monotherapies in subtherapeutic doses for over 30 years and the availability of substandard artemisinins likely drove the selection of the resistant phenotype. Resistance to artemisinin has been detected in Cambodia, Myanmar, Thailand, and Vietnam, and there has been emerging resistance in Laos.

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.

Tetracycline-group antibiotics (doxycycline, tetracycline) are commonly used. Chloramphenicol is an alternative medication recommended under circumstances that render use of tetracycline derivates undesirable, such as severe liver malfunction, kidney deficiency, in children under nine years and in pregnant women. The drug is administered for seven to ten days.

The treatment for bacillary angiomatosis is erythromycin given for three to four months.

As with many diseases in developing nations, (including trypanosomiasis and malaria) effective and affordable chemotherapy is sorely lacking and parasites or insect vectors are becoming increasingly resistant to existing anti-parasite drugs. Possibly due to the lack of financial return, new drugs are slow to emerge and much of the basic research into potential drug targets takes place in universities, funded by charitable organizations. Product Development Partnerships (PDPs) like Drugs for Neglected Diseases "initiatives" also work on the development of new treatments (combination treatments and new chemical entities) for visceral leishmaniasis.

The traditional treatment is with pentavalent antimonials such as sodium stibogluconate and meglumine antimoniate. Resistance is now common in India, and rates of resistance have been shown to be as high as 60% in parts of Bihar, India.

The treatment of choice for visceral leishmaniasis acquired in India is now Amphotericin B in its various liposomal preparations. In East Africa, the WHO recommended treatment is SSG&PM (sodium stibogluconate and paromomycin) developed by Drugs for Neglected Diseases "initiative" (DNDi)in 2010.

Miltefosine is the first oral treatment for this disease. The cure rate of miltefosine in Phase III clinical trials is 95%; Studies in Ethiopia show that is also effective in Africa. In HIV immunosuppressed people which are coinfected with leishmaniasis it has shown that even in resistant cases 2/3 of the people responded to this new treatment.

Miltefosine has received approval by the Indian regulatory authorities in 2002, in Germany in 2004 and in U.S.A. in 2014. It is now registered in many countries.

The drug is generally better tolerated than other drugs. Main side effects are gastrointestinal disturbance in the first or second day of treatment (a course of treatment is 28 days) which does not affect the efficacy. Because it is available as an oral formulation, the expense and inconvenience of hospitalization is avoided, and outpatient distribution of the drug becomes an option, making Miltefosine a drug of choice.

Incomplete treatment has been cited as a major reason of death from visceral leishmaniasis.

The nonprofit Institute for OneWorld Health has adopted the broad spectrum antibiotic paromomycin for use in treating VL; its antileishmanial properties were first identified in the 1980s. A treatment with paromomycin costs about $15 USD. The drug had originally been identified in the 1960s. The Indian government approved paromomycin for sale and use in August 2006.

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.

Other important issues related to the treatment of hookworm are reinfection and drug resistance. It has been shown that reinfection after treatment can be extremely high. Some studies even show that 80% of pretreatment hookworm infection rates can be seen in treated communities within 30–36 months. While reinfection may occur, it is still recommended that regular treatments be conducted as it will minimize the occurrence of chronic outcomes. There are also increasing concerns about the issue of drug resistance. Drug resistance has appeared in front-line anthelmintics used for livestock nematodes. Generally human nematodes are less likely to develop resistance due to longer reproducing times, less frequent treatment, and more targeted treatment. Nonetheless, the global community must be careful to maintain the effectiveness of current anthelmintic as no new anthelmintic drugs are in the late-stage development.