Ordanza, Svendson P.

OLFU COM D1 Group 8

Small Group Discussion in Biochemistry: Amoebiasis 1. Discuss how water is regulated in the body. Why is there excessive water loss in Cholera infection? Water is regulated by the body through different body systems that interact with each other to facilitate bodily functions and excretion. It involves intake of water through our digestive system and absorption of it in the colon, water reabsorption in the kidneys, excretion of water through the urinary system, skin and lungs.
In Amebiasis, the amount of dehydration seen on the client varies, usually mild or

moderate which could be easily treated in the health care facility if proper case management will be met.
In Cholera infection, A soluble toxin elaborated in the intestinal tract by the Vibrio

cholerae bacterium activates the adenylate cylase of the mucosa, causing active secretion of an isotonic fluid resulting in profuse watery diarrhea, extreme loss of fluid and electrolytes, and dehydration and collapse, but no gross morphologic change in the intestinal mucosa
2. Discuss the World Health Organization Criteria for Assessing Dehydration. Correlate

this with findings seen in the patient.

According to the WHO Integrated Management of Adolescent and Adult Illnesses

(IMAI), assessing dehydration is under the Diarrhea Category, you should ask first if the patient has diarrhea:

If yes, -For how long? - If more than 14 days, have you been treated before for persistent diarrhoea? - If yes, with what? When? - Is there blood in the stool? Then look and feel for: Is the patient lethargic or unconscious? Look for sunken eyes. Is the patient: Not able to drink or drinking poorly? Or Drinking eagerly, thirsty? Pinch the skin of the inside of the forearm. Does it go back: - Very slowly (longer than 2 seconds)? - Slowly?

Then Classify clients according to Dehydration.

If diarrhoea for 14 days or more and no blood, And if blood in stool,

Blood in the stool DYSENTERY Treat for 5 days with an oral antibiotic recommended for Shigella in your area Advise when to return immediately Follow up in 2 days
3. Discuss the World Health Organization Treatment plan for Rehydration. How do you

prepare home-made Oral Rehydrating Solution?

To classify dehydration and to select one of the following treatment plans:

Plan ATreat Diarrhoea at Home Plan BTreat Some Dehydration with ORS Plan CTreat Severe Dehydration Quickly

All three plans are described on the TREAT THE CHILD chart. Each plan provides

fluid to replace water and salts lost in diarrhoea. An excellent way to both rehydrate and prevent dehydration in a child is to give him or her a solution made with oral rehydration salts (ORS). IV fluid should be used only in cases of SEVERE DEHYDRATION.
Antibiotics are not effective in treating most diarrhoea. They rarely help and

make some children sicker. Unnecessary use of antibiotics may increase the resistance of some pathogens. In addition, antibiotics are costly. Money is often wasted on ineffective treatment. Therefore, do not give antibiotics routinely. Only give antibiotics to diarrhoea cases with SEVERE DEHYDRATION with cholera in the area and to cases with DYSENTERY.
Never give antidiarrhoeal drugs and antiemetics to children and infants. They

rarely help in treating diarrhoea, and some are dangerous. The dangerous drugs include antimotility drugs (such as codeine, tincture of opium, diphenoxylate, loperamide) or drugs to treat vomiting (such as chlorpromazine). Some of these harmful drugs can cause paralysis of the gut, or they can make the child

abnormally sleepy. Some can be fatal, especially if used in infants. Other antidiarrhoeal drugs, though not dangerous, are not effective diarrhoea treatments. These include adsorbents such as kaolin, attapulgite, smectite and activated charcoal. Using antidiarrhoeal drugs may cause delay in ORT treatment.
The age or weight of the child, the degree of dehydration and the number of

stools passed during rehydration will all affect the amount of ORS solution needed. The child will usually want to drink as much as he needs. If the child wants more or less than the estimated amount, give him what he wants. Another way to estimate the amount of ORS solution needed (in ml) is described below the box. Multiply the childs weight (in kilograms) by 75. For example, a child weighing 8 kg would need: 8 kg x 75 ml = 600 ml of ORS solution in 4 hours Notice that this amount fits in the range given in the box. The box will save you this calculation. Giving ORS solution should not interfere with a breastfed babys normal feeding. The mother should pause to let the baby breastfeed whenever the baby wants to, then resume the ORS solution. For infants under 6 months who are not breastfed, the mother should give 100-200 ml clean water during the first 4 hours in addition to the ORS solution. The breastmilk and water will help prevent hypernatraemia in infants. 4. Compare components of the original WHO ORS solution, WHO reformulated ORS, Lactated Ringers Solution, and Gatorade. Is it advisable to use Gatorade in place of ORS in Rehydration? Why was the ORS formula reformulated?
The old ORS solution involves only sugar and some salts, reformulated solution

has more balance fluid and electrolytes. Lactated Ringers has a lactate and will be converted into bicarbonate when it is in the instestines so it would not be advisable to use this during amoebiasis. Gatorade couldnt be used in replace of ORS in Amoebiasis because Gatorade is a hypotonic solution and it lacks the salts that is needed to treat the loss of salts due to persistent diarrhea
5. Discuss the epidemiology, signs and symptoms and prevention of Amoebiasis

brought about by Entamoeba histolytica infection.

Amebiasis

is infection with the parasitic intestinal protozoan Entamoeba histolytica. Most infections are probably asymptomatic, but E. histolytica can cause disease ranging from dysentery to extraintestinal infections, including liver abscesses. trophozoite stage. Infection of which humans are the natural host is acquired by ingestion of cysts contained in fecally contaminated food or water or, more rarely, through oral-anal sexual contact. Cysts survive stomach acidity and excyst within the small intestine to form the 20- to 50-m trophozoite stage. Trophozoites can live within the large-bowel lumen without causing disease or can invade the intestinal mucosa, causing amebic colitis. In some cases, E. histolytica trophozoites invade through the mucosa and into the bloodstream, traveling through the portal circulation to reach the liver and causing amebic liver abscesses. Motile trophozoites may be excreted into the stoola diagnostically important eventbut are rapidly killed upon exposure to air or stomach acid and

E. histolytica exists in two stages: a hardy multinucleate cyst form and the motile

therefore are not infectious. Trophozoite cysts within the large bowel are excreted in the stool, continuing the life cycle. Molecular diagnostics continue to clarify what was once a confusing picture of the true incidence and prevalence of E. histolytica infection and disease. It was a staple of most textbooks that 10% of the world's population was infected with E. histolytica. We now know that most asymptomatic individuals harboring amebic trophozoites or cysts in their stools are infected with a noninvasive species: Entamoeba dispar or Entamoeba moshkovskii. E. dispar appears not to cause disease, even in the most profoundly immunosuppressed individuals; furthermore, at this time, there is little evidence to suggest that E. moshkovskii causes disease, although epidemiologic studies of this species are in their infancy. In contrast, E. histolytica infection can cause disease, although not all patients develop symptoms. It remains unclear how frequently people infected withE. histolytica do develop symptoms; in one study in a highly endemic area, only 10% of infected patients developed symptoms over a 1-year observation period. A remarkable feature of amebiasis is its more common occurrence in men than in women, although the prevalence of infection with E. histolytica does not appear to differ between the sexes. This pattern is particularly pronounced for amebic liver abscess, whose prevalence is 7 times higher among men than among women. The explanation for this difference remains unknown, but less efficient complement-mediated killing of amebic trophozoites by serum from men than by serum from women has been reported. E. histolytica infections are most common in areas of the world where poor sanitation and crowding compromise the barriers to contamination of food and drinking water with human feces. Endemic areas include parts of Mexico, India, and nations in the tropical regions of Africa, South and Central America, and Asia. E. histolytica was present in 2.1% of individuals presenting with diarrhea in a large series from Bangladesh and in 1.4% of the asymptomatic control group. In 2007, amebiasis was listed as the sixth most common cause of disease in Mexico, with an incidence of 544 cases per 100,000 population. In the United States and other developed countries, disease is unusual and is found almost exclusively in travelers or immigrants from endemic areas. Rarely, outbreaks take place in institutionalized populations, and infections have been documented with increased frequency among men who have sex with men; however, most of the latter cases have been asymptomatic and probably represent E. dispar infections. Signs and Symptoms Intestinal Amebiasis Most patients harboring Entamoeba species are asymptomatic, but individuals with E. histolytica infection can develop disease. Symptoms of amebic colitis generally appear 26 weeks after ingestion of the cyst form of the parasite. Diarrhea (classically heme-positive) and lower abdominal pain are the most common symptoms. Malaise and weight loss may be noted as disease progresses. Severe dysentery, with 1012 small-volume, blood- and mucuscontaining stools daily, may develop, but only 40% of patients are febrile. Fulminant amebic colitis, with even more profuse diarrhea, severe abdominal pain (including peritoneal signs), fever, and pronounced leukocytosis are rare,

disproportionately affecting young children, pregnant women, individuals being treated with glucocorticoids, and possibly individuals with diabetes or alcoholism. Paralytic ileus and colonic mucosal sloughing may be seen; intestinal perforation occurs in >75% of patients with this fulminant form of disease. Mortality rates from fulminant amebic colitis exceed 40% in some series. Recognized complications of amebic colitis also include toxic megacolon (documented in 0.5% of patients with colitis), with severe bowel dilation and intramural air, and the aforementioned ameboma, which presents as an abdominal mass that may be confused with colon cancer. Amebic Liver Abscess Just a century ago, amebic liver abscessthe most common extraintestinal manifestation of amebiasiswas almost always fatal; however, with current rapid diagnostic methods and effective medical treatment, mortality rates are now 1 3%. Disease begins when E. histolytica trophozoites penetrate through the colonic mucosa, travel through the portal circulation, and reach the liver. Most individuals with amebic liver abscess do not have concurrent signs or symptoms of colitis, and most do not have E. histolytica trophozoites in their stools. The exceptions are individuals with fulminant amebic colitis, in which concurrent amebic liver abscess is not uncommon. Disease can arise from months to years after travel to or residence in an endemic area; therefore, a careful travel history is key in making the diagnosis. The classic presentations of amebic liver abscess are right-upper-quadrant pain, fever, and hepatic tenderness. The pace of disease is usually acute, with symptoms lasting <10 days. However, a more chronic presentation, with weight loss and anorexia as prominent accompanying features, does occur. Jaundice is unusual, but dullness and rales at the right lung base (secondary to pleural effusion) are common. The most common laboratory findings are leukocytosis (without eosinophilia), an elevated alkaline phosphatase level, mild anemia, and an elevated erythrocyte sedimentation rate. Other Extraintestinal Complications of Amebiasis Right-sided pleural effusions and atelectasis are common in cases of amebic liver abscess and generally require no treatment. However, the abscess ruptures through the diaphragm in 10% of patients, causing pleuropulmonary amebiasis. Suggestive symptoms are sudden-onset cough, pleuritic chest pain, and shortness of breath. In some patients, pleuropulmonary amebiasis is the presenting manifestation of amebic liver abscess and may be confused with bacterial pneumonia and empyema. A dramatic complication is the development of a hepatobronchial fistula, in which patients can cough up the contents of the liver abscesscopious amounts of brown sputum that may contain E. histolytica trophozoites. In 13% of cases, the amebic liver abscess ruptures into the peritoneum, and peritoneal signs and shock develop. Even rarer is rupture of an amebic liver abscess into the pericardium; the signs and symptoms are those commonly seen with pericarditis (chest pain, pericardial rub, dyspnea, tachypnea, or cardiac tamponade), and nearly 30% of cases end in death. Cerebral abscesses complicate <0.1% of cases of amebic liver abscess and are associated

with the sudden onset of headache, vomiting, seizures, and mental status changes and a high mortality rate. Cutaneous amebiasis (which usually involves the anal and perianal regions), genital disease (including rectovaginal fistulas), and urinary tract lesions are rare but reported complications of amebiasis. Prevention: Proper Handwashing, proper preparation of food and thourough cooking, Proper disposal of feces, and avoidance of fecal-oral sexual intercourse. Avoidance of the ingestion of food and water contaminated with human feces is the only way to prevent E. histolytica infection. Travelers to endemic areas should exercise the same measures used to reduce the risk of travelers' diarrhea (Chap. 117). Treatment of asymptomatic persons who pass E. histolytica cysts in the stool may help reduce opportunities for disease transmission. There is no evidence for any effective prophylaxis, and no vaccine is available. 6. Discuss the mechanism of intestinal infection by Entamoeba histolytica: Direct cell cell interaction and secreted products (proteases). E. histolytica trophozoites possess a potent repertoire of adhesins, proteinases, pore-forming proteins, and other effector molecules that enable them to lyse cells and tissue, induce both cellular necrosis and apoptosis, and resist both innate and adaptive immune defenses. Disease begins when E. histolytica trophozoites adhere to colonic mucosal epithelial cells. Disruption of the colonic mucin barrier is seen in pathologic sections from the diseased colon, but it is not clear whether this disruption is caused by the parasite, facilitating its adherence to mucosal cells, or occurs as a consequence of the adhesion event, with subsequent mucosal damage. Adherence is mediated primarily by a family of surface lectin molecules capable of binding to galactose and N-acetylgalactosamine residues. E. histolytica can lyse host cells upon contact through a family of amphipathic peptides called amoebapores that form barrel-stave pores in target cell membranes. Both cellular necrosis and apoptosis can occur after E. histolytica comes into contact with host cells, and which outcome predominates may relate to inherent characteristics of the target cell or the tissue environment. One consistent and unequivocal finding is the important role played by amebic cysteine proteinases in the disease process. E. histolytica possesses a large family of cysteine proteinases that are capable of lysing the extracellular matrix between host cells (thus detaching cells and facilitating invasion) and cleaving host defense molecules (including complement components and antibodies). Studies in animal models, including chimeric mice with human intestinal xenografts, have shown that inhibition of E. histolytica cysteine proteinase activity, via either direct gene targeting or chemical inhibitors, significantly reduces disease. The ultimate effect of all these amebic virulence factors on the human colon is the production of small ulcers that have heaped borders and contain focal areas of epithelial cell loss, a modest inflammatory response, and mucosal hemorrhage. The intervening mucosa is usually normal, but diffuse hyperemia is sometimes seen. E. histolytica trophozoites can then invade laterally through the submucosal layer, creating the classic flask-shaped ulcers that appear on pathologic examination as narrow-necked lesions, broadening in the submucosal region, with E. histolytica trophozoites at the margins between dead and live tissues (Fig. 209-3). Ulcers tend to stop at the muscularis layer, and full-thickness lesions and colonic perforation are unusual. Amebomas, a rare complication of intestinal disease, are granulomatous mass lesions protruding

into the bowel lumen, with a thickened edematous and hemorrhagic bowel wall that can cause obstructive symptoms. In some individuals with E. histolytica colonic infection, trophozoites invade the portal venous system and reach the liver, where they cause amebic liver abscesses. E. histolytica trophozoites must resist lysis by serum complement to survive in the bloodstream. Amebic liver abscesses have a characteristic appearance on pathologic examination: the roughly circular abscesses contain a large necrotic center resembling anchovy paste that is surrounded by a narrow ring of a few inflammatory cells, fibrosis, and occasionally a few amebic trophozoites. The adjacent liver parenchyma is usually completely normal. Results in experimental rodent models of amebic liver abscess suggest that initial lesions may have more inflammatory cells and that lysis of neutrophils by E. histolytica trophozoites may contribute to tissue damage. In murine models of disease, apoptosis is a prominent component of hepatocyte death and the blockade of caspase activity can significantly reduce liver abscess formation, but whether any of these factors is applicable to human disease is unclear. The role of innate and adaptive immunity in preventingE. histolytica infection or controlling disease needs further clarification. Studies of children in a highly endemic area have suggested that prior E. histolytica intestinal infection may stimulate mucosal IgA antibodies to amebic antigens, thereby reducing the likelihood of subsequent infections; this protection is relatively short lived. In contrast, among individuals in an area of Vietnam with a high prevalence of amebic liver abscess, a prior episode of disease did not reduce the risk of a second case, despite the presence of serum antibodies. Studies of animal models suggest that cell-mediated immunity may play a role in host defense, and glucocorticoid use has been associated with worse outcomes in patients with amebic colitis. However, individuals with HIV/AIDS do not appear to be at increased risk for infection with E. histolytica, and there is no evidence that they develop more severe disease than do immunocompetent hosts.

7. Discuss the role of leptin, the role of trophozoites in mucus layer dissolution and ingestion of apoptotic cells. What components of trophozoites induce host immune response?
Adherence is mediated primarily by a family of surface lectin molecules capable

of binding to galactose and N-acetylgalactosamine residues. E. histolytica can lyse host cells upon contact through a family of amphipathic peptides called amoebapores that form barrel-stave pores in target cell membranes. Both cellular necrosis and apoptosis can occur after E. histolytica comes into contact with host cells, and which outcome predominates may relate to inherent characteristics of the target cell or the tissue environment. One consistent and unequivocal finding is the important role played by amebic cysteine proteinases in the disease process. 8. How will you manage this case?

 Management of this would be based on the WHO Guidelines in IMAI up to follow up care.

Amoebiasis
Cause Caused by the protozoan parasite Entamoeba histolytica. Transmission Transmission occurs via the faecaloral route, either directly by person-to-person contact or indirectly by eating or drinking faecally contaminated food or water. Nature of the disease The clinical spectrum ranges from asymptomatic infection, diarrhoea and dysentery to fulminant colitis and peritonitis as well as extraintestinal amoebiasis. Acute amoebiasis can present as diarrhoea or dysentery with frequent, small and often bloody stools. Chronic amoebiasis can present with gastrointestinal symptoms plus fatigue, weight loss and occasional fever. Extraintestinal amoebiasis can occur if the parasite spreads to other organs, most commonly the liver where it causes amoebic liver abscess. Amoebic liver abscess presents with fever and right upper quadrant abdominal pain. Geographical distribution Occurs worldwide, but is more common in areas or countries with poor sanitation, particularly in the tropics. Precautions Food and water hygiene (Chapter 3). No vaccine is available.

What is amebiasis?
Amebiasis is a disease caused by a one-celled parasite calledEntamoeba histolytica.

Who is at risk for amebiasis?

Although anyone can have this disease, it is more common in people who live in tropical areas with poor sanitary conditions. In the United States, amebiasis is most common in:

People who have traveled to tropical places that have poor sanitary conditions Immigrants from tropical countries that have poor sanitary conditions People who live in institutions that have poor sanitary conditions Men who have sex with men

How can I become infected with E. histolytica?

E. histolytica infection can occur when a person: Puts anything into their mouth that has touched the feces (poop) of a person who is infected with E. histolytica. Swallows something, such as water or food, that is contaminated with E. histolytica. Swallows E. histolytica cysts (eggs) picked up from contaminated surfaces or fingers.

What are the symptoms of amebiasis?

Only about 10% to 20% of people who are infected with E. histolytica become sick from the infection. The symptoms are often quite mild and can include loose feces (poop), stomach pain, and stomach cramping. Amebic dysentery is a severe form of amebiasis associated with stomach pain, bloody stools (poop), and fever. Rarely, E. histolytica invades the liver and forms an abscess (a collection of pus). In a small number of instances, it has been shown to spread to other parts of the body, such as the lungs or brain, but this is very uncommon.

If I swallowed E. histolytica, how quickly would I become sick?

Only about 10% to 20% of people who are infected with E. histolytica become sick from the infection. Those people who do become sick usually develop symptoms within 2 to 4 weeks, though it can sometimes take longer.

What should I do if I think I have amebiasis?

See your health care provider.

How is amebiasis diagnosed?

Your health care provider will ask you to submit fecal (poop) samples. Because E. histolytica is not always found in every stool sample, you may be asked to submit several stool samples from several different days. Diagnosis of amebiasis can be very difficult. One problem is that other parasites and cells can look very similar to E. histolytica when seen under a microscope. Therefore, sometimes people are told that they are infected with E. histolytica even though they are not. Entamoeba histolyticaand another ameba, Entamoeba dispar, which is about 10 times more common, look the same when seen under a microscope. Unlike infection with E. histolytica, which sometimes makes people sick, infection with E. dispar does not make people sick and therefore does not need to be treated. If you have been told that you are infected with E. histolytica but you are feeling fine, you might be infected with E. dispar instead. Unfortunately, most laboratories do not yet have the tests that can tell whether a person is infected with E. histolytica or with E. dispar. Until these tests become more widely available, it usually is best to assume that the parasite is E. histolytica. A blood test is also available but is only recommended when your health care provider thinks that your infection may have spread beyond the intestine (gut) to some other organ of your body, such as the liver. However, this blood test may not be helpful in diagnosing your current illness because the test can be positive if you had amebiasis in the past, even if you are no longer infected now.

How is amebiasis treated?

Several antibiotics are available to treat amebiasis. Treatment must be prescribed by a physician. You will be treated with only one antibiotic if your E. histolytica infection has not made you sick. You probably will be treated with two antibiotics (first one and then the other) if your infection has made you sick.

I am going to travel to a country that has poor sanitary conditions. What should I eat and drink there so I will NOT become infected with E. histolytica or other such germs?
The following items are safe to drink:

Bottled water Tap water that has been boiled for at least 1 minute Carbonated (bubbly) water from sealed cans or bottles Carbonated (bubbly) drinks (like soda) from sealed cans or bottles

*You can also make tap water safe for drinking by filtering it through an "absolute 1 micron or less" filter and dissolving chlorine, chlorine dioxide, or iodine tablets in the filtered water. "Absolute 1 micron" filters can be found in camping/outdoor supply stores. More on: Personal Preparation and Storage of Safe Water More on: Guide to Water Filters The following items are NOT safe to drink or eat:

Fountain drinks or any drinks with ice cubes Fresh fruit or vegetables that you did not peel yourself Milk, cheese, or dairy products that may not have been pasteurized. Anything sold by street vendors

Should I be concerned about spreading the infection to others?

Yes, but the risk of spreading infection is low if the infected person is treated with antibiotics and practices good personal hygiene. This includes thorough handwashing with soap and warm water after using the toilet, after changing diapers, and before handling food.

Causal Agent:
Several protozoan species in the genus Entamoeba colonize humans, but not all of them are associated with disease. Entamoeba histolytica is well recognized as a pathogenic ameba, associated with intestinal and extraintestinal infections. The other species are important because they may be confused with E. histolytica in diagnostic investigations.

Life Cycle: Causal Agent:

Several protozoan species in the genus Entamoeba colonize humans, but not all of them are associated with disease. Entamoeba histolytica is well recognized as a pathogenic ameba, associated with intestinal and extraintestinal infections. The other species are important because they may be confused with E. histolytica in diagnostic investigations.

Life Cycle:

Cysts and trophozoites are passed in feces

. Cysts are typically found in formed stool, whereas trophozoites are in fecally occurs in the small intestine and trophozoites are released, , and both stages

typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts contaminated food, water, or hands. Excystation are passed in the feces which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts

. Because of the protection conferred by their walls, the cysts can survive days to weeks in

the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body, and if ingested would not survive exposure to the gastric environment. In many cases, the trophozoites remain confined to the intestinal lumen ( : noninvasive infection) of individuals who are asymptomatic : intestinal : extraintestinal carriers, passing cysts in their stool. In some patients the trophozoites invade the intestinal mucosa ( disease), or, through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (

disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E. histolyticaand E. dispar. These two species are morphologically indistinguishable unless E. histolytica is observed with ingested red blood cells (erythrophagocystosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective).

Cysts and trophozoites are passed in feces

. Cysts are typically found in formed stool, whereas trophozoites are in fecally occurs in the small intestine and trophozoites are released, , and both stages

typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts contaminated food, water, or hands. Excystation are passed in the feces which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts

. Because of the protection conferred by their walls, the cysts can survive days to weeks in

the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body, and if ingested would not survive exposure to the gastric environment. In many cases, the trophozoites remain confined to the intestinal lumen ( : noninvasive infection) of individuals who are asymptomatic : intestinal : extraintestinal carriers, passing cysts in their stool. In some patients the trophozoites invade the intestinal mucosa ( disease), or, through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (

disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E. histolyticaand E. dispar. These two species are morphologically indistinguishable unless E. histolytica is observed with ingested red blood cells (erythrophagocystosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective).