It is a protozoan parasite that causes amebiasis, a gastrointestinal infection. The epidemiology of E. histolytica varies by region and is influenced by several factors, including sanitation, hygiene practices, water supply, and socioeconomic status. 

In locations with limited access to clean water and poor sanitation, the prevalence of E. histolytica infection tends to be higher. In contrast, the incidence of infection is lower in areas with good sanitation and access to clean water. E. histolytica is also more commonly found in developing countries with widespread poverty. 

The transmission mode for  E. histolytica is ingesting cysts in contaminated food or water. The cysts can survive for weeks in the environment and resist chlorine disinfection. 

Individuals most at risk for infection include those who travel to endemic areas, those who have poor hygiene practices, and those who have sex with men.   

E. histolytica infection can range from asymptomatic colonization to severe disease. Symptoms of infection include abdominal pain, diarrhea, and fever. In severe cases, the parasite can invade the intestinal wall and spread to other organs, causing liver abscesses and other complications.

Structure and Classification 

It is a single-celled organism with a simple structure, lacking any discontinuing or complex structures. Here is a brief overview of the structure and Classification of Entamoeba histolytica: 

• Morphology: E. histolytica is a unicellular organism with a characteristic ameboid shape. It lacks cilia, flagella, and a distinct cell wall. 
• Classification: E. histolytica belongs to the phylum Amoebozoa, which consists of a diverse group of unicellular organisms that move using pseudopodia. Within the phylum, E. histolytica belongs to the class Archamoebae, a small group of ancient amoebae lacking mitochondria. 
• Life cycle: E. histolytica has a complex life cycle that involves both an infective cyst stage and an invasive trophozoite stage. The cysts are passed in the feces of infected individuals and can survive in the environment for several weeks. When ingested, the cysts release trophozoites in the intestine, which can invade the intestinal wall and cause tissue damage. 
• Virulence factors: E. histolytica produces several virulence factors contributing to its pathogenicity. These include enzymes that degrade host tissues, adhesion molecules that help the parasite attach to host cells, and toxins that cause cell damage. 

There are two antigenic types of E. histolytica: 

• Pathogenic type: This type causes disease in humans. It is also known as the invasive type because it invades the host’s tissues, causing damage and inflammation. The pathogenic type is characterized by the Gal/GalNAc lectin on the parasite’s surface. 
•  Non-pathogenic type: This type does not cause disease in humans and is typically found in the intestines of other animals. It is also non-invasive because it does not invade the host’s tissues. The non-pathogenic type does not have the Gal/GalNAc lectin on its surface.

Not all strains of E. histolytica are pathogenic, and some individuals can carry the parasite without exhibiting any symptoms. The pathogenicity of E. histolytica appears to be related to a combination of parasite virulence factors and host immune responses. 

The pathogenesis of E. histolytica involves several steps, including colonization, invasion, tissue destruction, and immune evasion. 

Colonization: E. histolytica is transmitted through ingesting contaminated food or water-containing cysts, which then transform into trophozoites in the large intestine. Trophozoites attach to the colonic mucosa using surface adhesion molecules, such as the galactose/N-acetyl galactosamine-inhibitable lectin (GAL/GALNAC), initiating the pathogenesis process. 

Invasion: The trophozoites of E. histolytica can penetrate the colonic mucosa by producing collagenase and other proteases, which degrade the extracellular matrix. Once inside the tissues, trophozoites use pseudopodia to move and invade more profoundly into the mucosa and submucosa, where they can cause ulceration, abscess formation, and perforation. 

Tissue destruction: E. histolytica trophozoites can directly damage host tissues by inducing necrosis, apoptosis, and inflammation. They can also induce apoptosis of host immune cells, such as neutrophils and macrophages, to evade host defenses and promote their survival. Releasing cytotoxic molecules and reactive oxygen species can further exacerbate tissue damage. 

Immune evasion: E. histolytica has developed several strategies to evade the host immune response. For example, trophozoites can alter their surface molecules, such as the primary surface antigen (MSA), to evade recognition and attack by host antibodies. They can also secrete molecules that suppress host immune responses, such as interleukin-10 (IL-10) and transforming growth factor-beta (TGF-β). 

Overall, the pathogenesis of E. histolytica is complex and multifaceted, involving several mechanisms that allow this parasite to colonize, invade, and damage host tissues while evading host defenses. 

The host defenses against E. histolytica include both innate and adaptive immune responses. Here are some of the host defenses against  E. histolytica: 

• Innate immunity is the first defense against invading pathogens, including E. histolytica. The innate immune response to E. histolytica involves phagocytosis by macrophages and neutrophils. These cells engulf and destroy the parasites by releasing enzymes and toxic molecules. 

• Adaptive immunity: The adaptive immune response to E. histolytica involves activating T and B cells. T cells recognize and kill infected cells, while B cells produce antibodies that neutralize the parasites. The adaptive immune response is essential for long-term protection against E. histolytica. 

• Mucosal immunity: The mucosal immune system plays a crucial role in defending against E. histolytica because the parasite infects the intestinal mucosa. Mucosal immunity involves the production of immunoglobulin A (IgA) antibodies, which can prevent the parasite’s attachment to the intestinal epithelium. 

• Complement system: A complement system is a group of proteins that can be activated by invading pathogens. The activated complement proteins can directly kill the parasites or enhance the activity of phagocytes. 

• Cytokines: Cytokines are small proteins secreted by immune cells and are vital in coordinating the immune response. Several cytokines, such as interferon-gamma (IFN-ã) and tumor necrosis factor-alpha (TNF-á), are involved in the defense against E. histolytica by activating macrophages and T cells. 

The clinical manifestations of Entamoeba histolytica infection can depend on how severe the infection is. 

Here are some common clinical manifestations of Entamoeba histolytica infection: 

Diarrhea: The most common symptom of Entamoeba histolytica is diarrhea, which can range from moderate to severe. In severe cases, the diarrhea may be bloody. 

• Abdominal pain and cramping: Abdominal pain and cramping are common symptoms of Entamoeba histolytica infection. 

• Fever: Some people with Entamoeba histolytica infection may develop a fever. 

• Fatigue: Fatigue is a common symptom of Entamoeba histolytica infection, especially in severe diarrhea cases. 

• Weight loss: Severe Entamoeba histolytica infection can lead to weight loss. 

• In some cases, Entamoeba histolytica infection can cause a liver abscess. Symptoms of a liver abscess may include pain in the upper right abdomen, fever, and nausea. 

Spread to other organs: Rarely, Entamoeba histolytica infection can spread to other organs, including the lungs and brain, leading to symptoms such as cough, chest pain, and confusion. 

Diagnosing Entamoeba histolytica infection can be challenging, as it often presents nonspecific symptoms that can be confused with other illnesses. Here are some standard methods used to diagnose Entamoeba histolytica infection: 

• Stool examination: A stool sample is collected and examined under a microscope for Entamoeba histolytica cysts or trophozoites. However, this method is not always reliable, as the cysts of Entamoeba histolytica can be morphologically like those of other non-pathogenic amoebae. 

• Serology: Blood samples are collected and tested for antibodies against Entamoeba histolytica. This method is more reliable in detecting the presence of the parasite, but it cannot differentiate between current and past infections. 

• Polymerase chain reaction (PCR): This method detects the parasite’s DNA in stool or tissue samples. PCR is a susceptible and specific method of detecting Entamoeba histolytica but requires specialized equipment and expertise. 

• Imaging studies: Imaging studies such as ultrasound, CT scan, or MRI can be used to detect the presence of liver abscesses, common complications of amoebiasis. 

To control Entamoeba histolytica: 

• Practice good hygiene: good hygiene is crucial to prevent the spread of Entamoeba histolytica. Washing hands properly with soap and water after changing, using the loo, and eating a baby’s diaper can help prevent infection. 

• Ensure safe drinking water: Entamoeba histolytica can spread through contaminated water. Boiling water or using a water filter can help remove the parasite from the water. 

• Proper sanitation: Proper sanitation, including the safe disposal of human waste, is essential in preventing the spread of Entamoeba histolytica. 

• Cook food thoroughly: cooking food can help kill the parasite. 

• Medications: Several medications are available to treat Entamoeba histolytica infections, including metronidazole, tinidazole, and paromomycin. You should see a doctor for proper diagnosis and treatment if you suspect an infection. 

• Prevention of re-infection: It is essential to prevent re-infection with Entamoeba histolytica. It can be achieved by treating infected individuals and their contacts and improving hygiene and sanitation practices. 

• Entamoeba Histolytica: Updates in Clinical Manifestation, Pathogenesis, and Vaccine Development – PMC (nih.gov) 

• Risk factors for Entamoeba histolytica infection in an agricultural community in Hanam province, Vietnam – PMC (nih.gov)