Amebiasis (Amoebic Dysentery) | Pathogenesis, Clinical presentation, Diagnosis & Treatment

amabiosis also known as amoebic dysentery is caused by entamoeba histolytica a unicellular protozoan that is found worldwide the highest prevalence of ammobiasis is in developing nations whose sanitary facilities are poor worldwide approximately 50 million cases of invasive and amoeba histolytica disease occur each year resulting in as many as forty thousand to one hundred thousand deaths amibiosis is the second leading cause of death due to parasitic diseases the first one is being malaria so in this video i'm going to discuss about entamoeba histolytica and its life cycle pathogenesis of amabiosis its clinical presentation diagnosis and finally the treatment and prevention of amibiosis first let's discuss about an amoeba histolytica and its life cycle entamoeba histolytica is a pseudopod forming non-flagellated protozoal parasite that has the ability to cause tissue lysis hence the species name histolytica the organism colonizes in the human large intestine to cause disease there are two main stages in the life cycle trophazoid stage and cyst stage trophazoid is the growing and model stage of entamoeba it has a single nucleus on the cytoplasm entamoeba uses pseudopods to engulf food particles bacteria and red blood cells trophizoid is the stage which invades the intestinal mucosa to cause disease cyst is the infective stage of entamoeba histolytica this means that only the ingestion of entamoeba cysts can cause disease even though cyst has no ability to invade the intestinal mucosa ingestion of only trophazoides may not cause the disease this is due to the ability of the cyst to withstand the high gastric acidity however in order to cause disease cyst has to form trophizoids within the large intestine cyst stage is non-model and consists of one to four nuclei amibiasis is mainly transmitted via the ingestion of fecally contaminated food and water often the food is contaminated by asymptomatic food handlers who chronically shed the pathogen in feces in addition house flies act as mechanical vectors in transmitting the disease sexual transmission is possible especially in a no oral sex therefore men who have sex with men are at high risk of getting the disease high-risk groups for developing emma biases include the following children especially neonates pregnant and postpartum women people who are on long-term corticosteroid therapy patients with malignancies malnourished individuals and travelers to endemic areas this image is from the cdc official website it shows the life cycle of entamoeba histolytica infected individuals and asymptomatic cyst passers shed both trophizoids and cysts in feces at this stage both the trophizoid and cysts are visible on a microscope so an entamoeba histolytical life cycle both the trophizoid and cyst are considered as diagnostic stages in order to get the disease mature cysts should be ingested by the individual ingestion of only a small amount of cysts is enough to cause the disease once the cysts reach the terminal ileum of the small intestine and colon they undergo a process called excess station during excess station a single cyst has the ability to formate trophizoids these trophizoids can multiply asexually and increase their number meanwhile they attach to the colonic mucosa and invade the intestinal tissue trophazoids also form cysts to complete the cycle the individual sheds these cysts in stools and they can survive in the environment for a long period of time multiplying trophizoids may not cause disease in every individual sometimes there may be only a non-invasive colonization sometimes they may cause intestinal disease only and sometimes they may penetrate the intestinal tissue and reach the other organs to cause extra intestinal disease let's discuss about them in detail in the following sections now let's come to the pathogenesis of amabiosis pathogenesis depends upon parasitic virulence factors and host protective mechanisms parasitic virulence factors include the following adhesion molecules which enable the binding of the parasite to the host tissues the major type of these molecules is galactus and acetyl galactose a mine binding lectin this molecule binds to the galactus and an acetyl galactose amine residues in the host tissues amoeba pores which are a family of peptides capable of forming pores in lipid by layers proteolytic enzymes like cysteine protein aces contact dependent killing ability and phagocytosis which is mediated by transmembrane kinases host defensive mechanisms include gut motility gut bacteria inflammatory response against entamoeba and cell-mediated immunity remember that the cell-mediated immunity is extremely important in limiting the disease and preventing recurrences now let's discuss about the mechanism of tissue invasion by entamoeba histolytica at first trophazoids adhere to the large intestinal mucosa parasitic adhesion molecules facilitate this binding then the parasite penetrates the epithelial cell lining and extracellular matrix of the colonic epithelium proteolytic enzymes and contact dependent killing mechanisms facilitate this penetration then the organism reaches the submucosal layer of colon and forms flask-shaped ulcers with unaffected submucosa in between here is a gross image of a colonic tissue specimen infected by entamoeba histolytica these are the initial superficial erosions caused by the parasite these yellow colored arrows indicate the unaffected submucosa in between those ulcers as trophozoites invade submucosa huge amounts of neutrophils and macrophages infiltrate into the affected area this is due to the secretion of various chemical mediators by the epithelial cells including interleukin-1 interleukin-8 and cyclooxygenases then the neutrophils and macrophages get activated by interferon gamma secreted by the surrounding cells and kill the trophazoids and halt the infection the killing process occurs via nitric oxide oxidative pathways and non-oxidative pathways however remember that the above description of processes occur only if the host immunity is adequate to halt the infection if the person is severely immunocompromised the immune response may not be able to contain the infection trophozoites then may secrete more and more proteolytic enzymes and penetrate the muscle and serous layers of the colon to reach the peritoneal cavity meanwhile contact dependent killing of the monocytes and macrophages occur after reaching the peritoneal cavity the trophocytes then invade the surrounding tissues to cause extra intestinal ammobiasis the commonest form of extra-intestinal ammobiasis is the amoebic liver abscess this condition occurs when the trophazoids invade the portal vein and reach the hepatic tissue in addition peritonitis pleura pulmonary ammobiasis pericarditis and brain abscesses are some other types of extra-intestinal disease now let's discuss about the clinical presentation of amabiosis the incubation period of entomoeba histolytica is usually two to four weeks but it may range from a few days to years approximately ninety percent of the people with amibiasis are asymptomatic intestinal conditions resulting from entamoeba histolytica infection include the following asymptomatic infection symptomatic non-invasive infection amoebic colitis fulminant colitis toxic megacolon chronic amoeba colitis and amaboma extra-intestinal conditions result from entamoeba histolytica infection include the following amoebic liver abscesses peritonitis plural pulmonary ammobiasis pericarditis brain abscesses and cutaneous ammobiasis amoeba colitis is the most common type of intestinal amabiasis it is gradual in onset with symptoms persisting over one to two weeks diarrhea is the most common symptom patients with amoebic colitis typically present with cramping abdominal pain watery or bloody diarrhea anorexia and weight loss fever is noted in 10 to 30 percent of patients sometimes intestinal ammo biases may mimic acute appendicitis rectal bleeding without diarrhea can occur especially in children fulminant colitis is a rare complication of amoebic dysentery it presents with the rapid onset of severe bloody diarrhea severe abdominal pain evidence of peritonitis and high grade fever in addition dehydration may occur due to the fluid loss the ulceration is massive and the affected area of the colon may undergo necrosis predisposing factors for fulminant colitis include poor nutrition pregnancy corticosteroid use and very young age intestinal perforation is common in fulminant colitis patients may develop toxic megacolon which is usually associated with the use of corticosteroids feminine colitis could be extremely fatal if left untreated which carries a mortality rate exiting 40 percent chronic amoebic colitis is clinically similar to inflammatory bowel disease recurrent episodes of bloody diarrhea and vague abdominal pain develop in about 90 of patients sometimes these patients are treated with corticosteroids for suspected inflammatory bowel disease keep in mind that it is important to rule out chronic amoebic colitis before treatment of suspected inflammatory bowel disease because corticosteroids will down regulate the immune system and worsen the condition ameboma is a less common form of intestinal disease arises from the formation of annular colonic granulations in response to the infecting organisms which results in a large local lesion of the bowel it presents as a right lower quadrant abdominal mass which may be mistaken for carcinoma tuberculosis crohn's disease or lymphoma biopsy findings assist in establishing the correct diagnosis amoebic liver abscess is the commonest form of extra-intestinal ammobiasis it occurs in about five percent of patients with symptomatic intestinal ammobiasis and it is ten times more frequent in men than in women approximately eighty percent of patients with amoebic liver abscess present to the clinic within two to four weeks of the infection right lobe of the liver is commonly affected most typical presentation is fever right upper quadrant pain and tenderness persist for less than 10 days duration involvement of the diaphragmatic surface of the liver may lead to right side pleuritic pain and referred shoulder pain associated gastrointestinal symptoms occur in 10 to 35 percent of patients including nausea vomiting abdominal distension and diarrhea or constipation plural pulmonary ammobiasis is most commonly the result of contiguous spread from a liver abscess rupturing through the diaphragm however hematogenous spread is also possible it occurs in about 10 percent of the patients with amoebic liver abscess symptoms of pleural pulmonary ammobiasis include cough pleuritic pain and dyspnea cutaneous ambibiasis occurs due to intestinal or hepatic fistulae which extend to the cutaneous surfaces perianal and urogenital ulceration is common here is a crude diagram of the overall picture of amabiosis green colored lesions indicate the intestinal disease and if the trophizoids penetrate the intestinal wall and reach the liver via the portal vein it can cause amoebic liver abscesses and if the liver abscess ruptures and trophizoids reach the pleural surfaces it can cause plural pulmonary ammobiasis hematogenous spread of trophozoites to the brain tissue causes cerebral ammobiasis formation of intestinal and hepatic fistula causes cutaneous ammobiasis and perianal ulceration now let's come to the diagnosis of amabiosis there are several methods available to diagnose amabiosis including microscopy culture antigen detection antibody detection pcr assay and imaging studies laboratory diagnosis of amibiasis in developing countries still relies on methods involving staining and microscopic examination of fresh stool samples presence of trophizoids with ingested red blood cells is a diagnostic event amoeba histolytica infection examination of three stool samples yields an about 85 to 95 sensitivity however routine microscopy cannot be relied on to distinguish the pathogenic entamoeba histolytica from non-pathogenic and amoeba disper and to meeba bangladeshi and entamoeba moshkov sky because they are morphologically similar to each other only the trophizoids with ingested red blood cells indicate the invasive disease and an acute dysentery trophozoites are predominant in stools in chronic amoebic colitis cysts are more prominent in stools and amoeba histolytica and all those non-pathogenic organisms mentioned above contain one to four nuclei in their cysts so presence of cysts in a stool sample does not tell whether the person have ammo biases or not and cystoventomy bicoli who is also non-pathogenic contains more than four nuclei in addition to trophizoids and cysts stool leukocytes may be found and in amoebic liver abscesses stool examination findings are usually negative culture can be performed on stool samples rectal biopsy specimens and liver abscess aspirates it has a success rate of about 50 to 70 percent but culture is technically difficult so overall culture is less sensitive than microscopy entamoeba histolytica antigens can be detected by enzyme linked to immunosorbent assay samples are taken from feces serum and liver aspirates antigen detection has an excellent sensitivity and specificity serum antibodies against entamoeba histolytica present in about seventy to ninety percent of patients with symptomatic intestinal ammobiasis and about ninety nine percent of patients with amoebic liver abscesses however antibody detection cannot distinguish between past and recent infection because the antibodies produced against entamoeba histolytica present in the serum for more than a year pcr assays can detect entamoeba histolytica specific genes and it can be done on feces and liver aspirate samples imaging studies are usually performed to diagnose amoebic liver abscesses these include radiography ultrasonography ct and mri finally let's come to the treatment and prevention of emma biosis treatment includes pharmacologic therapy and surgical intervention most people with amabiasis are treated on outpatient basis but in conditions like severe colitis and hypovolemia liver abscesses peritonitis and fulminant colitis inpatient care is required in endemic areas a symptomatic infection is not treated with drugs but in non-endemic areas a symptomatic infection should be treated luminal agents that are minimally absorbed in the gi tract like paramomas and aniodonal are best suited for such therapy metronidazole is the mainstream therapy for invasive ammobiasis in addition broad spectrum antibiotics may given to treat super infection in addition to pharmacologic therapy surgical intervention may required in severe conditions including the following perforated amoebic colitis massive gi bleeding toxic mega colon bacterial super infection in amoebic liver abscesses failure to respond to metronidazole after four days treatment and large left sided amoebic liver abscesses which have the potential to rupture into the pericardium the best way of preventing ammobiasis is avoiding fecal contamination of food and water this can be done by improved sanitation hygiene and water treatment and early treatment of carriers in non-endemic areas entamoeba cysts are not killed by soap or low concentrations of chlorine therefore water should be boiled for more than one minute and vegetables should be soaked in vinegar or acetic acid before consumption avoiding sexual practices involving fecal oral contact is also another way to prevent the transmission you