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Introduction: Amoebiasis protozoal infection of human beings initially involves the colon, but may spread to soft tissues, most commonly to the liver or lungs, by contiguity or hematogenous or lymphatic dissemination. Amoebiasis is the third leading parasitic cause of death worldwide, surpassed only by malaria and schistosomiasis. On a global basis, amoebiasis affects approximately 50 million persons each year, resulting in nearly 100,000 deaths. Etiologic Agent:

Enatamoeba Histolytica Prevalent in unsanitary areas Common in warm climate Acquired by swallowing Cysts survives a few days outside of the body Cyst passes to the large intestine and hatch into trophozoites. It passes into the mesenteric veins, to the

portal vein, to the liver, thereby forming amoebic liver abscess. Entamoeba Histolytica has two developmental stages: 1.

2.

Trophozoites/vegetative form Trophozoites are facultative parasites that may invade the tissues or may be found in the parasitized tissues and liquid colonic contents. Cyst

Cyst is passed out with formed or semi-formed stools and are resistant to environmental conditions. This is considered as the infective stage in the cycle of E. histolytica Source: Human Excreta Incubation Period: The incubation period in severe infection is three days. In subacute and chronic form it lasts for several months. In average cases the incubation period varies from three to four weeks Period of Communicability: The microorganism is communicable for the entire duration of the illness. Modes of Transmission: 1. 2. 3. The disease can be passed from one person to another through fecal-oral transmission. The disease can be transmitted through direct contact, through sexual contact by orogenital, oroanal, and proctogenital sexual activity. Through indirect contact, the disease can infect humans by ingestion of food especially uncooked leafy vegetables or foods contaminated with fecal materials containing E. histolytica cysts.

Food or drinks maybe contaminated by cyst through pollution of water supplies, exposure to flies, use of night soil for fertilizing vegetables, and through unhygienic practices of food handlers. Clinical Manifestations: 1. Acute amoebic dysentery

2.

Slight attack of diarrhea, altered with periods of constipation and often accompanied by tenesmus. Diarrhea, watery and foul smelling stool often containing blood-streaked mucus Colic and gaseous distension of the lower abdomen Nausea, flatulence, abdomnal distension and tenderness in the right iliac region over the colon

Chronic amoebic dysentery Attack dysentery that lasts for several days, usually succeeded by constipation Tenesmus accompanied by the desire to defacate Anorexia, weight loss, and weakness Liver may be enlarged The stool at first is semifluid but soon becomes watery, bloody, and mucoid Vague abdominal distress, flatulence, constipation or irregularity of bowel Mild toxemia, constant fatigue and lassitude Abdomen loses its elasticity when picked up between fingers


3.

On sigmoidoscopy, scattered ulceration with yellowish and erythematous border The gangrenous type (fatal cases) is characterized by the appearance of large sloughs of intestinal

tissues in the stool accompanied by hemorrhage. Extraintestinal forms 1. Hepatic Pain at the upper right quadrant with tenderness of the liver Abscess may break through the lungs, patient coughs anchovy-sauce sputum Jaundice Intermittent fever

Loss of weight or anorexia Clinical Features: 1. 2. 3. Onset is gradual Diarrhea increases and stool becomes bloody and mucoid In untreated cases:

Anatomy and Physiology: Amebiasis is an intestinal illness thats typically transmitted when someone eats or drinks something thats contaminated with a microscopic parasite called Entamoeba histolytica (E. histolytica). The parasite is an amoeba, a single-celled organism. Thats how the illness got its name amebiasis. In many cases, the parasite lives in a persons large intestine without causing any symptoms. But sometimes, it invades the lining of the large intestine, causing bloody diarrhea, stomach pains, cramping, nausea, loss of appetite, or fever. In rare cases, it can spread into other organs such as the liver, lungs, and brain. I. Structure. The GI System consists of the oral structures, esophagus, stomach, small intestine, large intestine and associated structures. A. Oral Structuresinclude the lips, teeth, gingivae and oral mucosa, tongue, hard palate, soft palate, pharynx and salivary glands. B. The esophagus is a muscular tube extending from the pharynx to the stomach. 1. Esophageal openings include: a. The upper esophageal sphincter at the cricopharyngeal muscle. b. The lower esophageal sphincter (LES), or cardiac sphincter, which normally remains closed and opens only to pass food into the stomach.

C. The Stomach is a muscular pouch situated in the upper abdomen under the liver and diaphragm. Te stomach consists of three anatomic areas: the fundus, body (i.e., corpus), and antrum (i.e., pylorus) D. Sphincters. The LES allows food to enter the stomach and prevents reflux into the esophagus. The pyloric sphincter regulates flow of stomach contents (chyme) into the duodenum. E. The small intestine, a coiled tube, extends from the pyloric sphincter to the ileocecal valve at the large intestine. Sections of the small intestine include the duodenum, jejunum and ileum F. The large intestine is a shorter, wider tube beginning at the ileocecal valve and ending at the anus. The large intestine consists of three sections: 1. The cecum is a blind pouch that extends from the ileocecal valve to the vermiform appendix. 2. The colon, which is the main portion of the large intestine, is divided into four anatomic sections: ascending, transverse, descending and sigmoid. 3. The rectum extends from the sigmoid colon to the anus. G. The ileocecal valve prevents the return of feces from the cecum into the small intestine and lies at the upper border of the cecum. H. The appendix, which collects lymphoid tissues, arises from the cecum. I. The GI tract is composed of five layers. 1. An inner mucosal layer lubricates and protects the inner surface of the alimentary canal. 2. A submucosal layer is responsible for secreting digestive enzymes. 3. A layer of circular smooth muscle fibers is responsible for movement of the GI tract. 4. A layer of longitudinal smooth muscle fibers also facilitates movement of the GI tract. 5. The peritoneum, an outer serosal layer, covers the entire abdomen and is composed of the parietal and visceral layers. II. Function. The GI system performs two major body functions: digestion and elimination. A. Digestion of food and fluid, with absorption of nutrients into the bloodstream, occurs in the upper GI tract, stomach and small intestines. 1. Digestion begins in the mouth with chewing and the action of ptyalin, an enzyme contained in saliva that breaks down starch. 2. Swallowed food passes through the esophagus to the stomach, where digestion continues by several processes. a. Secretion of gastric juice, containing hydrochloric acid and the enzymes pepsin and lipase ( and renin in infants) b. Mixing and churning through peristaltic action 3. From the pylorus, the mixed stomach contents (i.e. chyme) pass into the duodenum through the pyloric valve. 4. In the small intestine, food digestion is completed, and most nutrient absorption occurs. Digestion results from the action of numerous pancreatic and intestinal enzymes (e.g., trypsin, lipase, amylase, lactase, maltase, sucrase( and bile. B. Elimination of waste products through defacation occurs in the large intestines and rectum. In the large intestine, the cecum and ascending colon absorb water and electrolytes from the now completely digested material. The rectum stores feces for elimination. Pathophysiology Laboratory Diagnosis: 1. 2. Stool exam (cyst, white and yellow pus with plenty of amoeba) Blood exam (Leukocytosis)

3. Proctoscopy/Sigmoidoscoppy Diagnosis of amoebiasis 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 histolytica and 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. dispardoes 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 may still be positive if you had amoebiasis in the past, even if you are no longer infected now. Complications: 1. Amebic colitis Fulminant or necrotizing colitis

2.

Toxic megacolon Ameboma

Rectovaginal fistulas Amebic liver abscess Intrathoracic or intraperitoneal rupture with or without secondary bacterial infection Direct extension to pleura or pericardium

3. Brain abscess Treatment: 1. 2. 3. 4. Metronidazole (Flagyl) 800mg TID X 5 days Tetracyline 250 mg every 6 hours Ampicillin, quinolones sulfadiazine Streptomycin SO4, Chloramphenicol

5. Lost fluid and electrolytes should be replaced Several antibiotics are available to treat amoebiasis. 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. Nursing Management: 1. 2. Observe isolation and enteric precaution Provide health education and instruct patient to Boil water for drinking or use purified water Avoid washing food from open drum or pail Cover leftover food

Wash hands after defacation and before eating Avoid ground vegetables (lettuce, carrots, and the like) Methods of Prevention: 1. 2. 3. 4. 5. Health education Sanitary disposal of feces Protect, chlorinate, and purify drinking water Observe scrupulous cleanliness in food preparation and food handling Detection and treatment of carriers

6. Fly control (they can serve as vector) Resources: http://www.emedicine.com http://en.wikipedia.org http://kidshealth.org http://cdc.gov

Amebiasis is infection with Entamoeba histolytica. It is commonly asymptomatic, but symptoms ranging from mild diarrhea to severe dysentery may occur. Extraintestinal infections include liver abscesses. Diagnosis is by identifying E. histolytica in stool specimens or by serologic tests. Treatment for symptomatic disease is with metronidazole or tinidazole followed by paromomycin or other drugs active against cysts in the lumen. Three species of Entamoeba are morphologically indistinguishable, but molecular techniques show that they are different species: E. histolytica (pathogenic) E. dispar (harmless colonizer, more common) E. moshkovskii (harmless colonizer)

Disease is caused by E. histolytica and tends to occur in regions with poor socioeconomic conditions and poor sanitation. Most infections occur in Central America, western South America, western and southern Africa, and the Indian subcontinent. In developed countries (eg, US), most cases occur among recent immigrants and travelers returning from endemic regions. Worldwide each year, an estimated 40 to 50 million people develop amebic colitis or extraintestinal disease, and about 40,000 to 70,000 die.

Pathophysiology
Entamoeba sp exist in 2 forms: Trophozoite Cyst

The motile trophozoites feed on bacteria and tissue, reproduce, colonize the lumen and the mucosa of the large intestine, and sometimes invade tissues and organs. Trophozoites predominate in liquid stools but rapidly die outside the body. Some trophozoites in the colonic lumen become cysts that are excreted with stool. Cysts predominate in formed stools and resist destruction in the external environment. They may spread directly from person to person or indirectly via food or water. Amebiasis can also be sexually transmitted by oral-anal contact. E. histolytica trophozoites can adhere to and kill colonic epithelial cells and PMNs and can cause dysentery with blood and mucus but with few PMNs in stool. Trophozoites also secrete proteases that degrade the extracellular matrix and permit invasion into the intestinal wall and beyond. Trophozoites can spread via the portal circulation and cause necrotic liver abscesses. Infection may spread by direct extension from the liver to the right lung and pleural space or, rarely, through the bloodstream to the brain and other organs.

Symptoms and Signs

Most infected people are asymptomatic but chronically pass cysts in stools. Symptoms that occur with tissue invasion include intermittent diarrhea and constipation, flatulence, and cramping abdominal pain. Tenderness over the liver or ascending colon may occur, and stools may contain mucus and blood. Amebic dysentery: This form, common in the tropics, manifests with episodes of frequent semiliquid stools that often contain blood, mucus, and live trophozoites. Abdominal findings range from mild tenderness to frank abdominal pain, with high fevers and toxic systemic symptoms. Abdominal tenderness frequently accompanies amebic colitis. Between relapses, symptoms diminish to recurrent cramps and loose or very soft stools, but emaciation and anemia may develop. Symptoms suggesting appendicitis may occur. Surgery in such cases may result in peritoneal spread of amebas. Chronic amebic infection: This infection can mimic inflammatory bowel disease and manifests as intermittent nondysenteric diarrhea with abdominal pain, mucus, flatulence, and weight loss. Chronic infection may also manifest as tender, palpable masses or annular lesions (amebomas) in the cecum and ascending colon. Extraintestinal amebic disease: Extraintestinal disease originates from infection in the colon and can involve any organ, but a liver abscess, usually single and in the right lobe, is the most common. It can manifest in patients who had no prior symptoms, is more common among men than among women (7:1 to 9:1), and may develop insidiously. Symptoms include pain or discomfort over the liver, which is occasionally referred to the right shoulder, as well as intermittent fever, sweats, chills, nausea, vomiting, weakness, and weight loss. Jaundice is unusual and low grade when present. The abscess may perforate into the subphrenic space, right pleural cavity, right lung, or other adjacent organs (eg, pericardium). Skin lesions are occasionally observed, especially around the perineum and buttocks in chronic infection, and may also occur in traumatic or operative wounds.

Diagnosis
Intestinal infection: Microscopic examination and, when available, enzyme immunoassay of stool Extraintestinal infection: Imaging and serologic testing or a therapeutic trial

Nondysenteric amebiasis may be misdiagnosed as irritable bowel syndrome, regional enteritis, or diverticulitis. A right-sided colonic mass may also be mistaken for cancer, TB, actinomycosis, or lymphoma. Amebic dysentery may be confused with shigellosis, salmonellosis, schistosomiasis, or ulcerative colitis. In amebic dysentery, stools are usually less frequent and watery than those in bacillary dysentery. They characteristically contain tenacious mucus and flecks of blood. Unlike stools in

shigellosis, salmonellosis, and ulcerative colitis, amebic stools do not contain large numbers of WBCs because trophozoites lyse them. Hepatic amebiasis and amebic abscess must be differentiated from other hepatic infections and tumors. Diagnosis of amebiasis is supported by finding amebic trophozoites, cysts, or both in stool or tissues; however, pathogenic E. histolytica are morphologically indistinguishable from nonpathogenic E. dispar and E. moshkovskii. Intestinal infection : Identification of intestinal amebas may require examination of 3 to 6 stool specimens and concentration methods (see Table 1: Approach to Parasitic Infections: Collecting and
Handling Specimens for Microscopic Diagnosis of Parasitic Infections

). Antibiotics, antacids, antidiarrheals,

enemas, and intestinal radiocontrast agents can interfere with recovery of the parasite and should not be given until the stool has been examined. E. histolytica also has to be distinguished from nonpathogenic amebas such as E coli, E. hartmanni, Endolimax nana, and Iodamoeba btschlii. In symptomatic patients, proctoscopy often shows characteristic flask-shaped mucosal lesions, which should be aspirated, and the aspirate should be examined for trophozoites. Biopsy specimens from rectosigmoid lesions may also show trophozoites. Extraintestinal infection: This infection is more difficult to diagnose. Stool examination is usually negative, and recovery of trophozoites from aspirated pus is uncommon. If a liver abscess is suspected, ultrasonography, CT, or MRI should be done. They have similar sensitivity; however, no technique can differentiate amebic from pyogenic abscess with certainty. Needle aspiration is reserved for lesions of uncertain etiology, those in which rupture seems imminent, and those that respond poorly to drug therapy. Abscesses contain thick, semifluid material ranging from yellow to chocolate-brown. A needle biopsy may show necrotic tissue, but motile amebas are difficult to find in abscess material, and amebic cysts are not present. A therapeutic trial of an amebicide is often the most helpful diagnostic tool for an amebic liver abscess. Serologic tests are positive in about 95% of patients with an amebic liver abscess, in > 70% of those with active intestinal infection, and in 10% of asymptomatic carriers. Enzyme immunoassay (EIA) is the most widely used. Antibody titers can confirm E. histolyticainfection but may persist for months or years, making it impossible to differentiate acute from past infection in residents from areas with a high prevalence of infection. E. histolytica, E. dispar, and E. moshkovskii are morphologically indistinguishable, so microscopic examination cannot be used to differentiate them. A sensitive and specific antigen detection assay for the E. histolytica adherence lectin has been developed and is available. PCR-based assays are available in research settings.

Treatment
Metronidazole or tinidazole initially Iodoquinol , paromomycin , or diloxanide furoate subsequently for cyst eradication For mild to moderate GI symptoms, oral metronidazole

500 to 750 mg tid in adults (12 to 17 mg/kg tid in children) for 7 to 10 days is recommended. Metronidazole

should not be given to pregnant women. Alcohol must be avoided because of the drug's disulfiram

-like effect. Alternatively, tinidazole

2 g po once/day in adults (50 mg/kg [maximum 2 g] po once/day in children > 3 yr) for 3 days can be used. When taken with alcohol, tinidazole

also has a disulfiram

-like effect, and it should not be used during pregnancy; however, in terms of GI adverse effects, it is generally better tolerated than metronidazole

. For severe intestinal and extraintestinal amebiasis, metronidazole

750 mg tid in adults (12 to 17 mg/kg tid in children) for 7 to 10 days is used. Alternatively, tinidazole

2 g po once/day in adults (50 mg/kg [maximum 2 g] po once/day in children > 3 yr) for 5 days can be used. A course of metronidazole

or tinidazole

should be followed by a 2nd oral drug to eradicate residual cysts in the lumen. Options are Iodoquinol 650 mg po tid in adults (10 to 13 mg/kg [maximum of 2 g/day] tid in children) for 20 days Paromomycin 8 to 11 mg/kg tid for 7 days Diloxanide furoate 500 mg po tid in adults (7 mg/kg po tid in children) for 10 days Diloxanide furoate

is not available commercially in the US. Therapy should include rehydration with fluid and electrolytes and other supportive measures. Asymptomatic people who pass E. histolytica cysts should be treated with paromomycin

,iodoquinol

, or diloxanide furoate

(see above for doses). Although metronidazole

andtinidazole

have some activity against E. histolytica cysts, it is not sufficient for them to be used for cyst eradication. Treatment is not necessary for E. dispar or E. moshkovskii infections. However, if fecal antigen testing to differentiate them from E. histolytica is not available, the decision to treat is made clinically (eg, by the likelihood of exposure to E. histolytica).

Prevention
Contamination of food and water with human feces must be preventeda problem complicated by the high incidence of asymptomatic carriers. Uncooked foods, including salads and vegetables, and potentially contaminated water and ice should be avoided in developing areas. Boiling water kills E. histolytica cysts. The effectiveness of chemical disinfection with iodine- or chlorine-containing compounds depends on the temperature of the water and amount of organic debris in it. Portable filters provide various degrees of protection. Work continues on the development of a vaccine, but none is available yet.