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Jun 19 12 9:10 AM

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Just wanted to create a separate thread for information regarding histolytica 

Here is the red book info 

http://www.unboundmedicine.com/redbook/ub/view/RedBook/187095/all/Ameboma

Red Book

Amebiasis

Clinical Manifestations


Clinical syndromes associated with Entamoeba histolytica infection include noninvasive intestinal infection, intestinal amebiasis, ameboma, and liver abscess. Disease is more severe in the very young, the elderly, and pregnant women. Patients with noninvasive intestinal infection may be asymptomatic or may have nonspecific intestinal tract complaints. People with intestinal amebiasis (amebic colitis) generally have 1 to 3 weeks of increasingly severe diarrhea progressing to grossly bloody dysenteric stools with lower abdominal pain and tenesmus. Weight loss is common, but fever occurs only in a minority of patients (8%-38%). Symptoms may be chronic and may mimic inflammatory bowel disease. Progressive involvement of the colon may produce toxic megacolon, fulminant colitis, ulceration of the colon and perianal area, and rarely, perforation. Progression may occur in patients inappropriately treated with corticosteroids or antimotility drugs. An ameboma may occur as an annular lesion of the cecum or ascending colon that may be mistaken for colonic carcinoma or as a tender extrahepatic mass mimicking a pyogenic abscess. Amebomas usually resolve with antiamebic therapy and do not require surgery.

In a small proportion of patients, extraintestinal disease may occur. Although the liver is the most common extraintestinal site, the lungs, pleural space, pericardium, brain, skin, and genitourinary tract also may be involved. Liver abscess may be acute, with fever, abdominal pain, tachypnea, liver tenderness, and hepatomegaly; or chronic, with weight loss, vague abdominal symptoms, and irritability. Rupture of abscesses into the abdomen or chest may lead to death. Evidence of recent intestinal infection usually is absent.


Etiology


The genus Entamoeba includes 6 species that live in human intestine. Three of these species are identical morphologically: E histolytica, Entamoeba dispar , and Entamoeba moshkovskii . The pathogenic E histolytica and the nonpathogenic E dispar and E moshkovskii are excreted as cysts or trophozoites in stools of infected people.


Epidemiology


E histolytica can be found worldwide but is more prevalent in people of lower socioeconomic status who live in economically developing countries, where the prevalence of amebic infection may be as high as 50% in some communities. Groups at increased risk of infection in industrialized countries include immigrants from or long-term visitors to areas with endemic infection, institutionalized people, and men who have sex with men. E histolytica is transmitted via amebic cysts by the fecal-oral route. Ingested cysts, which are unaffected by gastric acid, undergo excystation in the alkaline small intestine and produce trophozoites that infect the colon. Cysts that develop subsequently are the source of transmission, especially from asymptomatic cyst excreters. Infected patients excrete cysts intermittently, sometimes for years if untreated. Transmission occasionally has been associated with contaminated food, water, and enema equipment. Sexual transmission also may occur.

The incubation period is variable, ranging from a few days to months or years but commonly is 2 to 4 weeks.


Diagnostic Tests


A presumptive diagnosis of intestinal infection depends on identifying trophozoites or cysts in stool specimens. Examination of serial specimens may be necessary. Specimens of stool, endoscopy scrapings (not swabs), and biopsies should be examined by wet mount within 30 minutes of collection and fixed in formalin or polyvinyl alcohol (available in kits) for concentration and permanent staining. E histolytica is not distinguished easily from the noninvasive and more prevalent E dispar and E moshkovskii , although trophozoites containing ingested red blood cells are more likely to be E histolytica . Polymerase chain reaction, isoenzyme analysis, and monoclonal antibody-based antigen detection assays can differentiate E histolytica, E dispar , and E moshkovskii .

The indirect hemagglutination (IHA) test has been replaced by commercially available enzyme immunoassay (EIA) test kits for routine serodiagnosis of amebiasis. The EIA test detects antibody specific for 
E histolytica in approximately 95% of patients with extraintestinal amebiasis, 70% of patients with active intestinal infection, and 10% of asymptomatic people who are passing cysts ofE histolytica . Patients may continue to have positive test results even after adequate therapy.

Ultrasonography and computed tomography can identify effectively liver abscesses and other extraintestinal sites of infection. Aspirates from a liver abscess usually show neither trophozoites nor leukocytes.


Treatment


Treatment involves elimination of the tissue-invading trophozoites as well as organisms in the intestinal lumen. E dispar and E moshkovskii infections do not require Treatment. Corticosteroids and antimotility drugs administered to people with amebiasis can worsen symptoms and the disease process. In settings where tests to distinguish species are not available, Treatment should be given to symptomatic people on the basis of positive results of microscopic examination. The following regimens are recommended:


  • Asymptomatic cyst excreters (intraluminal infections): treat with a luminal amebicide, such as iodoquinol, paromomycin, or diloxanide.

  • Patients with mild to moderate or severe intestinal symptoms or extraintestinal disease (including liver abscess): treat with metronidazole or tinidazole, followed by a therapeutic course of a luminal amebicide (iodoquinol or paromomycin). Nitazoxanide also may be effective for mild to moderate intestinal amebiasis, although it is only approved by the US Food and Drug Administration for Treatment of diarrhea caused by 
Giardia species or Cryptosporidium species.
Dehydroemetine followed by a therapeutic course of a luminal amebicide may be considered for patients for whom Treatment of invasive disease has failed or cannot be tolerated. However, dehydroemetine has significant toxicity and should be used with caution. An alternate Treatment for liver abscess is chloroquine phosphate concomitantly with metronidazole or tinidazole, followed by a therapeutic course of a luminal amebicide.
Surgical aspiration occasionally may be required when response of the abscess to medical therapy is unsatisfactory. To prevent spontaneous rupture of an abscess, patients with large liver abscesses may benefit from percutaneous or surgical aspiration.

Follow-up stool examination is recommended after completion of therapy, because no pharmacologic regimen is effective in eradicating intestinal infection completely. Household members and other suspected contacts also should have adequate stool examinations performed and be treated if results are positive for 
E histolytica .



Isolation of the Hospitalized Patient


In addition to standard precautions, contact precautions are recommended for the duration of illness.


Control Measures


Careful hand hygiene after defecation, sanitary disposal of fecal material, and Treatment of drinking water will control the spread of infection. Sexual transmission may be controlled by use of condoms and avoidance of sexual practices that may permit fecal-oral transmission.


Footnotes


1 . For further information, see Drugs for Parasitic Infections.


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Jun 19 12 9:11 AM



http://www.unboundmedicine.com/redbook/ub/view/RedBook/187196/all/Table_4_9__Drugs_for_Parasitic_Infections?q=drugs%20histolytica(copy and paste link if it doesnt work directly)

Table 4.9. Drugs for Parasitic Infections

Table 4-9







With increasing travel, immigration, use of immunosuppressive drugs and the spread of AIDS, physicians anywhere may see infections caused by parasites. The table below lists first-choice and alternative drugs for most parasitic infections. Table 4.10 summarizes the known prenatal risks of antiparasitic drugs. The brand names and manufacturers of the drugs are listed in Table 4.11.




This table is continued in the following:
Table 4-9a
Table 4-9b
Table 4-9c
Table 4-9d


Infection




Drug




Adult dosage




Pediatric dosage




ACANTHAMOEBA keratitis


Drug of choice:




see footnote1




AMEBIASIS (Entamoeba histolytica)


asymptomatic


Drug of choice:




Iodoquinol2




650 mg PO tid X 20d




30–40 mg/kg/d (max. 2g) PO in 3 doses X 20d




OR


Paromomycin3




25–35 mg/kg/d PO in 3 doses X 7d




25–35 mg/kg/d PO in 3 doses X 7d




OR


Diloxanide furoate4*




500 mg PO tid X 10d




20 mg/kg/d PO in 3 doses X 10d




mild to moderate intestinal disease


Drug of choice:5




Metronidazole




500–750 mg PO tid X 7–10d




35–50 mg/kg/d PO in 3 doses X 7–10d




OR


Tinidazole6




2 g once PO daily X 3d




>3yrs: 50 mg/kg/d (max. 2g) PO in 1 dose X 3d




either followed by


Iodoquinol2




650 mg PO tid X 20d




30–40 mg/kg/d (max. 2g) PO in 3 doses X 20d




OR


Paromomycin3




25–35 mg/kg/d PO in 3 doses X 7d




25–35 mg/kg/d PO in 3 doses X 7d




  severe intestinal and extraintestinal disease


Drug of choice:




Metronidazole




750 mg PO tid X 7–10d




35–50 mg/kg/d PO in 3 doses X 7-10d




OR


Tinidazole6




2 g once PO daily X 5d




>3yrs: 50 mg/kg/d (max. 2g) PO in 1 dose X 3d




either followed by


Iodoquinol2




650 mg PO tid X 20d




30–40 mg/kg/d (max. 2g) PO in 3 doses X 20d




OR


Paromomycin3




25–35 mg/kg/d PO in 3 doses X 7d




25–35 mg/kg/d PO in 3 doses X 7d






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#2 [url]

Jun 19 12 9:52 AM

Mayo clinic info

Amebiasis

Amebiasis is defined by the World Health Organization (WHO) and Pan American Health Organization (PAHO) as infection with Entamoeba histolytica, regardless of symptomatology. This protozoan parasite has a global distribution and an especially high prevalence in countries where poor socioeconomic and sanitary conditions predominate. In resource-rich nations, infections may be seen in travelers to and emigrants from endemic areas. Most infections are asymptomatic, but tissue invasion may result in amebic colitis, life-threatening hepatic abscesses, and even hematogenous spread to distant organs. Importantly, disease can occur months to years after exposure and must remain in the differential diagnosis in at-risk populations.

Advances in molecular technologies have revolutionized our understanding of this organism. Most notably, 2 additional Entamoeba species that are morphologically indistinguishable from E histolyticahave been recognized in humans. As our knowledge of the global epidemiology and pathogenicity ofEntamoeba spp increases, new clinical algorithms are developed. The latest nomenclature and recommendations, although unfamiliar and confusing to many, are important for appropriate patient care. Our review discusses what is known about these 3 Entamoeba spp and clarifies the currently accepted recommendations for diagnosis and treatment.

The “New” Entamoeba Species: Entamoeba Dispar and Entamoeba Moshkovskii

It is a long-held misconception that 10% of the world’s population is infected with E histolytica. In fact, most of these infections should be attributed to the morphologically identical but nonpathogenicE dispar. Emile Brumpt first proposed the existence of 2 indistinguishable Entamoeba spp, one pathogenic and one nonpathogenic, in 1925. However, not until 1978 was evidence for the existence of 2 separate entities provided by new technology (isoenzyme analysis). More recent studies using methodologies capable of distinguishing the 2 species suggest that E dispar is up to 10 times more prevalent in asymptomatic patients than E histolytica in endemic regions. Little is currently known about their epidemiology in resource-rich nations, where the incidence of both is rare, but previous reports of infection with E histolytica based only on morphology likely represent E dispar.

The discovery of a third morphologically identical Entamoeba spp further complicated our understanding of the epidemiology of E histolytica. The new species, named E moshkovskii, was first recognized as a ubiquitous freeliving organism in 1941; it has been reported in humans from both resource-rich and resource-poor nations. Although largely nonpathogenic, some recent evidence suggests that it may have a role in human intestinal disease. Much remains unknown regarding the pathogenicity and epidemiology of E moshkovskii.

The Definitive Pathogen: E Histolytica

E histolytica is the pathogenic species responsible for amebic colitis throughout the world. It infects people of both sexes and all ages; however, populations at risk may vary with geographic location, host susceptibility, and differences in organism virulence. People in highly endemic areas probably have recurrent asymptomatic infections, thus accounting for the high reported prevalence. In developed countries, amebic colitis is most commonly found in travelers to or emigrants from endemic countries, institutionalized persons, and patients infected with human immunodeficiency virus. Men who have sex with men were previously thought to have an increased incidence of infection, but this supposition was based on morphologic studies. New evidence suggests that these men were colonized primarily with E dispar rather than E histolytica.

The simple life cycle of E histolytica begins when infectious cysts are ingested in fecally contaminated food or water. This association with poor sanitation explains why resource-poor nations carry the bulk of the world’s disease. After ingestion and passage through the stomach, the organism excysts and emerges in the large intestine as an active trophozoite. Trophozoites multiply by simple division and encyst as they move further down the large bowel. Cysts are then expelled with the feces and may remain viable in a moist environment for weeks to months. Amebae typically subsist on a diet of intestinal bacteria and partially digested host food but are capable of tissue invasion and dissemination. Most infections (90%) remain asymptomatic, suggesting that tissue invasion is an aberration rather than a typical behavior.

Invasive intestinal disease may occur days to years after initial infection and is characterized classically by abdominal pain and bloody diarrhea. Watery or mucus-containing diarrhea, constipation, and tenesmus may also occur. This clinical picture corresponds histologically with trophozoites invading and laterally undermining the intestinal surface to form the so-called flask-shaped ulcers (Figure 1). The right side of the colon is commonly involved. Severe cases of amebic colitis are characterized by copious bloody diarrhea, diffuse abdominal pain, and (rarely) fever. Extensive fulminant necrotizing colitis, the most severe form of intestinal disease, is often fatal. Patients at increased risk of severe disease include those who are very young, very old, malnourished, or pregnant and those who are receiving corticosteroids. Some evidence suggests that patients infected with human immunodeficiency virus are at increased risk of severe disease, but this is not universally accepted. Complications of intestinal disease include stricture, rectovaginal fistulas, formation of an annular intraluminal mass (ameboma), bowel obstruction, perianal skin ulceration, toxic megacolon, perforation, peritonitis, shock, and death. Chronic intestinal amebiasis is also well described; patients with this condition can have years of intermittent abdominal pain, diarrhea, and weight loss.

Figure 1

Figure 1. “Flask-shaped” ulcer of invasive intestinal amebiasis (hematoxylin-eosin, original magnification x50). Note that the apex of the ulcer at the bowel lumen is narrower than the base, accounting for the flask shape. This is formed as trophozoites invade through the mucosa and move laterally into the submucosa (direction of ulcer expansion is marked by arrows). Microscopically, trophozoites are localized to the advancing edges of the submucosal ulcer. Image courtesy of John Williams, CBiol, MIBiol, London School of Hygiene and Tropical Medicine.

On rare occasions, E histolytica trophozoites enter the bloodstream and disseminate to other body sites, most commonly the liver via spread from the intestine through the portal vein. The right lobe is 4 times more likely to be involved than the left because it receives the bulk of the venous drainage from the right colon. Adult men aged 20 to 40 years are most frequently affected, although people of both sexes and all ages may develop an amebic liver abscess (ALA). Disease can occur years after exposure and may follow the onset of immunosuppression.

Hepatic invasion by amebic trophozoites results in marked tissue destruction with neutrophil recruitment, cellular necrosis, and formation of microabscesses that gradually coalesce. Most patients (65%–75%) present with a single abscess; however, multiple abscesses may also be formed. Abscesses consist of soft, necrotic, acellular yellow-brown debris, described as “anchovy paste.” Amebae are seldom identified in aspirates because they are located at the periphery of the lesion. White blood cells are also not usually seen, presumably because they have been destroyed by the amebic trophozoites.

Clinical presentation of ALA is highly variable and commonly includes tender hepatomegaly and pain in the right upper quadrant. Unlike amebic colitis, ALA is commonly accompanied by fever, as well as by rigors, chills, and profuse sweating. Most patients do not have concurrent colitis and cysts, and trophozoites are not always seen on fecal smears, posing an important diagnostic challenge. Jaundice is not typically present; elevated bilirubin levels are seen in less than 50% of patients, but elevated alkaline phosphatase levels are common. Complications include secondary bacterial infection; perforation into peritoneal, pleural, and pericardial cavities; septic shock; and death.

Perhaps the most serious complication is amebic metastasis from the liver. Rarely, trophozoites end up in other regions of the body, such as the brain, spleen, lungs, and genitourinary tract, through hematogenous or direct spread. Brain abscesses are extremely rare and are associated with high mortality rates. Like patients with ALA, those with disseminated disease do not usually have concomitant amebic colitis. Disseminated disease is not an adaptive mechanism for the parasite because its life cycle cannot be completed outside the intestine.

Radiologic and Endoscopic Features of Intestinal and Extraintestinal Disease

When amebiasis is suspected, radiologic and endoscopic examination may lend further support for a diagnosis. Colonoscopy can provide a wide spectrum of findings, from rare large-bowel ulcers in mild disease to diffuse mucosal ulceration, hemorrhage, colonic stricture, and presence of an ameboma. Grossly, these findings may resemble those seen with inflammatory bowel disease; therefore, correlation with histopathology and laboratory results is essential. Endoscopy is contraindicated in patients with evidence of peritonitis, severe dehydration, or shock.

Radiologic studies may also be helpful in evaluating a patient with possible ALA. Chest and abdominal radiography often reveal a pleural effusion and raised hemidiaphragm overlying the involved liver lobe. Ultrasonography reveals lesions that are typically hypoechoic and well defined with rounded edges. Computed tomography and magnetic resonance imaging can further characterize an abscess and allow for better detection of smaller lesions. All 3 techniques may facilitate guided needle biopsy and drainage if indicated. An abscess can usually be distinguished from solid lesions and biliary tract disease, but the differentiation between bacterial and amebic abscesses is less clear. Gallium scans may have a role in this differential diagnosis because amebic abscesses are usually “cold” on scan because of the lack of white blood cells in the abscess, whereas bacterial abscesses are typically “hot.”

Definitive Diagnosis of E HistolyticaE Dispar, and E Moshkovskii Infections

Clinically, it is desirable to definitively distinguish E histolytica from E dispar and E moshkovskiibecause, of the 3, it is the only proven human pathogen. The diagnosis of invasive amebiasis is usually suggested by the patient’s presenting symptoms, exposure history, and radiologic findings but should be confirmed with microbiological laboratory results. Many laboratory methods exist for identification of E histolytica, E dispar, and/or E moshkovskii, and the clinician should be aware that tests vary considerably in price, sensitivity, specificity, and the ability to definitively differentiate among the 3 species.

Light microscopic examination of fecal specimens (ie, “ova and parasite” examination) is often the first step in diagnosis; the characteristic trophozoites and cysts can often be identified through direct, concentrated, and/or permanently stained smears (Figure 2). Because organisms may appear intermittently, current recommendations call for submission of 3 stool specimens on different days during a period of 10 days. As mentioned previously, stool specimens from patients with disseminated disease may not contain cysts and trophozoites, despite repeated examinations.

Figure 2

FIGURE 2. Classic cyst morphology of Entamoeba histolytica/dispar/moshkovskii (iron hematoxylin stain of fecal sample, original magnification x1000). Cysts range from 10 to 16 µm in diameter (mean, 12.5 µm) and contain up to 4 nuclei, each with a central irregular dot and peripheral rim of chromatin. As seen above, all 4 nuclei are rarely visible in the same plane of focus. Chromatoid bodies (crystallized ribosomes) are also commonly seen (dark staining mass; arrow). Although this morphology allows for identification of these 3 organisms, exact speciation requires further testing. Image courtesy of Professor John Williams, London School of Hygiene and Tropical Medicine.

If stool cannot be examined in the fresh state (within 15 minutes) for motile trophozoites, then it should be placed immediately in an appropriate fixative to prevent deterioration of organisms. Unfortunately, microscopy alone cannot differentiate E histolytica from E dispar and E moshkovskii; additional tests are required for definitive speciation. The rare exception is when trophozoites containing ingested red blood cells are identified; they are strongly (but not definitively) indicative of invasive amebiasis. Trophozoites may also be identified in intestinal biopsy specimens, scrapings, or aspirates, allowing a diagnosis of amebiasis to be made if mucosal invasion and ulceration are also observed.

When only examination of stool specimens is available, the WHO/PAHO recommends that morphologically consistent cysts and trophozoites receive the nonspecific diagnosis E histolytica/E dispar, which could now be augmented to include E moshkovskii. The clinician must then interpret this laboratory result in the context of the individual patient and determine whether treatment is warranted.

When possible, E histolytica should be definitively identified. Identification methods include biopsy, serology, antigen detection, and molecular assays. Culture may be performed by some large specialty laboratories but is technically challenging and time-consuming. Furthermore, a negative culture result from intestinal samples does not exclude E histolytica because sensitivity is less than 100%. Culture followed by isoenzyme analysis is the criterion standard in diagnosis; however, it will likely be replaced by molecular assays in the near future.

Serologic tests detect the presence of species-specific antibodies in the patient’s serum. They are particularly useful in nonendemic countries where prevalence is low and have a good sensitivity and specificity for detecting invasive intestinal disease. They are also the test of choice for ALA because titers are typically high and test sensitivities and specificities exceed 95% with most assays. The primary disadvantage of serologic tests is that they cannot distinguish between past and current infection unless IgM is detected; IgM antibodies to E histolytica are short-lived and rarely detected. In contrast, IgG antibodies are longlived but highly prevalent in endemic settings because of past exposure. Serologic assays, which are also less sensitive in asymptomatic infection, take 7 to 10 days to appear in the bloodstream, resulting in possible false-negative results. Enzyme-linked immunosorbent assay is the most popular test in the diagnostic setting because of its speed and ease of use.

Fecal antigen detection tests use specific monoclonal or polyclonal antibodies to detect E histolyticaantigens. They are rapid, highly sensitive, and widely used in the diagnostic laboratory. Antigen tests are useful for confirming microscopic findings and providing a diagnosis in patients with negative fecal smear results. They are also helpful for interpreting positive results on amebic serology in patients from endemic countries because positive results on an antigen test indicate current rather than past infection. Some antigen detection kits can also be used on serum and material obtained from aspirated abscesses, offering greater sensitivity than microscopy for extraintestinal disease. Not all commercial kits are capable of speciation; some demonstrate cross-reactivity between E histolyticaand E dispar. Antigen detection methods are also not as sensitive as polymerase chain reaction assays, and may have low specificity in nonendemic regions. Clinicians should be familiar with the specifications of the kits used in their laboratory and confirm a suspected diagnosis if indicated.

The highest sensitivity and specificity for the diagnosis of E histolytica are offered by DNA-based tests. Many assays are available, including conventional and real-time polymerase chain reaction formats; however, they are currently used primarily by research and reference laboratories. Like most molecular amplification assays, they remain impractical for resource-limited settings because of their equipment, personnel, and facility requirements.

Differential Diagnosis

The differential diagnosis of amebic colitis must include bacterial (eg, Salmonella and Shigella spp,Mycobacterium tuberculosis), parasitic (eg, Schistosoma mansoni, Balantidium coli), and noninfectious (eg, inflammatory bowel disease, carcinoma, ischemic colitis, diverticulitis) causes of dysentery. When present, amebomas may mimic carcinoma, tuberculosis, or an appendiceal mass. Diagnostic tests in the work-up of patients with dysentery might include stool cultures for bacteria, ova, and parasites (other than E histolytica) and assays for bacterial toxins. Biopsy specimens of intestinal ulcers are useful for confirming the presence of trophozoites and for excluding other etiologies. Given its varied clinical presentation and possible delay of onset, the diagnosis of ALA may not be straightforward. The differential diagnosis includes bacterial abscess, echinococcal cyst, tuberculosis, and primary or metastatic tumor, all which would have vastly different treatments. Radiology can differentiate between many noninfectious and infectious etiologies; however, bacterial and amebic abscesses may appear remarkably similar. In comparison with bacterial abscesses, ALAs are more likely to be solitary, subcapsular, and located in the right lobe of the liver, but these findings are not always reliable. Occasionally, ALA may cause a pneumonia-like presentation with pleuritic pain, cough, and dyspnea. Radiologic imaging, clinical history, findings on physical examination, and serologic results are essential for including or excluding the diagnosis of ALA.

Treatment

The WHO/PAHO recommendations state that, when possible, E histolytica should be differentiated from morphologically similar species and treated appropriately. Given the small but substantial risk of invasive disease and the potential to transmit the infection to others, WHO/PAHO recommends treating all cases of proven E histolytica, regardless of symptoms. If E dispar is the only species identified, then no treatment should be given and other causes should be sought as appropriate.

In resource-poor countries, the standard but less optimal approach is to treat all patients with cysts and trophozoites identified on stool examination without additional testing for speciation. This method results in vast overtreatment and may hasten the development of drug resistance in E histolytica. Thus, WHO/PAHO recommends withholding treatment from asymptomatic patients when only a morphologic diagnosis by stool examination is available (ie, E histolytica/E dispar/E moshkovskii), unless another reason to suspect E histolytica infection exists. Even if patients diagnosed as being infected with E histolytica/E dispar/E moshkovskii have symptoms, other causes of disease, such as bacterial colitis, should not be excluded until further testing is done. Prophylaxis for E histolytica infection with amebicides is not recommended under any circumstances.

The medications recommended to treat confirmed amebiasis vary with clinical manifestation. Asymptomatic intestinal infection with E histolytica should be treated with luminal amebicides, such as paromomycin and diloxanide furoate. These medications will eradicate the luminal amebae and prevent subsequent tissue invasion and spread of the infection through cysts. Paromomycin, more widely available in the United States, has the advantage of not being absorbed in the bowel. Abdominal cramps and nausea are the most commonly reported adverse effects. A 10-day course at 30 mg/kg per day (divided into 3 daily doses) is typical. Some recommend follow-up stool examination to confirm eradication of cysts.

Compared with asymptomatic infection, intestinal and extraintestinal invasive disease are aerobic processes and should be treated with tissue amebicides, such as 5-nitroimidazoles (eg, metronidazole), which are readily absorbed into the bloodstream. Metronidazole (750 mg, 3 times a day, for 5–10 days) is the most commonly used drug in the United States for invasive amebiasis. Because little metronidazole reaches the lumen of the colon, treatment should be followed by administration of a luminal agent to eradicate any potential intestinal reservoirs. Most uncomplicated cases respond to a 5-day course of metronidazole; however, a 10-day course is useful in severe cases. Metronidazole may also be given parenterally to critically ill patients and can be supplemented with an antibiotic to cover secondary sepsis with bowel flora. The most common adverse effects of metronidazole are abdominal discomfort and nausea; most patients, however, are able to complete a full 5- to 10-day course. Serious adverse drug reactions include confusion, ataxia, and seizures.

A promising new regimen for invasive amebiasis is a 3-day course of nitazoxanide. This drug is effective against both luminal and invasive forms and has the added benefit of eliminating other intestinal parasites, including helminths. Surgery may be necessary in cases of perforation, abscess, obstruction, stricture, or toxic megacolon. However, given the friable nature of the inflamed mucosa, bowel repair is risky and should be avoided when possible.

Like amebic colitis, ALA typically responds well to a 5- to 10-day course of metronidazole, which should also be followed with a luminal amebicide. Metronidazole is the drug of choice in this setting, given its fast intestinal absorption, excellent bioavailability in tissue, and good abscess penetration. Surgical or percutaneous drainage of ALAs is generally not recommended because of the risk of content spillage and/or bacterial superinfection; exceptions are cases of imminent rupture, failure to respond to treatment after 4 to 5 days, and secondary bacterial infection. After treatment, ultrasonography may be used to monitor abscess regression, which occurs slowly during a period of 3 to 12 months. Small cystic defects may remain indefinitely.

Amebae rarely disseminate beyond the portal circulation. Given the small number of cases, no definitive treatment guidelines are available for management of extraintestinal, extrahepatic disease. As mentioned previously, infections with E dispar do not require treatment. Less is known about E moshkovskii, but it is likely that this infection also would not require treatment in most cases.

Conclusion

Recent discoveries have revolutionized our understanding of the epidemiology of Entamoeba spp infections and have led to important treatment and diagnostic recommendations. To avoid unnecessary and possibly harmful therapies, clinicians should follow the precise guidelines promulgated by the WHO/PAHO in 1997, including definitive differentiation of E histolytica from morphologically identical nonpathogenic species. Such definite differentiation is especially important in countries with adequate sanitation measures, where the predominant organism identified from morphologic stool examination will be E dispar. Because they have the highest sensitivity and specificity, molecular technologies offer the greatest diagnostic potential for laboratories in resource-rich countries at this juncture; however, some antigen detection tests can also provide reliable speciation. When speciation is impossible, we recommend using the phrase “E histolytica/E dispar/ E moshkovskii” to describe the morphologically identical species seen on stool examination. Continued use of new technologies will be crucial in elucidating the true epidemiology and pathogenesis ofEntamoeba spp, including the less well-studied E moshkovskii. Continued development of affordable, sensitive, and specific diagnostic tools will be required for use in resource-poor settings, where the incidence of disease is highest.

Reprinted from Pritt BS, Clark G: Amebiasis. 
Mayo Clin Proc. 2008;83:1154-1160. References omitted. Used with permission. The complete article is available online at www.mayoclinicproceedings.com.

A. It is a common misconception that the microscopic examination of stool for the presence of parasites (eg, #50016 Parasitic Examination) is the preferred test in all situations. When there is a clinical suspicion of giardiasis, the direct enzyme-linked immunosorbent assay (ELISA) for detection of stool Giardia antigens (#80231 Giardia Antigen, Feces) is a more sensitive and specific test than the traditional stool microscopic examination, with a sensitivity of 96%, and specificity of 97%. This test also has a high-positive predictive value (95%) given that giardiasis is the most common intestinal parasitic infection in the United States. While the microscopic examination of stool would allow detection of other parasites such as helminths, these parasites are extremely unlikely unless the patient has additional risk factors such as travel to endemic areas. The Parasitic Investigation of Stool Specimens Algorithm (included in this issue) is useful for guiding the selection of tests based on clinical and exposure history.

Q.The stool sample I submitted for parasitic examination came back with the following result: “Negative for parasites,” and the comment: “This assay doesn’t replace individual testing for Cryptosporidium, Cyclospora, and Microsporidia.” Since I still do not know the etiology of my patient’s symptoms, should I now order tests for these 3 additional organisms?

A.It is rarely appropriate to order all 3 additional tests. The above comment is added to negative Parasitic Examination results since these organisms are not typically detected by this method. However, these 3 parasites occur in specific clinical scenarios, some or all of which may not be applicable to your patient. For example, human infections with Microsporidia spp have been reported most frequently in patients with acquired immunodeficiency syndrome (AIDS) and are associated with chronic diarrhea, weight loss, and malabsorption. Cryptosporidiosis also occurs in patients with AIDS, but can cause a self-limited moderate diarrhea in young children, especially daycare attendees. Alternately, infection with Cyclospora cayatenensis is typically seen in travelers to developing countries, and in outbreaks due to contaminated food or water. It would be unlikely for one patient to have risk factors for all 3 parasites. The Parasitic Investigation of Stool Specimens Algorithm can help guide your decision to order additional testing by considering factors such as immune status and exposure history.

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#3 [url]

Jun 19 12 10:06 AM

About the Author

Dr. Omar M. Amin, Ph. D. is a professor of Parasitology at Arizona State University, Tempe, Arizona and the Director of the Institute of Parasitic Diseases (IPD) and it's Diagnostic and Educational Laboratory (DEL), Phoenix, Arizona. He is a recognized authority in the field of Parasitology with over 100 major scientific articles and books to his credit.

SYMPTOMS, NEGATIVE TESTS, AND PERIODICITY IN PARASITIC INFECTIONS - BY DR. OMAR M. AMIN, MD, USA

©Copyright 1999 by Dr. Omar M. Amin, MD, USA

(Explore Issue: Volume 9, Number 1)



Parasitological investigations of large patient populations are rarely conducted in the United States where the illusion of freedom from parasitic infections still predominate. Such investigations are considerably more common in most third world countries where endemic parasitosis are more readily documented.



Single and concurrent infections of 5 species of protozoans have been diagnosed in 378 symptomatic and asymptomatic patients from 644 samples examined in the summer of 1996 at the Diagnostic and Educational Laboratory (DEL) of the Phoenix based Institute of Parasitic Diseases (IPD) using a concentration-sedimentation technique (Amin, 1997). Fifty-four (8.4%) were infected with Blastocystis hominis, 13 (2.0%) with Cyclospora cayetanensis, 50 (7.8%) with Entamoeba coli, 53 (8.2%) with E. hartmanni, 99 (15.4%) with E. histolytica/E. dispar, 28 (4.3%) with Entamoeba spp., 9 (1.4%) with E. coli and E. hartmanni, 53 (8.2%) with B. hominis and Entamoeba spp., and 17 (2.6%) with other combinations of protozoan species. More females were represented in the infected, especially the multiply infected, patients than in the uninfected. The patient population varied between 0 and 78 years of age. Very young children were not multiply infected and only adults were infected with C. cayetanensis. All single and multiple infections were represented in symptomatic and asymptomatic patients. (Table 1)



Table 1. Prevalence of protozoan infections in stool samples of 644 symptomatic and asymptomatic patients examined during the summer of 1996 at DEL-IPD.

CategoriesNo. Tested (%)
Patients with Symptoms
No. Tested (%)
Patients without Symptoms
Single infections233 (43.8%)38 (33.9%)
Blastocystis hominis44 (8.3%)10 (8.9%)
Cyclospora cayetanensis10 (1.9%)3 (2.7%)
Entamoeba coli47 (8.8%)3 (2.7%)
E. hartmanni44 (8.3%)9 (8.0%)
E. histolytica88 (16.5%)11 (9.8%)
Multiple infections (above)95 (17.8%)12 (10.7%)
Other combinations14 (2.6%)3 (2.7%)
Total infected328 (61.6%)50 (44.6%)
Not infected204 (38.4%)62 (55.4%)
Total examined532 (100%)112 (100%)

Enteric and extra-intestinal symptoms were associated with presumably "harmless commensals" like E. coli and E. hartmanni. Symptomatic patients infected with E. histolytica/E. dispar markedly out-numbered those without symptoms.



It is clear from Table 1 that a number of patients had sub-clinical infections and showed no overt intestinal or extra-intestinal symptoms. These patients have been treated and their overall health improved after having been tested, and their parasites identified, at DEL-IPD.



The most common intestinal symptoms include bloating, diarrhea, flatulence, cramps, constipation, maldigestion, and malabsorption. Less frequently a patient may experience bleeding, irritable bowel, ulcerative colitis, leaky gut, and excess mucus secretion. Extra-intestinal symptoms often include fatigue, allergies, nausea, nervous/sensory disorders (memory loss, brain fog, irritability, poor coordination), skin disorders, pain, and muscle problems. Less frequent extra-intestinal symptoms may include fever, headache, immune deficiency, insomnia, weight changes, respiratory and hepatic symptoms, and peritonitis.



It is also clear from Table 1 that a number of symptomatic patients had no parasites that were detectable from fecal samples provided. These cases are probably related to one or both of the following reasons:



1. Other pathogenic organisms, ex., pathogenic bacteria, can cause symptoms comparable to those produced by typical parasites. These may include enterotoxigenic Escherichia coli, Salmonella, Shigella and/or Campylobactor among others; see Paredes et al. (1996). Like the typical parasites, these bacterial parasites are also amenable to treatment with herbal products.

2. Because of the heterogeneous distribution and the cyclic nature of some of the most common human parasites, infections may not be detected in fecal samples if collected when parasites are not running in the main fecal flow; e.g., intervals of many days may intervene between amoebic "runs" which may make the microscopic examination of many stool specimens necessary to confirm a positive Entamoeba histolytica infection (Amin, 1994-95; Hiatt et al., 1995; Kelsall and Ravdin, 1994). The same kind of periodicity and/or adherence to the intestinal lining are also known to occur in Giardia lamblia (see Amin, 1994-95, Walterspiel and Pickering, 1994) and Cyclospora cayetanensis (see Amin, 1998). This explains the intermittent shedding and cyclic recovery of these parasites in fecal samples collected for testing. It is important to test for cyclic parasites when they are "running." The DEL-IPD kit is designed to collect 2 separate fecal samples on 2 different days to maximize parasite recovery rate. On some occasions, however, testing may have to be repeated.



References

1. Amin, O. M. 1994-95. Relationships in parasitology: Parts I, II. Explore! for the Professional 5(5-6): 5-8, 6(1): 19-22.
2. Amin, O. M. 1997. Prevalence and host relationships of intestinal protozoan infections during the summer of 1996. Explore! for the Professional 8(2): 29-35.
3. Amin, O. M. 1998. Seasonal prevalence and host relationships of Cyclospora cayetanensis in North America during 1996. Parasitology International 47:53-58.
4. Hiatt, R. A., E. K. Markell, and E. NG. 1995. How many stool examinations are necessary to detect pathogenic intestinal protozoa? American Journal of Tropical Medicine and Hygiene 53:36-39.
5. Kelsall, B. L. and J. I. Ravdin. 1994. Amebiasis: Human infection with Entamoeba histolytica. In progress in Parasitology (Sun, T. Ed.) pp 27-54. CRC Press, Ann Arbor.
6. Paredes, P., S. Campbell-Forrester, H. L. DuPont, D. V. Ashley, J. J. Mathewson, S. Thompson, and R. Steffen. 1996. The etiology of travelers diarrhea on a Caribbean Island. Abstract no. 74, 45th Annual Meeting of the American Society of Tropical Medicine and Hygiene, Baltimore, Maryland, (December 1-5).
7. Walterspiel, J. N. and L. K. Pickering. 1994. Giardia and giardiasis. In Progress in Parasitology (Sun, T. ed.) pp 1-26, CRC Press, Ann Arbor.

Write Dr. Omar Amin in care of Explore Publications. Here you may also obtain his 60 pg. research from Vol. 8, #6, Explore!, free one time to current subscribers or $14.00 for others. Telephone 360-424-6025, or Fax 360-

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#4 [url]

Jun 19 12 10:08 AM


[Prevalence of iron and iodine deficiency, and parasitosis among children from Arandas, Jalisco, Mexico].

[Article in Spanish]
Vásquez-Garibay EMRomero-Velarde ENápoles-Rodríguez FNuño-Cosío METrujillo-Contreras FSánchez-Mercado O.

Source

Instituto de Nutrición Humana, Unidad de Investigación en Ciencias de la Salud, Edificio Anexo al Hospital Civil Dr. Juan I. Menchaca, 3o. Piso, Salvador Quevedo y Zubieta #750, 44340, S.L. Guadalajara, Jalisco, México. inhu@cucs.udg.mx

Abstract

OBJECTIVE:

To estimate the prevalence of iron deficiency, iodine deficiency and parasitosis in children attending the Instituto Alteño para el Desarrollo de Jalisco (Highlands Institute for Development of Jalisco State, INADEJ), Arandas, Jalisco, Mexico.

MATERIAL AND METHODS:

A cross-sectional study was conducted between 1997 and 1999, among 432 children aged 12 to 120 months attending the INADEJ. Measurements included hematological values, urine iodine concentration, and presence of parasites. Student's t test chi square tests were used for parametric and nonparametric analysis.

RESULTS:

The prevalence figures of anemia (20 vs 7.4%, p = 0.007) and iron deficiency (60.9 vs 44.4%, p = 0.02) were higher in preschool than in school children. Iodine deficiency was found in 29% (10.5% moderate or severe) and parasitosis in 47.2% of children, mainly E. histolytica (30.2%) and G. lamblia (28.9%). Low income, male gender and lack of social security policy holding were associated to parasitosis.

CONCLUSIONS:

The high prevalence rates of iron deficiency, iodine deficiency, and parasitosis, should be addressed by state health services with effective interventions to restrain these preventable diseases. The English version of this paper is available at: http://www.insp.mx/salud/index.html.




The vitamin B1 status among young Egyptian males in relation to infection with parasites.

Hussein LArafah AGaafar S.

Source

National Research Center, Nutrition Department, Giza, Egypt.

Abstract

Erythrocytic transketolase activity and thiamin pyrophosphate effect (TPP%) were used to define the nutritional thiamin status of an age stratified sample of 66 young males with parasitic infection. The results revealed that 6% of the control group were biochemically deficient in vitamin B1 compared with a percentage incidence of 42% among the parasitized subjects. Intestinal infection with Entamoeba histolytica, Hymenolepsis nana or with more than one parasite had the most depleting effect on the tissue thiamin status.




The salutary effect of milk on amoebiasis and its reversal by iron.

Murray MJMurray AMurray CJ.

Abstract

Observations among milk-drinking African nomads showed an unusual freedom from infection with Entamoeba histolytica compared with similar nomads taking a mixed diet. A controlled study among Maasai pastoralists showed that the administration of iron to correct their dietary iron deficiency sharply increased their susceptibility to amoebiasis. Examination of the milk of their Zebu cattle showed that it not only had a concentration of iron below the minimum necessary for the growth of E histolytica but also contained partly saturated lactoferrin and transferrin, which may actively compete with the parasite in the colon for ambient iron. These observations suggest the possibility of a long-standing ecological compromise between nomads, their milk diet, and E histolytica.

PMID:
 
7388537
 
[PubMed - indexed for MEDLINE] 
PMCID:
 
PMC1601833
 
Free PMC Article



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#5 [url]

Jun 19 12 10:10 AM

From Badbugs.com

Some therapeutic failures with metronidazole in patients with invader amebiasis and some reports of resistance to it
In vitro sensitivity of Entamoeba 
histolytica to metronidazole
Aguirre-Cruz ML, Valadez-Salazar A, Munoz O. 
Arch Invest Med (Mex). 1990;21 Suppl 1:23-6 
Unique in that it is effective both in the bowel lumen and in tissues, metronidazole has been reported to eradicate only up to 50% of luminal infections 
This statement has support from a study of 36 patients with amoebic liver abscess for whom the hepatic lesions were cleared; but 20 were recolonized in the intestine, 16 asymptomatically. This was ascribed to the pharmacokinetics of metronidazole cycling in the liver and the action of metronidazole against trophozoites but not invariable eradication of cysts, creating E. 
histolytica carrier states.

Current recommendations suggest the use of metronidazole or tinidazole PLUS the luminal amoebicide diloxanide furoate or iodoquinol, with other combinations (including paromomycin, tetracycline, and chloroquine) depending on the severity of the infection and site, i.e., whether it is intraluminal, invasive, or abscessed. 
Drug Targets and Mechanisms of Resistance in the Anaerobic Protozoa 
Peter Upcroft* and Jacqueline A. Upcroft 
Queensland Institute of Medical Research and The Tropical Health Program, Australia
(italics & caps added by author of this site)
During 4 years of chronic digestive symptoms Gary had been diagnosed with the parasite Entamoeba histolytica twice - once by stool antigen and once by saliva antibody testing. Ova and parasite, stool antibody, saliva antigen, stool antigen and a blood antibody test had all been negative.

As the negative results outweighed the positive, and drs questioned the results of 
saliva antibody testing, f
inding a doctor who believed he was actually infected with E.
histolytica proved a challange. In an effort to find an answer to his illness Garey consulted more than ten doctors over four years. Despite a number of Flagyl treatments his symptoms remained unchanged. (cont. below)
Garey managed to keep the worst of the symptoms at bay with anti-parasitic herbs. In hindsight he realises this may have contributed to the negative results because some herbs and drugs not only reduce the number of parasites colonising the bowel, but may also alter the appearance of the parasite. This change in appearance makes it more difficult for the lab technician to identify the parasite microscopically. Drugs can also alter sensitivity of stool antigen testing during and after drug treatment.

Keeping the symptoms under control did not always work in Garey's favour:"We have a fairly sophisticated infectious disease clinic at the medical school complex here in Portland. At one point I tried to make an appointment about my infection via a naturopathic doctor based on a positive lab test through Great Smokies Diag. I was refused to be seen. The reason given was that I was not thought to be sick enough to require the services of a specialist".

After four years of searching Garey eventually found a specialist endocrinologist with an interest in treating parasites, who "thought outside the square" and was willing to taking into consideration Garey's positive result for E.histolytica combined with chronic health problems. The specialist agreed to treat Garey with a combination of Humatin and Nitazoxinide resulting in a complete recovery. 

Garey wrote to his first primary care physician outlining the extent of his search for a treatment, enduring misdiagnosis and inadequate treatment for four years until he finally found a dr who would help him. The doctor replied, by registered mail, informing Garey he 
"would no longer be willing to see me for any reason". 

Garey wrote: 
"I can corroborate about the lack of knowledge doctors often have about parasites, symptoms, testing and treatment. I have heard many times that Eh is not pathological. I saw about 10 different doctors. It is remarkable the ignorance of this very serious infection."

Garey took 
Nitazoxanide 600mg 4 x daily for four days and Paromomycin 250mg 3 x daily for five days. If this treatment helps you please drop me a line. Your experience will help others make an informed decision about their own treatment.
March 2004
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#6 [url]

Jun 19 12 10:21 AM

Treatment for asymptomatic /silent histolytic infection

Paromomycin and diloxanide furoate are the drugs recommended for the treatment of asymptomatic Entamoeba histolytica infection.1 These agents have been used in clinical practice for more than 30 years. The efficacy of either agent against E. histolytica is reported to be greater than 80 percent,2 although some have suggested that paromomycin is preferable because of a lower cure rate reported with the use of diloxanide furoate in symptomatic patients.3 However, the efficacy of these medications was evaluated before the identification of E. dispar as a separate nonpathogenic species, which is morphologically indistinguishable from E. histolytica and which also colonizes the human gut.4 Because the prevalence of E. dispar worldwide is believed to be 10 times as high as that of E. histolytica, previous studies may have reflected primarily the effectiveness of these medications against E. dispar.

We report the results of a randomized trial comparing the efficacy of diloxanide furoate with that of paromomycin for the treatment of asymptomatic carriers of E. histolytica. Subjects were identified by screening adult members of 372 households in Phu Cat, Hué, Vietnam (33 percent of all households). Stool specimens were obtained from 1040 subjects (87 percent of those eligible) and analyzed with the use of a real-time polymerase-chain-reaction (PCR) assay that is specific for E. histolytica, according to a method described previously.5 A total of 93 asymptomatic carriers of E. histolytica were identified, of whom 71 agreed to participate in the study. The study was approved by the scientific review board of the Medical College of the University of Hué. Written informed consent was obtained from all subjects.

Thirty-four subjects (13 men with a mean [±SD] age of 37.6±11.2 years and 21 women with a mean age of 36.8±10.5 years) were randomly assigned to receive paromomycin, and 37 subjects (18 men with a mean age of 39.2±11.2 years and 19 women with a mean age of 36.8±11.0 years) were assigned to receive diloxanide furoate. Both drugs were given at the recommended oral dose of 500 mg three times a day for 10 days. The taking of medication was directly observed in 44 of the subjects (62 percent). For all subjects, the presence of E. histolytica in the stool was reassessed with the use of the PCR assay 10 and 20 days after the termination of therapy. There was no loss to follow-up.

Evaluation on day 20 indicated a significantly higher cure rate among the subjects randomly assigned to treatment with paromomycin than among those assigned to treatment with diloxanide furoate (85 percent vs. 51 percent, P=0.003) (Table 1TABLE 1Efficacy of Paromomycin as Compared with Diloxanide Furoate for the Treatment of AsymptomaticEntamoeba histolyticaInfection.). The findings were similar when the comparison was limited to the subjects whose regular intake of medication was directly observed. In two subjects who received paromomycin and one subject who received diloxanide furoate, stool samples were negative for parasites on day 10 after therapy but were positive on day 20. Since the reinfection rate for E. histolytica in the studied population is only 4 percent per year, it is likely that the reappearance of the parasite was due to incomplete efficacy of the drug, resulting in a transient reduction of the parasite load to a level below the threshold of detection. Since both drugs are well tolerated and their costs are similar, the results support the use of paromomycin as the first-line agent for the treatment of asymptomatic E. histolytica infection.

Joerg Blessmann, M.D.
Egbert Tannich, M.D.
Bernhard Nocht Institute for Tropical Medicine, 20359 Hamburg, Germany 
tannich@bni.uni-hamburg.de

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#7 [url]

Jun 19 12 12:03 PM

Effect of vitamin A and zinc supplementation on gastrointestinal parasitic infections among Mexican children.

Long KZRosado JLMontoya Yde Lourdes Solano MHertzmark EDuPont HLSantos JI.

Source

Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA. k.long@uq.edu.au

Abstract

OBJECTIVE:

Gastrointestinal parasites continue to be an important cause of morbidity and stunting among children in developing countries. We evaluated the effect of vitamin A and zinc supplementation on infections by Giardia lamblia, Ascaris lumbricoides, and Entamoeba histolytica.

METHODS:

A randomized, double-blind, placebo-controlled trial was conducted among 707 children who were 6 to 15 months of age and from periurban areas of Mexico City, Mexico, between January 2000 and May 2002. Children, who were assigned to receive either vitamin A every 2 months, a daily zinc supplement, a combined vitamin A and zinc supplement, or a placebo, were followed for 1 year. The primary end points were the 12-month rates and durations of infection for the 3 parasites and rates of parasite-associated diarrheal disease as determined in stools collected once a month and after diarrheal episodes.

RESULTS:

G. lamblia infections were reduced and A. lumbricoides infections increased among children in the combined vitamin A and zinc group or the zinc alone group, respectively. Durations of Giardia infections were reduced among children in all 3 treatment arms, whereas Ascaris infections were reduced in the vitamin A and zinc group. In contrast, E. histolytica infection durations were longer among zinc-supplemented children. Finally, E. histolytica- and A. lumbricoides-associated diarrheal episodes were reduced among children who received zinc alone or a combined vitamin A and zinc supplement, respectively.

CONCLUSIONS:

We found that vitamin A and zinc supplementation was associated with distinct parasite-specific health outcomes. Vitamin A plus zinc reduces G. lamblia incidence, whereas zinc supplementation increases A. lumbricoides incidence but decreases E. histolytica-associated diarrhea.

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#8 [url]

Jun 19 12 12:08 PM

Entamoeba histolytica uses ferritin as an iron source and internalises this protein by means of clathrin-coated vesicles


http://www.sciencedirect.com/science/article/pii/S0020751908003676


Entamoeba histolytica uses ferritin as an iron source and internalises this protein by means of clathrin-coated vesicles.

López-Soto FGonzález-Robles ASalazar-Villatoro LLeón-Sicairos NPiña-Vázquez CSalazar EPde la Garza M.

Source

Departamento de Biología Celular, Centro de Investigación y de Estudios Avanzados del IPN, México DF 07000, Mexico.

Abstract

Entamoeba histolytica is a parasitic protozoan that produces dysentery and often reaches the liver, leading to abscess formation. Ferritin is an iron-storage protein that is mainly found in liver and spleen in mammals. The liver contains a plentiful source of iron for amoebae multiplying in that organ, making it a prime target for infection since iron is essential for the growth of this parasite. The aim of this study was to determine whether trophozoites are able to take up ferritin and internalise this protein for their growth in axenic culture. Interaction between the amoebae and ferritin was studied by flow cytometry, confocal laser-scanning microscopy and transmission electron microscopy. Amoebae were viable in iron supplied by ferritin. Trophozoites quickly internalised ferritin via clathrin-coated vesicles, a process that was initiated within the first 2 min of incubation. In 30 min, ferritin was found colocalizing with the LAMP-2 protein at vesicles in the cytosol. The uptake of ferritin was time- temperature- and concentration-dependent, specific and saturated at 46 nM of ferritin. Haemoglobin and holo-transferrin did not compete with ferritin for binding to amoebae. Amoebae cleaved ferritin leading to the production of several different sized fragments. Cysteine proteases of 100, 75 and 50 kDa from amoeba extracts were observed in gels copolymerised with ferritin. For a pathogen such as E. histolytica, the capacity to utilise ferritin as an iron source may well explain its high pathogenic potential in the liver.

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#9 [url]

Jun 19 12 1:19 PM

The intestinal bacterial milieu may be important in the treatment of protozoan infestation, especially for colonic oprganisms like E. histolytica.  Pathogenic strains of Entameba histolytica are able to evade lysis by both classical and alternative pathways of complement. 

Intestinal bacteria, E. coli in particular, are necessary for complement resistance and for amebic virulence[63]. Mirelman has suggested that ingested bacteria lower the redox potential within the parasite and allow the amebae to escape destruction by oxidative enzymes[64] He has reported that one can reversibly change the zvmodeme patterns of Entameba histolytica isolates from non-pathogenic to invasive by culturing amebae with the gut flora of patients who have either invasive disease or no symptoms.[65] [66]. 

Optimal treatment of protozoan infection requires not only the administration of antimicrobial substances, but strategies aimed at enhancing the function of intestinal resistance factors like secretory IgA and phagocyte function and creating a bacterial milieu that is not parasite friendly. 

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#10 [url]

Jun 19 12 1:30 PM

Awesome compilation! Especially the redbook! I just wish doctors would USE the lab test handbooks or the redbooks if someone comes with a bowel problem. And it also explains why my partner is better off: He used to drink a LITER of milk a day! 

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linenup

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#11 [url]

Jun 19 12 10:42 PM

Entamoeba histolytica uses ferritin as an iron source and internalises this protein by means of clathrin-coated vesicles

-iloveisabelle

Lactoferrin binds the iron up thus preventing biofilm proliferation as well.   Don't know the studies on lacto & e histo but I would suspect that it would be helpful. 

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linenup

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#12 [url]

Jun 19 12 11:27 PM

The intestinal bacterial milieu may be important in the treatment of protozoan infestation, especially for colonic oprganisms like E. histolytica.  Pathogenic strains of Entameba histolytica are able to evade lysis by both classical and alternative pathways of complement. Intestinal bacteria, E. coli in particular, are necessary for complement resistance and for amebic virulence[63]. Mirelman has suggested that ingested bacteria lower the redox potential within the parasite and allow the amebae to escape destruction by oxidative enzymes[64] He has reported that one can reversibly change the zvmodeme patterns of Entameba histolytica isolates from non-pathogenic to invasive by culturing amebae with the gut flora of patients who have either invasive disease or no symptoms.[65] [66]. Optimal treatment of protozoan infection requires not only the administration of antimicrobial substances, but strategies aimed at enhancing the function of intestinal resistance factors like secretory IgA and phagocyte function and creating a bacterial milieu that is not parasite friendly. 

-iloveisabelle

So the way I would interpret this is that probiotics do not help in protozoa infections which has been an ongoing discussion.   When I talked to the lab company that Dr. Jonathan Wright owns, the lab tech said that the sickest people had no beneficial e coli which is a vital probiotic and is overlooked in the US.   So my suspicion is that the body sequesters or limits probiotic colonies to keep the protozoa infection at bay.   Comments?

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#13 [url]

Jun 19 12 11:57 PM

Very very good research iloveisabelle!!!

@lineup: I think that (protozoal) infections in generel trigger a dysbiosis. How this dysbiosis show up depends of the individual case. Everyone had another mixture of good bacteria before the infection came. And not everybody has the same infection. Some have just entamoeba, some have a mixture from entamoeba, ppt and bh and so on.

In my case my colis are even to high and my bifidos are down.

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linenup

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#14 [url]

Jun 20 12 12:14 AM

joechip:  yes, I think it is difficult to get a final answer on this as there are many possibilities.   I have read that protozoa (which species?) eat bacteria for survival.   So many questions.   

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#15 [url]

Jun 20 12 6:24 AM






So the way I would interpret this is that probiotics do not help in protozoa infections which has been an ongoing discussion.   When I talked to the lab company that Dr. Jonathan Wright owns, the lab tech said that the sickest people had no beneficial e coli which is a vital probiotic and is overlooked in the US.   So my suspicion is that the body sequesters or limits probiotic colonies to keep the protozoa infection at bay.   Comments? 



-linenup





Lineup I would love to hear any other info from the lab about clues to repopulating beneficial e.coli.

The one has me scratching my head. 

I have been tested as having no beneficial e.coli.  I got a hold of a package of mutaflor (november?) and began taking two a day in addition to two mutaflor implants. Im not sure on the time frame but sometime after my bloating went higher up in my small intestines and I started to gain 2 pounds a week (I was already overweight). I kept taking it, not knowing for sure if there was a direct connection. Then lower bloating got worse and over the course of a month and a half I had gained 15 lbs! 
I stopped the mutaflor , still havent lost the weight (seems like water weight/edema) but have managed to get the bloat down so that I am not uncomfortable.  

Im still wondering if it was just my time to gain that much weight -though in past years Ive only gained at most 2-3 lbs per year- or if I was feeding the infection-or was this part of the healing process?

Questions

1. Did my low/no beneficial e.coli allow for the infection (infection did begin after intravenous antibiotics)?
2. Did the infection eat/crowd out all my beneficial e.coli?
3. If e.coli helps control gut infections why didnt it prove to be help in my case?
4. Is it necessary once an infection had taken over that it needs to be eradicated before beneficial e.coli can re-colonize?
5. I did get a mild die off from the implant. Perhaps some infection in my small intestines was able to consume and grow from taking the beneficial e.coli by mouth?
6. Perhaps and just perhaps all the extra bloating and weight gain were a sign that it was doing something positive and I just needed to keep going? (hmm.. I dont know that was some scary fast weight gain..up two sizes) Bifidus and sauerkraut also cause me bloating

Should I try the mutaflor again after the histolytica treatment? Now I am afraid of feeding whatever it was I was feeding.

Any one know of a natural source of e.coli? I dont understand how one could permanently loose all beneficial e.coli and have no natural way of re-establishing growth if it is so important. Perhaps when the infection is gone my apendix will repopulate the gut

http://www.sciencedaily.com/releases/2009/08/090820175901.htm



We need an e.coli thread too.




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#16 [url]

Jun 20 12 6:57 AM

There is one thing that I basically don´t understand. I always thought that colis and bifidos are mainly living in the large intestine and that protozoans live in the small intestine. So how could these two beneficial bacterias be influenced by the protozoans?

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#17 [url]

Jun 20 12 9:21 AM

I am adding this post from "Tracemins" who eradicated his  Blastos infection with some of the drugs recommended for histolytica, also he references psyllium which inhibits growth of histolytica. Cahill claims that Blastos does not cause infection. 

http://pptu.lefora.com/2012/03/10/tracemins-success/

March 2012

" Lineup, this has been a great blog and I learned a few things here. I was dealing w/Blast for the last couple years. I was finally able to get rid of it.

To summarize, I had tried some of the herbal formulas, oregano, wormwood, cloves, etc, etc. Many of them. I found the wormwood help the most, as symptoms would clear, but they would come back when I stopped taking it.

I finally decided to go to my MD. Of course he recommended 3 prescription drugs. He's a great doctor here in Santa Cruz that's open to natural therapies as well, but often is just not aware of them. The bottom line is he had done some investigating some time back and came across a protocol put together by an MD in San Francisco. The key here was taking the prescription meds with psyllium fiber. I believe this helps get the meds down into the lower intestines to help kill the Blasto Hom where they reside. This is the key.

Well, the first time I didn't realize that the fiber was all that important, so I took the meds w/out the fiber. The symptoms cleared temporarily but came back in 2-3 weeks after I stopped taking them. I retested a month after I stopped taking them, and was positive for Blasto Hom.

The 2nd time I took them w/the fiber and it worked. I did another stool test through MetaMetrix and tested negative for Blasto. I did test positive for "Parasite present; taxonomy unavailable", but at least the Blasto is gone. I had waited 5 weeks before retesting to make sure.

The natural herbs would have probably worked if I had taken the fiber w/them as well. But, I didn't realize that at the time. I take a variety of supplements as it is, and actually work for a vitamin company in sales and have been taking supplements for over 20 years. I have to admit that the herbs were harder on my system (causing fatigue) then the meds. I believe the reason is because the herbs have so many different compounds in them, that some could cause side effects. Whereas the meds only have the one chemical in the drug (though I was taking 3 of them). For whatever reason it was much easier to take.

I also just came across the article:. 

The presence of antiamoebic constituents in psyllium husk  

http://www.ncbi.nlm.nih.gov/pubmed/11807972

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#18 [url]

Jun 20 12 9:25 AM


The presence of antiamoebic constituents in psyllium husk.

Zaman VManzoor SMZaki MAziz NGilani AU.

Source

Department of Microbiology, The Aga Khan University Medical College, Karachi 74800, Pakistan.

Abstract

The crude extract of psyllium husk (ispaghula) and its active constituent (petroleum fraction) caused varying degrees of growth inhibition in three different species of Entamoeba, i.e. Entamoeba histolytica, E. invadens and E. dispar. The inhibitory effect of the crude extract was in the dose range of 1-10 mg/mL, whereas a similar inhibitory effect was obtained with the petroleum fraction at a much lower dose (0.1-1.0 mg/mL), indicating that the active chemical(s) is/are concentrated in the petroleum fraction. These data support the traditional use of psyllium husk in amoebic dysentery.


Copyright 2002 John Wiley & Sons, Ltd.

PMID:
 
11807972
 
[PubMed - indexed for MEDLINE]


Question..was it the psyllium that inhibited the histolytica or did the psyllium change the gut to inhibit infection?

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#19 [url]

Jun 20 12 9:50 AM


-- from the Doctor who's protocol Tracmins refers to:

http://www.jonkaiser.com/educate/ask/77.html


Dr. Kaiser replies:


Alberto, You ask an excellent question that is relevant to many other people both with and without HIV. The treatment of parasites with Flagyl is often unsuccessful due to the resistance many parasites have developed to this medication over time. Taking only a natural treatment is also very likely to be unsuccessful. Your best bet is a combination approach with Humatin (aka paromomcyin) 250 mg two capsules 3X/day PLUS Iodoquinol 650 mg one capsule 3X/day for the first fourteen days followed by a second fourteen days of Iodoquinol three times per day by itself. You should also take the ParaGone-Psyllium combination with the above medication program for the full twenty-eight days. Both during and after the above, take two months of high dose acidophilus supplementation. This may sound like a lot to take but it is all necessary to clear Blastocystis which is a very persistent parasite that often does not want to leave. As always, you need to retest to make sure that the treatment was successful. Good luck!


-------------------------


Both Humatin (paromo) and Iodoquinol are used for histolytica.


I have read in older publications that one could eradicate histolytica by killing off histolytica's symbiotic host. Perhaps Blastos is this symbiotic host? I dont know if the articles mean that the symbiotic host is always the same pathogen or differs per infection. (anyone know?)



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#20 [url]

Jun 20 12 9:58 AM

Tracemins protocol:


"Here is the email from my Doc. 
This was for Blastocystis Homonis. 

The 3 drug regimen is twice daily, taken on empty stomach with full glass of water or juice with psyllium and Lglutamine mixed in. I sometimes prescribe only a 2 drug regimen, in which case it is 3 x/day. The one you have is more effective.
Sincerely, Bruce Eisendorf, M.D.

These were the medications:
ALBENDAZOLE 200 MG PO TABS - Take 1 Tab by mouth twice
Daily. X 14 days
PAROMOMYCIN SULFATE 250 MG PO CAPS - 2 caps twice daily x 14
days
IODOQUINOL 650 MG PO TABS - Take 1 Tab by mouth three times
daily with meals. X 20 days



They were 3 different meds. I took them between meals, and w/psyllium. 
One medium heaping TBS w/each does of meds. 


Took the psyllium 3 x's/day. First thing in the morning w/my meds, then ate bfast an hr later. 
1 hr before lunch I took my meds again and psyllium together. 
1-2 hrs before dinner I took them again. 

No side effects. It's only for a few weeks while you take your meds. I don't believe that will cause any mineral deficiencies. If you are low, then just supplement w/those minerals. I"m not sure why you are low in minerals. If you take mineral supplements you should be fine. 

Yes, 3 grams Glutamine plus the med
s. "

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