Amoebiasis

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This article is about the infection. For the Amoebic Ensemble album, see Amoebiasis (album).
Amoebiasis
SpecialtyInfectious diseases Edit this on Wikidata
Life-cycle of the Entamoeba histolytica

Amoebiasis, or Amebiasis, refers to infection caused by the amoeba Entamoeba histolytica.[1][2] The term Entamoebiasis is occasionally seen but is no longer in use;[citation needed] it refers to the same infection. Likewise amoebiasis is sometimes incorrectly used to refer to infection with other amoebae, but strictly speaking it should be reserved for Entamoeba histolytica infection. Other amoebae infecting humans include:[3]

Except for Dientamoeba, the parasites above are not thought to cause disease.

A gastrointestinal infection that may or may not be symptomatic and can remain latent in an infected person for several years, amoebiasis is estimated to cause 70,000 deaths per year world wide.[8] Symptoms can range from mild diarrhea to dysentery with blood and mucus in the stool. E. histolytica is usually a commensal organism.[9] Severe amoebiasis infections (known as invasive or fulminant amoebiasis) occur in two major forms. Invasion of the intestinal lining causes amoebic dysentery or amoebic colitis. If the parasite reaches the bloodstream it can spread through the body, most frequently ending up in the liver where it causes amoebic liver abscesses. Liver abscesses can occur without previous development of amoebic dysentery. When no symptoms are present, the infected individual is still a carrier, able to spread the parasite to others through poor hygienic practices. While symptoms at onset can be similar to bacillary dysentery, amoebiasis is not bacteriological in origin and treatments differ, although both infections can be prevented by good sanitary practices.

Transmission

Amoebiasis is usually transmitted by the fecal-oral route, but it can also be transmitted indirectly through contact with dirty hands or objects as well as by anal-oral contact. Infection is spread through ingestion of the cyst form of the parasite, a semi-dormant and hardy structure found in feces. Any non-encysted amoebae, or trophozoites, die quickly after leaving the body but may also be present in stool: these are rarely the source of new infections. Since amoebiasis is transmitted through contaminated food and water, it is often endemic in regions of the world with limited modern sanitation systems, including México, Central America, western South America, South Asia, and western and southern Africa.[10]

Amoebic dysentery is often confused with "traveler's diarrhea" because of its prevalence in developing nations. In fact, most traveler's diarrhea is bacterial or viral in origin.

Prevention

Amoebic Ulcer Intestine

To help prevent the spread of amoebiasis around the home :

To help prevent infection:

  • Avoid raw vegetables when in endemic areas, as they may have been fertilized using human feces.
  • Boil water or treat with iodine tablets.
  • Avoid eating Street Foods especially in public places where others are sharing sauces in one container

Good sanitary practice, as well as responsible sewage disposal or treatment, are necessary for the prevention of E.histolytica infection on an endemic level. E.histolytica cysts are usually resistant to chlorination, therefore sedimentation and filtration of water supplies are necessary to reduce the incidence of infection.[11]

Nature of the disease

Most infected people, about 90% [12], are asymptomatic, but this disease has the potential to make the sufferer dangerously ill. It is estimated that about 40,000 to 100,000 people die due to amoebiasis annually worldwide[13].

Infections can sometimes last for years. Symptoms take from a few days to a few weeks to develop and manifest themselves, but usually it is about two to four weeks. Symptoms can range from mild diarrhoea to dysentery with blood and mucus. The blood comes from amoebae invading the lining of the intestine. In about 10% of invasive cases the amoebae enter the bloodstream and may travel to other organs in the body. Most commonly this means the liver, as this is where blood from the intestine reaches first, but they can end up almost anywhere.

Onset time is highly variable and the average asymptomatic infection persists for over a year. It is theorised that the absence of symptoms or their intensity may vary with such factors as strain of amoeba, immune response of the host, and perhaps associated bacteria and viruses.

In asymptomatic infections the amoeba lives by eating and digesting bacteria and food particles in the gut, a part of the gastrointestinal tract.[citation needed] It does not usually come in contact with the intestine itself due to the protective layer of mucus that lines the gut. Disease occurs when amoeba comes in contact with the cells lining the intestine. It then secretes the same substances it uses to digest bacteria, which include enzymes that destroy cell membranes and proteins. This process can lead to penetration and digestion of human tissues, resulting first in flask-shaped ulcers in the intestine. Entamoeba histolytica ingests the destroyed cells by phagocytosis and is often seen with red blood cells inside when viewed in stool samples. Especially in Latin America,[citation needed] a granulomatous mass (known as an amoeboma) may form in the wall of the ascending colon or rectum due to long-lasting immunological cellular response, and is sometimes confused with cancer.[14]

"Theoretically, the ingestion of one viable cyst can cause an infection."[15]

Diagnosis of human illness

Immature E. histolytica/E. dispar cyst in a concentrated wet mount stained with iodine. This early cyst has only one nucleus and a glycogen mass is visible (brown stain). From CDC’s Division of Parasitic Diseases

Asymptomatic human infections are usually diagnosed by finding cysts shed in the stool. Various flotation or sedimentation procedures have been developed to recover the cysts from fecal matter and stains help to visualize the isolated cysts for microscopic examination. Since cysts are not shed constantly, a minimum of three stools should be examined. In symptomatic infections, the motile form (the trophozoite) can often be seen in fresh feces. Serological tests exist and most individuals (whether with symptoms or not) will test positive for the presence of antibodies. The levels of antibody are much higher in individuals with liver abscesses. Serology only becomes positive about two weeks after infection. More recent developments include a kit that detects the presence of amoeba proteins in the feces and another that detects ameba DNA in feces. These tests are not in widespread use due to their expense.

Amoebae in a colon biopsy from a case of amoebic dysentery.

Microscopy is still by far the most widespread method of diagnosis around the world. However it is not as sensitive or accurate in diagnosis as the other tests available. It is important to distinguish the E. histolytica cyst from the cysts of nonpathogenic intestinal protozoa such as Entamoeba coli by its appearance. E. histolytica cysts have a maximum of four nuclei, while the commensal Entamoeba coli cyst has up to 8 nuclei. Additionally, in E. histolytica, the endosome is centrally located in the nucleus, while it is usually off-center in Entamoeba coli. Finally, chromatoidal bodies in E. histolytica cysts are rounded, while they are jagged in Entamoeba coli. However, other species, Entamoeba dispar and E. moshkovskii, are also commensals and cannot be distinguished from E. histolytica under the microscope. As E. dispar is much more common than E. histolytica in most parts of the world this means that there is a lot of incorrect diagnosis of E. histolytica infection taking place. The WHO recommends that infections diagnosed by microscopy alone should not be treated if they are asymptomatic and there is no other reason to suspect that the infection is actually E. histolytica.

Typically, the organism can no longer be found in the feces once the disease goes extra-intestinal.[citation needed] Serological tests are useful in detecting infection by E. histolytica if the organism goes extra-intestinal and in excluding the organism from the diagnosis of other disorders. An Ova & Parasite (O&P) test or an E. histolytica fecal antigen assay is the proper assay for intestinal infections. Since antibodies may persist for years after clinical cure, a positive serological result may not necessarily indicate an active infection. A negative serological result however can be equally important in excluding suspected tissue invasion by E. histolytica.[citation needed]

Relative frequency of the disease

In older textbooks it is often stated that 10% of the world's population is infected with Entamoeba histolytica.[citation needed] It is now known that at least 90% of these infections are due to E. dispar. Nevertheless, this means that there are up to 50 million true E. histolytica infections and approximately seventy thousand die each year, mostly from liver abscesses or other complications. Although usually considered a tropical parasite, the first case reported (in 1875) was actually in St Petersburg in Russia, near the Arctic Circle.[16] Infection is more common in warmer areas, but this is both because of poorer hygiene and the parasitic cysts surviving longer in warm moist conditions.[10]

Treatment

Main article: Amoebicide

E. histolytica infections occur in both the intestine and (in people with symptoms) in tissue of the intestine and/or liver.[10] As a result, two different classes of drugs are needed to treat the infection, one for each location. Such anti-amoebic drugs are known as amoebicides.

Complications

In the majority of cases, amoebas remain in the gastrointestinal tract of the hosts. Severe ulceration of the gastrointestinal mucosal surfaces occurs in less than 16% of cases. In fewer cases, the parasite invades the soft tissues, most commonly the liver. Only rarely are masses formed (amoebomas) that lead to intestinal obstruction.(Mistaken for Ca caecum and appendicular mass) Other local complications include bloody diarrhea, pericolic and pericaecal abscess.

Complications of hepatic amoebiasis includes subdiaphragmatic abscess, perforation of diaphgram to pericardium and pleural cavity, perforation to abdominal cavital (amoebic peritonitis) and perforation of skin (amoebic cutis).

Pulmonary amoebiasis can occur from hepatic lesion by haemotagenous spread and also by perforation of pleural cavity and lung. It can cause lung abscess, pulmono pleural fistula, empyema lung and broncho pleural fistula. It can also reach brain through blood vessel and cause amoebic brain abscess and amoebic meningoencephalitis. Cutaneous amoebiasis can also occur skin around site of colostomy wound, perianal region, region overlying visceral lesion and at the site of drainage of liver abscess.

Urogenital tract amoebiasis derived from intestinal lesion can cause amoebic vulvovaginitis (May's disease), rectovesicle fistula and rectovaginal fistula.

Entamoeba histolytica infection is associated with malnutrition and stunting of growth.[17]

Food analysis

E. histolytica cysts may be recovered from contaminated food by methods similar to those used for recovering Giardia lamblia cysts from feces. Filtration is probably the most practical method for recovery from drinking water and liquid foods. E. histolytica cysts must be distinguished from cysts of other parasitic (but nonpathogenic) protozoa and from cysts of free-living protozoa as discussed above. Recovery procedures are not very accurate; cysts are easily lost or damaged beyond recognition, which leads to many falsely negative results in recovery tests.[18]

Outbreaks

The most dramatic incident in the USA was the Chicago World's Fair outbreak in 1933 caused by contaminated drinking water; defective plumbing permitted sewage to contaminate water.[19] There were 1,000 cases (with 58 deaths). In 1998 there was an outbreak of amoebiasis in the Republic of Georgia.[20] Between 26 May and 3 September 1998, 177 cases were reported, including 71 cases of intestinal amoebiasis and 106 probable cases of liver abscess.

See also

References

  1. ^ WHO (1969). "Amoebiasis. Report of a WHO Expert Committee". WHO Technical Report Series. 421: 1–52. PMID 4978968.
  2. ^ WHO (1997). "WHO/PAHO/UNESCO report. A consultation with experts on amoebiasis. Mexico City, Mexico 28–29 January 1997". Epidemiological Bulletin. 18 (1): 13–14. PMID 9197085.
  3. ^ Berger SA, Marr JS. Human Parasitic Diseases Sourcebook. Jones and Bartlett Publishers: Sudbury, Massachusetts, 2006.
  4. ^ Visvesvara GS, Moura H, Schuster FL (2007). "Pathogenic and opportunistic free-living amoebae: Acanthamoeba spp., Balamuthia mandrillaris, Naegleria fowleri, and Sappinia diploidea". FEMS Immunol. Med. Microbiol. 50 (1): 1–26. doi:10.1111/j.1574-695X.2007.00232.x. PMID 17428307. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  5. ^ "Orphanet: Amoebiasis due to free living amoebae". Retrieved 2009-01-17. at Orphanet
  6. ^ "EyeRounds.org:Acanthamoeba Keratitis: 39-year-old contact lens wearer with persisting keratitis & pain". Retrieved 2009-01-17.
  7. ^ Recavarren-Arce S, Velarde C, Gotuzzo E, Cabrera J (1999). "Amoeba angeitic lesions of the central nervous system in Balamuthia mandrilaris amoebiasis". Hum. Pathol. 30 (3): 269–73. doi:10.1016/S0046-8177(99)90004-7. PMID 10088544. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  8. ^ WHO (1998). Life in the 21st Century: a vision for all. The World Health Report 1998. World Health Organization, Geneva, Switzerland.
  9. ^ Haque R, Mondal D, Duggal P; et al. (2006). "Entamoeba histolytica infection in children and protection from subsequent amebiasis". Infection & Immunity. 74 (2): 904–909. doi:10.1128/IAI.74.2.904-909.2006. PMC 1360358. PMID 16428733. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  10. ^ a b c Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. pp. 733–8. ISBN 0-8385-8529-9. {{cite book}}: |author= has generic name (help)
  11. ^ Brock Biology of Microorganisms; Madigan (et al.); Pearson Education Inc., 2003; pgg. 947-948
  12. ^ "Amebiasis". NEJM. United States NEJM: Massachusetts Medical Society. 2003-04-17. Retrieved 2012-04-12.
  13. ^ Atlas of Human Infectious Diseases, First Edition. Heiman F.L. Wertheim, Peter Horby and John P. Woodall., 2012, Blackwell Publishing Ltd.
  14. ^ Day, David W. (2003). Morson and Dawson's Gastrointestinal Pathology. John Wiley & Sons, Inc. ISBN 978-0-632-04204-3. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  15. ^ "Foodborne Pathogenic Microorganisms and Natural Toxins Handbook: Entamoeba histolytica". Bad Bug Book. United States Food and Drug Administration: Center for Food Safety & Applied Nutrition. 2007-12-28. Retrieved 2009-07-13.
  16. ^ Lösch, F. (1875) Massenhafte Entwickelung von Amöben im Dickdarm. Virchow's Archiv 65: 196-211.
  17. ^ Mondal D, Petri Jr WA, Sack RB; et al. (2006). "Entamoeba histolytica-associated diarreal illness is negatively associated with the growth of preschool shildren: evidence from a prospective study". Trans R Soc Trop Med H. 100 (11): 1032–38. doi:10.1016/j.trstmh.2005.12.012. PMID 16730764. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  18. ^ "FDA Bacteriological Analytical Manual". Retrieved 2008-03-26.
  19. ^ Markell EK (1986). "The 1933 Chicago outbreak of amebiasis". West. J. Med. 144 (6): 750. PMC 1306777. PMID 3524005. {{cite journal}}: Unknown parameter |month= ignored (help)
  20. ^ Kreidl P, Imnadze P, Baidoshvili L, Greco D (1999). "Investigation of an outbreak of amoebiasis in Georgia". Euro Surveill. 4 (10): 103–104. PMID 12631887. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

External links

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