At least 4 species of amoebae live in the human intestinal tract :
o Entamoeba histolytica, o E. dispar o Entamoeba coli o Endolimax nana o Iodamoeba butschlii. The intestinal amoebae have 2 stages in their life cycles, a motile trophozoite and a cyst. E. histolytica is the only proven pathogen among the amoebae producing both intestinal and extraintestinal lesions. Naegleria fowleri This is a freeliving amoebae found in soil and !ater. "uman infections have been reported from many parts of the !orld and result from s!imming in contaminated !ater. #nfection by $aegleria appears to be more common than by Acanthamoeba. Acanthamoeba castellani %bi&uitous, free living amoebae found in soil and !ater. "uman infections have been reported from many parts of the !orld 'esult from s!imming in contaminated !ater. (an also result from infected contact lens solutions #nfection by $aegleria appears to be more common than by Acanthamoeba. )isease Amoebiasis #nfection by E. histolytica is found !orld!ide, but occurs most fre&uently in tropical countries *S+ areas !ith poor sanitation About ,2- of pple in %S are affected. The disease is !idely prevalent among male homosexuals Primary amoebic meningoencephalitis (PAM) This is a purulent meningitis and a rapidly fatal encephalitis (linically the condition is described as /primary amoebic meningitis0 1+A23 as the central nervous system is primarily involved, unli4e infections !ith *ntamoeba histolytica in !hich brain involvement is usually secondary. 5ranulomatous amoebic encephalitis15A*3 This can cause a brain infection too, but progresses more slo!ly. (an become chronic. Amoebic 4eratitis S4in or lung lesions 6ife cycle (ysts are passed in feces . #nfection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, !ater, or hands. *xcystation occurs in the small intestine and trophozoites are released, !hich migrate to the large intestine. The ingested cysts differentiate into trophozoites in the ileum 7%T tend to colonize the rectum and colon The trophozoites multiply by binary fission and produce cysts , !hich are passed in the feces . 7ecause of the protection conferred by their !alls, the cysts can survive days to !ee4s in the external environment and are responsible for transmission. 1Trophozoites can also be passed in diarrheal stools, but are rapidly destroyed once outside the body, and if ingested !ould not survive exposure to the gastric environment.3 %bi&uitous in nature, found in fresh !ater la4es and ponds Three life cycle stages 8 amoeba !ith pseudopodia 8 motile biflagellate form 8 resistant cyst stage Amoebae #n many cases, the trophozoites remain confined to the intestinal lumen 1 : noninvasive infection3 of individuals !ho are asymptomatic carriers, passing cysts in their stool. #n some patients the trophozoites invade the intestinal mucosa 1 : intestinal disease3, or, through the bloodstream, extraintestinal sites such as the liver, brain, and lungs 1 : extraintestinal disease3, !ith resultant pathologic manifestations. Trophozoites invade the colonic epithelium and secrete enzymes that cause localized necrosis 6ittle inflammation occurs at the site As the lesions reaches the muscularis layer, a typical flas4 shaped ulcer forms that can undermine and destroy large areas of the intestinal epithelium +rogression into the submucosa leads to invasion of portal circulation by the trophozoites 7y far the most fre&uent site of systemic disease is the liver !here abscesses containing trophozoites form #t has been established that the invasive and noninvasive forms represent t!o separate species, respectively E. histolytica and E. dispar, ho!ever not all persons infected !ith E. histolytica !ill have invasive disease. These t!o species are morphologically indistinguishable. Stages Trophozoites 2otile 9eeding Stage (yst form is infective Amoebae stage 1trophozoite stage3 infective Stages in life cycle Trophozoite (yst 'oute of Transmission :rganism is ac&uired by ingestion of cysts that are tm primarily by the fecal oral route in contaminated food and !ater Anal oral transmission among the male homosexuals, also occurs 9ecal exposure during sexual contact 1in !hich case not only cysts, but also trophozoites could prove infective3. There is $: animal reservoir +ossible entry through respiratory tract, eyes, s4in $:T* nasal route of infection is not as common as in $aegleria 2ay aspirate !ater into the lungs and get infection in lung 8 (an infect the eye or s4in by direct trauma 8 +resumed hematogenous dissemination to the ($S 8 #nfection associated !ith debilitation or immunosuppression 16evinson says that the infection occurs primarily in immunocompromised pple for Acanthamoeba, !hile $aegleria infections occur in other!ise healthy pple usually children3 (arriage Asymptomatic cyst passers may transmit disease Since cysts are the transmissible stage, and cysts are not passed in diarrhea $o carriers Amoeba is free living in environment $o carriers Amoeba is free living in environment hence !ill not get amoebiasis from the diarrhea stools 1(;STS only found in $:'2A6 ST::6S3 +athogenesis Non- Invasive: Amoebae on mucosa surface (an either be an Asymptomatic cyst passer carriers :' $ondysenteric diarrhea1T"#S #S $:T 76::); "*$(* $:T );S*$T*';3, cramps, abdominal discomfort Invasive: $ecrosis of mucosa < ulcer due to destruction of mucosa )ysentery )iarrhea !ith mucus and blood in stools $ote that dysentery can be either amoebic or bacterial. "ence should loo4 for "ematophagous trophozoites present in stools characteristic of amoebic dysentery Metastases- Extraintestinal Amoebiasis: )issemination primarily via blood stream *.g. portal vein !hich !ill affect liver 1+'*):2#$A$T S#T* A99*(T*)3 'esults in amoebic abscess :ther sites infre&uent 7rain, cutaneous, pulmonary $:T* that cutaneous amoebiasis is 'A'* #n cases of *=T'A#$T*ST#$A6 A2:*7#AS#S Amoebafree stools common should not be surprised $:T to find amoeba in stools because the amoeba move out of the gut. (linical +resentation #ntestinal Amoebiasis: Asymptomatic cyst passer 1. Symptomatic $ondysenteric infection 1colitis3 2. Amoebic dysentery 1acute3 3. Amoeboma 1amoebic granuloma3 4. Amoebic appendicitis (omplications and se&uelae of intestinal amoebiasis ,. 9ulminant colitis 2. +ost dysenteric colitis >. Stricture 4. #ntussusception ?. +erforation and peritonitis @. +erianal ulceration "epatic Amoebiasis: This is a big problem !ith amoebiasis 1acute nonsuppurative and liver abscess3 o 9ever o 6iver enlargement o 6iver tenderness +rimary Amoebic 2eningoencephalitis 1+A23 The infection occurs for Acanthamoeba occurs primarily in immunocompromised pple 7%T $aegleria infections occur in other!ise healthy pple usually children #nfection !ith these organisms should be suspected in individuals !ith meningoencephalitis !ho have been s!imming in fresh !ater pools, ponds or hot springs > to A days previously. 8 ,,4 days incubation period 8 #nfection introduced through nasal cavity and olfactory bulbs 8 Symptoms usually !ithin a fe! days after s!imming in !arm still !aters 8 Symptoms include headache, lethargy, disorientation, coma 1fairly non specific3 8 'apid clinical course, death in 4? days after onset of symptoms 8 24 survivors B:'6)B#)* Chronic granulomatous amoebic encephalitis (GAE) 8 A type of meningoencephalitis, Cgranulomatous amoebic encephalitis0 15A*3 is caused by Acanthamoeba spp. 8 (an be subacute or chronic disease !ith focal granulomatous lesions in the brain. :n postmortem examination, 8 2icroscopic examination of the infected brain sho!s nests of amoebae !ith extensive haemorrhagic reaction mostly involving the basilar portion of the cerebrum and cerebellum. 8 #n Acanthamoeba infections cysts and trophozoites may also be found. amoebae not detected in spinal fluid. 8 The route of ($S invasion is thought to be hematogenous, !ith the primary site being s4in, respiratory tract or eyes 8 :nset insidious !ith headache, personality changes, slight fever 8 +rogresses to coma and death in !ee4s to months Inections o the s!in o 6iver abscess o +us is bro!nish yello! !ith consistency of anchovy paste Complications o liver abscess" o 'upture or extension o 7acterial infection o "aematogenous spread to other organs. #nvolvement of other organs 1lung, brain, spleen, etc3 may occur !ithout manifest liver involvement. 8 S4in lesions have also been associated !ith Acanthamoeba infections. Amoebic inection o the eye Pre#isposing actors 8 :cular trauma 8 (ontact lens 1contaminated cleaning solutions3 this has become the most common disease associated !ith acanthamoeba infection $ymptoms 8 :cular pain 8 (orneal lesions 1refractory to usual treatments3 8 Amoebic 4eratitis can also occur 8 Together !ith %veitis and corneal ulceration 8 #nfections have been seen in both hard and soft lens !earers. (omplications o %lcer enlargement o (olitis o +eritonitis o 2etastasis 1see extraintestinal amoebiasis3 o :ccasional amoeboma 1can form a tumor li4e mass. 5ranulomatous type mass that can obstruct the intestine and loo4 li4e a tumor3 )iagnosis Intestinal Amoebiasis" ,. Stool examination for trophozoitesDcysts #t ta4es a trained microbiologist to differentiate E. histolytica for the other protozoa in intestine particularly *.dispar 2. Sigmoidoscopy 6oo4 for ulcers in the large intestine lining. At most can inspect li4e less than a meter of intestine %eaptic Amoebiasis" ,. Stool examination Stool sample may be ta4en 7%T because this is extraintestinal, hence stool samples may be negative 2. Serology >. #maging This is the preferred method. %se (T scan or ultrasound )iagnosis is usually at autopsy Microscopy o C$& )iagnosis can be made by microscopic examination of the (S9 !hich may reveal the presence of the trophozoites. (S9 may sho! red cells and is bacteriologically sterile. Culture o organism The amoebae can also be cultured by inoculating (S9 on to nonnutrient agar plates previously seeded !ith *schericia coli. 'n post mortem 2icroscopic examination of the infected brain sho!s nests of amoebae !ith extensive haemorrhagic reaction mostly involving the basilar portion of the cerebrum and cerebellum. Amoebic Eeratitis: )emonstration of amoebae in corneal scrapings Microscopic examination o the C$& )iagnosis can be made by microscopic examination of the (S9 8 Bhich 2A; reveal the presence of the trophozoites. 8 The (S9 may sho! red cells and is bacteriologically sterile. 8 Amoebae not detected in spinal fluid 8 (ysts and trophozoites detectable in histological specimens Culture The amoebae can also be cultured by inoculating (S9 on to nonnutrient agar plates previously seeded !ith *schericia coli. 4. Abscess aspiration 1seldom need to do this to diagnose no!, only aspirate !hen the lesion is about to rupture and spread it to other organs o 'eddish bro!n li&uid Trophozoites at abscess !all 1not in the li&uid. Bhen aspirating fluid, !ill locate the parasites at the tail end of the drainage of the abscess !hen they drop off the !all3 Fecal Examination Techniques that can be used to identify E.histolytica )irect Bet Smear Saline #odine (oncentration 1sedimentation and flotation3 9ormalinethyl acetate sedimentation Finc sulphate flotation Treatment The treatment of choice for symptomatic intestinal amoebiasis or hepatic abscesses is 2*T':$#)AF:6* 196A5;63 or tinidazole "epatic abscesses need not be drained Asymptomatic cyst carriers should be treated !ith ido&uinol or paromomycin Amphotericin 7 &rom (evinson +rognosis ho!ever is poor even in treated cases )ifficult, limited success 8 (orneal grafts often re&uired These may be effective in acanthamoeba infections +entamidine Eetoconazole 9lucytosine +revention +revention involves avoiding fecal contamination of food and !ater and observing good personal hygiene such as hand !ashing +urification of municipal !ater supplies is usually effective, but outbrea4s of amebiasis in city d!ellers still occurs !hen contamination is heavy +rohibit use of night soil 1human feces3 for fertilization of crops #n areas of endemic infection, vegetables should be coo4ed