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Amebiasis↗
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Cytopathogenic mechanisms of Entamoeba histolytica.
Cinemicrography of Entamoeba histolytica destruction of Chinese hamster ovary (CHO) cells shows that ameba cytopathogenicity consists of separate components: a contact-dependent cytolethal effect, and phagocytosis. Cells not in contact with amebae remain intact. Quantitation of ameba destruction of CHO cells by applying the one-hit hypothesis confirms that the cytoethal effect of amebae is contact dependent. Studies with 111Indium oxine-labeled cells provide further evidence of extracellular killing by E. histolytica and indicate that > 94% of the target cells are killed before phagocytosis. When we examined for a cytotoxin release by E. histolytica, we found no effect on CHO cells with filtrates of amebae, and a nonspecific effect of cell rounding and release with sonicates of amebae. The ameba sonicate effect was time-dose dependent, was not cytolethal, was reversible, and was inhibited by alpha II macroglobulin. Cytochalasin B altered ameba motility and morphology, and monolayer experiments confirmed that cytochalasins A, B, or D inhibited CHO cell destruction by E. histolytica. Cytochalasin D also inhibited extracellular killing of CHO cells by amebae in pellets, apparently independent of effects on ameba motility or phagocytosis. Colchicine and vinblastine, alone or in combination with cytochalasin D, did not inhibit E. histolytica cytopathogenicity, which indicates that microtubule function is not required for target cell killing by amebae.
Amebiasis↗
Entamoeba histolytica: chemoattractant activity for gerbil neutrophils in vivo and in vitro.
The kinetics of the host's cellular response in the peritoneal cavity of gerbils toward axenic pathogenic and nonpathogenic Entamoeba histolytica strains were examined. Amebae contained in diffusion chambers or free in the peritoneum elicited a neutrophilic response accompanied by decreased levels of macrophages and lymphocytes. Pathogenic amebae (IP:0682:1 strain) elicited a neutrophilic response greater than the nonpathogenic DKB and "entamoeba-like" Laredo amebae. The neutrophil eliciting factor was found in high levels in disrupted freeze-thawed amebae (53% elicited neutrophils vs 8% for control), glutaraldehyde fixed amebae (45%) and amebic membranes (65%), and low levels in conditioned amebic medium (15%) and the supernatant fraction of amebae (16%). The factor was heat stable to high temperature (100 C for 30 min) and at various pH (6 to 9). The neutrophil eliciting factor in amebic membranes was lowered following pretreatment for 30 min with 1% immune and nonimmune gerbil or human sera (34-48% lowered neutrophil response vs control), acidic pH (less than 3, 69%), proteolytic digestion [trypsin (68%) and alpha-chymotrypsin (72%), 100 micrograms/ml], and 2% Triton X-100 (75%). Peritoneal neutrophils isolated following stimulation with amebic membranes or thioglycollate medium demonstrated higher chemotaxis in vitro toward live pathogenic amebae and amebic membranes (IP:0682:1 strain) compared to either the supernatant fraction or the nonpathogenic DKB or Laredo amebae. The results of this study indicate that membrane bound proteins of pathogenic amebae are chemotactic for gerbil neutrophils which may be important in the pathogenesis and pathology of amebiasis.
Animals↗
Detection of Balamuthia mitochondrial 16S rRNA gene DNA in clinical specimens by PCR.
Balamuthia mandrillaris is a free-living ameba that causes granulomatous amebic encephalitis in both immunocompromised and immunocompetent individuals. Because of a lack of pathognomonic symptoms and the difficulty in recognizing amebas in biopsied tissues, most cases are not diagnosed or effectively treated, leading to a >95% mortality. We report here on five cases of balamuthiasis that were diagnosed by indirect immunofluorescence (IIF) staining of serum for anti-Balamuthia antibodies (titer > or = 1:128) and confirmed by IIF of unstained brain tissue sections and/or detection of amebas in hematoxylin-eosin-stained slides. Additionally, we have used the PCR for the detection of mitochondrial 16S rRNA gene DNA from the ameba in clinical specimens such as brain tissue and cerebrospinal fluid (CSF) from individuals with Balamuthia encephalitis. Balamuthia DNA was successfully detected by the PCR in clinical samples from all five individuals. It was detected in brain tissue from three cases, in CSF from three cases, and in one of two samples of lung tissue from two individuals, but not in two samples of kidney tissue tested. One sample of unfixed brain tissue was culture positive for Balamuthia. In order to test the sensitivity of the PCR for detection of Balamuthia DNA, CSF specimens from two individuals negative for amebic infection were spiked with Balamuthia amebas. We found that it was possible to detect Balamuthia DNA in the PCR mixtures containing mitochondrial DNA from 1 to as little as 0.2 ameba per reaction mixture. A single Balamuthia ameba contains multiple mitochondrial targets; thus, 0.2 ameba represents multiple targets for amplification and is not equivalent to 0.2 of an ameba as a target.
Amebiasis↗
Role of adherence in cytopathogenic mechanisms of Entamoeba histolytica. Study with mammalian tissue culture cells and human erythrocytes.
The enteric pathogen, Entamoeba histolytica, appears to cause disease by adhering to and then destroying mucosal barriers. Using an in vitro method of studying the interaction of E. histolytica with target cells (Chinese hamster ovary [CHO] and human erythrocytes [RBC]), we examined the mechanism of amebic adherence and its role in lysis of target cells. Killing and phagocytosis of target cells by amebas ceases at 4 degrees C, allowing observation of adherence. Amebas adhere to CHO cells at 4 degrees C, 78.9% formed rosettes (amebas with >/=3 adherent CHO cells each) at 2 h. At 37 degrees C, cytochalasins B and D inhibit adherence of amebas to CHO cells (P < 0.0005). Amebas adhere to and kill CHO cells in media with <0.1 muM calcium and magnesium plus 10 mM EDTA, indicating that divalent cations are not required in the medium. Adherence of amebas to human RBC was not ABO blood group specific and showed greater adherence to human than bovine or sheep RBC (P < 0.005). Neither Fc nor complement receptors were found on amebas by standard rosette studies. The amebic adherence receptor is not trypsin (0.125%) sensitive nor inhibited by trypan blue (1 mM). N-acetyl-d-galactosamine (GALNAc) inhibited the adherence of amebas to CHO cells and human RBC (0.1 g/100 ml or 4.5 mM GALNAc, P < 0.005) by binding to a receptor on the amebic surface. GALNAc abolishes amebic cytolysis of target CHO cells (determined by (111)Indium oxine release from CHO cells, P < 0.001) but not amebic phagocytosis of CHO cells. By suspending ameba-CHO cells rosettes in dextran, we found that GALNAc (1%) reversibly inhibits amebic adherence (P < 0.0005) and that cytochalasins decrease amebic killing of adherent CHO cells (P < 0.025). These findings indicate that the adherence of E. histolytica to target cells requires microfilament function, is via a specific amebic receptor that has affinity for GALNAc, and is required to lyse cells. Inhibition of the adherence of E. histolytica may alter the pathogenicity of this organism.
Acetylgalactosamine↗
Adherence of Entamoeba histolytica trophozoites to rat and human colonic mucosa.
We studied the adherence of [3H]thymidine-labeled axenic Entamoeba histolytica (strain HM1-IMSS) to in vitro preparations of rat and human colonic mucosa. Studies were performed with fixed or unfixed rat colonic mucosa, unfixed rat mucosa exposed to trypsin, unfixed rat submucosa, and fixed human colonic mucosa. Twenty percent of the amebae adhered to fixed rat colonic mucosa; adherence was specifically inhibited by N-acetyl-D-galactosamine (GalNAc), galactose, and asialofetuin. The adherence of amebae to fixed human colonic mucosa was also GalNAc inhibitable. Greater adherence was found with unfixed rat colonic mucosa (40.9%) and was not GalNAc inhibitable unless the tissue was first exposed to trypsin. However, GalNAc did inhibit the adherence of amebae to unfixed rat submucosa. Glutaraldehyde fixation of amebae inactivates known amebic adhesion proteins; there was a markedly decreased adherence of fixed amebae to trypsin-exposed mucosa or fixed rat colonic mucosa. However, fixed or viable amebae had equal levels of adherence to unfixed rat colonic mucosa, suggesting the presence of a host adhesion protein that binds to receptors on amebae. Human (10%) and rabbit (5%) immune sera reduced the adherence of viable amebae to fixed rat colonic mucosa. We concluded that the GalNAc-inhibitable adhesion protein on the surface of E. histolytica trophozoites mediated adherence to fixed rat mucosa, fixed human colonic mucosa, trypsin-exposed unfixed rat mucosa, and unfixed rat submucosa. The surface of unfixed rat colonic mucosa contained a glutaraldehyde- and trypsin-sensitive host adhesion protein, perhaps in the overlying mucus blanket, which bound viable or fixed E. histolytica trophozoites.
Acetylgalactosamine↗
Environmental isolation of Balamuthia mandrillaris associated with a case of amebic encephalitis.
This report describes the first isolation of the ameba Balamuthia mandrillaris from an environmental soil sample associated with a fatal case of amebic encephalitis in a northern California child. Isolation of the ameba into culture from autopsied brain tissue confirmed the presence of Balamuthia: In trying to locate a possible source of infection, soil and water samples from the child's home and play areas were examined for the presence of Balamuthia: The environmental samples (plated onto nonnutrient agar with Escherichia coli as a food source) contained, in addition to the ameba, a variety of soil organisms, including other amebas, ciliates, fungi, and nematodes, as contaminants. Presumptive Balamuthia amebas were recognized only after cultures had been kept for several weeks, after they had burrowed into the agar. These were transferred through a succession of nonnutrient agar plates to eliminate fungal and other contaminants. In subsequent transfers, axenic Naegleria amebas and, later, tissue cultures (monkey kidney cells) served as the food source. Finally, the amebas were transferred to cell-free axenic medium. In vitro, the Balamuthia isolate is a slow-growing organism with a generation time of approximately 30 h and produces populations of approximately 2 x 10(5) amebas per ml. It was confirmed as Balamuthia by indirect immunofluorescence staining with rabbit anti-Balamuthia serum and human anti-Balamuthia antibody-containing serum from the amebic encephalitis patient. The environmental isolate is similar in its antimicrobial sensitivities and identical in its 16S ribosomal DNA sequences to the Balamuthia isolate from the deceased patient.
Amebiasis↗
Changes in isoenzyme patterns of a cloned culture of nonpathogenic Entamoeba histolytica during axenization.
The axenization of an Entamoeba histolytica isolate with a nonpathogenic isoenzyme electrophoretic pattern (zymodeme) was recently achieved for the first time (15). Forty days after the cells were transferred to the medium used for axenic cultivation, the amebae developed virulence properties, and the zymodeme converted to a pathogenic pattern. To exclude the possibility that the original isolate consisted of two zymodeme populations and that conditions of growth selected for a particular population, the experiment was repeated with a cloned culture of a nonpathogenic (zymodeme III) strain, E. histolytica SAW 1734R clAR, isolated by and obtained from P. G. Sargeaunt. Axenization was accomplished, as before, by transferring trophozoites to TYI-S-33 medium containing a mixture of antibiotics to suppress the growth of the associated bacterial flora and a nutritional supplement consisting of gamma-irradiated bacteria. A change in the hexokinase and phosphoglucomutase isoenzyme pattern was observed 21 days after the amebae had been transferred to the axenic medium but before complete axenization of the amebae had occurred. The change in zymodeme was accompanied by an increase in virulence, as evidenced by the ability of fewer amebae to induce hepatic abscesses in hamsters. A reverse conversion to a nonpathogenic zymodeme was also accomplished by reassociating and subculturing the newly converted pathogenic trophozoites of strain SAW 1734R clAR with the bacterial flora that accompanied this ameba in the original xenic culture. The electromobilities of the hexokinase isoenzymes changed back to their original pattern 7 days after the amebae were returned to xenic growth conditions. Our in vitro results demonstrate that culture conditions and bacterial flora can cause changes in the zymodeme and virulence of a cloned ameba isolate and raise the concern that this could happen also in vivo. Thus, the finding of a particular zymodeme in a culture of E. histolytica isolated from a carrier should not be used to predict a clinical condition or serve as a basis for the recommendation of therapy.
Animals↗
Electron microscope studies of experimental Entamoeba histolytica infection in the guinea pig. I. Penetration of the intestinal epithelium by trophozoites.
Germ-free guinea pigs were inoculated intracecally with Entamoeba histolytica and the enteric flora derived from a human patient with acute amebic colitis. Aanimals were killed at post-inoculation intervals of 7 to 12 days. The mode of penetration of cecal epithelium by the ameba was examined by light and electron microscopy. The following sequence was reconstructed from numerous individual observations. When the amebae were in moderately close proximity to the brush, border, the microvilli became shortened, irregular, and sometimes disappeared. Dense material was observed between the amebae and microvilli. When the ameba was very close to the epithelium the apical portion of epithelial cytoplasm projected into the lumen contacting the organism, thus becoming detached from adjoining cells. This produced spaces between epithelial cells through which amebae invaded interepithelial spaces. Initially the ameba penetrated the interglandular epithelium. Later, it penetrated equally the glandular and interglandular epithelium barrier. There were marked alterations of cytoplasmic components of epithelial cells. Polymorphonuclear leukocytes migrated into the epithelium filling these spaces; these often showed a variety of degenerative processes. Amebae, utilizing their pseudopodia, moved further through the intercellular spaces and reached the lamina propria.
Animals↗
Experimental Acanthamoeba infections in mice pretreated with methylprednisolone or tetracycline.
Human infections due to free-living amebas of the genus Acathamoeba have been reported sporadically, occasionally in individuals with underlying diseases. To determine if such infections may be considered opportunistic, groups of laboratory mice were pretreated with either methylprednisolone or tetracycline and inoculated intranasally with 1.075 times 10(4) Acanthamoeba castellanii isolated from a natural fresh water well. Results were compared with controls receiving either drug or amebas alone and with controls receiving saline injections with and without amebas. The mortality rate for those animals receiving methylprednisolone and amebas (50%) was found to be greater than the mortality in ameba controls (10%) (P equal 0.074). Similarly, the mortality rate for animals receiving tetracycline and amebas (60%) was higher than the mortality in the ameba controls (10%) (P equal 0.0286). Precise mechanisms for the increased mortality were unknown but were suspected to be due to the capacity of either corticosteroids or tetracycline to suppress host defenses, particularly those depending on neutrophils. The findings suggest a potentially pathogenic role for naturally occurring Acanthamoeba sp in humans with depressed host immunity.
Amebiasis↗
Intracellular digestion of human erythrocytes by Entamoeba histolytica: a kinetic study in vitro.
The objective of this investigation was to quantitatively evaluate, by using light and transmission electron microscopy, the intracellular digestion of human erythrocytes (HE), ingested by Entamoeba histolytica trophozoites in vitro. Amebas fed 10 min with HE were postincubated 3-12 h at 36.5 degrees C without HE, and fixed with glutaraldehyde. After staining by the benzidine reaction, HE per ameba, and percent of amebas containing at least one HE were determined by light microscopy. Trophozoites ingested an average of eight HE per ameba and 92% of them contained HE after the 10 min pulse. Erythrocytes were clearly observed as reddish-brown corpuscles in the amebic cytoplasm. During postphagocytosis incubations progressive loss of HE staining, as well as changes in size of food vacuoles, were observed, thus proving the intracellular digestion of HE. The hydrolysis of HE was corroborated with the electron microscope, the HE cytoplasmic matrix being the first structure catabolized and later the plasma membrane. Quantitative analysis demonstrated decrease of 56% of ameba containing HE, and 1.35 HE per ameba on average, after 3 h postphagocytosis. Afterwards, both parameters decreased at a slow rate until HE disappeared. The t1/2 of HE within amebas was 2 h.
Animals↗
Electron microscope studies of experimental Entamoeba histolytica infection in the guinea pig. II. Early cellular and vascular changes accompanying invasion of the lamina propria.
Early cellular and vascular changes in response to invasion of lamina propria by Entamoeba histolytica were studied sequentially, at the ultrastructural level, in germfree guinea pigs inoculated intracecally with amebae and enteric flora derived from patients with acute amebic colitis. Approximately one week post-inoculation the animals developed acute colitis with mucosal invasion by trophic amebae. Although epithelial cells at the sites of amebic invasion showed progressive cytoplasmic changes and desquamation resulting in microerosions, most mesenchymal elements in the lamina propria appeared normal without cytopathic changes even when in direct contact with invading amebae. Only the polymorpho-nuclear leukocytes (PMN) apposed or topographically close to amebae exhibited degenerative changes which were characterized by condensation of nucleoplasm and cytoplasm, extra-cellular release of cytoplasmic components including granules, and, finally, lysis of cell membranes. Capillaries and venules in the lamina propria showed a variety of changes such as swelling and gap formation at the intercellular endothelial junctions and more rarely at the fenestrae. Blood vessels physically close to amebae showed formation of endothelial cytoplasmic blebs which pinched off into the vascular or extravascular space. Platelet and fibrin thromboses were common in the more severely damaged capillaries and venules. Fragments or clumps of fibrin-like material were found also in the extracellular spaces. Amebic invasion of the lamina propria, then, is accompanied by continued epithelial shedding, PMN degeneration, and changes in both capillaries and venules consisting of endothelial damage and occlusive thrombosis. The vascular changes appeared to be closely related to PMN degeneration resulting from interaction of PMN with invading amebae.
Amebiasis↗
Entamoeba histolytica: effect of growth conditions and bacterial associates on isoenzyme patterns and virulence.
In xenic culture, isolates of Entamoeba histolytica from asymptomatic carriers are characterized, with rare exception, by possession of a nonpathogenic zymodeme. During the process of axenizing such an isolate, strain CDC:0784:4, a change in the pattern of the isoenzymes from nonpathogenic zymodeme I to pathogenic zymodeme II was observed 40 days after the amebae had been transferred from a medium for xenic cultivation to one used for axenic cultivation, but before axenization of the amebae had actually occurred. Axenization was accomplished by feeding the amebae lethally irradiated bacteria while suppressing and finally eradicating with antibiotics the bacterial flora accompanying the amebae in the original xenic culture. The change in zymodeme was accompanied by a change in virulence as evidenced by the ability of the amebae to produce hepatic abscesses in hamsters and to destroy monolayers of tissue culture cells. Two explanations are offered for the observed changes in zymodeme and virulence: a zymodeme is not a stable inherent property of the ameba. Alternatively, the original isolate consisted of two zymodeme populations and the conditions of growth selected for one or the other of the populations. In either case, our results suggest that the finding of a particular zymodeme in a culture of E. histolytica isolated from an asymptomatic carrier of the parasite cannot be used to predict a clinical condition or serve as a basis for the recommendation of therapy.
Amebiasis↗
Molecular cloning of ras and rap genes from Entamoeba histolytica.
To better understand growth regulation in the protozoan parasite Entamoeba histolytica, ameba genes homologous to the ras oncogene and rap (Krev-1) anti-oncogene were cloned. Two putative ameba ras genes (Ehras1 and Ehras2) were identified, which contain 205 and 203 amino acid (aa) open reading frames (ORFs), respectively. The Ehras1 ORF shows an 91% positional identity with that of Ehras2, a 55% identity with Dictyostelium discoideum (Dd) ras, and a 47% identity with human (Hs) ras. Two ameba rap genes (Ehrap1 and Ehrap2) were identified, both of which contain 184-aa ORFs. The Ehrap1 ORF shows a 93% positional identity with that of Ehrap2, a 60% identity with Dd rap, a 61% identity with Hs Krev-1, and a 45% identity with that of Ehras1. Conserved aa in each ameba ras and rap ORF include GTP-binding sites, effector site, site of ADP-ribosylation by Pseudomonas exoenzyme S, and COOH-terminus CAAX. As all Xs = Leu or Phe, ameba ras and rap proteins may be gerenylgerenylated and not farnesylated. Both ras and rap genes are transcribed by trophozoites. A single 21-kDa ameba ras protein reacts with the rat Y13-259 anti-ras monoclonal antibody, which is located on the cytosolic side of the plasma membrane. These are the first ras and rap genes identified from a protozoan parasite.
Amino Acid Sequence↗
Oriented thick and thin filaments in Amoeba proteus.
Actin and myosin filaments as a foundation of contractile systems are well established from ameba to man (3). Wolpert et al. (19) isolated by differential centrifugation from Amoeba proteus a motile fraction composed of filaments which moved upon the addition of ATP. Actin filaments are found in amebas (1, 12, 13) which react with vertebrate heavy meromyosin (HMM), forming arrowhead complexes as vertebrate actin (3, 9), and are prominent within the ectoplasmic tube where some of them are attached to the plasmalemma (1, 12). Thick and thin filaments possessing the morphological characteristics of myosin and actin have been obtained from isolated ameba cytoplasm (18, 19). In addition, there are filaments exhibiting ATPase activity in amebas which react with actin (12, 16, 17). However, giant ameba (Chaos-proteus) shapes are difficult to preserve, and the excellent contributions referred to above are limited by visible distortions occurring in the amebas (rounding up, pseudopods disappearing, and cellular organelles swelling) upon fixation. Achievement of normal ameboid shape in recent glycerination work (15) led us to attempt other electron microscope fixation techniques, resulting in a surprising preservation of A. proteus with a unique orientation of thick and thin filaments in the ectoplasmic region.
Actins↗
Maintenance of integrity, viability, and adhesion of Entamoeba histolytica trophozoites in different incubation media.
We have determined the integrity, viability and adhesion of Entamoeba histolytica HK9 and HM1 trophozoites during their incubation in two basal culture media (TP and TYI) and three saline media ("maintenance medium" MM-1 and two others buffered with HEPES). In basal culture media, more than 70% of the trophozoites maintained their integrity and adhesion to human red blood cells (RBC) for up to 4 h, and the proportion of those excluding Trypan blue decreased slowly after 2 h. In saline media, the number of ameba-RBC complexes reached a maximum after 20-30 min and then decreased rapidly (and fastest in MM-1), less than 10% of the amebae were intact after 3-4 h, and dye exclusion fell abruptly from the start of incubation. The number of ameba-RBC complexes formed and the rate of adhesion were highest in basal TP medium. Normal nonvacuolated refringent (NVR) trophozoites deteriorated progressively in all media--although much faster in the saline ones--to vacuolated refringent (VR), nonrefringent, and disrupted. Trypan blue was excluded by all NVR and a fraction of the VR trophozoites. Horse serum helped to maintain ameba integrity and viability, but inhibited adhesion in a concentration-dependent manner. We conclude that E. histolytica trophozoite integrity and adhesion are adequately preserved and should be characterized only in basal culture media, that refringence without vacuolization is a more stringent characteristic of ameba quality than Trypan blue exclusion, and that some serum component inhibits ameba adhesion.
Animals↗
Chemosensory responses of Acanthamoeba castellanii: visual analysis of random movement and responses to chemical signals.
A visual assay slide chamber was used in conjunction with time-lapse videomicroscopy to analyze chemotactic behavior of axenically grown Acanthamoeba castellanii. Data were collected and analyzed as vector scatter diagrams and cell tracks. Amebas responded to a variety of bacterial products or potential bacterial products by moving actively toward the attractant. Responses to the chemotactic peptide formyl-methionyl-leucyl-phenylalanine (fMLP), lipopolysaccharide, and lipid A were statistically significant (P < or = 0.03), as was the response to fMLP benzylamide (P < or = 0.05). Significant responses to cyclic AMP, lipoteichoic acid, and N-acetyl glucosamine were also found. Chemotactic peptide antagonists, mannose, mannosylated bovine serum albumin, and N-acetyl muramic acid all yielded nonsignificant responses (P > 0.05). There was no single optimal concentration for response to any of the attractants tested, and amebas responded equally over the range of concentrations tested. Pretreatment of amebas with chemotactic peptides, bacterial products, and bacteria reduced the directional response to attractants. Amebas that had been grown in the presence of bacteria appeared more responsive to chemotactic peptides. Treatment of amebas with trypsin reduced the response of cells to chemotactic peptides, though sensitivity was restored within a couple of hours. This suggests the ameba membrane may have receptors, sensitive to these bacterial substances, which are different from the mannose receptors involved in binding bacteria to the membrane during phagocytosis. The rate of movement was relatively constant (ca. 0.40 microns/s), indicating that the locomotor response to these signals is a taxis, or possibly a klinokinesis, but not an orthokinesis. Studies of the population diffusion rate in the absence of signals indicate that the basic population motility follows the pattern of a Levy walk, rather than the more familiar Gaussian diffusion. This suggests that the usual mathematical models of ameboid dispersion may need to be modified.
Acanthamoeba↗
Introductory remarks: bacterial endosymbionts or pathogens of free-living amebae1.
Free-living amebae are ubiquitous in the environment and can be isolated from a variety of habitats including water, soil, air, hospital water systems, dental units, contact lens cases, and cooling towers. The interaction of amebae with other microorganisms in their environment is varied. Bacteria are a major food source for free-living amebae. However, some bacteria have established a stable symbiotic relationship with amebae. Recent reports indicate an association of amebae with intracellular bacterial pathogens. Such amebae may serve as reservoirs for maintaining and dispersing pathogenic bacteria in the environment or as vectors of bacterial disease in humans.
Amoeba↗