Acanthamoeba species are ubiquitous, occupying diverse habitats, including moist soils and freshwater environments. In these natural habitats, they prey on bacteria, controlling the bacterial population, which ultimately results in the recycling of nutrients back into the ecosystem [1]. However, some bacterial species have evolved ways to evade digestion and persist within the protozoa as endosymbionts [1,2]. Acanthamoeba can withstand hostile environmental conditions such as chlorination and high temperatures. It also displays resistance to numerous disinfectants and may exist as cysts, thus providing bacteria that may be less tolerant to environmental stresses, an enticing environment to live in [3]. Acanthamoeba are found virtually everywhere, and the ongoing interaction between protozoa and bacteria, particularly pathogenic bacterial strains are of great concern. A particular species, Acanthamoeba polyphaga, have been implicated in serving as a potential reservoir for methicillin-resistant Staphlyococcus aureus (MRSA), Campylobacter jejuni, Vibrio cholera and Escherichi coli O157. Thus, these amoeba serve as vectors for the spread of life-threatening infections [2]. Several studies have demonstrated that pathogenic bacteria species that are capable of evading digestion by amoeba can proliferate within the host and emerge as more virulent forms [4]. Therefore, it is important to study the protozoa-bacteria interactions and understand how this relationship impacts human health.
MRSA are able to replicate within the intracellular environment of A. polyphaga. Huws et al. 2004 have shown that in about 50% of amoebae isolated in the study, viable MRSA were detected within phago-lysosomes, and viable cocci can be detected within the cytoplasm. In a co-culture with amoeba and MRSA, extracellular numbers of bacteria were significantly larger compared to bacteria alone, demonstrating a 1000-fold difference in the number of bacteria in the presence of A. polyphaga relative to its absence. Due to the ability of protozoa to form cysts, it can also entrap MRSA and provide a means of infection via aerosilization. Therefore, this study suggests that A. polyphaga can impact the proliferation of MRSA, and be involved in its dispersal in both community and nosocomial settings [4].
Another study, performed by Axelsson-Olsson et al., demonstrated the protozoa’s role in supporting the life cycle of C. jejuni. Previous studies have shown that these bacteria can avoid the bactericidal effects of chlorination by residing in protozoa, and that in a co-culture, C. jejuni displayed over a 50-fold increase in resistance to chlorine compared to pure cultures. These researchers also demonstrated that these bacteria can accumulate within amoebic vacuoles and persist in the intracellular environment provided by A. polyphaga for a longer period of time when compared to co-cultures. Ultimately, the study demonstrated that C. jejuni are capable of infecting A. polyphaga, and avoid degradation by the host and proliferate intracellularly suggesting that the protozoa are capable of serving as a reservoir for C. jejuni [3]. This has important implications because infection by C. jejuni , although it is usually non-lethal, is responsible for over 2 million cases of gastroenteritis in the U.S. which can be transmitted via uncooked poultry or untreated water [5].
Vibrio cholera, particularly strains O1 and O139, causes potentially life-threatening dysentery with a 25-50% fatality rate if left untreated, is the agent responsible for the continual pandemic in South America, Africa and Asia. An individual can contract cholera by consumption of water contaminated with feces. Natural water samples obtained in Sudan, where cholera is endemic, V. cholera can be found associated with Acanthamoeba. Although it is commonly affiliated with A. castellanii, studies have demonstrated that it also interacts with A. polyphaga. These bacteria can be found within the vacuoles of the amoeba , and a co-culture demonstrated that neither species diminished the growth of the other [6]. In fact, they seemed to support each other’s growth, in that 89% of V. cholera were found associated with Acanthamoeba. By residing in Acanthamoeba, V. cholera can escape the selective pressures of chlorination and even the actions of antibiotics and contribute to the severity of human illness. Thus, it is important to understand the interactions between these two organisms to develop an efficient way to combat the spread of disease [6,7].
Escherichia coli O157:H7 are responsible for haemolytic uraemic syndrome outbreaks in North America, and this strain is highly transmissible, and only requires ingestion of about 100 bacterial cells. In 1997, mud contaminated with E. coli O157 may have been the source of the outbreak, suggesting that an environmental source may be responsible for its continual recycling in the environment causing re-current infections in cattle. Studies suggest that a possible source may be ubiquitous organisms, such as amoeba like A. polyphaga. These protozoa could prey on E. coli and use it as a food source, but there are cases where E. coli can escape digestion and proliferate within vacuoles. However, the exact mechanism of how certain E. coli evade digestion remains unknown. In any case, studies suggest that because E. coli can live within Acanthamoeba, the amoeba may serve as a vector for possible E. coli infections [8].
Although Acanthamoeba species are more commonly associated with amoebic infections such as keratitis and potentially fatal granulomatous encephalitis, its role as a potential reservoir for certain pathogenic bacteria have been overlooked. Their ability to inhabit diverse areas and resist environmental stresses makes them very attractive hosts for bacteria which are less tolerant. It remains to be discovered the mechanisms of how certain bacteria are able to evade digestion and proliferate within the intracellular environment by the amoeba, and how it provides a selective environment for more pathogenic strains. However, its ability to play host to a plethora of bacterial organisms has important implications in the spread and maintenance of disease both in nosocomial and community settings.
Works Cited
1. Barker J, Brown MRW (1994) Trojan Horses of the microbial world: protozoa and the survival of bacterial pathogens in the environment. Microbiology 140: 1253–1259. Available:http://mic.sgmjournals.org/cgi/doi/10.1099/00221287-140-6-1253. Accessed 10 November 2011.
2. Huws SA, Morley RJ, Jones MV, Brown MRW, Smith AW (2008) Interactions of some common pathogenic bacteria with Acanthamoeba polyphaga. FEMS microbiology letters 282: 258–265. Available:http://www.ncbi.nlm.nih.gov/pubmed/18399997. Accessed 13 August 2011.
3. Axelsson-Olsson D, Waldenström J, Broman T, Olsen B, Holmberg M (2005) Protozoan Acanthamoeba polyphaga as a potential reservoir for Campylobacter jejuni. Applied and environmental microbiology 71: 987–992. Available:http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=546671&tool=pmcentrez&rendertype=abstract. Accessed 10 November 2011.
4. Huws SA, Smith AW, Enright MC, Wood PJ, Brown MRW (2006) Amoebae promote persistence of epidemic strains of MRSA. Environmental microbiology 8: 1130–1133. Available:http://www.ncbi.nlm.nih.gov/pubmed/16689734. Accessed 10 November 2011.
5. Campylobacter jejuni (2011). Available:www.cdc.gov. Accessed 11 October 2011.
6. Sandström G, Saeed A, Abd H (2010) Acanthamoeba polyphaga is a possible host for Vibrio cholerae in aquatic environments. Experimental parasitology 126: 65–68. Available:http://www.ncbi.nlm.nih.gov/pubmed/19815016. Accessed 12 November 2011.
7. Shanan S, Abd H, Hedenström I, Saeed A, Sandström G (2011) Detection of Vibrio cholerae and Acanthamoeba species from same natural water samples collected from different cholera endemic areas in Sudan. BMC research notes 4: 109. Available:http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3080310&tool=pmcentrez&rendertype=abstract. Accessed 12 November 2011.
8. Barker J, Humphrey TJ, Brown MW (1999) Survival of Escherichia coli O157 in a soil protozoan: implications for disease. FEMS microbiology letters 173: 291–295. Available:http://www.ncbi.nlm.nih.gov/pubmed/10227158. Accessed 12 November 2011.
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