Helicobacter Pylori and Houseflies: Are They Really to Blame?
abstracts & commentary
Sources: Grübel P, et al. Detection of Helicobacter pylori DNA in houseflies (Musca domestica) on three continents. Lancet 1998;352:788-789. Osato M, et al. Houseflies are an unlikely reservoir or vector for Helicobacter pylori. J Clin Microbiol 1998;36:2786-2788.
Grübel and colleagues have already shown that the humble housefly has the potential for harboring Helicobacter pylori for at least 30 hours after being fed pure cultures of the bacterium and have now shown the presence of the gene for isocitrate dehydrogenase (icd) elaborated by H. pylori among 97 groups of five flies collected from around North America, Poland, and Egypt. They used a PCR technique and found a positive reaction in one of 14 groups of flies collected from a dairy farm in South Carolina, four of 17 groups collected on a dairy farm in Florida, and five of 13 groups collected in a residential area in California. Similarly, five of the 14 groups of flies collected in Krakow, Poland, were positive as were three of the nine groups collected in Cairo, Egypt. However, none of the flies collected in three different Japanese cities were positive, nor were any of those collected at a turkey farm in North Carolina, from a pig farm and a chicken farm in South Carolina, or a dairy farm in Iowa. The specificity of the PCR was determined using other Helicobacter species, other bacteria, flies raised in the laboratory, and fecal material from patients known not to harbor H. pylori. Thus, Grübel et al conclude that the DNA found must represent colonization of the flies with H. pylori lending further weight to their argument that the housefly is both a vector and reservoir of the bacterium it acquires by eating infected feces.
Osato and colleagues doubt this conclusion and set about to disprove it by feeding the same species of laboratory-raised domestic houseflies fresh fecal material from a volunteer known to harbor H. pylori and another known to be free of infection. One group of flies was fed feces from the H. pylori positive volunteer, another group was fed feces from the negative volunteer, and the third group was fed the same feces seeded with almost 100 million viable H. pylori. Groups of five flies were killed at six hourly intervals between 24 and 72 hours after exposure, but H. pylori was not found in any of their mid-gut samples. Osato et al had already taken the precaution of removing all other sources of water to be sure that the flies were forced to eat the fecal material. Apparently, contrary to common belief, the domestic housefly, Musca domestica, does not have a predilection for feces although his subtropical cousin Musca domestica vicina does. This makes it unlikely that the domestic housefly acquires H. pylori in the first place. The experiments done by Osato et al indicate that even higher levels of H. pylori need to be present in fecal material if the fly is to become infected, much less become a carrier. Such levels are unlikely outside the stomach of an infected individual.
Comment by J. Peter Donnelly, PHD
So, we are left with a conundrum. If one has to force-feed houseflies with feces loaded with unattainably high numbers of viable H. pylori, how did the DNA get there? It is tempting to dismiss the positive results as contamination but, in fact, neither group has proved their case beyond all reasonable doubt. It is a pity that Grübel et al didn’t culture the flies and that Osato et al didn’t attempt to detect the icd gene. It is also tempting to inquire why anyone should be trying so hard to implicate the housefly as a vector of this gastric pathogen. If it is proven, will this lead to an attempt to protect potential victims from contact with the ubiquitous insect or, even more futile, a drive to eradicate the poor thing altogether? It seems much more likely that people acquire H. pylori like they do many other micro-organisms, namely, feces to fingers to mouth. There seems no need to invoke any role for the housefly.
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