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Dear Sir:
In response to the letter of Hung and others regarding our results published in the American Journal of Tropical Medicine and Hygiene,1 we wish to make some comments. The aim of this work was to analyze a group of patients with human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) for sociodemographic variables and immunologic indicators that could be risk factors for infection with Entamoeba histolytica and/or E. dispar. It is with this intention that we conducted our study in an HIV/AIDS group at the AIDS Clinic at Hospital 1 de Octobre at the Instituto de Salud y Seguridad Social para los Trabajadores del Estado in northwestern Mexico City, Mexico. Mexico is an area endemic for amebiasis.1–3 Given that HIV infection represents a human model of naturally acquired immunodeficiency, areas endemic for parasitic infections can be a handicap per se for these HIV/AIDS patients.
Hung and others disagree with selection of our control group because of possible selection bias caused by weakening of the correlation between the two infections since the two groups may share the same environment and risk of exposure to E. histolytica and E. dispar. We use this group of close relatives or non-HIV-infected sexual partners to ensure that both the experimental group and the reference group were exposed to the same source of parasitic infection.
We found a statistically significant difference (P = 0.04) in overall parasite prevalence between the HIV/AIDS group (17.2%) and HIV contacts (26.4%) (Table 1).1 Differences in the frequencies of parasites observed by microscopic examination of samples from both groups were not statistically significant. This suggests that both groups were exposed to similar environmental sources of parasites.
The second point of Hung and others deals with the observation of non-significant differences in prevalence values of E. histolytica between the HIV/AIDS group (25.3%) and the non-HIV reference group (18.4%) (P = 0.16). We agree that the lack of statistical significance may be due to small sample size (Table 2).1 Taking into account that both species (E. histolytica and E. dispar) share similar biologic cycles, ecologic niches, and modes of transmission in humans, we decided to group E. histolytica- and/or E. dispar-infected individuals as one group in both study groups. We found a statistically significant difference between the HIV/AIDS patients (34.1%) and the non-HIV-infected group (21.5%) (P = 0.019). Further analysis showed that the observed difference was due to a greater prevalence of E. dispar, 22.2% in HIV/AIDS patients, compared with 3.8% in non-HIV-infected individuals (P = 0.001).
The third comment of Hung and others involves the relative risk of E. histolytica infection analyzed by a polymerase chain reaction (PCR) in homosexual and bisexual individuals in the HIV/AIDS group compared with HIV-uninfected control subjects. We did not calculate the relative risk in accordance with sexual preference. In Table 2,1 we show the prevalence of Entamoeba detected by PCR to be 25.3% in HIV/ AIDS group and 18.4% in HIV contact group (P = 0.16).
I agree with Hung and others that some sexual practices in homosexual or heterosexual populations are strongly associated with transmission of many different infections; amebiasis has been considered a sexually transmitted disease since 1979.4 Unfortunately, we did not investigate this particular risk of infection in either study population; this was also mentioned in the discussion of our report.
The relative risk for acquisition of E. histolytica and/or E. dispar infection relative to a particular sexual preference was calculated in the HIV/AIDS patients (colonized versus non-colonized HIV/AIDS patients) (Table 3).1 Our results showed no significant association between sexual preferences and the E. histolytica and/or E. dispar colonized condition (P = 0.52).
The fourth comment of Hung and others deals with our conclusion regarding the low virulence of E. histolytica strains prevalent in this particular community. Our observations suggest a prevalence of E. histolytica strains with a low pathogenic potential based on the lack of antecedents (six months before), diarrhea outcomes attributable to invasive E. histolytica infection over a period of 12 months, and no significant association of high levels of antibodies to amebae (IgA or IgG) and E. histolytica in feces. Conversely, there was no association between the immunologic state of the HIV/AIDS group (low CD4+ lymphocyte counts) and E. histolytica and/ or E. dispar colonization. We emphasize that there is substantial evidence for extensive polymorphisms in both E. histolytica and E. dispar.5–8
The high morbidity rates of invasive amebiasis and asymptomatic infections caused by E. histolytica in different geographic regions and in some risk groups (homosexuals)6,7,9 suggest that morbidity rates in a particular area or community can be strongly associated with genetically determined virulence of prevalent strains of E. histolytica. This statement is not a consequence of our study design, but is based on long-term epidemiologic observations on amebiasis in Mexico and other disease-endemic areas.9–13
With regard to serologic analysis, studies in Mexico and other Latin American countries have shown no association between high levels of antibodies to E. histolytica and parasites in stool samples (E. histolytica sensu stricto).9,14 However, in other regions, studies have shown a correlation between E. histolytica infection and high titers of specific antibodies.10–12 These differences can be caused by antibody detection techniques, type of antigen used in the detection of such antibodies, high or low exposure of the host to the parasite and efficient mechanisms of transmission of E. histolytica invasive strains in a specific population. I agree with Hung and others that more epidemiologic studies are needed on this type of co-infection in geographic areas of high parasite prevalence.
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