Becker Daniel J, Oloya James, Ezeamama Amara E
Odum School of Ecology, University of Georgia, Athens, Georgia, United States of America.
Department of Epidemiology & Biostatistics, College of Public Health, University of Georgia, Athens, Georgia, United States of America.
PLoS Negl Trop Dis. 2015 Sep 14;9(9):e0004080. doi: 10.1371/journal.pntd.0004080. eCollection 2015.
Cryptosporidium are parasitic protozoa that infect humans, domestic animals, and wildlife globally. In the United States, cryptosporidiosis occurs in an estimated 750,000 persons annually, and is primarily caused by either of the Cryptosporidium parvum genotypes 1 and 2, exposure to which occurs through ingestion of food or water contaminated with oocytes shed from infected hosts. Although most cryptosporidiosis cases are caused by genotype 1 and are of human origin, the zoonotic sources of genotype 2, such as livestock, are increasingly recognized as important for understanding human disease patterns. Social inequality could mediate patterns of human exposure and infection by placing individuals in environments where food or water contamination and livestock contact is high or through reducing the availability of educational and sanitary resources required to avoid exposure.
METHODOLOGY/PRINCIPAL FINDINGS: We here analyzed data from the National Health and Nutritional Examination Survey (NHANES) between 1999 and 2000, and related seropositivity to Cryptosporidium parvum to correlates of social inequality at the household and individual scale. After accounting for the complex sampling design of NHANES and confounding by individual demographics and household conditions, we found impaired household food adequacy was associated with greater odds of Cryptosporidium seropositivity. Additionally, we identified individuals of non-white race and ethnicity and those born outside the United States as having significantly greater risk than white, domestic-born counterparts. Furthermore, we provide suggestive evidence for direct effects of family wealth on Cryptosporidium seropositivity, in that persons from low-income households and from families close to the poverty threshold had elevated odds of seropositivity relative to those in high-income families and in households far above the poverty line.
CONCLUSIONS/SIGNIFICANCE: These results refute assertions that cryptosporidiosis in the United States is independent of social marginalization and poverty, and carry implications for targeted public health interventions for Cryptosporidium infection in resource-poor groups. Future longitudinal and multilevel studies are necessary to elucidate the complex interactions between ecological factors, social inequality, and Cryptosporidium dynamics.
隐孢子虫是一种寄生原生动物,在全球范围内感染人类、家畜和野生动物。在美国,估计每年有75万人感染隐孢子虫病,主要由微小隐孢子虫基因型1和2引起,通过摄入受感染宿主排出的卵囊污染的食物或水而接触到这些病原体。虽然大多数隐孢子虫病病例由基因型1引起且源于人类,但基因型2的人畜共患病源,如家畜,对于理解人类疾病模式的重要性日益得到认可。社会不平等可能通过将个体置于食物或水污染以及与家畜接触风险高的环境中,或者通过减少避免接触所需的教育和卫生资源的可及性,来介导人类接触和感染模式。
方法/主要发现:我们分析了1999年至2000年美国国家健康与营养检查调查(NHANES)的数据,并将微小隐孢子虫血清阳性与家庭和个体层面的社会不平等相关因素联系起来。在考虑了NHANES的复杂抽样设计以及个体人口统计学和家庭状况的混杂因素后,我们发现家庭食物充足性受损与隐孢子虫血清阳性几率增加有关。此外,我们确定非白种人和非白人种族以及在美国境外出生的人比白人、在美国出生的同龄人感染风险显著更高。此外,我们提供了家庭财富对隐孢子虫血清阳性有直接影响的暗示性证据,即低收入家庭和接近贫困线家庭的人血清阳性几率相对于高收入家庭和远高于贫困线家庭的人有所升高。
结论/意义:这些结果反驳了关于美国隐孢子虫病与社会边缘化和贫困无关的说法,并对资源匮乏群体中针对隐孢子虫感染的公共卫生干预措施具有启示意义。未来需要进行纵向和多层次研究,以阐明生态因素、社会不平等和隐孢子虫动态之间的复杂相互作用。