Intestinal Cryptosporidiosis in a 6-Year-Old Child with Alpha1-Antitrypsin Deficiency

Background

Human enteric infections caused by intestinal protozoa of the genus Cryp­to­sporidium exhibit a large, yet still insufficiently quantified disease burden worldwide (Shirley DA et al., Curr Opin Infect Dis 2012; 25: 555–563). Children and individuals with cell-mediated immunodeficiency (e. g., HIV infection) are at highest risk of developing severe diarrheal illness (Leav BA et al., Clin Infect Dis 2003; 36: 903–908). Large food- and waterborne outbreaks, zoonotic transmission, and occurrence in pediatric hospital settings have led to the recognition of crypto­sporidiosis as an emerging infectious disease. A recently published multi-country case-control study identified Crypto­sporidium spp. as one of the 5 most important intestinal pathogens giving rise to moderate-to-severe diarrhea in children aged below 5 years in developing countries (Kotloff KL et al., Lancet 2013; 382: 209–222).

Besides HIV infection, several primary immunodeficiencies (e. g., selective IgA deficiency), malignant diseases and solid organ transplantation have been identified as risk factors for severe and prolonged cryptosporidiosis (Hunter PR, Nichols G. Clin Microbiol Rev 2002; 15: 145–154). In vitro data suggest that the human serine protease inhibitor alpha1-antitrypsin (AAT) may reduce the intestinal infectivity of Cryptosporidium oocysts due to inhibitory effects on crucial proteolytic steps of the parasite’s life cycle (Forney JR et al., J Parasitol 1997; 83: 771–774). Here, we describe the first clinical report of a potential association between AAT deficiency and intestinal Cryptosporidium infection, and support our findings with a brief literature review.