Chapter 16, Problem 1EDCS

Microsporidiosis

Darius is sick, which is not surprising for an HIV-infected man. But he is sick in several new ways. Sick of having to stay within 20 feet of a toilet. Sick of the cramping, the gas, the pain, and the nausea. Sick with irregular but persistent, watery diarrhea. He is losing weight because food is passing through him undigested. Most days over the past seven months have been disgusting despite his use of over-the-counter remedies, which provide a few days of intermittent relief. His belief that these normal days signaled the end of the ordeal have kept him from the doctor. But now his eyes have begun to hurt, and his vision is blurry. Whatever it is, it’s attacking him at both ends. Time to get stronger drugs from his physician.

Microscopic examination of Darius’s stool sample reveals that he is being assaulted by Encephalitozoon intestinalis, a member of a group of opportunistic emerging pathogens called microsporidia. The single-celled pathogens are also seen on smears from Darius’s nose and eyes. Microsporidia were long thought to be simple single-celled animals, but genetic analysis and comparison with other organisms reveal that they are closer to zygomycete yeasts.

Microsporidia appear to infect humans who engage in unprotected sexual activity, consume contaminated food or drink, or swim in contaminated water. People with active T cells rarely have symptoms, but people with suppressed immunity become easy targets for the fungus.

Microsporidia attack by uncoiling a flexible, hollow filament that stabs a host cell and serves as a conduit for the microsporidium’s cytoplasm to invade. In this way, the pathogens become intracellular parasites. They can destroy the intestinal lining, causing diarrhea, and spread to the eyes, muscles, or lungs.

Fortunately for Darius, an antimicrobial drug, albendazole, kills the parasite, and the effects of the infection are reversed. Unfortunately for Darius, the loss of helper T cells in AIDS means that another emerging, reemerging, or opportunistic infection is likely to follow.

1. 1. Why are microsporidia considered to be opportunistic pathogens?
2. 2. How could the discovery that microsporidia are fungi rather than animals improve treatment of microsporidiosis?
3. 3. Microsporidia are intracellular pathogens. Which immune cells likely fight off the infection in people with a normal immune system?