Faculty Bibliography

Meat-eating primates avoid scavenging for dietary protein and micronutrients even when carrion is relatively fresh. Chimpanzees, baboons, and modern hunter-gatherers supplement their diets of high-energy, low-protein fruit with protein obtainedfrom leaves, insects, and animal prey. Most primates, especially leaf-eating primates, digest the cellulose cell walls of ingested plant material in a well developed caecum and/or large intestine through fermentation caused by enzymes released by their normal gut flora. The primate digestive strategy combines a rapid passage through the stomach and prolonged digestion in the ileum of the small intestine and caecum, and this combination increases the likelihood of colonization of the small intestine by ingested bacteria that ai-e the cause of gastrointestinal disease. Carrion is very quickly contaminated with a high bacterial load because the process of dismemberment of a car-cass exposes the meat to the bacteria from the saliva of the predator, from the digestive tracts of insects, and from the carcasses' own gut. Thus, the opportunistic eating of uncooked carrion or even unusually large quantities of fresh-killed meat by nonhuman primates or humans is likely to result in gastrointestinal illness. We propose that among meat-eating primates, carrion avoidance is a dietary strategy that develops during their lifetime as a response to the association of gastrointestinal illness with the ingestion of contaminated meat from scavenged carcasses. This has important implications for our understanding of early hominid behavior

Human parvovirus B19, which infects and lyses erythroid precursors, can cause severe anemia in patients with immunodeficiency. The incidence of parvovirus infection in adult acquired immunodeficiency syndrome (AIDS) patients is unknown. Eighty-one archival formalin-fixed, paraffin-embedded (FFPE) bone marrow biopsies from 73 AIDS adults were immunostained with monoclonal R92F6 against B19 VP1 and VP2 capsid proteins using streptavidin peroxidase and streptavidin alkaline phosphatase techniques. In addition, the same tissues were hybridized in situ with a digoxigenin-labeled parvovirus B19 DNA probe. Five FFPE bone marrows, from 3 HIV-negative patients with positive immunoglobulin M (IgM) serology for parvovirus B19, and 1 parvovirus B19-infected fetal liver were positive controls. By immunoperoxidase, all tissues were negative with R92F6 except the fetal liver, which exhibited strong positivity predominantly in viral inclusions. With immunoalkaline phosphatase, all positive controls were immunoreactive with R92F6; however, the AIDS marrows were negative. With in situ hybridization (ISH), all positive controls and 7 of 81 (8.6%) of AIDS marrows were positive for B19 parvovirus DNA. We conclude that ISH is more sensitive than R92F6 immunohistochemistry in parvovirus B19 detection. A small but significant number of bone marrows from AIDS adults shows evidence of human parvovirus B19 infection

Despite the tendency to rely considerably on laboratory test results for the differential diagnosis of Lyme disease, considerable problems exist with such testing. In this article we compare the effectiveness of five main categories of laboratory tests used for the detection of Lyme disease. Our goal is to enable the reader to better understand the limitations of different test methods and to realize that until better tests become available, diagnosis of Lyme disease still must be made clinically. Clinical data, however, can be used to increase the predictive power of any laboratory test as well as to help judge its validity