JOHNS HOPKINS U N I V E R S I T Y Department of Pathology 600 N. Wolfe Street / Baltimore MD 21287-7093 (410) 955-5077 / FAX (410) 614-8087 Diviision of Medical Microbiology THE JOHNS HOPKINS MICROBIOLOGY NEWSLETTER Vol. 25, No. 22 Tuesday, November 21, 2006 A. Provided by Sharon Wallace, Division of Outbreak Investigation, Maryland Department of Health and Mental Hygiene. There aren’t any outbreaks available at this time. B. The Johns Hopkins Hospital, Department of Pathology, Information provided by, Andrea Subhawong, M.D. Clinical presentation: A 38 year old male with HIV diagnosed in 1996 was non-compliant with HAART therapy and antimicrobial prophylaxis (last CD4 count 51, undetectable viral load), and had a history of chronic diarrhea, HSV proctitis, Pneumocystis pneumonia, cryptococcal meningitis, esophageal candidiasis, MAI cervical lymphadenitis, shigellosis, and MRSA axillary cellulitis. He has been followed at JHH for several years with known microsporidial diarrhea, with failure to take albendazole. He now presents with several weeks of worsened diarrhea and acute renal failure with severe metabolic derangements (potassium 2.6, creatinine 3.9, calcium 6.6, and bicarbonate 10). Many Cryptosporidium spp. oocysts were noted by trichrome and acid fast stains on stool O&P smears. Microsporidia were seen as well. Cryptosporidiosis Background: Cryptosporidium parvum and C. hominis are intracellular protozoan parasites that infects digestive and respiratory tract epithelial cells of vertebrates. Human infection is usually caused by drinking water contaminated by the feces of animals, but can also occur from direct contact with infected animals. Prior to the AIDS epidemic, Cryptosporidium spp. were known to cause a self-limited diarrheal illness in children and travelers. However, in the clinical setting of advanced AIDS, Cryptosporidium spp. have become a frequent cause of serious intestinal infections. In fact, detection of Cryptosporidium spp. in patients of unknown immune status should prompt specific HIV testing. Waterborne transmission is a major problem because the oocysts are resistant to chlorination. The incidence of cryptosporidiosis in North American AIDS patients is estimated at 16% to 33%. In developing countries, 55% of AIDS patients are infected. Clinical presentation: Patients usually present with watery diarrhea, at times with severe dehydration, malabsorptive syndromes, electrolyte derangements, and weight loss. Dull abdominal pain with bloating is common, and can be accompanied by nausea and vomiting, anorexia, and low grade fever. Diagnosis: The homogenous, red-staining, spherical oocysts (4-6 microns in diameter) can be identified in fecal smear acid fast stains. Enzyme immunoassays for antigen detection also exist, but the sensitivity of this approach is a point of contention. Diagnosis also can be made in hematoxylin and eosin-stained tissue biopsy sections by identifying the tiny oocysts on the villi epicellular surfaces lining epithelial cells. Therapy: Albendazole, paromomycin, atovaquone, nitazoxanide, and azithromycin can be used, with only temporary effects, along with supportive treatment using loperamide and tincture of opium. The severity of symptoms in AIDS patients correlates with lower CD4 cell counts; therefore, the use of antiretroviral therapy and concomitant increase in CD4 count may help resolve symptoms. References 1. Pensa E, Borum M. The AIDS Reader. 10(6):347-358, 2000. 2. Gelb A, Miller S. AIDS and gastroenterology. Am J Gastroenterol. 1986;81:619-622. 3. Wyatt SH, Fishman EK. The acute abdomen in individuals with AIDS. Radiol Clin North Am. 1994;32:1023-1043. 4. Garone MA, Winston BJ, Lewis JH. Cryptosporidiosis and the stomach. Am J Gastroenterol. 1986;81:465-470. 5. Ramratnam B, Flanigan TP. Cryptosporidiosis in persons with HIV infection. Postgrad Med J. 1997;73:713-716. 6. Flanigan T, Whalen C, Turner J, et al. Cryptosporidium infection and CD4 counts. Ann Intern Med. 1992;15:840-842.