Affiliations: 1. Division of Healthcare Quality Promotion, Centers for Disease Control and Prevention, Atlanta, Georgia; 2. Center for Evidence-Based Practice, University of Pennsylvania Health System, Philadelphia, Pennsylvania; 3. Division of Infectious Diseases, The Ohio State University, Columbus, Ohio. Received July 7, 2011; accepted July 15, 2011; electronically published September 1, 2011. This article is in the public domain, and no copyright is claimed. 0899-823X/2011/3210-0001. DOI: 10.1086/662025 editor’s note

https://www.cambridge.org/core/services/aop-cambridge-core/content/view/S0195941700040698

Guideline for the prevention and control of norovirus gastroenteritis outbreaks in healthcare settings.

The biologic principles for the global eradication of poliomyelitis are as follows: Poliovirus causes acute, nonpersistent infections, virus is transmitted by infectious humans or their waste, survival of virus in the environment is finite, humans are the only reservoir, and immunization with polio vaccine interrupts virus transmission. These principles appear to be sound. The potential for prolonged virus excretion by immunocompromised patients requires further definition, although there is no epidemiologic evidence of a threat to eradication. Survival of poliovirus in the environment is highly variable, but viral inactivation is usually complete within months. Higher primates may be infected with poliovirus, but they are unlikely reservoirs in nature. The only poliovirus reservoir remaining after eradication will be laboratory stocks. Serious attention must be given to reducing this potential source of infection. Polio eradication through immunization is evidenced by the documented absence of poliomyelitis in an increasing number of countries and the progressive disappearance of poliovirus genotypes.

The Biologic Principles of Poliovirus Eradication

Chronic diarrhoea among HIV-infected adult patients in Nairobi, Kenya

Chronic excretion of a norovirus in a child with cartilage hair hypoplasia (CHH)

Prospective surveillance of 63 human immunodeficiency virus (HIV)-positive patients and 9 HIV-negative partners over 5-27 months yielded 51 adenoviruses from 18 HIV-positive patients. These were serotyped and compared by restriction enzyme analysis (REA) together with 24 isolates from 19 other HIV-positive patients. The actuarial risk of infection at 1 year in HIV-positive patients was 28% (17% with entry CD4 cell count of > 200/mm3 and 38% with CD4 cell count of < or = 200/mm3, P = .03). The most frequent site of infection was gastrointestinal (17/18 patients) with mainly subgenus D adenoviruses, while urinary infection was caused by subgenus B or D. Prolonged fecal excretion (2-27 months) was associated with CD4 cell counts < 150/mm3. Identical strains were seen in 2 HIV-positive partners and 2 unrelated patients. Gastrointestinal infection was temporally associated with diarrhea in only 7 (41%) of 17 cases. The remainder (59%) were asymptomatic or minimally symptomatic, and diarrhea was often caused by other opportunistic pathogens.

Adenovirus Infections in Human Immunodeficiency Virus-Positive Patients: Clinical Features and Molecular Epidemiology

Diarrhoea is the most common manifestation of acquired immunodeficiency syndrome (AIDS) in Africa. Numerous parasitic or bacterial agents have been implicated, but a pathogen-specific aetiology has not been found. Enteric viruses (i.e., rotavirus, small round structured viruses, coronavirus, and adenovirus) were detected by enzyme-linked immunosorbent assay or electron microscopy in faecal specimens of 17% of 198 consecutive adult admissions to a general medical ward of an urban hospital in Kinshasa, Zaire. Overall, 57% of patients were seropositive for infection with human immunodeficiency virus (HIV) 1; of these, 50% were classified as World Health Organization AIDS stage IV. The prevalence of enteric viruses in stool specimens did not differ significantly between patients with and without HIV infection, and was not associated with acute or chronic diarrhoea, or constitutional symptoms. However, a trend (P = 0.14) towards greater frequency of virus in stools from patients in the lower 3 quintiles of the CD4/CD8 T cell ratio was seen. This trend approached statistical significance (P = 0.07) with stratification by HIV infection. Although we found no evidence in this population to support a major pathogenic role for these viruses alone in the enteropathy of AIDS, increased viral shedding was weakly associated with immunodeficiency.

Uvoya Atido

Papers

Prevalence of enteric viruses among hospital patients with AIDS in Kinshasa Zaire.