By Carol A. Kemper, MD

Encouraging Needlestick Reporting

Source: Haiduven DJ, et al. Hosp Infect 1999;41:151-154.

Failure to report needlestick injuries is remarkably common, especially among physicians and medical students (Donnelly JP. Infect Dis Alert 1999;18:81-82; Osborn EH, et al. Ann Intern Med 1999;130:45-51). Haiduven and colleagues distributed confidential surveys to healthcare personnel at a public teaching hospital in San Jose between 1992 and 1995. A total of 549 individuals responded to the survey, 83% of whom were nurses and 7% of whom were physicians. The remaining subjects included operating room technicians, dentists, and other hospital personnel.

About one-half of the nurses and physicians and 84% of the remaining personnel reported at least one percutaneous needlestick injury within the previous five years. However, 46% failed to report all of their injuries, including 80% of the physicians and 45% of registered nurses. Reasons for nonreporting included the perception that the stick was sterile or clean (39%), or represented no risk (26%), too busy (9%), and dissatisfaction with follow-up (8%).

While educational interventions regarding actual risk may enhance reporting behaviors, establishing user-friendly mechanisms by which needlestick injuries can be dealt with quickly and appropriately, as well as adequate follow-up, is essential. The use of the ER for after-hours injuries is, in my experience, inadequate in that patients are often required to wait longer than that recommended for the administration of post-exposure prophylaxis (< 1 hour), and the management is often inconsistent and occasionally incorrect. This is despite the availability of approved hospital protocols. A designated 24-hour hotline, such as the one established at the San Francisco General Hospital, (which, after-hours, usually rings a knowledgeable fellow or faculty member) appears to more consistently meet the needs of their hospital personnel. The hotline number is prominently posted in blazing colors throughout the hospital to encourage reporting.

Penile Chiggers in Kids

Source: Smith GA, et al. Pediatr Emerg Care 1998;14:116-118.

Chigger bites causing an acute penile hypersensitivity syndrome in boys in the summer months is apparently quite common and well known to emergency room physicians, although I had never heard of it. Chiggers are those nonhuman mites that are unable to burrow under human skin and suck blood like human scabies, but instead can only attach to the surface skin where they inject saliva and feed on tissue fluids. Like scabies, however, mite bites usually occur around the waist and groin where clothing is tighter, and the immune response is generally more marked in those sensitized by prior infestations. Hence, the resulting penile swelling and severe pruritis found in young males (typically 1-10 years of age). An additional 33% of patients may complain of dysuria. Although only half of the patients have an obvious papule or bite on the penis, bites may be found on other parts of the body. The symptoms usually last about two weeks and eventually respond to topical remedies, such as camphorated oil and baking soda, cold compresses, and antihistamines. Because the mites are usually long-gone, treatment with permethrin is not necessary, but consideration can be given to treating clothing in those with recurrent infestations.

Progression in a Nonprogressor

Source: Greenough TC, et al. N Engl J Med 1999;340:236-237.

An earlier report from green-ough and colleagues documented the presence of HIV-infection in a long-term nonprogressor infected with only nef-deleted forms of HIV-1 (Kirchhoff F, et al. N Engl J Med 1995;332:228-232). Nef-deficient virus has been associated with decreased virulence and has, therefore, been proposed for possible use in an attenuated viral vaccine. Beginning in January 1997, however, the patient’s CD4+ cell count began to mysteriously decline (from a peak of 713 to as low as 216/mm3), although plasma levels of HIV remained undetectable (< 50 particles/mL). Despite repeated attempts, HIV was cultured from blood on only one occasion in 1994, and levels of viral DNA in peripheral blood mononuclear cells have remained low (20-164 copies/106 CD4+ cells).

Despite evidence of low-level infection, several findings in vitro suggest continued HIV-1 antigenic stimulation, including the presence of HIV-specific cytotoxic T-cell responses, increased levels of activated CD8+ cells, and strong CD4 T-lymphocyte proliferative responses to gag antigen. The pathogenetic basis for this patient’s declining CD4+ cell count, despite barely detectable HIV replication, remains uncertain. But this individual case suggests that factors other than readily demonstrable viral replication, which have not yet been elucidated, may be responsible for declines in CD4+ count.