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By Carol A. Kemper, MD, FACP
Newer lab tests for GC/Chlamydia
Centers for Disease Conrol and Prevention. Recommendations for the laboratory-based detection of Chlamydia trachomatis and Neisseria gonorrhoeae - 2014. MMWR 2014;63(RR02);1-19.
Our county-based HIV/AIDS Clinic in San Jose, California provides STD screening of the rectum, oropharynx, and urethra for all new and returning HIV+ patients with increasingly alarming results. In calendar year 2013, a total of 500 men who have sex with men (MSM) were screened for GC/Chlamydia using nucleic acid amplification testing (NAAT; APTIMA GenProbe Unisex swab testing kit) (informal data, Wilson Ly, Pharm. D.). The patients did self-swabbing of all 3 sites, under the supervision of the HIV Pharmacy Specialist, who assists with the initial intake visit. Overall, 14% of cultures from all sites were positive for at least one organism. The highest prevalence of GC was 11% in the oropharynx; and the highest prevalence for Chlamydia was 23% from the rectum. Most of these infections were asymptomatic. Follow-up proof of cure NAAT testing is provided for anyone testing positive for GC.
Revised CDC guidelines now recommend routine laboratory screening for GC and chlamydia of all genital and extra-genital sites for all sexually active MSM and they are specifically recommending the routine use (for all 3 sites) of the newer NAAT laboratory screening tests, which are superior to earlier screening laboratory STD tests. While earlier non-culture tests based on DNA or RNA sequences frequently failed to detect a good number of infections (especially chlamydia), the newer tests are much more sensitive and specific.
The CDC cautioned that laboratories should maintain capability for culturing these organisms for several reasons: for suspect cases of treatment failure for GC; for sexual assault cases (where the reliability of the NAAT screening tests is not known); and to monitor for evolving antibacterial resistance.
Hospitals should remain alert for MERS-CoV
Arabi YM, et al. Clinical course and outcomes of critically ill patients with Middle East respiratory syndrome coronavirus infection. Ann Intern Med 2014; 160:389-97; and accompanying editorial: Perl TM, et al. Medusa’s ugly head again: From SARS to MERS-CoV. Ann Intern Med 2014; 160: 432-433.
Since the world was alerted September 15, 2012 to (another) new virus more than 200 cases of MERS-CoV have been reported, and new cases continue to occur. Similar to SARS, MERS-CoV results in a severe respiratory illness for which there is no effective therapy. It tends to affect middle-aged persons and spare children. All cases have been directly or indirectly linked to travel to or from key countries within the Arabian Peninsula. In this article, Arabi and colleagues report on 12 consecutive cases with severe respiratory failure and sepsis requiring critical care, with a mortality of 68%. All of the patients had comorbidities including diabetes, kidney disease or heart disease. One-third of these cases were hospital-acquired.
It is still not clear whether infections are occurring from episodic contact with infected animal sources (both bats and camels have been implicated), or from low-level sustained transmission between humans. But what is clear is that many of the cases have occurred in health care personnel. Of the first 160 reported cases, 30 (18.6%) were in HCWs. The rapid recognition of a suspect case on first presentation is therefore critical.
• Patients who should be immediately screened and placed in airborne and contact isolation include: (1) A person with fever (≥38 C, 100.4 F) and pneumonia or acute respiratory distress syndrome (based on clinical or radiological evidence); and either
(2a) history of travel from countries in or near the Arabian Peninsula within 14 days before symptom onset; or (2b) close contact with a symptomatic traveler who developed fever and acute respiratory illness (not necessarily pneumonia) within 14 days after traveling from countries in or near the Arabian Peninsula; or (2c) is a member of a cluster of patients with severe acute respiratory illness (e.g., fever and pneumonia requiring hospitalization) of unknown etiology in which MERS-CoV is being evaluated.
The Arabian Peninsula or neighboring countries include: Bahrain, Iran, Iraq, Israel, Jordan, Kuwait, Lebanon, Palestinian territories, Oman, Qatar, Saudi Arabia, Syria, the United Arab Emirates, and Yemen.
All hospitals should have Infection Control Guidelines developed for known or suspected MERS-CoV infection, and work with their Emergency Room and critical care personnel to be alert to potential travelers at risk who meet the above criteria. The World Health Organization and the CDC split on the need for airborne precautions (the CDC favors airborne precautions), since the exact mode of transmission of the virus is not known. Earlier outbreaks were apparently thwarted in the Al-Hasa province of Saudi Arabia using intensive surveillance and contact and droplet precautions alone.
Fortunately, preliminary modeling of the Basic Reproductive Number (Ro) for MERS-CoV is estimated to be 0.6 to 0.69. This provides a mathematical estimate of the number of secondary infected individuals produced by an individual in its lifetime. In comparison, the Ro for SARS is variously estimated at 0.19 to 1.08, depending on the location of the outbreak examined, and Ebola has an Ro of 1.34-1.83. It is a grim reminder that >90% of cases in the SARS outbreak in Toronto were hospital-acquired.
Heart disease in HIV
Post WS, et al. Associations between HIV infection and subclinical coronary atherosclerosis. Ann Intern Med 2014; 160:458-467.
Primary care of my aging HIV patient population has become much like primary care for any patient group it’s all about diabetes, HTN, heart disease, and the usual colds and flus - with the added twist of monitoring and managing generally well-controlled HIV infection. But as many HIV+ patients stare down 60 years of age the question remains whether HIV and /or HIV medications are significantly associated with an increased risk of heart disease. Studies have been inconsistent on this point, although they suggest an increased relative risk of about 50% compared with the rest of the population. Increased levels of systemic inflammation and immune system activation associated with HIV infection may be responsible, although mechanisms of plaque development and stenosis are not well understood.
The Multicenter AIDS Cohort Study (MACS) is a well-established cohort study with a well-matched control group, created to examine the natural history of HIV. Now in its third decade, it continues to track more than 7,000 gay men, including both HIV+ and HIV- men, at four different sights in the United States, including UCLA, Northwestern University in Chicago, the University of Pittsburgh, and Johns Hopkins. The cumulative dropout rate over two and half decades is astoundingly low at 15%. The project even rates its own Wikipedia page.
These authors examined the degree of coronary artery plaque characteristics and severity in a group of HIV+ and HIV- men ages 40-70, weighing < 200 lbs, and having no history of cardiac surgery or intervention. In all, a total of 1001 men were studied, including 618 HIV+ men. More HIV+ men were smokers, had longer cumulative smoking years, lower body mass index, and higher serum creatinine. They also had lower LDL and HDL levels, but higher triglyceride levels; and one-third were using lipid lowering agents.
All of the participants underwent non-contrast cardiac CT scan, which were reviewed by blinded readers. Coronary arteries were defined as normal, or containing non-calcified, mixed, or calcified plaque — and the extent of the plaque was graded as mild, moderate or severe. Stenosis was also graded, and a composite score was created for each scan. In addition, 759 men underwent coronary arteriography. In all, 53% of HIV+ men had evidence of any coronary calcium compared with 52% of non-infected men. After adjusting for age, race, and cohort, HIV+ men had a higher rate of coronary artery calcium and plaque, including both non-calcified (p < .001) and mixed plaque (p< .004) than un-infected men. Scores measuring both the extent of plaque and the segment involvement were greater for HIV+ men compared with their HIV- cohort. In addition, HIV+ men had a higher prevalence of coronary artery stenosis (>50%) compared with the HIV- cohort (16.9% vs 14.6%), although this difference did not appear statistically significant, even after adjusting for age, race and cohort. However, a longer duration of antiretroviral therapy and a lower nadir CD4 count were both associated with an increased risk of coronary stenosis (> 50%) (p = .005).
Both the extent and severity of non-calcified coronary artery plaque is significantly greater in HIV+ men compared with their uninfected counterparts. An interesting clue to the mechanism of plaque development may be the greater degree of coronary artery involvement in persons who have ever had more advanced HIV/AIDS disease, presumably reflecting a period of sustained immune system impairment.