February 2019

Emerging Infectious Diseases Journal

Highlights: Emerging Infectious Diseases, Vol. 25, No. 2, February 2019

Important Note: Not all articles that EID publishes represent work done at CDC or by CDC staff. In your stories, please clarify whether a study was conducted by CDC (“a CDC study”) or by another institution (“a study published by CDC in the EID journal”). Opinions expressed by authors contributing to EID do not necessarily reflect the opinions of CDC or the institutions with which the authors are affiliated. EID requests that, when possible, you include a live link to the actual journal article in your stories. Once the embargo lifts, this month’s articles will be found in the Ahead of Print section of the EID website at https://wwwnc.cdc.gov/eid/ahead-of-print.

The articles of interest summarized below will appear in the February 2019 issue of Emerging Infectious Diseases, CDC’s monthly peer-reviewed public health journal. This issue will feature Emerging Viruses. The articles are embargoed until January 16, 2019, at 12 p.m. EDT.


1.     Lassa Fever in Travelers from West Africa, 1969–2016, Aaron Kofman et al.

Lassa fever is a potentially fatal disease caused by the rodentborne Lassa virus and is common to West Africa, where it was first discovered in 1969. Although nearly 80% of persons infected with the virus experience only mild symptoms (e.g., light fever, general malaise, and weakness), about 20% suffer more serious disease, which can include hemorrhaging, respiratory distress, and shock. Lassa fever is fatal in approximately 1% of cases, and even for the patients who recover, neurologic complications, including hearing loss, can be permanent. Diagnosis of Lassa fever in patients arriving from West Africa can be challenging for healthcare providers unfamiliar with the disease. To survey the clinical and epidemiologic characteristics of Lassa fever, researchers at CDC reviewed all 33 reported cases of Lassa fever imported from West Africa during 1969–2016. They found that only half of imported cases had distinctive clinical features, delays in clinical suspicion of Lassa fever were common, and secondary transmission of Lassa fever to contacts with high-risk exposures (typically defined as contacts with substantial direct contact with patients or their body fluids) did occur — although rarely. With the ease and frequency of international travel, healthcare providers in countries where Lassa fever is not endemic will continue to encounter Lassa fever. Strict maintenance of standard infection control precautions in healthcare settings will help prevent secondary transmission of Lassa virus. Recognizing distinctive clinical features promptly, treating patients earlier, and focusing public health responses on high-risk contacts are essential components of future responses to imported cases of Lassa fever.

Contact: CDC Media Relations, 404-639-3286 or media@cdc.gov


2.   Zika Virus IgM Detection and Neutralizing Antibody Profiles 12–19 Months after Illness Onset, Isabel Griffin et al.

Diagnosing Zika virus infection and distinguishing between infection with Zika virus and closely related viruses (in the genus Flavivirus) is often difficult. Several methods of testing are used to diagnose Zika virus infection: detection of Zika virus RNA (which is most effective only during the first week of infection) and detection of IgM and neutralizing antibodies (which are detectable longer than RNA but for which cross-reactions make it difficult to distinguish Zika virus from other flavivirus infections). Data on the duration of IgM antibody duration following Zika virus infection are lacking, but IgM antibodies against other flaviviruses can last for months to years following infection. Neutralizing antibodies develop shortly after IgM antibodies, persist for many years, and may confer lifelong immunity. To determine the duration of detectable Zika virus antibodies, researchers measured IgM antibody responses in patients 12–19 months after confirmed (RNA detection) Zika virus infection. The findings demonstrate that 73% of patients still had detectable levels of Zika virus IgM antibodies. As expected, 100% patients had neutralizing antibodies against Zika virus, but more than half (63%) also had neutralizing antibodies against dengue virus.  The results highlight the complexity of using serologic diagnosis, both for determining the specific timing of a recent infection, which is particularly important for pregnant women and complicates the diagnosis of new Zika virus infections in areas with known previous outbreaks, and for determining the specific flavivirus responsible for recent infection.

Contact: Olga Connor, Director of Communications, Florida Department of Health in Miami-Dade County—Epidemiology, Disease Control, and Immunization Services, 8323 NW 12th Street, Miami, FL 33126, USA; email: olga.connor@flhealth.gov; phone: 786-336-1276.


3.     Macrophage Activation Marker Soluble CD163 Associated with Fatal and Severe Ebola Virus Disease in Humans, Anita K. McElroy et al.

Ebola virus disease (EVD) is often severe, even fatal. Data suggest that EVD severity may be exacerbated by an abnormal immune response. The immune system produces proteins called cytokines. Levels of proinflammatory cytokines are increased by proliferation and activation of two types of cells: macrophages and T cells in two diseases similar to EVD: macrophage activation syndrome and hemophagocytic lymphohistiocytosis. To explore whether a similar situation occurs in EVD, researchers evaluated two groups of EVD patients: one from Uganda, 2000–2001, and one from Georgia, USA, 2014. By looking for biomarkers in the blood, they found that severe and fatal EVD was associated with activation of macrophages (indicated by biomarker sCD163) but not T cells (indicated by biomarker sCD25). Furthermore, in patients with fatal EVD, they found increased numbers of CD163 + macrophages in association with virus infected cells.  . These data suggest that in patients with EVD, activation of macrophages leads to increased production of proinflammatory cytokines and that this activation contributes to increased inflammation and severity of disease. Therapies aimed at decreasing inflammation could thus benefit patients with EVD.

Contact: CDC Media Relations, 404-639-3286 or media@cdc.gov.

 

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Page last reviewed: January 14, 2019