(IM) is usually caused by the . Typically, once a person acquires EBV, it stays in their body for life. However, such a person isn’t always infectious ( , ). Though seasonal changes in IM incidence have been observed in a few studies, they don’t all find peak incidence at the same time of the year, and some studies found no seasonal pattern whatsoever.
Studies that show IM incidence is higher or peaks in spring (defined as March, April, May in the Northern Hemisphere)
- Oxford, UK, 1954-1956, n = 342 ( ). Peak IM incidence from April to July.
- England and Wales, 1973-1992, n = 4769; Scotland, 1983-1993, n = 3294; England and Wales, Northern Ireland, Eire, Channel Islands, Isle of Man, 1980-1984, n = 74552 (4). Peak IM incidence in March.
- University of Minnesota college students, USA, 2006-2007, n = 66 ( , 6). Peak IM incidence in March.
Studies that show IM incidence isn’t higher in spring
- Hospital IM cases, Malmo, Sweden, 1954-1960, n = 424 (7). No clear pattern but slight increase in October.
- Metropolitan Atlanta, Georgia, USA, 1968, n = 575 (8). Two IM peaks, major one in January–February, smaller one in April-May.
- 19 colleges across the USA, 1969-1970, n = 2811 (9). No consistent seasonal pattern.
- Military personnel, Israel, January 1978 to December 1991, n = 590 ( ). Peak IM incidence from June to August.
- Military personnel, Israel, January 1978 to December 2009 (11). Peak IM incidence in August.
Thus, IM doesn’t seem to be always more active in summer. While spring-summer peaks were observed in 2 studies from the UK and one from the USA, 1 study each from Sweden and the USA found no consistent pattern while 2 studies from Israel found a peak in August and one study from the USA in January-February. Not only different peaks in different countries but also different results from 3 studies in the USA.
Though some of these few studies hint at a seasonal disposition to IM, i.e., greater likelihood of spread from infected individuals at some times of the year compared to other times, season isn’t the only factor in IM infectiousness. IM could also spread if a person became temporarily immunosuppressed, under heavy stress or due to vitamin D deficiency for example, two factors that often precede IM symptoms (6). Means can’t go by season alone to avoid getting IM from someone who’s already infected.
3. Hobson, F. G., Barbara Lawson, and Mary Wigfield. “Glandular fever: a field study.” British medical journal 1.5075 (1958): 845.
4. Douglas, A. Stuart, Tom Brown, and Daniel Reid. “Infectious mononucleosis and Hodgkin’s disease—a similar seasonality.” Leukemia & lymphoma 23.3-4 (1996): 323-331.
5. Balfour, Henry H., et al. “Behavioral, virologic, and immunologic factors associated with acquisition and severity of primary Epstein–Barr virus infection in university students.” Journal of Infectious Diseases 207.1 (2013): 80-88.
6. Lossius, Andreas, et al. “Season of infectious mononucleosis and risk of multiple sclerosis at different latitudes; the EnvIMS Study.” Multiple Sclerosis Journal (2013): 1352458513505693.
7. Belfrage, S. “Infectious Mononucleosis An Epidemiological and Clinical Study.” Acta Medica Scandinavica 171.5 (1962): 531-541.
8. HEATH, CLARK W., ALLAN L. BRODSKY, and ABRAHAM I. POTOLSKY. “Infectious mononucleosis in a general population.” American journal of epidemiology 95.1 (1972): 46-52.
9. BRODSKY, ALAN L., and CLARK W. HEATH. “Infectious mononucleosis: epidemiologic patterns at United States colleges and universities.” American journal of epidemiology 96.2 (1972): 87-93.
10. Grotto, I., et al. “Clinical and laboratory presentation of EBV positive infectious mononucleosis in young adults.” Epidemiology and infection 131.01 (2003): 683-689.
11. Levine, H., et al. “Secular and seasonal trends of infectious mononucleosis among young adults in Israel: 1978–2009.” European journal of clinical microbiology & infectious diseases 31.5 (2012): 757-760.