Issue: February 2014
Disclosures: Kaye and Pollack report no relevant financial disclosures.
February 01, 2014
4 min read

MERS vs. SARS: Compare and contrast

Issue: February 2014
Disclosures: Kaye and Pollack report no relevant financial disclosures.
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The severe acute respiratory syndrome outbreak in 2002 and 2003 led to more than 8,000 infections worldwide and killed close to 10% of those infected.

It was caused by a coronavirus that made a species jump from bats to humans through the intermediate host of farmed civet cats bred for human consumption in China. From recognition of the outbreak to identification of the agent and animal reservoir, to containment and resolution, the outbreak occurred during a 9-month period.

Similarities and differences of disease

As of mid-January, the time of preparation of this editorial, we are now in the 18th month of the Middle East respiratory syndrome (MERS) outbreak. It is of interest at this point to evaluate the current status of the outbreak, which is far from being contained or, for that matter, from being understood in terms of the epidemiology. Perhaps because there have been fewer than 200 cases of MERS, with fewer than 100 deaths, and very limited spread outside of the Arabian Peninsula has something to do with it. Add to that the observation that severe disease has been seen primarily in older individuals with comorbidities, whereas, in contrast to severe acute respiratory syndrome (SARS), young, healthy individuals tend to have asymptomatic-to-mild disease. Clearly, the threat level to the world is perceived as much less with MERS than it was with SARS.

Because SARS started and spread in China, which has formidable scientific expertise, and then spread to Western countries with their scientific resources may explain the differences in response to and knowledge about the MERS and SARS epidemics. There seems to be a large discrepancy between the worldwide scientific resources thrown into the SARS outbreak, which seem to dwarf the resources applied to the MERS outbreak. This could be a result of limited scientific resources in the countries primarily involved, as well as the fact that SARS spread to “the backyards” of industrialized nations while MERS has not. Alternatively, perhaps the novelty of a coronavirus that was lethal for humans in the case of SARS attracted more attention of scientists and funding than the second-place MERS. Regardless of the explanation, the result is that we clearly know less about MERS than we did about SARS, despite the much longer duration of the MERS outbreak.

Marjorie P. Pollack

Donald Kaye

We know that the novel coronaviruses responsible for both SARS and MERS probably originated in bats and then spread to an intermediate mammalian host from which humans were infected. The discovery of civet cats as an infection source of SARS for humans occurred about 4 months after the international recognition that there was an outbreak of a new disease. In contrast, it was not until 10 months after the recognition of MERS that camels were suspected as the possible intermediate host.

Camels may not be to blame

In fact, although camels throughout the Middle East are serologically positive for a virus similar to or identical to the virus of MERS, there is no evidence that the camel is an important intermediate host — only nine cases thus far have reported a definite history of exposure to camels (or other farm animals) during the period preceding onset of disease. Furthermore, the whole virus has not been isolated from camels. RNA fragments have been sequenced, and some have similar fragments as the viruses infecting individuals with known contact with these camels. However, until the whole virus is sequenced, we cannot be certain that it is the same virus that is infecting people. The other compounding question is whether these camels were the source of the infection for the people, or if the ill people were the source of the infection for the camels. Furthermore, most of the cases did not have known contact with camels. It is safe to say that, at present, we still do not know the identity of the intermediate host.

The SARS epidemic, with only a 10% mortality rate, spread rapidly from person-to-person worldwide, aided by super spreaders. In an 8-month period, there were more than 8,000 cases of SARS. Despite a more than 40% mortality rate with MERS, the slower spread of the disease, with fewer than 200 cases worldwide in an 18-month period, with virtually all of those directly or indirectly related to transmission in the Arabian Peninsula, has not elicited the sense of urgency that SARS did. In fact, the actual mortality rate for MERS is most likely lower than the reported more than 40% because mild or even asymptomatic infections have been reported, and it is likely that others remain unrecognized.

In the SARS outbreak, the cases were primarily seen in young healthy individuals, whereas more than half of the MERS cases have been in individuals older than 50 years. More than 70% of severe disease and deaths in MERS occurred in people with comorbidities. SARS affected males and females equally, whereas more than 65% of MERS sporadic cases have been in men. The male predominance may possibly suggest either an occupational or cultural relationship.

It is clear that both SARS and MERS have caused nosocomial outbreaks involving health care workers as well as other patients, probably related to suboptimal respiratory precautions and, possibly, procedures that resulted in aerosolization of respiratory secretions. Although MERS is clearly less infectious than SARS in terms of person-to-person spread, both in and outside of hospitals, the advent of super spreaders or a mutation in the MERS virus could change the dynamics of the outbreak.

Approach to the epidemic

From the experience thus far, it seems likely that the MERS outbreak will continue to limp along with sporadic cases occurring primarily in the Arabian Peninsula followed by nosocomial outbreaks when first introduced into a health care facility. This may change when the routes of transmission to the sporadic cases are clearly identified, or if there is a change in the virus leading to the super spreader phenomenon observed with SARS or a change in virulence of the virus. Without definitive identification of the non-human animal reservoir, there is unlikely to be a practical approach to stopping the epidemic.

Even if camels are proven to be the animal reservoir, an approach to containment will be difficult without a vaccine. Unlike the civet cat in China, camels are important to the daily lives and economies of the countries in the Middle East and elimination of camels is unlikely to occur.

For more information:

Donald Kaye, MD, is a professor of medicine at Drexel University College of Medicine, associate editor of the International Society for Infectious Diseases’ ProMED-mail, section editor of news for Clinical Infectious Diseases and is an Infectious Disease News Editorial Board member.
Marjorie P. Pollack, MD, is deputy editor of ProMED-mail and an independent consultant medical epidemiologist with a focus on developing world issues following CDC training. She is based in New York City.

Disclosure: Kaye and Pollack report no relevant financial disclosures.