What makes covid19 different from...?

 Today I had a conversation with an MD and public health leader concerning the data on Covid19. He asked me a question to which I did not have the answer. What makes covid19 different from H1N1, SARS, and MERS which had relatively few deaths? I did not have the answer so I started researching. I learned a lot including that "virulence" is a mortality measure and "infectivity" is the correct term for how fast things spread.

Here is what I found in my research: conclusions, followed by the data to back it up.

There is a perfect storm for a deadly pandemic. 1) You need a virus which does not kill its host too quickly. If the host gets too sick too quickly they will not adequately spread the virus and the virus will die out before it has spread widely. 2) you need a virus where a large percentage of those infected do not get sick enough to stop their daily tasks (e.g. 2-14 days before symptoms). 3) you need a virus that kills a high percentage of the hosts--in the later stages of infection.

MERS and SARS both have high virulence and do not spread quickly before running their course. So both are too deadly to spread--but if they did spread, wow. Combined with a serious response from the medical and policy communities, neither became significant global threats. H1N1 was virulent, but not too virulent, and we found two drugs that worked effectively for treatment in somewhere less than 30 days. In 1918 we had no antibiotics at all to treat the 1918 version of H1N1.

My conclusion is that covid19 meets the standard for the worst case. Incubation period is as short as 2 days and as long as 14 during which time an individual does not know that they are sick and can actively spread the virus. Around 80% of infected cases are not bad enough to make a person seek medical treatment which means the discovered and verified cases will always be lower than the true cases out in the wild; perhaps by a factor of 5. Mortality rate looks to be around 4.56% (based on a model discussed in yesterday's post) so it is not likely to burn itself out. To date, there is no known effective treatment though there is some hope for improved patient outcomes in the near future; if we can slow down the rate of spread we may be able to minimize health and economic impact.

Data:

H1N1 2009 started as a highly virulent disease killing over 6.4% of the first 1600 patients to contract it. 25% of patients required hospitalization. Symptoms show between 2 and 14 days after infection (this will start to sound familiar). The infectivity was well above 1, but not too bad--1300 became 1600 cases in one day. Fortunately within weeks, the CDC tested 4 antivirals and found two which worked. 31 days after patient zero was found (in California, not Mexico as I had thought) the CDC released 25% of the millions of doses on hand and the mortality rate plummeted making it, in retrospect, not a particularly bad flu, particularly considering the last few flu years. 18,036 people died from H1N1 out of 60.8 million cases.

 SARS The WHO reports that SARS killed 774 of 8,096 patients across 29 countries. Symptoms show between 2 and 14 days after infection. Spread is via sputum. Global virulence was 9.56% in 2003 and 2004. There is no known cure.

 MERS Since 2012, MERS has caused 2,494 confirmed cases in 27 countries and killed 858 people. Symptoms show between 2 and 14 days after infection. Spread is via sputum. Virulence i.s extremely high for MERS at 34.4%. Patients sick with MERS are so sick that they barely spread it at all giving the virus a low overall infectivity. There is no known cure.

 H1N1 started as a significant threat with a 2-12 day incubation period which allowed infected hosts to spread the virus to others before becoming too sick to spread, a virulence of 6.4%, and an infectivity on the high side with cases multiplying by about 1.25 a day. This likely would have been a very serious event had an effective treatment not been discovered in less than 30 days. With treatment, mortality dropped from 6.4% to 0.0297%. Without effective treatment could have resulted in 3.9 million deaths assuming it did not burn itself out sooner. 1918 should inform this.

 Finally I considered the 1918 H1N1 epidemic which killed somewhere between 27 and 50 million people globally or 5 to 10% of infections resulted in death. Estimates on infections are around 500 million people. The virus shared DNA with the 2009 swine Flu so we could have seen similar results. What was different? A common flu and swine respiratory disease circulated at the same time. Penicillin, the first antibiotic, was not discovered until 1928. The first sulfa drug was not discovered until 1935. In 1918 there was no effective treatment for a flu of this kind. Had we had antibiotics, this story would have been different. How different we cannot say, but it is safe to say that far fewer would have died.

 From the CDC site on the 1918 H1N1 pandemic, "With no vaccine to protect against influenza infection and no antibiotics to treat secondary bacterial infections that can be associated with influenza infections, control efforts worldwide were limited to non-pharmaceutical interventions such as isolation, quarantine, good personal hygiene, use of disinfectants, and limitations of public gatherings, which were applied unevenly."

 Here is a timeline that I compiled, mostly from the US CDC, but other sources also considered. This shows the way H1N1 spread and how quickly.

Day 1, March 25, 2009: patient zero, California

Day 10, April 4, 2009: outbreak in veracruz

Day 21, April 15, 2009: 10 year old diagnosed in California (1)

Day 22, April 16, 2009: 8 year old tested 130 miles away as part of a flu survey (1)

Day 27, April 22, 2009: CDC activated emergency operations center (EOC) (1)

somewhere around this time the cdc began testing antivirals on the samples obtained from the two California patients. "Testing showed that these two viruses were resistant to the two antiviral drugs amantadine and rimantadine, but susceptible to the antiviral drugs oseltamivir and zanamivir." (1)

Day 30, April 25, 2009: 18 confirmed cases in Mexico City (including 6 deaths)

Day 30, April 25, 2009: 1300 suspected cases, 81 deaths (source CNN)

81/1300 = 6.23% virulence/morbidity rate

Day 30, April 25, 2009: WHO declared public health emergency of international concern

Day 31, April 26, 2009: WHO recognition that containment is impossible

Day 31, April 26, 2009: ***The US began releasing 25% of stores of the two antiviral drugs oseltamivir and zanamivir to which H1N1 was discovered to be vulnerable...this was no longer a runaway virus and there was now a path to global treatment.

Day 32, April 27, 2009: 1600 suspected cases, 400 hospitalized, 103 deaths

103/1600 = 6.4375% virulence

At this point in time we can see that swine flu H1N1 was putting 25% of suspected cases in the hospital, and morbidity exceeded 6.2%

Day 33 , April 29, 2009: WHO Phase 5 (pandemic) -note that pandemic means the virus has spread everywhere.

A global pandemic does not speak to the exact threat of a particular virus, merely indication that it is a threat everywhere. It also does not consider the improvement in care that usually occurs once health care providers understand the disease, secondary infections, and preferred treatment thereby drastically improving patient outcomes.

Day 33 , April 29, 2009: Morbidity rate plummets due to available treatment...

and just like that, H1N1 becomes a blip, not a global tragedy. But there were still many casualties. Recent studies looking at the global casualties estimate as many as 100,000 died.

 notable: 2009 H1N1 did not come from swine--it was circulating among people. (cdc.gov)

 sources:
https://www.cdc.gov/flu/pandemic-resources/2009-h1n1-pandemic.html
http://www.cidrap.umn.edu/news-perspective/2010/03/study-shows-1918-and-2009-pandemic-viruses-share-key-feature
https://www.sciencedaily.com/releases/2009/04/090430111640.htm
https://www.cdc.gov/flu/pandemic-resources/1918-pandemic-h1n1.html