Mumps on ice

The mumps vaccine was licensed in the US in 1967 and recommendations regarding use of the vaccine have varied since its introduction. As described in the CDC Manual for the Surveillance of Vaccine-Preventable Diseases, the Advisory Committee on Immunization Practices (ACIP)

made an official recommendation for one dose of mumps vaccine for all children at any age after 12 months in 1977. In 1989, children began receiving two doses of mumps vaccine because of the implementation of a two-dose measles vaccination policy using the combined measles, mumps, and rubella vaccine (MMR) vaccine. In 2006, a two-dose mumps vaccine policy was recommended for school-aged children, students at post high school educational institutions, healthcare personnel, and international travelers.

Mumps vaccine has had a profound impact on the annual incidence of mumps in the US. In 1968 more than 152,000 cases reported, while in 2003 only 231 cases were reported. Recently, however, the nation has witnessed a resurgence of the disease, and an apparently ongoing outbreak of mumps in the National Hockey League (NHL) illustrates how the mumps virus continues to circulate in the general population. The NHL outbreak has, so far, affected 15 players on five teams, and another three cases are suspected. A timeline of events surrounding the cases suggests the outbreak originated in October.

Doni Bloomfield wrote an article this week (which also contains "mumps on ice" in the title) that, in one vivid passage, illustrates potential infection pathways for mumps virus in professional hockey. Bloomfield quotes James Conway of the University of Wisconsin School of Medicine and Public Health:

You watch these guys taking a big hit up against the boards, there’s snot and boogers and all sorts of stuff flying around as the guy gets hit hard enough, so I don’t think it would surprise me at all that there’s some transmission just by stuff flying around during the games. It’s a sloppy, messy sport.

That's colorful imagery for sure, but in addition to how, it's important to ask why this and other recent outbreaks are occurring. Mumps is, after all, a vaccine preventable disease. 

It's possible that this group of players belongs to a demographic that has lower vaccine coverage, potentially due to parental reticence to vaccinate. However, at least one player is known to have had two doses of vaccine: one childhood dose, consistent with ACIP guidelines in the late 1980s, and another in preparation for foreign travel in February of 2014. Tara Haelle wrote an article recently on the mumps vaccine in which she quotes Paul Offit discussing the rate of waning immunity associated with this vaccine. Offit notes that

If you look at the three [MMR component] vaccines, measles and rubella induce larger memory in B and T cells . . . They have longer lasting immunity. Mumps is the weak sister of the three. You start to see vulnerability 10 years after the first dose and 10 years after the second dose.

Waning vaccine-associated immunity could thus play a role in this outbreak, and in potential future ones as well. Boosters have been used to compensate for waning immunity in past mumps outbreaks. Might a third dose of vaccine be appropriate for the general population at some point in the future?

(image source: CDC)

Hepatitis in the summer of '69

A remarkable epidemic took place in 1969 at the College of the Holy Cross in Worcester, Massachusetts. In the autumn of that year, the college was forced to cancel the football season after the first two games due to an outbreak of hepatitis. 

The first football game of that season was against Harvard and took place on September 27th; Holy Cross lost 13-0. The team appeared sluggish to fans, and one player missed the game due to fever. Michael Neagle described what happened next in a 2004 essay:

Players began dropping out during the week leading up to the team’s next game at Dartmouth [on October 4th]. What had been described as a “flu bug” by newspapers during the week was confirmed as hepatitis the day of the game. Eight players did not make the trip because of illness. Some got sick on the drive up. More were sidelined when they fell ill during the game . . .

Holy Cross lost 38-6. There were interesting facets to this outbreak, as told in a 1972 Associated Press story:

The outbreak was somewhat puzzling because faculty members, the freshman football team, and others on the Worcester, Mass., campus before formal opening of classes were not affected. Food services were studied and did not produce suspicious leads.

Neagle describes what was eventually pieced together:

. . . [the] season was doomed after just the second day of practice. On Aug. 29, a hot summer day in Worcester, on the practice fields where the Hart Center now stands, players drank water from a faucet that was later found to be contaminated with hepatitis. Though investigators almost immediately suspected the drinking fountain as the source of the illness, it took nearly a year to determine conclusively the sequence of events that led to the contamination.

On that fateful day, firefighters battled a blaze on nearby Cambridge Street. This caused a drop in the water pressure, allowing ground water to seep into the practice field’s irrigation system. That ground water had been contaminated by a group of children living near the practice facility who were already infected with hepatitis. Once the players drank from the contaminated faucet, they too became infected.

A 1972 study by Morse et al described the epidemiology of the event:

Of 97 persons exposed, 90 were infected, 32 experienced typical icteric [jaundice] disease, 22 were anicteric but symptomatic, and 36 asymptomatic players were recognized as having significantly elevated serum glutamic pyruvic transaminase values (> 100 units). Other athletes, using the same facilities but arriving six days after the established date of exposure, were unaffected. The decision to obtain blood samples from the entire team, as soon as the initial cases were recognized, resulted in the demonstration of an unexpectedly high attack rate of 93% . . .

An attack rate of 93% is remarkable, but potentially consistent with a high inoculum that could have been delivered by contaminated water. Friedman et al returned to the event in a 1985 study. Using a radioimmunoassay to test stored serum samples for IgM antibody to hepatitis A virus, they found that

Only individuals with icteric hepatitis were found to have IgM anti-HAV in serum; those with presumed anicteric illness were shown not to be infected with hepatitis A virus. The attack rate was thus only 34%, not 93% as originally reported, and the incidence of icteric illness in those infected was 100%, not 33%.

What made the other players sick thus remains a mystery, though one can speculate about potential pathogens in the environment that could have contaminated the practice field faucet given the negative pressure scenario. I'm always intrigued by disease events that seem so open-and-shut based on the technology of one era but less so when analyzed with the technology of another. This is one of those events.

(image source: Wikipedia)