You’re also too pretty for math

I wasn’t going to raise this comment en blogge, but with Dr. Isis’ new post, it becomes more relevant. From Rick Fletcher on the “you’re too pretty” post:

It’s a major issue if your department won’t hire your or promote you because you are a woman. It’s no surprise that a retail clerk at a small shop in a downtown area is not the smoothest operator.

25 years ago it was a common response when I was introduced as a PhD chemist: “You don’t seem like a scientist.” Now it’s a common response when introduced, “Why are you single?” People say some dumb things. Not exactly the news.

But again, it’s an issue if the people who matter to your career hold you back because of your gender or appearance. Is that the case? No?

You can’t tweet the science but you can blog your indignation over getting hit on. Check your issues bag, it might be time for spring cleaning.

I already responded in the thread so I won’t rehash here, but via Isis comes this lovely reminder of why it’s more than just the people who hold my career back who matter–it’s an all-too-pervasive attitude, and it’s not just about me. Isis caught this screenshot from the store Forever21 (a store that I think we have in our mall here; I’ll have to see if they carry this particular product):

Yes, for less than $4, you too can tell the girls in your life that they’re too attractive for math. As Dr. Isis notes:

This is the kind of nonsense that frightens me. Washed up old fucks like Harvey Mansfield don’t worry me. I worry more about the small messages that pervade popular culture. The messages that we have to defend our girls against when we take them to the mall or the market.

Things like this make me realize just how far we have to go.

Bingo. *This* is why comments like that matter and aren’t just some kind of harmless flirty pick-up line, or just my “issues” that I need to “spring clean.” It affects all of us, and we all need to be aware of it and respond, rather than sweep it under the rug and dismiss it.

The Epidemic: Typhoid at Cornell

In the United States, we tend to take our clean drinking water for granted. Even though there are periodic concerns which bubble up about pharmaceuticals or other chemicals in our water supply, we typically believe–with good reason–that we have little to fear when it comes to contamination from microbes. Our drinking water, while far from perfect, is heads and shoulders above what it once was–something many of us forget or have never realized. There have been notable breakdowns, such as the 1993 outbreak of Cryptosporidium in Milwaukee that sickened over 400,000 individuals, but these days such events are few and far between.

This hasn’t always been the case. In the early 1900s, the safety of the water supply even in many large U.S cities wasn’t monitored, and there were no standards in place to guarantee that individuals receiving pumped water wouldn’t be made ill by it. This is the setting for David DeKok’s new book, “The Epidemic,” detailing a 1903 outbreak of typhoid fever (caused by Salmonella enterica serovar Typhi) in Ithaca, New York, that hit at least 512 homes in the town and left 82 dead, including 29 Cornell students. It’s estimated that 10 percent of the populace was sickened, one of the last of the major typhoid outbreaks in the U.S.

The book begins with a description of those behind Ithaca’s water supply back in the day. It was an ugly mess of local businessmen and members of Cornell’s Board of Trustees, who unwittingly set the outbreak in motion with the 1901 sale of Ithaca Water Works to local businessman William Morris. Morris was a Cornell alum, a lawyer and entrepreneur who had previously invested in power companies. He had agreed to buy the Water Works only as a side deal that provided him with his main interest, Ithaca Gas Light Company. The deal was financed in part by Cornell University, with some of Morris’s buddies on the Board of Trustees greasing the deal.

Morris had never run a water company before and while others in town had suggested adding in a filtration plant upon Morris’s purchase of the company, Morris ultimately refused, and began construction on a huge new dam. For this, he hired Italian workers–from an area of Italy where typhoid was still endemic. This was prior to the discovery of the carrier state for typhoid, so while the workers appeared to be quite healthy, at least one of them was unwittingly spreading the deadly organism. Coupled with the atrocious state of the dam construction site–including limited access to outhouses, so workers urinated and defecated near the creek where they were working–this assured that Six Mile Creek would be contaminated, and a good portion of Ithaca’s water supply along with it.

Soon, the cases started to roll in. From January 1903 until May of that year, they piled up even as students began to flee the campus, sometimes unknowingly taking their infection home with them to family members. What followed was a mess of blame-gaming and politicking, with no one taking responsibility and officials contending that the very victims of the outbreak were responsible by being careless about what they ate and drank. Even well into the epidemic, the need for boiling contaminated water was debated and put aside as students and townfolk were dying. Indeed, a letter from late February 1903–well into the epidemic–shows that university officials were still denying they carried any blame, or even that their students were drinking contaminated water.

DeKok uncovers a story that will make anyone interested in public health seethe in anger, and yet it’s one that can–and does–still happen today, as the good ol’ boys’ network and corporate interests trump the health of the populace. Our drinking water is much improved, but corporations are still allowed to pollute with little more than a slap on the wrist. Sadly, DeKok recounts how Morris’ wealthy friends ended up protecting him from any kind of fallout, while Andrew Carnegie came through and donated enough funds to cover medical and funeral bills for the affected students. Finally, in an ironic turn of events, DeKok also notes how Morris’ companies evolved over the years into the General Public Utilities Corporation, which ran the Three Mile Island nuclear power plant.

“The Epidemic” is a story of an outbreak that, with just a bit of foresight and concern for the public good over private profits, could have been prevented entirely. It sadly mirrors many public health controversies that still thrive today. For instance, one passage notes that any government funding for the water works was fear-mongered as “socialism,” a platform that could have come from our current Republican leadership. It’s a tragic reminder that we don’t always learn from our mistakes, and while our water may be safer today than in 1903, public health still gets trampled on by private industry. Will we ever learn?

Measles in Iowa

We’ve had pertussis and mumps, so it was only a matter of time.

State health officials declared a “public health emergency” Tuesday after a test confirmed a case of measles in an unvaccinated Dallas County baby who apparently picked up the disease in India.

They said people who might have been exposed included passengers on an Americans Airline flight from Chicago to Des Moines May 11 and people who were at Mercy Medical Center or a Mercy pediatric clinic in downtown Des Moines May 14.

Dr. Patricia Quinlisk, medical director for the Iowa Department of Public Health, said many Americans falsely recall measles as a benign childhood illness. “I get asked by medical students, ‘Which disease are you most afraid of?’ And they expect me to say Ebola or SARS or something like that – but, it’s measles,” she said. “I don’t think people understand how bad it can be, how many people can get seriously ill and, unfortunately, how many people can die from this disease. It’s bad and it’s probably the most spreadable disease we have in our society.”


Dr. Asha Madia, a Mercy pediatrician, said the patient is an 8-month-old boy who had a fever, a rash and a mild eye infection. He has recovered. She said the boy was not vaccinated because such vaccinations generally are not given before age 1. But she said his family believes in vaccinations and had immunized the boy’s older sibling.

So this is unique in that the index case isn’t from a family who has eschewed vaccination (unlike this case in 2004), but in a child who was unvaccinated nevertheless due to his age. This is one reason the CDC just last month recommended the MMR vaccine in infants who would be traveling abroad, even if they are below the traditionally recommended age.

Story still developing, but for now it appears that this is the only case recognized. However, as Maryn recently pointed out, *any* measles outbreak isn’t cheap, due to the diligent surveillance that must be undertaken to make sure no one else comes down with the infection. Full information available here from the Iowa Department of Public Health.

You’re too [pretty/young/female, take your pick] to be a microbiologist!

This wasn’t the post I wanted to write about the ASM conference. There’s been lots of great science discussed (I’ve tried to tweet some of it, but the wifi in both the conference center and my hotel have been spotty, so I’ve not had a chance to write anything comprehensive). Instead, I’m ticked off and venting via dashed-off blog rant.

[Me, trying to make a purchase]: Do you have any of these in a box that doesn’t say “from someone in New Orleans who loves you”? I was going to get them for my lab and that might be kind of creepy.

[Retail salesguy]: Your lab? I’m not sure those are good for dogs.

[Me]: No, not the dog lab. A science lab. My laboratory. The people who work for me.

[RSG]: Oh, you’re here for the science conference?

[Me]: Yes, microbiology. I study germs.

[RSG]: But you can’t be a scientist!

[Me]: I can’t?

[RSG]: No, you don’t look like a microbiologist.

[Me]: Um, what exactly does a microbiologist look like, then?

[RSG]: Uh…

[Me]: Because I’m pretty sure that I am one. (Rummaging through bag, digging out ASM nametag). Yep, that’s my name, and that’s the microbiology conference logo right there.

[RSG]: But you’re too pretty! You should be in Hollywood.

[Me]: (picking up bag, leaving unpurchased boxes on counter) I bet you’ve had dozens of scientists just like me through your store today, and never even realized it because of the stereotypes you hold. Conference runs through tomorrow, so I hope you’ll say hello to a few of them.

I know Mr. Salesguy was trying to be nice and probably thought he was flattering me, but fer chrissakes, that is NOT the way to go about it. Women in science already frequently feel like “The Other,” that we’re “too XX” to be good at what we do, that our possession of breasts surely must mean that we’re too much of a fragile flower to be able to handle the “man’s work” involved in science and academia, and that we need to go above and beyond what our male colleagues do just to feel the same level of acceptance and appreciation. I’m sure Mr. Salesguy has never thought about the plight of women in science before tonight (and I doubt that my conversation really made him think about it for more than a few fleeting seconds), but it really dragged down what had otherwise been a very nice few days of unadulterated sciencey goodness.

Of course, it’s not only science meetings or clueless salespeople; atheist meetings have their unthinking men too, as was recently demonstrated yet again. From now on, maybe I’ll print out this post and keep a copy in my bag, just for situations like today.

Pigs with Ebola Zaire: a whole new can o’ worms

Ebola has long been associated with wildlife. From the early days, bats were viewed as a potential reservoir (though it wasn’t confirmed that they actually harbored the virus until 2005). Contact with wild animals–particularly primates which were butchered for food–was also long thought to be a risk factor, and now we know that primates can become ill with Ebola and pass the virus to humans.

What hadn’t been examined until 2008 were pigs. I mean, it’s not exactly the animal you associate with central Africa, where many of the Ebola cases have been concentrated. However, pigs are much more plentiful in the Philippines, where another Ebola subtype–Ebola Reston–is thought to lurk. The Reston strain actually was first documented in the United States, where twice it was associated with outbreaks in primates originating from the Philippines. When the facility in the Philippines was closed down in 1997, Reston disappeared for 11 years–until it surfaced in pigs in 2008.

The ecology of Ebola Reston in the Philippines isn’t known–unlike African Ebola strains (and their cousin, Marburg), no bats have been caught in that country and tested positive for the virus, though they probably serve as a reservoir of the virus in the Philippines just as they do in Africa. So it was a huge surprise when pigs from that country tested positive for Ebola Reston–and so did 6 of their human caretakers, suggesting cross-species transmission. (I should note here that the Reston strain has yet to be linked to any symptomatic infections in humans–the pig farmers who tested positive probably had no idea they’d been infected and did not show any clinical signs of illness). Pigs hadn’t previously been linked to any Ebola infection, so this brought in a whole other wrinkle when it came to Ebola transmission–the possibility of being exposed to Ebola via contaminated food, and the potential for pig populations to harbor the filovirus (and transmit it to their caretakers, as we have seen with outbreaks of Nipah and Hendra viruses).

A new study delves further into Ebola in pigs. Instead of using the Reston strain, they use the much-more-deadly Zaire strain. This is the one that movies are made about; the one which can cause outbreaks so nasty that they kill up to 90% of those who are infected. Why use Zaire instead of the Reston strain–the one which has actually infected pigs in nature? Well, the researchers wanted to find an animal that’s easier to work with than primates (there are all kinds of very strict regulations when it comes to working with non-human primates), so if pigs could work as a good model for human Ebola disease, that would make studying the virus just a bit easier. (In any case, for any live Ebola work, it still needs to be done in a biosafety level 4 environment, meaning complete spacesuits and the whole works).

The authors did 2 studies. In the first, they inoculated 6 pigs with Ebola Zaire, via a combination of intranasal, intraocular, and oral routes of infection. (Interestingly, no injection, which can be a key way Ebola is spread). They had an additional 2 pigs that they inoculated the same way with a saline solution, and housed them separately from the Ebola-inoculated animals. The goal of this experiment was to look at the pathogenesis of a virulent Ebola strains in the pig model. The infected animals all developed fevers and respiratory disease, with some internal hemorrhaging and evidence of airway replication by Ebola. Infectious virus was found at low levels in nasal washes and oral and rectal swabs; one animal also had a low level of virus in the blood. Higher levels of virus were found in various organs, including the heart and bladder, while the highest levels were found in lung tissue.

In the second experiment, they inoculated 3 new pigs in the same fashion, but then added in 4 additional (uninoculated) animals to stay with them, and kept 2 additional control animals in a separate area so that they could investigate pig-to-pig transmission of the virus. They did find viral RNA from the mucosa of all contact animals, and infectious virus was detected from 2 of 4, demonstrating that the virus can be passed among pigs. Not stated in the article was if the authors thought this was due to direct contact with respiratory secretions among the pigs, or via airborne transmission (a much more concerning route of transmission, as in humans, Ebola Zaire doesn’t seem to transmit well via air–typically it’s spread via close direct contact and bodily fluids).

Notably, pigs didn’t seem to develop severe systemic disease from Ebola, as primates do–the main symptoms exhibited were respiratory, which the pathology supports (finding little virus in the blood, but a lot in the lungs). This suggests that even for Ebola Zaire, infection in a pig could be mistaken for other respiratory diseases, such as influenza or PRRS virus (porcine respiratory and reproductive syndrome virus, which the initial pigs in the Phillipenes were co-infected with). So, Ebola may be circulating even more than we realize in the pig population, disguised by its commonplace symptoms.

A commentary published in tandem with the research article ponders the issue of foodborne Ebola, suggesting that this is a remote possibility and noting that butchering infected animals in the wild in Africa has certainly spread the virus. However, solely eating meat as a means of infection hasn’t been reported, and cooking likely destroys any risk (similar to influenza viruses). Like influenza virus, Ebola doesn’t seem to survive long in most environments, but it’s also noted that differences in African food storage (with little refrigeration) versus more typical cold storage may affect that as a risk factor, possibly prolonging the life of the virus when held in the cold. I think foodborne transmission is unlikely, but it can’t be completely ruled out right now.

Because of the respiratory symptoms, does this mean Ebola could enter the population via meat from animals that farmers don’t consider very ill, or put butchers at a heightened risk of infection during slaughter? This to me is more concerning than simple foodborne transmission. With Reston, at least no human symptoms have been observed, but if pigs (and potentially other animals?) can present with Ebola Zaire as a rather generic respiratory infection…well, that could spell trouble in a lot of different ways. It means that telling individuals to simply avoid sick-looking primates (and bats) is going to be even more woefully inadequate than it already is. Plus, it raises the remote-but-not-completely-outside-the-realm-of-possibility of someone intentionally spreading the virus via animals that are infected in this manner.

Science fiction? Maybe. Probably. Hopefully. But this research opens the door on many new lines of investigation and once again, raises even more questions.

Kobinger GP, Leung A, Neufeld J, Richardson JS, Falzarano D, Smith G, Tierney K, Patel A, & Weingartl HM (2011). Replication, Pathogenicity, Shedding, and Transmission of Zaire ebolavirus in Pigs. The Journal of infectious diseases PMID: 21571728

Ebola in Uganda: current and past outbreaks

Via H5N1 and other sources, there’s at least one new Ebola case in Uganda:

The rare and deadly Ebola virus has killed a 12-year-old Ugandan girl and health officials said on Saturday they expected more cases.

The girl from Luwero district, 75 km (45 miles) north of the capital Kampala, died on May 6, said Anthony Mbonye, the government’s commissioner for community health, in the first outbreak of the virus in Uganda in four years.

“Laboratory investigations have confirmed Ebola to be the primary cause of the illness and death. So there is one case reported but we expect other cases,” he said.

Though we’ve known about Ebola in Africa since 1976, Ebola wasn’t recognized in Uganda until a bit over 10 years ago. Now, this is the third outbreak in this amount of time. The first occurred in August of 2000; the first case died in Gulu on the 17th of September. Despite an investigation, doctors were unable to determine where or how she had contracted the disease. Her death was followed by the deaths of her husband, two children, and several other family members. This was reported to the Ministry of Health in October of that year, near the peak of the epidemic. An investigation and intervention to control the disease followed, and the epidemic was declared to be over in January of 2001. A total of 425 patients from 3 villages (Gulu, Masindi, and Mbarara) across Uganda were identified based on symptoms and/or laboratory data. 224 of them died, with a resulting mortality rate of 53%; an eerie echo of the 1976 Ebola outbreak in Sudan. Indeed, sequence analysis showed the infecting strain to be the Sudan subtype of Ebola; the first time this type had surfaced since the 1979 outbreak in Sudan. It is hypothesized that Sudanese rebels, who carried out regular attacks around Gulu, may have accidentally introduced the virus in some manner, though this has not been confirmed.

Ebola returned to Uganda in August of 2007, causing 149 illnesses and 37 deaths until the outbreak was declared over in February of 2008. This mortality (36%) was significantly lower than most Ebola outbreaks. Interestingly, when scientists tested this virus, it also reacted strangely with their assays. Therefore, they determined the entire molecular sequence of the virus, and found that it was a whole new strain of Ebola, which they named Ebola Bundibugyo.

I couldn’t find any other details about the current outbreak–how she was infected, if she’s actually the index case or if there were previous deaths that have not yet been confirmed. (The girl died at the hospital–previous deaths may have gone unrecognized if they had died at home). I’m sure more details will be coming in the next days and weeks. What we’re left with now is the knowledge that in 11 years’ time, Uganda is now on its third Ebola outbreak. These have occurred in 3 different areas of the country (Gulu is toward the north, Kampala region in the south near Lake Victoria, and Bundibugyo in the southwest, almost due west of Kampala) and with 2 different strains (thus far). This again feeds my morbid fascination with the virus–what does this mean about Ebola reservoirs in Uganda? Are these cases bat-acquired? Other wildlife? Spillover from other countries, as suggested with the 2000-1 outbreak? As always, Ebola outbreaks tend to raise more questions than they answer.

[UPDATE: via Crawford Killian, CDC says current outbreak is due to Sudan strain.]

MRSA, Meat, and Motown

It’s been not even a month since the last paper looking at MRSA in meat, and up pops another one. So far here in the US, we’ve seen studies in Rhode Island (no MRSA found); Louisiana (MRSA found in beef and pork, but “human” types: USA100 and USA300); the recent Waters et al study sampling in California, Florida, Illinois, Washington DC, and Arizona, finding similar strains (ST8 and ST5, associated with USA300 and USA100, respectively). Now a new study has collected MRSA samples in Detroit, collecting 289 samples from 30 retail stores in the city.

For this study, they collected only beef, turkey, and chicken–a bit odd, since pork has been the meat product typically linked to MRSA to date. The paper is short on methods so it doesn’t say how the sampling was done, which is a bit frustrating as they found levels of S. aureus that were quite a bit lower than those found in the Waters paper. Unlike the Pu and Waters papers, *all* of the Detroit samples were USA300. No typing data was given for the S. aureus that were susceptible to methicillin.

There’s also something interesting about some of the USA300 isolates–they’re resistant to tetracycline. Resistance to this antibiotic is relatively rare in human S. aureus isolates, but it was found in 3 chicken samples–all a molecular type called t2031. The other isolates were resistant to erythromycin, and one was additionally resistant to ciprofloxacin and levofloxacin, suggesting (like the Waters paper) that multi-resistant S. aureus are present in our meat supply. Unfortunately, there’s no information letting us know whether these positive isolates–especially the unique t2031 strains–were from the same brands of meat product, same stores, etc.

So what’s going on here? The authors suggest that human contamination is probably at play here, and that’s quite possible. No ST398 (“livestock-associated”) MRSA has been found yet in published papers examining U.S. meat, though Waters did find ST398 in their S. aureus which were methicillin-susceptible. That suggests that farm-origin Staph can make it through the processing chain, but is human contamination along the line a bigger issue in the U.S.? This is different than the situation in The Netherlands, where they found ST398 MRSA almost exclusively in the meat products they tested. But–the prevalence of humans carrying MRSA in that country is also much, much lower than it is in the U.S., so it may simply be an issue of relative colonization rates (more MRSA in Dutch animals versus their human population, while we may have more in American humans versus our animals–but additional surveillance would be needed to confirm that).

So what we’re left with here is another piece of the puzzle, but one that unfortunately doesn’t yet add a whole lot to the bigger picture.

Bhargava K, Wang X, Donabedian S, Zervos M, da Rocha L, Zhang Y. (2011). Methicillin-resistant Staphylococcus aureus in Retail Meat, Detroit, Michigan, USA Emerging Infectious Diseases : 10.3201/eid1706.101095

MRSA and bedbugs?

An ahead-of-print paper in Emerging Infectious Diseases is generating some buzz in the mainstream media. While the findings are interesting, I’m honestly not sure how they got published, being so preliminary.

Like many areas, Vancouver, British Columbia has seen a jump in the prevalence of bedbugs. After finding impoverished patients infested with the bugs, researchers decided to collect some and test them for pathogens–specifically, methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant Enterococcus (VRE). So, they tested 5 bugs from 3 patients. That’s it–it doesn’t even appear to be 5 bugs apiece, but just 5 total. And the bugs were simply homogenized and streaked–not an uncommon way to test bugs for microbes, but one that has pretty severe limitations if you’re really looking at transmission via biting.

They did find MRSA (and VRE)–obviously, or it wouldn’t have made news. VRE was isolated from 1 bug each from 2 patients; MRSA was isolated from 3 bedbugs from the remaining patient. At first read, I thought they’d confirmed the MRSA strains were USA300, but they didn’t even do that–all they did was note the antibiotic susceptibility profiles of the isolates were consistent with USA300 (though headlines are already screaming “flesh eating bacteria isolated from bedbugs!” as you can see from the link up top). However, what we don’t know if whether the bedbugs were simply externally contaminated (perhaps from close contact with their human hosts), or if they were actually carrying the organisms in their salivary glands (as has been previously reported for S. aureus). If it’s the latter, an infection risk seems more plausible, although I suppose a bite from an externally-contaminated bedbug could also introduce organisms into an open wound.

Still, the paper is really, really, really sparse on data. I’ll sum up with words expressed in the newspaper story above:

Medical health officer Dr. Reka Gustafson said the St. Paul’s study is so small that no public health warning is necessary. She noted the superbug MRSA can be found on “doctors’ ties” and chairs in public places and that it’s more important to counsel people “to wash their hands thoroughly and use antibiotics wisely.”

Lowe CF, Romney MG (2011). Bedbugs as Vectors for Drug-Resistant Bacteria Emerging Infectious Diseases

Epidemiological studies–why don’t people participate?

Maryn McKenna was awesome enough to take some time out of her vacation to blog about our recent ST398 paper, finding “livestock-associated” S. aureus in a daycare worker. She raised one question I didn’t really address previously, regarding our participation by kids and workers at the facility (eight kids out of 168, and 24 out of 60 staff members).

(Staph screening is very non-invasive, by the way; it effectively involves twirling a long-handled Q-tip inside the front of your nostrils. Kinda makes you wonder why families would not have wanted to participate. On the other hand, since Iowa is the pig-growing capital of the U.S., they may have been motivated not to want to know.)

I thought I’d chat a bit about enrollment for this project, since getting people to participate is one of the most difficult parts of these types of studies. First, there really wasn’t any mention of MRSA and swine for this particular study, so I doubt protecting the pig industry was high on anyone’s list for reasons not to participate. However, anytime we do these type of studies, we’re relying on the generosity of individuals in the community–particularly when we didn’t really have participation incentives, as was the case in this project, which was done on a shoestring budget. (We passed out mini hand sanitizer bottles for adults, and had some little toys for the children).

We ran into several challenges for the research which limited our ability to enroll children. Along with a swab, we also had a questionnaire for parents and employees to fill out (as well as a third questionnaire for the director of the facility). For parents and employees, we asked about exposures: did they spend time in hospitals, around animals, at the gym? Had they recently had an infection? etc. For the directors, we asked about cleaning routines at the facility, as well as facility size (number of children and employees). So it wasn’t only the swabs, but also a decent amount of paperwork to fill out when you include the informed consent forms. We also had to do all of this at the facility; because of the way we were sampling, parents didn’t have a chance to take the questionnaire home to fill it out and then return it. So only parents (and employees) who had some spare time during either child drop-off or pick-up really had the chance to participate.

This particular study also started in roughly March 2009–right around the same time as the emergence of novel H1N1. There was a lot of news about the swabs that were taken to test for flu, which are more invasive than regular Staph swabs, so perhaps many potential participants had the mistaken assumption that the swab collection would be more uncomfortable than it really is. (When we were able to swab the child participants, most of them giggled and said that the swab tickled).

Finally, I should note that this facility was one of the larger ones we sampled, and to do this, my grad student returned several times during the day to try and catch parents during common drop-off/pick-up times (and employees who worked different shifts). However, even with this, we certainly missed a number of children and employees, such as those who were part-time and simply didn’t attend or work the day that we were there. We did have higher participation rates at some of the other facilities.

So, I think timing and misinformation–rather than any kind of fear of finding out things they might not want to know–led to our lower participation rate at this facility.