Monday, November 9, 2015

Ebola one year later: an open letter to Robert J. Vickers

Dear Mr. Vickers,

One year ago today I arrived in Sierra Leone where I worked in the Maforki Ebola Treatment Centre in Port Loko. Saturday, November 7, 2015, Sierra Leone was declared Ebola-free. Two incubation periods have passed since the last case of Ebola virus disease (EVD) was diagnosed in that country.

Since returning to the U.S., I have given several presentations on EVD including a presentation to an ethics class at Pacific Lutheran University, a global health class at University of Washington, Tacoma, and, most recently, a presentation at the Washington State Public Health Association annual conference on the experiences of health workers returning to the U.S. after working in Ebola treatment facilities in West Africa. This is an image that I have included in some of those presentations:

On October 31, 2014, the Seattle Times published an opinion piece you wrote titled, Ebola aid workers can't be trusted. In it, you criticized Kaci Hickox and Craig Spencer, two health care providers who had worked in Ebola treatment facilities in West Africa. Craig Spencer is the only person to have developed EVD while being monitored for symptoms of the disease since the Centers for Disease Control and Prevention (CDC) published its guidelines for monitoring people with potential Ebola virus exposure. Dr. Spencer is also the only health worker to have developed EVD after returning to the U.S.

Kaci Hickox
Time Person of the Year 2014

Mr. Vickers, it had been established long before you wrote your article that ebolaviruses are not transmitted by asymptomatic people. It had also been established that at the onset of the "dry" stage of the disease, the stage at which Dr. Spencer presented himself for isolation and treatment, the amount of virus in the blood is usually too low to be detected by polymerase chain reaction (PCR). That is why EVD cannot be ruled out until 72 hours after the onset of symptoms. It is not until the "wet" stage of the disease, characterized by diarrhea and vomiting, that a person with EVD person becomes infectious. This is the reason the CDC has never recommended quarantining asymptomatic health workers who wore appropriate personal protective equipment (PPE) while caring for people with EVD.

Those of us who have worked in Ebola treatment facilities have watched people die from the disease. It is an ugly, painful death. We have also watched people recover from EVD and know that survival is dependent upon aggressive fluid and electrolyte replacement. It seems absurd to me that someone could think that those of us who have seen this disease would jeopardize our own probability of survival or the safety of those around us by ignoring or failing to disclose symptoms of the disease.

I find it ironic that you suggested a comparison between health workers, like me, and Gaëtan Dugas, who was erroneously identified as "patient zero" in the AIDS epidemic. Ironic, because a number of authors have compared the hysteria around Ebola and stigmatization of health workers to the hysteria around AIDS and stigmatization of people believed to be infected with HIV in the 1980s (See Davtyan et al., 2014 and Gonsalves & Staley, 2014). As the authors of Ethics and Ebola: public health planning and response wrote, “Similar to epidemics that have come before, the current Ebola epidemic reveals how social perceptions of infectious diseases can lead to unethical infringement of civil liberties and stigmatization of the ill, those who treat them, and those who otherwise come to be associated with them.”

I am fortunate that I returned to Washington State after working at Maforki. The Washington State Department of Health Guidance for local health jurisdictions regarding follow-up of asymptomatic persons with potential exposure to the Ebola virus is essentially the same as the CDC guidelines. By and large, there were no restrictions placed on my movements. I came home to my wife and son, I went to church where I was warmly received by the congregation that had prayed over me before I left, I went out to dinner with my family, and I spent a week playing with my little boy before I returned to work. If the weather had been warmer, I would have gone for a bike ride. If I had wanted to, I could have gone bowling.

Andrew, Halloween 2015
Many of my colleagues were not as fortunate. One of my colleagues in New York State wrote, “I was escorted out the main doors of the airport by two EMS, two National Guard, two Department of Health workers and two security guards. I felt like a criminal. I was then taken home in an ambulance with a National Guard escort." This was in full view of that person's neighbors. Several of my friends chose to spend three weeks in Europe rather than return to their home states to be unnecessarily quarantined. I have a friend who was harassed by her coworkers when she returned from Sierra Leone, another who was asked not to return to her apartment, and others who were told not to come to their families' holiday celebrations.

Kaci Hickox received a Diploma in Tropical Nursing from the London School of Tropical Medicine and Hygiene. I received a Master of Public Health and Tropical Medicine (MPH&TM) from the Tulane University School of Public Health and Tropical Medicine. Both schools are home to respected virologists who have studied ebolaviruses for decades. I also attended the CDC Safety Training Course for Healthcare Workers Going to West Africa in Response to the 2014 Ebola Outbreak before going to Sierra Leone. Those of us who donned PPE and worked with patients with EVD understand the risks and modes of transmission of ebolaviruses. Only a handful of U.S. health care personnel were infected and none of them transmitted the disease to anyone else.

Neither Kaci Hickox nor Craig Spencer placed the public at risk. The public's trust was betrayed by certain politicians and the media. I have singled you out, Mr. Vickers, not simply because my wife subscribes to the Seattle Times, but because I feel that your comments are representative of the most inflammatory and irresponsible statements I have heard from or read in the media regarding Ebola and the health workers who cared for people with the disease. There are, of course, others who bear greater responsibility for the shameful treatment that many of my colleagues received after sacrificing their time working to bring West African Ebola epidemic to a close. Perhaps worse than the abusive treatment of my colleagues, the stigmatization of health workers and threat of unnecessary quarantine may have dissuaded others from working in the Ebola response.


Matthew Rollosson, RN, MPH&TM

P.S. Couldn't you come up with a more contemporary cliché than Nurse Ratched? Kaci Hickox hadn't been born when the movie One Flew Over the Cuckoo's Nest was released.


I highly recommend reading Dr. Spencer's article in the New England Journal of Medicine (cited below). The following quote, taken from that article, eloquently describes what, I believe, many of us felt while caring for people with EVD:

"Every day, I looked forward to putting on the personal protective equipment and entering the treatment center. No matter how exhausted I felt when I woke up, an hour of profuse sweating in the suit and the satisfaction I got from treating ill patients washed away my fear and made me feel new again."


"Travelers from Sierra Leone entering the United States will continue to be funneled through one of five U.S. airports conducting enhanced entry screening (New York JFK, Washington-Dulles, Newark International, Chicago O’Hare, and Atlanta Hartsfield-Jackson). Travelers from Sierra Leone will continue to have their temperatures taken and answer questions about travel history and possible exposures to Ebola. Travelers will also provide their contact information so that the health department at their destination can connect with them, if needed. Under the modified entry screening, travelers from Sierra Leone with no enhanced risk factors will receive a version of the CARE kit that includes information about Ebola, a thermometer, and contact information for state and local health departments. Travelers will be encouraged to watch their health for 21 days after leaving Sierra Leone and to contact their local health departments if they develop symptoms consistent with Ebola.  Travelers from Sierra Leone will no longer need to be actively monitored by or be in daily contact with their health departments."

Two down, one to go!


Centers for Disease Control and Prevention. (2015). State and territorial Ebola screening, monitoring, and movement policy statements – United States, August 31, 2015. Morbidity and Mortality Weekly Report, 64(40), 1145-1146.

Davtyan, M., Brown, B., & Folayan, M. O. (2014). Addressing Ebola-related stigma: lessons learned from HIV/AIDS. Global Health Action, 7.

Gonsalves, G. & Staley, P. (2014). Panic, paranoia, and public health – the AIDS epidemic's lessons for Ebola. New England Journal of Medicine, 371(25), 2348-2349.

Infectious Diseases Society of America. (2014). IDSA statement on involuntary quarantine of healthcare workers returning from Ebola-affected countries.

Presidential Commission for the Study of Bioethical Issues. (2015). Ethics and Ebola: public health planning and response.

Spencer, C. (2015). Having and fighting Ebola – public health lessons from a clinician turned patient. New England Journal of Medicine, 372(12), 1089-1091.

Vickers, R. J. (October 31, 2014). Ebola aid workers can't be trusted. Seattle Times.

Sunday, August 23, 2015


I've taken a break from writing this blog. I have a couple of posts in the works, but I've put them on the back-burner while I enjoy the warm summer months.

I cut back my hours at work so I have a couple of days every month to take Andrew out and have daddy-and-son time together. Cutting back made a noticeable dent in my paycheck, but it's worth every penny! He and I have been taking a lot of bike rides together. The Scott Pierson Trail isn't as scenic as some of the other rides we take together, but it's not far from our house and we've been riding that trail a couple of times every week. We've gone out to Orting several times on our days out together to ride the Foothills Trail and, on the weekends, we ride the Five Mile Drive at Point Defiance Park (we go around the loop twice for a 10-mile ride).
Five Mile Drive: Andrew gets a nap, Holly gets a couple of toddler-free hours, and I get a work out; everyone wins!

Titlow Park

Titlow Park
Andrew loves going for rides with me, but he has the most fun running through wooded areas.

Snake Lake
Point Defiance Park
China Lake Park
This has been a good year for my pepper garden. This year I have all five of the domesticated species of chilies in my garden: Capsicum baccatum (aji yellow), C. chinense (habanero), C. frutescence (Tabasco), C. pubescens (rocoto), and several varieties of C. annuum (almapaprika, bell, and cayenne). I also have a couple of plants from seeds I brought back from Sierra Leone. I call them "Ebola peppers." I've been perusing a couple of Oaxacan cookbooks (The Food and Life of Oaxaca, Mexico and Oaxaca al Gusto) instead of reading references for this blog and planning what I'm going to grow next year.

Ebola peppers

Okra blossom
There have been a few disappointments this year. My tomatoes got hit with a bad fungus and, although the plants look great, I haven't seen a single pumpkin yet – I think the squirrels are eating them.

It's a lot of work, but Holly and I have created a pleasant space for our family to enjoy. So, please pardon me as I enjoy relaxing on this warm summer afternoon instead of writing about infectious diseases and vaccines.
Holly's piano studio


Sunday, June 28, 2015

Immune responses to vaccines: adaptive immunity

I love summer! I love riding my bike when it's hot. More than that, I love riding my bike with Andrew in tow. Andrew and I recently rode out the Foothills Trail between Orting and South Prairie. We found a little picnic area next to a pond where we feasted on peanut butter sandwiches and homemade cookies and then sat together watching frogs, tadpoles, and dragonflies.

My garden seems to love the hot weather too. I spend most of my weekends working in my garden while neglecting this blog.

One of my reasons to discussing the different types of immune responses to vaccines is to use this as a basis for discussing different types of vaccines, why some vaccines are much more effective than others, why some vaccines require "booster" doses and others do not, and why some vaccines contain adjuvants.

In my last post I gave an overview of innate immunity; skin, mucous membranes, and stomach acid that act as barriers to foreign invaders, complement that tears holes in cells that are not recognized as self, and white blood cells that kill infected cells and others that eat pathogens. Although the goal of immunization is to stimulate adaptive immune responses, antigen-presenting cells, which are part of innate immunity, are integral to adaptive immunity.


Adaptive immunity develops after the immune system encounters a foreign antigen – something that is non-self. One of the most important parts of adaptive immunity is antibodies. As we saw in The Fantastic Voyage, antibodies attach to foreign invaders. Specifically, antibodies attach to antigens. Each antibody attaches to a specific antigen. By attaching to antigens on the surface of a pathogen, the antibody can block the pathogen from attaching to its target cell and prevent it from killing or invading that cell. Antibodies can also help phagocytic white blood cells engulf and destroy a pathogen. For example, a number of pathogenic bacteria are covered with a polysaccharide capsule – they are literally sugar-coated – which protect them from phagocytosis. Antibodies can attach to polysaccharide epitopes, giving the phagocytic cell something to grab onto.

NIAID/Jeanne Kelly
Think of antibodies as keys that fit locks. Each antibody fits a specific antigen. Sometimes the lock is similar enough to another one that a key that wasn't made for it will fit. Antibodies that fit an antigen other than the one it was made for are known as cross-reactive antibodies. Cross-reactive antibodies are beneficial when they attach to pathogens other than the one it was originally made to fit. Cross-reactive antibodies can also be detrimental when they attach to self-antigens, which is what happens in autoimmune diseases.


B-lymphocytes, also known as B-cells, are the workhorse of adaptive immunity. B-cells transform into plasma cells and manufacture antibodies. The surface of B-cells is covered with B-cell receptors (BCR). These are essentially antibodies that are anchored to the cell membrane. Each B-cell receptor is made to attach to a specific non-self antigen, which is known as its cognate antigen; the antigen it "recognizes." Of course, a B-cell cannot see if its cognate antigen is actually attached to a pathogen, so it needs more information before it commits to cloning itself to make enough plasma cells to fight off an attack. One way is when there are many B-cell receptors on the surface of the B-cell engaged with many cognate antigens on the surface of a pathogen. Another is when there is a chemical messenger from other cells that tells the B-cell that there is a battle going on and its antibodies are needed. Sometimes B-cells need some help.


There are a lot of different types of T-cells. For this discussion, I'm just going to talk about helper T-cells. Helper T-cells interact with B-cells in several different ways. A B-cell can enlist the help of a T-cell to determine whether it needs to differentiate into a plasma cell and make antibodies. T-cells can help B-cells make antibodies that are a better fit for the target antigen and they also help with immune memory. Helper T-cells also act as intermediaries between antigen-presenting cells and B-cells; an antigen-presenting cell brings the antigen to a helper T-cell that then attaches to a B-cell to "teach" it to make antibodies to that antigen.

While B-cells "recognize" many different types of molecules, helper T-cells only recognize protein antigens. That means that antibody responses to antigens that are not proteins, like polysaccharides, are T-cell independent; the antibodies do not "fit" as well as those made during T-cell dependent responses and immune memory is not as robust – it takes the immune system longer to remember that it has previously fought a battle with the pathogen and it takes longer to mount an antibody response than with T-cell dependent responses.

Incidentally, the human immunodeficiency virus (HIV) kills helper T-cells. Symptoms of acquired immunodeficiency syndrome (AIDS) appear when there are not enough helper T-cells to fight off opportunistic infections.

Cell-mediated immunity

Helper T-cells that have been activated by antigen-presenting cells can "teach" other types of white blood cells to recognize and kill infected cells. Cell-mediated immunity is one of the reasons live virus vaccines are highly effective.

Again, this is a simple explanation of very complex processes that I plan to use as a basis for discussions on a number of vaccines.

Thanks to all of my readers for 20,000 pageviews!


Kroger, A. T., Pickering, L. K., Wharton, M., Mawle, A., Hinman, A. R., & Orenstein, W. A. (2015). Immunization. In J. E. Bennett, R. Dolin, & M. J. Blaser (Eds.) Mandell, Douglas, and Bennett's principles and practice of infectious diseases, 8th ed. [Electronic version]. Saunders.

Pickering, L. K & Orenstein, W. O. (2012). Active immunization. In S. S. Long, L. K. Pickering, & C. G. Prober (Eds.) Principles and practice of pediatric infectious diseases, 4th ed. [Electronic version]. Elsevier.

Playfair, J. H. L., & Chain, B. M. (2005). Immunology at a glance, 8th ed. Malden, MA: Blackwell Science.

Siegrist, C-A. (2013). Vaccine immunology. In S. A. Plotkin, W. A. Orenstein, & P. A. Offit (Eds.) Vaccines, 6th ed. [Electronic version]. Saunders

Sompayrac, L. (2003) How the immune system works, 2nd ed. Malden, MA: Blackwell Science.

Monday, May 25, 2015

Immune responses to vaccines: innate immunity

After spending most of the weekend working in my garden, I spent today relaxing, barbequing, and spending time with my family.

Andrew and my garden
Right to left: Andrew, his Grandpa Esvelt, and his Uncle Seth
I don't know about you, but I remember very little about the human immune system from grade school and high school. I remember that white blood cells eat (phagocytize) bad stuff and I remember Raquel Welch being attacked by antibodies in The Fantastic Voyage (Maybe you're not that old).

Of course, I learned more about the immune system in nursing school and in my postgraduate curriculum. A lot of what I've learned about the immune system is from my reading about the pathology and pathophysiology of malaria. Like a lot of other diseases, many of the symptoms of malaria are caused by immune responses to the infection. As I mentioned in my post on hepatitis, hepatotropic viruses themselves do not damage the liver. The damage is caused by immune responses that kill infected liver cells.

The immune system is much more complex than phagocytic leukocytes (Greek: phagō, to eat; leukos, white; kytos-, cell) and Raquel Welch. In fact, immunity is mediated through several systems that work together. White blood cells not only eat invading pathogens and secrete antibodies, they also produce chemical messengers like interleukins that mediate inflammation and other cytokines that mobilize other white blood cells. There are also dozens of different types and subtypes of white blood cells that perform different functions.

There is no way I can adequately discuss all of the intricacies of the subject of medical textbooks. My purpose is to introduce some of the major players in immune responses to diseases and vaccines. I started writing this several weeks ago and got bogged down in too many details, so I'm going to start with innate immunity and save adaptive immunity, that is, why we give vaccines in the first place, for a later post.

Self versus non-self

The first priority of the immune system is recognizing "self" from "non-self," that is, anything that isn't part of our bodies. There are molecules on the surface of cells that are used by the different components of the immune system to identify those cells as self. Likewise, there are molecules on the surfaces of pathogenic organisms that the components of the immune system recognize are non-self. Cells that are infected with certain pathogens will place those molecules on their surface to target themselves to be killed to prevent other cells from being infected.

Innate immunity

Innate immunity refers to non-specific mechanisms the body uses to protect itself from infection. Skin, mucous membranes, and stomach acid are barriers that prevent pathogenic organisms from entering the body. Complement is a system of proteins that, among other things, tears holes in cells that are not recognized as self. The aptly-named natural killer cells (NK) kill cells that are infected with viruses and some type of tumor cells.

Phagocytic cells like macrophages ("big eaters") and dendritic cells are antigen-presenting cells (APCs). They are part of the innate immune system, but they perform an essential function in mobilizing adaptive immune responses. Most cells use major histocompatibility complex (MHC) molecules to "present" part of proteins found inside of the cell on its surface. It allows specialized white blood cells to "see" what's happening inside of the cell. MCH proteins on cell infected with viruses present viral antigens on the cell surface. This allows NK cells and cytotoxic lymphocytes (CTL) to target the cell for destruction. Antigen presenting cells use MHC molecules to present proteins to white blood cells that are part of the adaptive immune system.

Inflammation is another innate response to injury or infection that stimulates adaptive immune responses.

Antigens are foreign substances that cause antibody response. Allergens are a type of antigen. An antigen may have several epitopes, which are areas on the molecule to which antibodies can attach. For example, an influenza virus has several antigens on its surface including hemagglutinin, neuraminidase, and M2 ion channel. Influenza vaccines use epitopes or "antigenic sites" of the hemagglutinin head to stimulate production of antibodies that will attach to that part of the virus. Unfortunately, the hemagglutinin head changes shape (antigenic drift) so that antibodies to those epitopes will not bind to the antigen. Some researchers have suggested using epitopes on the hemagglutinin stalk or on the M2 ion channel as vaccine antigens.
CDC, 2014

Next: adaptive immunity.


Kroger, A. T., Pickering, L. K., Wharton, M., Mawle, A., Hinman, A. R., & Orenstein, W. A. (2015). Immunization. In J. E. Bennett, R. Dolin, & M. J. Blaser (Eds.) Mandell, Douglas, and Bennett's principles and practice of infectious diseases, 8th ed. [Electronic version]. Saunders.
Pickering, L. K & Orenstein, W. O. (2012). Active immunization. In S. S. Long, L. K. Pickering, & C. G. Prober (Eds.) Principles and practice of pediatric infectious diseases, 4th ed. [Electronic version]. Elsevier.
Playfair, J. H. L., & Chain, B. M. (2005). Immunology at a glance, 8th ed. Malden, MA: Blackwell Science.
Siegrist, C-A. (2013). Vaccine immunology. In S. A. Plotkin, W. A. Orenstein, & P. A. Offit (Eds.) Vaccines, 6th ed. [Electronic version]. Saunders.
Sompayrac, L. (2003) How the immune system works, 2nd ed. Malden, MA: Blackwell Science.