Zika & Wolbachia II: Disease transmission

    I am back. I had some business to take care of, and then of course there was another visit to spend time with my nephew and fulfill my duties as a new aunt. But I am here and excited to resume our conversation about Zika.

    The first part of the Zika and Wolbachia story morphed into a biography of Wolbach, for whom Wolbachia was named. I provided a teaser about recent research that suggests Wolbachia can reduce Zika transmission by mosquitoes. But I didn’t actually talk about Zika at all, and even though it’s only been a short time (~4 weeks) several new Zika stories have come out. Lucky for us, scientists world-wide are ramping up their efforts to understand Zika, and continue research on other diseases like Ebola, which remain important even when not in the spotlight (ideally congress would agree).

Aedes aegypti (Image credit: James Gathany, Center for Disease Control and Prevention Public Health Image Library)

   In 2009, a group of 17 scientists from Australia and Brazil published a study showing that when the mosquito Aedes aegypti is infected with particular strains of Wolbachia, the mosquitoes were less competent disease vectors, and could reduce transmission of diseases such as dengue, chikungunya, and Plasmodium (malaria) (Moreira et al. 2009). Let's put this in perspective, 85 years after Wolbach and Hertig first discovered Wolbachia in a mosquito in Boston (Culex pipiens), and after decades of Wolbachia research resulting in hundreds of publications that have little to do with humans and disease transmission, scientists discovered that Wolbachia could reduce the number of humans contracting deadly viruses. If this is not a solid argument for exploratory research then go fishing. Listen in, and we will see how it works. But first, there are several pieces of information that will help you follow the story: 1) The three main players are mosquitoes, Wolbachia bacteria, and Drosophila fruit flies, 2) There are over 3500 species of mosquitoes and only a handful carry diseases (a.k.a disease vectors), 3) Some mosquito species carry one disease, some carry many diseases, most carry no diseases, 4) The main species of mosquito that carries dengue, chikungunya, and Zika is Aedes aegypti, which is not typically infected with Wolbachia in the wild, and 5) Wolbachia is a genus of bacteria comprising many different types/strains that infect a variety of different insects. The most well-studied strains of Wolbachia are from the model organism Drosophila melanogaster, a fruit fly we will inevitably revisit in future posts.

Drosophila melanogaster: Illustration by Katy Wiedemann (Wiedemann Illustrations)

    Moving on. Methods to reduce the number of humans contracting diseases carried by mosquitoes focus on prevention, either through the development of vaccines or use of bug spray to prevent mosquito bites. The other option is to try and get rid of mosquitoes. Methods of reducing mosquito populations include spraying copious amounts of DDT into houses with growing children, and introducing copepods that eat mosquito larvae.

     

    Between 2000 and 2008, data from several labs coalesced on a different kind of preventive method. By infecting A. aegypti mosquitoes with certain Wolbachia strains isolated from the fruit fly D. melanogaster, the life span of A. aegypti was reduced. From the perspective of limiting disease transmission, this is good because many mosquitoes die before they can transmit disease. At the same time, another group of scientists studying Wolbachia in D. melanogaster found that certain strains were beneficial to D. melanogaster individuals that had harmful insect viruses such as Drosophila C virus, Flock House virus, and Cricket paralysis virus.

    In 2009, Moreira and colleagues put these two things together and hypothesized that Wolbachia infected mosquitoes would be less effective disease vectors. The idea was to test whether A. aegypti mosquitoes infected with Wolbachia from D. melanogaster fruit flies would reduce disease transmission. The answer was yes. The authors showed that A. aegypti with Wolbachia are resistant to several diseases, which prevents the mosquito from being able to pass the diseases onto the next human they bite. The mechanism for how this works remains unclear. The authors suggest it has something to do with how the mosquito immune system reacts to the Wolbachia bacteria, but no direct link was found. The other possibility is that there is competition for resources between the disease and Wolbachia in the cells of the mosquito, and Wolbachia outcompetes the disease. But no conclusive evidence has been presented to support either hypothesis. Regardless of the mechanism, it is clear that Wolbachia infected mosquitoes offer a two-pronged approach for controlling disease transmission: they have a shorter life-span and they show resistance to several different diseases. As a result, non-profit groups such as Eliminate Dengue Program are using this approach to slow the spread of dengue (and other diseases) in multiple locations around the world.

Eliminate Dengue Program

    That was the status of things before the spread of Zika skyrocketed last year, and was declared a Public Heath Emergency of International Concern (PHEIC) on February 1st, 2016. Scientists were quick to react and on June 8^th, 2016, six Brazilian researchers published the results of a study demonstrating the effectiveness of Wolbachia to block two Zika strains currently being transmitted by A. aegypti mosquitoes in Brazil (Dutra et al. 2016). The release of Wolbachia infected mosquito eggs and adults is currently underway in Brazil and scientists are optimistic about the spread of the Wolbachia in Brazilian A. aegypti populations. All of this is very recent but at present it appears to be good news for humans, science, and exploratory research.

   Exactly how Wolbachia spreads in insect populations is an intriguing topic we will investigate next time. It is based on decades of exploratory research covering many different Wolbachia strains in many different types of insects.

Life

   Life caught up with me these last two weeks so I will have to continue the Zika & Wolbachia miniseries in the next post.

Logo credit

   On Saturday I had the pleasure of participating in a BioBlitz at Cabrillo National Monument in San Diego, CA. This event was part of the National Parks BioBlitz series to celebrate the 100^th anniversary of the National Parks System. What is a BioBlitz you ask? A BioBlitz is a 24-hour survey of the plants and animals that live in a defined area. Scientists specializing in everything from plants to mammals, birds, and insects convene and document their findings as a series of observations. While the goals of a BioBlitz are to document the biodiversity of a given area, they also serve to introduce the public to the flora and fauna of a specific place. Could a BioBlitz be conducted in your backyard? Definitely.

   During Saturday’s BioBlitz I was a member of the invertebrate team and helped survey for insects, primarily beetles. For entomologists, the BioBlitz can be a time consuming process. Unlike ornithologists that document sightings with photographs and can usually provide species identifications on the spot, entomologists need to collect and curate their specimens before identifications can be made. I collected throughout the day and sorted and pinned my specimens by 9pm. At 9:10pm I was running out of gas at a time when I needed it most, to start identifying. Do I sound like I am complaining here? I may be - just a little. The main reason is that identifying insects can be extremely time consuming. While there are some entomologists that invest huge amounts of time becoming familiar with the insects of a given region, this is often a thankless effort. And thus, people with this level of expertise are few and far between. Would I like to be one of these people? Yes. Do I have the time it takes to accomplish this? No. One of the reasons I don’t is because, unfortunately, these efforts are not often valued by employers and granting agencies. As a youngish scientist I invest my time collecting data for projects that have a chance of getting funded and being published in high profile journals. I do this to keep my scientific career afloat. I am a little torn about this method of prioritization, and have set a goal to invest at least a few hours every week (or two) with the beetles in my backyard.  

   I am not the only one that finds this upsetting, not to mention detrimental to scientific research in general. This was brought to my attention most recently by an article in Scientific American highlighting the loss of natural history courses at colleges and universities. Natural history classes such as botany (plants), entomology (insects), ornithology (birds), ichthyology (fishes), and herpetology (amphibians and reptiles), provide students with the nitty gritty of a specific group of organisms, an overview of their diversity, and how to identify them. The level of identification expertise is usually broad, but provides the foundation for continued refinement. The article highlighted the findings of a recent study published in BioScience that revealed that while over 90% of scientists agreed that natural history was important to their field, young scientists felt under prepared in this area.

   What does a frustrated entomologist do? Tell stories and find a way to communicate the relevance of a name, a species description, and a sound identification.

   I am also a newly minted aunt. Much of my time in the last two weeks has been devoted to my sister and brother-in-law during the birth of my nephew, Matteo Karolos Castañeda. I could not be more proud.

Zika & Wolbachia I: Wolbach

   “‘It was just curiosity-based work, total serendipity’ Dr. O'Neill said.” (Carl Zimmer quoting Dr. Scott O'Neill in his article Bacteria-Infected Mosquitoes Could Slow Spread of Zika Virus published in the New York Times May 4, 2016)

   Can I quote a quote? I did, and hopefully I provided enough citations to make it legit. I know it is not wise to try and out-zimmer Carl Zimmer but there is so much to write about here I am going for it. This quote encompasses the mission of this blog (**although - see my commentary below) and is a great example of the return on our investment in curiosity. In this case, the return is slowing down the spread of Zika and other diseases transmitted by insects using Wolbachia, an insect bacterial parasite. The reason we know about Wolbachia, and its potential to reduce the spread of viruses like Zika, is because of public and institutional support for unbridled curiosity. The Wolbachia-Zika story is part of a decades long history of research on Wolbachia that goes back to 1924.

   A brief introduction. As with last week and Ebola, Wolbachia has been covered extensively. And while there is not as much known about Zika, there are many articles describing what has been discovered thus far. We will establish a basis for the underlying biology and go from there. Wolbachia is a genus of bacteria (unicellular organisms that have all of the machinery necessary to replicate themselves). While not harmful to humans, Wolbachia live within the cells of insect hosts. Zika, on the other hand, is a virus that infects humans and has been linked with microcephaly in infants. Like Ebola, and all other viruses, Zika does not have the cellular machinery to replicate itself and must co-opt the machinery from the cells of an infected host. How are Wolbachia and Zika linked? To understand that we need to take a closer look at decades of work by a long list of scientists, including Scott O'Neill, that began in 1924 when Hertig and Wolbach first discovered (and which Hertig later named) Wolbachia.

Image credit: Seth Bordenstein (from EOL). Image description: Insect testes showing sperm DNA (red) and Wolbachia endoysymbionts (green).

   If we start from the beginning, however, I think we will need to break this up into multiple posts, which is okay. There is plenty here to keep us all fascinated. Today we will start with Simeon Burt Wolbach, after whom Wolbachia was named, and based on what I have seen so far he is deserving of his own post. Here is an excerpt from a tribute published in the Harvard Medical School Alumni Bulletin:

“S. Burt Wolbach, one of Harvard Medical School's most beloved as well as one of its most distinguished professors, died on March 19, 1954, in his seventy-fourth year, after a relatively brief illness, of cancer of the prostate. In the minds of many, both his scientific achievements and his personality present a perfect synthesis of the best in the past and in the present. Sound training in morphology, guided by imaginative insight, made it possible for him to place new and fruitful interpretations upon cellular structural mechanisms. In his personality too, one was aware of that blend of conventional and liberal attitudes, an appreciation of the traditions of the past and the freedoms of the present. Thus his stature, [equaled] by few, resulted from that rare integration of the austerity and vision of the scientist with the humanity and warmth of the guide and teacher. His name will be remembered with a lift of the heart and a quickening of the imagination by student, colleague and friend.” (Dr. Charlotte L. Maddock and Dr. Arthur T. Hertig (1954) Harvard Medical School Alumni Bulletin 28: 41-45).  

Figure 1 from Hubbard (1987). Figure caption: "S. Burt Wolbach, circa 1938. Etching, 300 x 251 mm, by Arthur Heintzelman (1891-1965)."

   Simeon B. Wolbach was a polymath (much like my beloved Schrank) growing up riding horses on the plains of Nebraska “…ranging free with the cowboys…..” in the late 1800s, and graduating cum laude from Harvard Medical School in 1903. Wolbach subsequently held a variety of esteemed posts at various institutions on the east coast where he pursued research in two fields of study, infectious disease and vitamin deficiency. The diseases he worked on included both viral (i.e influenza and Rocky Mountain spotted fever) and bacterial (tuberculosis, leprosy, syphilis, and typhus) pathogens. In fact, it was his work on typhus that led to the discovery of Wolbachia. While Wolbach’s work on disease transmission is the most relevant to this blog post, some think “[h]is most brilliant work was done on those disorders associated with vitamin deficiency and excess.” Among other distinctions, the quality and breadth of Wolbach’s research granted him induction to the National Academy of Sciences in 1938.

  The language used to describe Wolbach’s character is cryptic and intriguing. It outlines a person of genuine character that embodied both seriousness and a sound sense of humor. His lecture style was described as non-didactic, but his students clearly revered him as was demonstrated by two separate instances where they paid him tribute by coming to lecture with a red carnation in their lapel, something Wolbach did on a regular basis. While perhaps a tough nut to crack, it seems that upon cracking a plethora of goodness was exposed. He remained an avid outdoors-man through his academic pursuits and continued riding horses throughout his life. “It was there, along the banks of the Jeannotte River and Lac Castor, that his friends knew him best. There he became a boy again and would engage in an impromptu canoe race, or chase a moose in the lake until he could smack its rump with a paddle.” (All quotes from the previous two paragraphs are from the Maddock and Hertig tribute referenced above.)

   I could go on, and am surprised a more detailed biography of Wolbach has not been published. When I started looking for one I actually found that in addition to all of the accomplishments listed in the Harvard Medical School tribute, Wolbach appears to have written a biography of Hans Zissner, a physician, bacteriologist, and author of Rats, Lice, and History. !!. The more I find the more I am intrigued by these scientists, what amazing stories. I literally have about 20 tabs open in my web browser right now.

   I found an example of Wolbach’s non-didactic delivery method, combined with the foresight of a complex mind, in this passage from “The Glorious Past, the Doleful Present, and the Uncertain Future of Pathology”, a presentation he gave on Harvard Alumni Day in 1952 (his last public presentation) that was subsequently published in the Harvard Medical School Alumni Bulletin 28: 41-45:

“What do I mean by the Science of Pathology? Years ago, challenged by Theobald Smith, I defined Pathology as that branch of Biology which investigates the reactions of living things — unicellular to man — to injurious agents. Deleterious environments of all sorts are productive of pathological states and a super Darwin become pathologist would, I believe, have a grand time in attacking problems of phylogenesis from the viewpoint of a pathologist. The scientific use of the imagination is legitimate and I get satisfaction in believing that the adaptation of marine creatures to terrestrial conditions was the result of eons of responses in myriads of survivors of non-lethal injuries.”

I will give you, and myself, some time to ponder this and we will pick-up here next time.

PS **My issue with this quote, and this is my opinion only, is that the tone highlights an ongoing problem we all have of downplaying the importance of exploratory research. I do not know Dr. O'Neill and I want to make it clear that I am not slighting him; he and his colleagues have done amazing work, which we will look at next time. In all honesty, I think the quote reflects Dr. O'Neill’s humility while talking about his own research. But I am going to go all Sheryl Sandburg on this right now. I think we need to lean in to the immense impact of exploratory research. I think scientists, myself included, need to be careful about downplaying the importance of exploratory research. When I first read Dr. O'Neill’s quote I thought, bingo, perfect for the blog, and retweeted it. It wasn’t until I was typing it out for this post that I picked up on the tone, and thought about how much language can impact public perception. If we want curiosity driven research to be understood and funded by the public we need to be proud and put it on the pedestal it deserves. The same is true when we talk about taxonomy and natural history museums, which I have written about before. If we want our taxonomists to be rock stars and our museum collections respected, we cannot refer to them as a bunch of dead insects. Which happens, from places we should least expect it.

 

Again, I don't mean to diss anyone here, just highlighting the need to be more aware (and UConn got $500k, not $500).

Ebola, evolution, and the role of phylogenies

   As an evolutionary biologist I love phylogenies. Or, I love phylogenies so I became an evolutionary biologist. Except I did not always know what a phylogeny was. A phylogeny is similar to a family tree except we usually have to infer who the ancestors were. To do this, we collect and study present-day organisms and use the data to reconstruct what happened millions of years ago. In the end we are left with an illustration of relationships, a phylogeny, which gives us an idea of who is more closely related to whom. Are beetles more closely related to ants or cockroaches? Ants. Are pine trees more closely related to kelp or moss? Moss. In fact, there is a huge push to understand what is called the Tree of Life – a phylogeny that includes all the major extant (living) organismal lineages. An updated version was recently published and did a nice job of putting humans in our place. We are not as big of a deal as we like to think, evolutionarily speaking - we are merely a small nubbin on the twig of ‘Eukaryotes’.

Recently published phylogeny of the Tree of Life (Hug et al., 2016)

   Understanding phylogenetic relationships gives us a foundation to test hypotheses and tease out answers about how our world works. The information we retrieve tells us that birds are actually dinosaurs, neanderthals exchanged genes with humans, and that immune systems can evolve under pressure from viruses and other pathogens.

 

   That's where we are going today - using phylogenies to unpack the evolutionary dynamics of one-up-man-ship between a virus and the host immune system. The plan is to delve deep into stuff that will make you say, wow. First, a little background. I am not going into great detail about Ebola as this has been extensively covered. Briefly, Ebola is a filamentous virus, categorized as a filovirus, which infects humans (and other mammals) resulting in viral hemorrhagic fevers that can be fatal. In addition to researching treatment and vaccine options for Ebola, scientists are conducting research to understand how the virus ‘jumps’ from a non-human host to humans (a.k.a a spillover event). To do that, we first need to figure out what that non-human host is. Based on data showing remnants of filoviruses in fruit-eating bats and insect-eating bats, many researchers are focusing on bats as a likely reservoir. Of course there are many questions making this is an active area of research. One of those questions, investigated by Ng et al. (2015), is: how come bats do not seem susceptible to Ebola and other filoviruses? The short, brief, and tractable answer of the Ng et al. study is that some bats have a genetic mutation in the protein filoviruses use to bind to and infect the bat’s cells. It would be like playing a game of Pac-Man where the ghosts have gone wild and the only way Pac-Man can stay alive is by having a mutation that prevents the ghosts from recognizing him. Did I just date myself? Or, let’s try this analogy. Hackers recently found a way to generate ‘universal keys’ allowing them to break into cars with keyless entry systems. This would be our virus hacker, breaking into cars using sophisticated biochemical tactics. But, let’s say there is one type of car (the new Tesla Model 3?) that has changed its keyless entry system so it is no longer susceptible to hacking. The virus hacker tries its key against the lock but it doesn’t work. Now, of course, people with the resistant car are more likely to keep their cars in this hacking environment, and the desire to have this car spreads and they become more and more frequent. Tough luck for the hacker.

   And this is what Ng et al. (2015) found. The mutation that prevents Ebola virus from attaching to the bat’s cells is under positive selection, meaning that its frequency in the population increased rapidly relative to other genes. When researchers find evidence of positive selection it lends further support to the idea that something important is happening. Interestingly, Ng et al. found that not all bat species had the mutation.

   In walks the bat phylogeny. Bats are a diverse group of flying mammals with over 1200 species that live in many different habitats all over the world. 

Townsend's big-eared bat (Corynorhinus townsendii), a nice picture of a bat but not one included in the study by Ng et al. (Image Credit)

   If we want to understand disease dynamics, and how and why some bats have the mutation and others don’t, we can use the phylogeny as a forensic tool to reconstruct how resistance evolved. We can ask questions like: are bats with the mutation close relatives? Did they inherit it from an ancestor? Or, did the mutation evolve multiple times in different bat species? And, due to the innate curiosity of humans, there are phylogenies for lots of different animal groups, including bats. In 2007, Miller-Butterworth and colleagues put together an impressive genetic data set (over 11,000 base pairs of DNA) to essentially go back in time and figure out how different types of bats are related to each other. It is important to point out here that our estimates of phylogenetic relationships are just that, estimates. The reason is that any given phylogeny is a hypothesis, our best estimate given the data available. For a long time, biologists relied on morphological data to figure out who was most closely related to whom. Evidence of close relationship was inferred if two species shared a trait that was presumably inherited from a common ancestor. But you can imagine how this might lead to spurious relationships. Just because both bats and birds have wings, it doesn’t mean they are close relatives. We know from studying the morphology underlying bird and bat wings that these animals did not inherit wings from a common ancestor, they each evolved them independently; thus, it would be a mistake to infer they are close relatives because they both have wings. In the past few decades, researchers have been able to rely more heavily on genetic data to infer relationships. And while these data have their own set of problems, they provide an additional perspective to consider alongside morphological data. As new technologies are developed and our ability to accumulate more data improves, our phylogenies are continuously updated and remain dynamic. This may frustrate many students in introductory biology classes, but underscores the importance of understanding the process and history of scientific data collection and hypothesis testing.

  

   Back to bats. What Ng and colleagues found when they combined their data with the bat phylogeny was that the mutation preventing filovirus infection evolved once about 25 million years ago, and was passed down to descendant lineages. The researchers interpreted these results as evidence that bats have been evolving alongside filoviruses, and for much longer than previously thought. But what do we know about hackers that we should be thinking about here? They evolve too. Just because the Model 3 may be resistant to hackers now, the hackers are not going to sit idle and find another means of making a living. The hacker tactics will shift and evolve to overcome new car-locking technology. And Ng et al. found evidence of this happening between bats and Ebola too. What they see is multiple mutations with a signature of positive selection, which they suggest results from counter-attacks by the virus. In other words, the virus sees the bat mutation and raises it a mutation of its own. It is an arms race. Between the virus and its host. Between the hacker and the car company. It is known as the Red Queen Hypothesis (coined by Leigh Van Valen in 1973) and that is a story for another day.

“Now, HERE, you see, it takes all the running YOU can do, to keep in the same place.” (Lewis Carroll, Through the Looking Glass)

  P.S. There is a nice podcast on TWiEVO discussing the Ng et al. (2015) paper with some of the authors of the paper.

Schrank update

 

“Franz von Paula Schrank was a polymath in the true sense of the word.” (Edmund Launert)¹

   We first met Schrank back in February during our discussion of parasites and swellable microneedle adhesives. I promised to come back to Schrank, and I think about him often enough that I did not forget. Instead of going to the Stanford library, I submitted an interlibrary loan request for Annette Zimmerman’s biography on Schrank (Franz von Paula Schrank (1747-1835): Naturforscher zwischen Aufklärung und romantic) and got it over a month ago. 

 

Title page and table of contents of Zimmerman's biography on Schrank

And there it is, sitting on my kitchen table, filled with rich information on Schrank that I cannot read because I don’t speak German. It calls out to me on a daily basis (in English), taunting me to read it and learn about Schrank. I will have to return it soon, unread. (I am open to ideas for efficient translation to English if you have them.) Several of his publications have also been scanned by the Biodiversity Heritage Library and are available to read. But not only are these also in German, the intricate script makes it difficult to decipher the letters.

   I did track down a review of Zimmerman’s biography, written in English by Edmund Launert, by means of a second Interlibrary Loan (thank you UCSD library).¹ It is not a substitute by any means, but in combination with what is available from the Catholic Encyclopedia², it gives us a little information to fly with. Schrank was by all means a polymath, someone who is skilled and experienced in a variety of different subjects (not just math – the Greek translation of polymath is “having learned much”, derived from the Greek work ‘manthánein’). Schrank is on the list of Roman Catholic cleric-scientists and fulfilled the duties of priest, and professor of botany and zoology. While this may sound unusual to us given current perspectives of an oft-assumed divide between science and religion, this was very common historically, especially in 1774 when Schrank was ordained as a priest. Other notables on the list you may be familiar with are Nicolas Copernicus (mathematics and astronomy - a few hundred years before Schrank) and Gregor Mendel (genetics – a hundred years after Schrank). At age 15, Schrank became a Jesuit, a Catholic religious order well known for many things (good and bad) including its contributions to science. He was born into a well-respected family in Munich, Germany and started his studies at the Jesuit College of Passau when he was 9. 

   His interest in the natural world was inspired by Father Sluha (Szluha is the native spelling) when Schrank was a budding Jesuit student at Oedenburg collegium in Hungary. Father Sluha had been a Jesuit missionary in Brazil until he was put in a Portuguese jail when the Jesuits were expunged from Brazil in 1759.² There is very little known about Sluha, and another source (McKinley³) (who, unlike me, could read German) reported that Zimmerman was not able to find much out about Sluha when she was working on her biography of Schrank. Presumably, the idea is that as a missionary in Amazonian Brazil (1753-1760) Sluha acquired or refined his skills as a naturalist (probably focusing on botany), and opened the door of natural history to the young Schrank. Just to be clear, I am speculating on this, but the idea is not that far-fetched.

   Schrank was a Jesuit teacher until 1773 when the Jesuit religious order was repressed and abolished by Pope Clement XIV, the year before Schrank was ordained and received his doctorate in Theology. He started his academic career as a professor of mathematics and physics in 1776 at Amberg, and was a professor of botany, agriculture, mining, forestry, and zoology at the University of Ingolstadt starting in 1784 (with a subsequent move to Landshut). Schrank published his first scientific study (of over 40) during this time (Beiträge zur Naturgeschichte - Contributions to Natural History - in 1776). While many of Schrank’s publications were focused on natural history (botanical, zoological, and entomological), he also published papers in the fields of physics, chemistry, agriculture, travel, geology, mineralogy, theology, and poetry. Are you kidding me? And, all of this is inaccessible to me because it is written in German. An unfortunate outcome of growing up monolingual.

   In 1809, Schrank was appointed to be the first Director of the München Botanical Garden. His influence there was described by Stafleu & Cowan⁴ as follows: “The present state of the garden bears out Schrank’s early and wise judgment” (p. 325). In the same text, he was attributed with the quote: “Man würde weniger deräsonniren, wenn mann über nichts räsonnirete, was man nicht versteht.” When I type this into Google translate I get “One would less deräsonniren when man räsonnirete about anything you do not understand”, which is not super helpful. So I asked a German colleague of mine for help and he responded: “Hehe, ‘deräsonieren’ appears to be a word creation by the author. It means: the opposite of ‘reasoning’, maybe unreasoning, or reasoning in an unreasonable way.” I love this, he made up a word for something I can barely wrap my head around. But, essentially, he seems to be saying: One would have fewer mental issues if one did not speculate on things one does not know about. Seems like a good idea. My German colleague referred me to a similar quote from a German comedian, Dieter Nuhr: "Wenn man keine Ahnung hat, einfach mal die Fresse halten". Consider to shut up if you don’t know what’s going on. I don't think there is a moral here but thought it was interesting.......

München Botanical Garden (Image credit: Diego Delso)

¹E.E. Launert (1983) Natruforscher zwischen Aufklarun und romantic. Archives of Natural History 11: 362-363.

³ J. Stein (1912) Franz Paula von Schrank. In The Catholic Encyclopedia. New York: Appleton Company. Retrieved April 7, 2016 from New Advent:

² D. McKinley (1992) Adrien Lebreton, S.J. (1662-1736): A search for the identity of a neglected botanist in early Martinique. Huntia 8: 155-162.

⁴ F.A. Stafleu & Cowan, R.S. (1985) Taxonomic literature, a selective guide to botanical publications and collections, with dates, commentaries and types. 2ed. Vol. 5 (Sal-Ste) p. 323-325.