New publication: Environmental and Household-Based Spatial Risks for Tungiasis in an Endemic Area of Coastal Kenya
New publication! I started working on this cool project on tungiasis (jiggers) with colleagues in Kenya and Japan way back in 2014. Today, I am happy to say that after much ado our work has finally seen the light of day, thanks to Nagasaki PhD student (and soon to be Dr.) Ayako Hyuga. It appears today in the journal Tropical Medicine and Infectious Disease (MDPI).
Environmental and Household-Based Spatial Risks for Tungiasis in an Endemic Area of Coastal Kenya
“#Tungiasis is a #cutaneous #parasitosis caused by an embedded female sand flea. The distribution of cases can be spatially heterogeneous even in areas with similar risk profiles. This study assesses household and remotely sensed environmental factors that contribute to the geographic distribution of tungiasis cases in a rural area along the Southern Kenyan Coast. Data on household tungiasis case status, demographic and socioeconomic information, and geographic locations were recorded during regular survey activities of the Health and Demographic Surveillance System, mainly during 2011. Data were joined with other spatial data sources using latitude/longitude coordinates. Generalized additive models were used to predict and visualize spatial risks for tungiasis. The household-level prevalence of tungiasis was 3.4% (272/7925). There was a 1.1% (461/41,135) prevalence of infection among all participants. A significant spatial variability was observed in the unadjusted model (p-value < 0.001). The number of children per household, earthen floor, organic roof, elevation, aluminum content in the soil, and distance to the nearest animal reserve attenuated the odds ratios and partially explained the spatial variation of tungiasis. Spatial heterogeneity in tungiasis risk remained even after a factor adjustment. This suggests that there are possible unmeasured factors associated with the complex ecology of sand fleas that may contribute to the disease’s uneven distribution.” #environmental #kenya #NTD #NeglectedTropicalDisease #parasitology #globalhealth #publichealth
New publication: An urban-to-rural continuum of malaria risk: new analytic approaches characterize patterns in Malawi
12 years in the making! Our new paper from partners at the University of Michigan and the #Malawi College of Medicine on new approaches to defining urban and rural environments in the context of malaria risk is now out in #Malaria Journal.
It was the last chapter in my dissertation to be published (all the rest were published when I was still in grad school.)Short version: malaria is complicated and really local. Malaria transmits poorly in urban and environments and well in rural environments. There’s urban like spaces in “rural” areas and rural-like spaces in “urban” areas, demanding a more nuanced view of what those terms really mean.
We know that malaria is a “rural” problem, but not all “rural” spaces are the same. Even in the country, there are “urban like” spaces and in “rural like” spaces even in the largest cities in Sub-Saharan Africa. Could those spaces impact malaria risk? If so, shouldn’t we redefine what we mean by urban vs. rural to inform intervention strategies to better target resources?
Here, we combine GIS and statistical methods with a house to house malaria survey in Malawi to create and test a new composite index of urbanicity and apply that to create a more nuanced risk map.
The urban–rural designation has been an important risk factor in infectious disease epidemiology. Many studies rely on a politically determined dichotomization of rural versus urban spaces, which fails to capture the complex mosaic of infrastructural, social and environmental factors driving risk. Such evaluation is especially important for Plasmodium transmission and malaria disease. To improve targeting of anti-malarial interventions, a continuous composite measure of urbanicity using spatially-referenced data was developed to evaluate household-level malaria risk from a house-to-house survey of children in Malawi.
Children from 7564 households from 8 districts in Malawi were tested for presence of Plasmodium parasites through finger-prick blood sampling and slide microscopy. A survey questionnaire was administered and latitude and longitude coordinates were recorded for each household. Distances from households to features associated with high and low levels of development (health facilities, roads, rivers, lakes) and population density were used to produce a principal component analysis (PCA)-based composite measure for all centroid locations of a fine geo-spatial grid covering Malawi. Regression methods were used to test associations of the urbanicity measure against Plasmodium infection status and to predict parasitaemia risk for all locations in Malawi.
Infection probability declined with increasing urbanicity. The new urbanicity metric was more predictive than either a governmentally defined rural/urban dichotomous variable or a population density variable. One reason for this was that 23% of cells within politically defined rural areas exhibited lower risk, more like those normally associated with “urban” locations.
Are dogs associated with infections by a skin burrowing flea in Kenya? Masanobu Ono and I with Kensuke Goto, Satoshi Kaneko, mwatasa Changoma just published a paper on #tungiasis in the journal Tropical Medicine and Health.
Most people haven’t heard of tungiasis, an ectopic skin disease caused by the skin burrowing parasite, T. pentrans. It causes itching, pain, is associated with serious secondary bacterial infections, gangrene, social exclusion and debilitation. It primarily afflicts the very young and very old and is found almost exclusively in the poorest parts of the poorest parts of the world. It fits the classic definition of a neglected tropical disease.
We explored associations of wildlife and domesticated animals with household level tungiasis in Kenya using a two stage complex sampling based survey in an area adjacent to a wildlife preserve.
Tungiasis is a ectopic skin disease caused by some species of fleas in the Tunga genus, most notably T. penetrans. The disease afflicts poor and marginalized communities in developing countries. Transmission of tungiasis comprises a complex web of factors including domesticated animals and wildlife. This research explores animal and environmental risk factors for tungiasis in an area adjacent to a wildlife reserve in Kwale, Kenya.
A two-stage complex sampling strategy was used. Households were selected from three areas in and around Kwale Town, Kenya, an area close to the Kenyan Coast. Households were listed as positive if at least one member had tungiasis. Each household was administered a questionnaire regarding tungiasis behaviors, domesticated animal assets, and wild animal species that frequent the peridomiciliary area. Associations of household tungiasis were tests with household and environmental variables using regression methods.
The study included 319 households. Of these, 41 (12.85%) were found to have at least one person who had signs of tungiasis. There were 295 (92.48%) households that possessed at least one species of domesticated animal. It was reported that wildlife regularly come into the vicinity of the home 90.59% of households. Presence of dogs around the home (OR 3.85; 95% CI 1.84; 8.11) and proximity to the park were associated with increased risk for tungiasis infestation in humans in a multivariate regression model.
Human tungiasis is a complex disease associated with domesticated and wild animals. Canines in particular appear to be important determinants of household level risk.
We just spent the day driving around Kwale looking for snakes, and/or people who had been bitten by snakes. As the last post showed, snakebites are a persistent problem along the Kenyan Coast, with more then 5% of the households we survey indicating that at least one person in the household had been bitten in the past two years.
It wasn’t difficult to find them.
Snakes are universally feared all over Africa and the associations with witchcraft make it a common topic of discussion. Everyone knows someone who has been bitten. They often know all the details, including where it happened and what occurred following the bite. It’s never a happy story.
We went deep into Kinango, an extremely rural area west of Kwale Town and found a friendly lady who seemed to know everything about everyone. She was incredibly jolly, pulled out some plastic chairs for us to sit under and cracked jokes the whole time. I even got to copy her collection of Sangeya music which she had recorded on her phone (another post but you can hear some of it here) at some local music festivals. In total I got more than five hours of live Sengeya and Chilewa music. In the music world, these would be called “field recordings.” Here, this is just music she cooks and cleans to.
Switching back and forth between snakes and Sengenya (in Africa it seems to be possible to have multiple conversations at once), she told us about a kid who had been bitten two days previous. She even told us where to find her, so off we went.
The child was collecting firewood around a mango tree near her home, when she was suddenly bitten by a large green snake, not once but three times on the foot. The snake bit once skated away, decided it wasn’t enough and came back and bit her twice more.
Ants had moved into the dead tree and hollowed out the area underneath. Presumably, the snake moved in previously and came out to warm up during the day.
The mother thankfully took the child immediately to Kinango Hospital and treated was administered. The child was given a three day course of antivenom injections and charcoal was wrapped around the wounds to absorb any venomous discharge. Though the child complains of some numbness in the area, it looks as if there won’t be any permanent damage. Thankfully.
We were also told of an old woman who had been bitten more than 20 years ago, and was badly scarred, figured out where she was and off we went again.
As we pulled up a friendly young lady came out to greet us, and showed us the way to the house out back. In the distance, we could see an old lady walking with a limp. Otherwise, she was completely fit and seemed to be cutting her own firewood with a panga.
She brought us out some chairs and sat down to chat. In 1992, she had been out back collecting firewood (a pattern) and was bitten on the foot by puff adder, one of the deadliest snakes in the world. She was bitten on the foot, and became immobile for nearly a week. A series of witch doctors were brought in, who administered charcoal rubbed into small cuts in the skin.
Necrosis set in, and watery blood erupted out of the wound site. A large number of maggots appeared. Finally, someone had the good sense to take her to the hospital, where she spent an entire year.
The details were unclear, but it appeared that the gangrene was so severe that multiple infections were presents. They likely had her on intravenous antibiotics for an extended amount of time. Despite this, the foot did not heal. Some Christian missionaries came, and convinced her to convert to Christianity, which, she claimed, improved her condition. This is likely coincidental.
The doctors suggested a skin graft to improve the foot, but she refused. Necrosis was so deep that it permeated the bone and the foot is permanently curved as a result. The leg still shows sign of swelling even more than 24 years after the bite. In most cases, they probably would have simply amputated.
The lady was born in 1948, bore ten children, one of which was born just as she was bitten. She was unable to breast feed or care for the child. Regardless, the daughter has two children of her own now.
Snakebites are bad news. In this woman’s case, the disregard for proper medical care simply made a bad situation worse. She is truly lucky to be alive. If she had died, it is doubtful that the Mgangas would have admitted any responsibility.
Ebola is a cool disease. It transmits among fruit bats in the area in and around the Central African Republic. Apes live in and under the trees the bats live in and ingest their feces. Humans who ingest the apes pick up the virus when slaughtering the animal, or so some think. The truth is that no one really knows for sure.
Contacts between humans is increasing as settlements expand and a demand for meat increases. Lacking access to formal methods of employment, individual sellers happily take advantage of market demand and a thinly profitable trade in bushmeat profulgates. Meat equals success and in the place of professionally or pastorally raised beef, which is mostly unavailable to poor people in countries like Liberia and Sierre Leone, people eat the monkeys, chimps and many other of our cousins which are able to harbor the many of the same pathogens we do.
One person gets sick. He or she has no access to formal care because his or her government can’t or won’t provide it so he remains at home. The family consults the local herbalist who provides some medications which offer temporary psychological relief but nothing more. As time ticks on, the victim becomes even sicker until the situation becomes so serious that the family has no choice but to carry their dying loved one to a health clinic 20 km away from their house. Along the way, everyone carrying him or her touches infected feces and vomit and three weeks later the process is repeated.
This could have all been avoided if rural economies were developed enough so that a mass migration to urban areas wasn’t necessary, had there been safer sources of meat available for an affordable price, were there sufficient jobs which wouldn’t necessitate the bushmeat trade, were the governments of Liberia and Sierre Leone effective enough to place a proper health facility close by to patient 0’s house and if health care was dependable enough to be able to spot and deal with an Ebola case.
Ebola is a conflation of ecology, economics, sociology, culture and politics, all mixed together to create conditions for one of the worst health crises the African continent has seen since HIV. It’s going to erase any of the gains of the past decade and collapse the already struggling health systems of some of the poorest places on the planet.
Meanwhile, the United States is having another 9/11 moment and this is where I’m starting to get quite concerned. Panic is about to become policy. Fears of global terrorism prompted our entry into Afghanistan, which might have been justified. But it also paved the way for the invasion of Iraq, which, from the beginning, was a disaster waiting to happen. Out of 9/11, we got the Patriot Act, a massive expansion in government powers to search, seize and detain and America stood by and allowed it to happen with little debate.
I am not a Libertarian, though keep getting accused of being one. I believe in public schools, public health care and government oversight of dangerous industries. So there. John Galt wouldn’t be much into me (but I guess from the far, far left anyone looks like a Libertarian).
I am, however, despite my leftist pedigree, quite concerned with the rights of individuals and the potential for panic and ignorance to lead to a rhetoric that can quickly spiral out of control and veer seemingly caring people away from the direction that the moral compass would normally point us in. I am remembering how many Americans supported torture during Bush II and wondered how many of them would support torture were it to be practiced on their own children. Though seemingly alarmist, I think that we need to be extremely careful.
Enough about me. The reality of Ebola is that it is a man-made crisis. Forest dwelling locals have eaten bushmeat for as long as humans have lived there but there is little evidence that there has ever been a large scale outbreak like the one we are currently experiencing (though history in Africa is often obscure). As I noted earlier, many forces are at play, all of which are associated with the rapid social change that Sub-Saharan African states are currently experiencing.
Some of these forces are inevitable. Population growth, as it did in Europe and Asia before, has led to the creation of mega-cities. The connections, however, between the rural and the urban, however have not been severed. People are going to do what they do, regardless of risk, particularly if they can make a buck meeting some market demand.
Some forces, though, are avoidable. While health care did not initiate the crisis, it helped drag it along. Liberia and Sierre Leone can boast to have two of the worst health systems in the world, but their poor capabilities are hardly unique in Sub-Saharan Africa. NGOs and missionary groups work to plug some of the gaps, but the reality is that without a concerted and proactive effort from the governments of those countries, the system will never improve. International funding is too poor and weak national economies and top heavy tax structures can’t adequately fund these systems domestically. Poor funding leaves many clinics, particularly those in rural areas where these outbreaks begin, without supplies, trained staff and diagnostic equipment. In Kenya, Malawi and Tanzania, I’ve seen more than one rural clinic without power or clean water. Worse yet, Ebola outbreaks, though devastating, are infrequent so that more pressing needs like malaria, diarrheal disease and HIV eat up the brunt of the already scarce funds clinics receive. Pathogens not only compete in the wild, but also for funding and support. This leaves many rural health workers without the protective gear they need, so that they work are the highest risk for death from diseases like Ebola.
What can we do? First, we can calm down. In the United States, the reality is that one of far more likely to be killed by an oncoming car than from Ebola and the probability of sustained transmission extremely low. Though people like to view domestic transmission events such as the one in Texas as failure, the reality is that public health and medical resources move much more quickly and effectively in Texas than in troubled Liberia. Much is made over Ebola’s lethality, but a patient who is found to be infected in the United States has a vastly higher likelihood of surviving than one in Liberia.
Second, leaders can stop spreading and capitalizing on misinformation. While attractive, promoting hysteria only leads to bad policy. The tendency in America is to view as some kind of apocalyptic movie scenario. While fun (not to me), the reality is that there are people in the world who are dying who shouldn’t be. Moreover, closing schools because someone knows someone who knows a Liberian is just simply unwise and counterproductive in the long term.
Third, the international community needs to engage the governments of Liberia and Sierre Leone to improve their public health infrastructure. This is not an easy task. The histories of working relationships of international health bodies and developing countries governments are fraught with failure. Mutual distrust, corruption and indifference of political leaders to the plight of their constituencies has created a mostly untenable system. However, providing supplies and training come at little cost is a mostly uncontroversial affair.
How long will this last? No one knows but it is inevitable that, even if this epidemic is brought under control, it certainly won’t be the last of its kind. We don’t have time to waste.
I’m reading through news about the American rights hijacking of the Ebola crisis for their own political gain. Did this outbreak have to occur right before the midterms, and right before a Senate election? The awful toll it will take on West African states aside, the virus couldn’t have picked a worse time (or a better, depending on how you look at it).
Ebola is a scary virus, assuming that one ever has the misfortune to come into contact with it. “Contact” in this case, means that you have to have direct contact with the blood, feces or vomit of a person infected and symptomatic with Ebola. Unfortunately for the virus, people don’t really live that long once they become symptomatic with the disease and the people who survive appear to be immune to it
This is a terrible model for an infectious pathogen. The symptoms are so severe that all around the person will immediately run away (except health workers, who bear the brunt of the risk) and the host doesn’t live very long providing only a short window with which to infect other hosts.
So the duration of infectiousness is short, the pathways are really awful and repeat infections are unlikely.
To put this into perspective, looks at the most successful pathogens out there, pathogens like influenza. Influenza transmits easily, nearly two thirds of those infected show no symptoms and thus can happily shed viral particles to everyone they know undetected. When symptoms do occur, they aren’t so bad as to keep every outside of a 5 miles radius of you. Influenza mutates at an incredible rate, so that a single infection doesn’t provide much protection against later infections. Even better, though its rapid mutation rate sometimes leads to horribly virulent strains like the 1918 flu pandemic which killed millions, in most cases influenza spares a healthy host.
It has developed an incredibly efficient and effective survival strategy (and for this reason is far scarier than Ebola).
So I’ve been thinking of how a virus like Ebola might persist in the wild, given it’s odd mode of transmission.
Now, we know that Ebola is a zoonotic disease, that is, it is transmitted from animal to humans. Since humans have not developed genetic resistance to the disease, we are at particular risk for its worst effects. Many of the scariest diseases out there are zoonoses. Examples would include HIV, SARS and, of course, influenza. While not always true, we tend to make peace with pathogens that are old and exclusively human. Many of the bacteria which live happily in your gut would be examples. As we haven’t had sufficient time to make peace with Ebola or HIV, the outcomes can be far worse than those seen in their normal hosts.
Thus, it is possible that Ebola is far less serious in whatever host it is adapted for. Nipa virus, which has a case fatality rate (the percentage of all infections of a pathogen which result in death) of more than 90% does nothing to the fruit bats it happily resides in. It is possible that Ebola is also harmless to whatever host it depends on.
However, it is possible that Ebola might be harmless in some hosts, while deadly in others, and this difference might be the result of a successful evolutionary adaptation.
Ebola has been pegged as residing in bats possibly explaining its wide range over central Africa. [1-6] Bats are a pathogens dream. They multiply quickly, providing ample opportunities for transmission and for evolutionary adaptations to the pathogen which might insure its long term survival. Better yet, they fly so that pathogens can disperse themselves quickly over a large geographic space. This is particularly useful if the pathogens wants to maintain healthy genetic diversity (though the creation of multiple sub-populations) and if it can infect multiple hosts which may or may not be all that mobile.
Apes would be a good example of the latter. Apes, being fairly sensitive to environmental changes, don’t like to move around a whole lot (unlike humans which are highly adaptable to just about any environment on the planet) but still might be important to the survival of the pathogen.
Ebola has been found in apes and the disease is currently devastating local populations.[4, 7-10]
And this is where I get stuck. In nature, plenty of things happen for no reason at all, but with pathogens, even accidental occurrences can have implications for survival and are often part of the tool box with which diseases evolve and persist.
A bleeding ape on a forest floor will likely kill all of its relatives in quick fashion, assuming its family doesn’t just hightail it out in which case transmission is over anyway. But the dead ape might serve an important purpose. Predators and scavengers will quickly arrive to feast on the infected corpse, transmitting the virus to carnivorous animals all around the forest. This could provide ample opportunities for transmission to other species. Even though many of these species could be poor hosts for the disease, they could also represent new opportunities for survival.
HIV would be an example of this. From HIV’s standpoint (assuming a collective viral consciousness), the jump to humans was extremely fortuitous. Humans love to have sex with multiple people, often even after having already reproduced, and physiologically they proved resistant enough to allow the virus to hang out for a few years before dying, allowing for years of transmission possibilities.
Thus, while on the surface, blood based modes of transmission seem pretty useless, they could serve a larger purpose of insuring a pathogens survival on a macro-level. In the case of HIV, humans didn’t turn into a dead end host (as they are with diseases like Brucella) but rather a new opportunity for survival.
The deadly nature of the virus in apes and humans, then might be like an insurance policy. Like a retirement portfolio, a diversified package of stocks will keep you alive in retirement much better than a portfolio with a single stock. Work has been done on pathogens which infect multiple species, and, depending on the nature of the pathogen, species diversity can either work for or against the survival of the pathogen.[11-13]
In the case of Ebola, there is no real evidence that humans play a role in sustaining transmission, but blood and predation could be sustaining something like Brucella or Q Fever in the wild.
Now, in this article, I have rambled on and bored you to death (and bless you if you made it this far) but I have to point out that I am under no illusions that pathogens act consciously, though I have like many of my colleagues present it as such. Actually, no living thing really does have a long term plan outside of its narrow goals of producing offspring. But new opportunities for transmission do present new opportunities for the long term evolutionary survival or a biological entity. These lucky occurrences are not consciously sought out, but rather enable the pathogen to do what it does successfully.
It must be said that the ecology of Ebola is somewhat of a mystery. Not much work has been done on the subject, as the pathogen hides out in some of the most inaccessible areas of the planet, and conflict and political instability in places like the Central African Republic and Northern Uganda prevent researchers from doing extensive work on the pathogen.
1. Stan D: Ebola and Fruit Bats. Clinical Infectious Diseases 2006, 42(5):V.
2. Olival KJ, Islam A, Yu M, Anthony SJ, Epstein JH, Khan SA, Khan SU, Crameri G, Wang L-F, Lipkin WI et al: Ebola virus antibodies in fruit bats, bangladesh. Emerging infectious diseases 2013, 19(2):270.
3. Hayman DTS, Yu M, Crameri G, Wang L-F, Suu-Ire R, Wood JLN, Cunningham AA: Ebola virus antibodies in fruit bats, Ghana, West Africa. Emerging infectious diseases 2012, 18(7):1207.
4. Kumulungui B, Leroy EM, Swanepoel R, Gonzalez J-P, Pourrut X, Rouquet P, Yaba P, Paweska JT, Délicat A, Hassanin A: Fruit bats as reservoirs of Ebola virus. Nature 2005, 438(7068):575.
5. Vogel G: Infectious disease. Are bats spreading Ebola across sub-Saharan Africa? Science (New York, NY) 2014, 344(6180):140.
6. Hayman DTS, Emmerich P, Yu M, Wang L-F, Suu-Ire R, Fooks AR, Cunningham AA, Wood JLN: Long-term survival of an urban fruit bat seropositive for Ebola and Lagos bat viruses. PloS one 2010, 5(8):e11978.
7. Groseth A, Feldmann H, Strong JE: The ecology of Ebola virus. Trends in microbiology 2007, 15(9):408.
8. Vogel G: Ecology. Tracking Ebola’s deadly march among wild apes. Science (New York, NY) 2006, 314(5805):1522.
9. Leroy EM, Rouquet P, Formenty P, Souquière S, Kilbourne A, Froment J-M, Bermejo M, Smit S, Karesh W, Swanepoel R et al: Multiple Ebola Virus Transmission Events and Rapid Decline of Central African Wildlife. Science 2004, 303(5656):387.
10. Walsh PD, Biek R, Real LA: Wave-like spread of Ebola Zaire. PLoS biology 2005, 3(11):e371.
11. Renwick AR, White PCL, Bengis RG: Bovine tuberculosis in southern African wildlife: a multi-species host–pathogen system. Epidemiology and Infection 2007, 135(4):529.
12. Dobson A, Meagher M: The population dynamics of brucellosis in the Yellowstone National Park. Ecology 1996, 77(4):1026.
13. Dobson A: Population Dynamics of Pathogens with Multiple Host Species. The American Naturalist 2004, 164(S5):S64.
Tunga penetrans is native to South America, was brought to West Africa through the slave trade. In the mid 19th century it was brought on an English shipping vessel and made its way through trade routes and is now found everywhere throughout the continent.
Bacteria opportunistically invades the site and super-infections (multiple pathogens) are common. Victims suffer from itching and pain and multiple fleas are common. Due to the location of the bite, people often have trouble walking and due to the disgusting nature of the infection, victims are stigmatized and marginalized. Worse yet, the site can becomes gangrenous and auto-amputations of digits and feet and eventually death are not uncommon.
The Parliaments of both Kenya and Uganda have introduced bills in the past calling for the arrest of people suffering from jiggers. Of course, these ridiculous bills don’t come with public health actions to control the disease.
Jiggers are entirely preventable, treatable through either surgical excision or through various medications but risk factors for it are mostly unknown and the data contradictory and mostly inconclusive.
It sometimes occurs in travelers and is easily treated in a clinic on an outpatient basis but is a debilitating infection for poor communities. Thus, it is not taken seriously by international public health groups who choose to focus on big issues like HIV and malaria.
Jiggers are a classic example of the neglected tropical disease: it devastates the poorest of the poor but gets almost no attention from donors or the international press.
We gathered some data on jiggers back in 2011 along the coast of Kenya. Without presenting these results as official, I was drawn to the attached map.
Animals of various species have been implicated as reservoirs for the disease, most notably pigs and dogs. Less understood is the role of wildlife in maintaining transmission. On the map below, the large yellow dots represent cases. Note that they are nearly all located along the Shimba Hills Wildlife Reserve. I calculated the distance of each household to the park’s border (see the funny graph at the bottom), and found a graded relationship between distance and jiggers infections. Past 5km away from the park, the risk of jiggers is nearly zero.
What does this mean? I have ruled out domesticated animals, at least as a primary reservoir. People in this area tend to all own the same types and numbers of animals. Being Islamic, there are no pigs here, but dogs are found everywhere. Despite this, there are distinct spatial patterns which are associated with the park. Note that all of the cases are found between the parks border and a set of lakes, perhaps implying that certain wild animals are traveling there for water and food.
The ecology of jiggers is very poorly understood and, like many pathogens (like Ebola, for example), wildlife probably play an important role.
It’s worth paying me a lot of money to study it.