Wind-Borne Illness from Coastal Seas: Present and Future Consequences of Toxic Marine Aerosols

By John J Walsh

Wind-Borne Illness from Coastal Seas: Present and Future Consequences of Toxic Marine Aerosols explores the present and future human health consequences of marine aerosol poisons carried ashore by coastal winds. The book compiles relevant information on an interrelated toxicological, environmental sciences and public health problem that is combined with recent observations, extensive epidemiological data and case studies. It tackles this challenge with a small, interdisciplinary group of authors who dissect the underlying causes and potential remedies of increasing ill health issues on a planet that is covered by 70% seawater and subject to increasing sea spray-containing malign aerosols.

The book's authors outline the historical context of the situation, discuss the importance of recognizing toxic marine aerosols as a cause of wind-borne illness, and suggest operational forecasts for avoidance of onshore, wind-borne marine toxins, and crucially, present extensive epidemiological evidence. This resource will be useful to a wide variety of toxicologists, medical doctors and environmental scientists.

• Contains extensive epidemiological data and case studies on aerosol forms of windborne global marine toxins
• Presents information from an interdisciplinary author team
• Argues for future operational forecasts for avoidance of onshore, windborne marine toxins

• Language: English
• Publisher: Academic Press
• Release date: Jul 18, 2019
• ISBN: 9780128121320

Book preview

Wind-Borne Illness from Coastal Seas

Present and Future Consequences of Toxic Marine Aerosols

Edited by

John J. Walsh

Emeritus Distinguished University Professor of Marine Science, University of South Florida, United States

Table of Contents

Cover image

Title page

Copyright

Front plate

List of Contributors

Foreword

Chapter 1. Introduction

Abstract

1.1 Divergent protozoan predators

1.2 Fungal parasites

1.3 Size matters

1.4 Monsoon exchanges

1.5 Cincinnati boiler heating smoke laws

1.6 Mercury, arsenic, and carcinogen exports from Ohio River Valley

1.7 Lexington secondhand smoke ban

1.8 Smoke allergen, cancer cause, or competition cure within the looking glass?

1.9 The full Zorban catastrophe: top-down and bottom-up controls

1.10 Human bone collagens reflect phytoplankton bases of food webs

Chapter 2. Histories

Abstract

2.1 Greek experiences

2.2 Egyptian experiences

2.3 Roman experiences

2.4 American (New World) colonial experiences

2.5 African experiences

2.6 Antipodean experiences

2.7 Asian experiences

Chapter 3. Material transports

Abstract

3.1 Introduction

3.2 The coastal ocean circulation by local wind forcing

3.3 The coastal ocean circulation by deeper ocean forcing

3.4 Ecological applications

3.5 Ocean atmosphere exchange

3.6 Atmosphere transport

3.7 Concluding remarks on prediction

Chapter 4. Efficacies of imprudent top-down and time variant bottom-up controls over 1965–2011 as computed from a validated model of 35 state variables

Abstract

4.1 Introduction

4.2 IXTOC analog

4.3 Model constructs

4.4 Methodology

4.5 Competing dinoflagellates

4.6 Bacterioplankton

4.7 Ciliates

4.8 Riverine loadings

4.9 Carbon budgets

Chapter 5. Pharmacological antagonist interventions

Abstract

5.1 Serendipity of penicillin emergence

5.2 Quinine remedies for other infectious diseases

5.3 Methylene blue

5.4 Gulf of Guinea’s malaria versus asthma incidences

5.5 Ivory Coast’s phytoplankton succession at Abidjan

5.6 Ghana’s coastal and inland records

5.7 LD50 comparisons

Chapter 6. Future numerical consiliences

Abstract

6.1 Dust bowl land mismanagements replaced buffalo grass with wheat

6.2 Change of Asian dust silicosis agents to 100-fold more potent harmful algal blooms

6.3 European parallels

6.4 North American wetland harbingers under global warming

Backword

Bibliography

Index

End plate

Copyright

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Front plate

List of Contributors

J.M. Lenes,     Little Meadows Early Childhood Center, New York, United States

J.J. Walsh,     Emeritus Distinguished University Professor of Marine Science, University of South Florida, United States

Robert H. Weisberg,     College of Marine Science, University of South Florida, FL, United States

Foreword

Like all important things in life, this synthesis is a family affair.

Foremost, I honor the memory of my best friend and sage advisor, Orvita I. Poppell Walsh. While I scribbled, she took care of everything else. Her death from stage-four lung cancer, even though she was not a smoker, piqued my studies of the ongoing environmental origins of pulmonary disorders. My sister Kathy—a critical care nurse, lawyer, and government official involved in public health affairs—provided a practical perspective. My late sister Michele—a gourmet cook and sommelier, who held the family together in bad and good times—added the human perspective. My brother Chris—a member of the US National Academies of Science and Medicine—helped me write the last chapter, contributing biochemical and medical perspectives.

Of course, without the additional contributions written by Bob Weisberg and Jason Lenes, societal dealings with continued airborne poisons from coastal seas would have had a dim future. We must deal with human health consequences of marine microbial interactions (viral, bacterial, fungal, algal, and protozoan parasite vectors) with both more seaside trypanosomiasis parasite vectors and mineral (coal ash and desert dust), smoke, and harmful algal bloom (HAB) toxic allergens. Due to our binary immune system, land and marine allergens all exacerbate the malign impacts of chronic obstructive pulmonary disease, malaria, tuberculosis, silicosis, aspergillosis, histoplasmosis, coccidioidomycosis, and trypanosomiasis. Yet potential aerosol-induced deaths from Earth’s oceans and sea-shores can be kept within minimal historical ranges of other seafaring, fishing, and bathing hazards by following prudent guidelines of problem definitions, with eventual unanimity in their solutions.

A narrative fiction binary construct consisted of: I think novelists come in two types that includes the sort of fledgling novelist I was in 1970. Those who are bound for the more literary or serious side of the job examine every possible subject in the light of this question: What would writing this sort of story mean to me? Those whose destiny … is to include the writing of popular novels are apt to ask a very different one: What would writing this sort of story mean to others? The serious novelist is looking for answers and keys to the self; the popular novelist is looking for an audience (King, 1982, 2003, 2017). Since the major thrusts of this ecomedical synthesis are future ameliorations on a water planet of the past and present results of marine HAB-induced asthma exacerbations of another binary reality—that of our human immune system, trying to deal with both external wind-borne allergens and internal parasite vectors—I opted here for the latter vision.

John J. Walsh

Lexington, Kentucky

February 2019

Notes: The front and back end plates of this book were photographic depictions of potential large onshore fluxes of marine aerosol pollutants during tropical (generic Caribbean) and subtropical (Harvey 2017) hurricanes (cyclones), beyond the usual diel sea breezes and seasonal monsoons. Finally, the unpublished satellite images were kindly provided by Prof. Chuanmin Hu of the University of South Florida.

Chapter 1

Introduction

J.J. Walsh,    Emeritus Distinguished University Professor of Marine Science, University of South Florida, United States

Abstract

Present natural and anthropogenic global lung diseases annually impact ~2.4 billion humans, with synergistic interactions. These pulmonary ill events consist each year of ~370 million episodes of viral influenza; ~300 million asthmatics, compounded at times by fungal aspergillosis in adults; ~200 million victims of chronic pulmonary disease, including ~50 million emphysema patients; ~40 million cases of pneumonia as the leading cause also of ~1.3 million child deaths; ~20 million active tuberculosis infections; 14 million onsets of lung cancer; ~11.3 million episodes of fungal morbidities and deaths due to bronchopulmonary aspergillosis, with eightfold smaller mortality rates attributed to histoplasmosis and coccidioidomycosis, masquerading when present as instead 15%–30% of community-acquired pneumonia (CAP); similar annual losses of 0.40 millions from malaria, 0.45 millions from silicosis, 0.27 millions from black lung, and 0.19 millions from burning domestic wastes to yield inhaled PM2.5. Finally, prior fatal cases in 1990–2015, due to cardiac arrests and central nervous system failures of brain meningoencephalitus in Africa and South America, then roughly summed to annual respective losses from trypanosomiasis of 0.34 and 0.08 million deaths in sub-Saharan and Latin American countries, like those caused worldwide by malarial Plasmodium spp. Accordingly, consiliences of environmental and medical scientists, guided by imperfect numerical model results, are now required to build upon past inadequate data sets of combined microbial predator impacts on a binary human immune system of different cytokines, dealing with external protozoan, dust, ash, smoke allergens, in contrast to internal extracellular parasites drifting in your bloodstream.

Keywords

Harmful algal blooms (HABs); trypanosomiasis; malaria; airborne; tuberculosis; aspergillosis; coccidioidomycosis

There’s nothing more dangerous than a man who doesn’t appreciate the limitations of his data, unless it’s a mathematician who hasn’t any data.

Larkin (1977)

1.1 Divergent protozoan predators

Some dinoflagellate protozoan harmful algal blooms (HABs) have retained their marine heritage as part-time primary producers of coastal seas, but they were still also herbivores on other phytoplankton, routinely killed fish as a decomposing supply of recycled dissolved inorganic nutrients (Walsh et al., 2009), and were presumably inadvertent asthma triggers and poisoners of humans as well. But without winged hosts of mosquito, tsetse fly, and assassin bug carriers of viral, bacterial, and protozoan vectors of many diseases, these phytoplankton have yet to participate in the hematophagic strategies of human blood meals by those insects.

Nevertheless, some of the marine single-cell Borgian phytoplankton poisoners drove barely breathing humans away from global seashores (Walsh et al., 2017), with a palytoxin poison almost equivalent to the most deadly botulinum (Table 1.1). Of course, other protozoan instigators of malaria, Plasmodium spp., led to pulmonary edema and respiratory failure, once the victim’s lungs filled with fluid, like drowning at sea. More protozoan parasites Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense were also the major sources of human sleeping sickness (trypanosomiasis) in sub-Saharan Africa, albeit via the vector of biting African tsetse flies Glossima spp., instead of just mosquito and assassin bug carriers of other parasites.

Table 1.1

The tsetse flies acted as obligate hematophagic predators of mainly land mammals, while passage of protozoan parasites to humans, dogs, cattle, and wildlife occurred via their bites. Finally, other bites by the major South American assassin bug Triatoma infestans hosts of Trypanosoma cruzi parasites and their now return exports to the United States probably caused more cases of protozoan illnesses in the Americas than those due to malaria [World Health Organization (WHO), 2008].

1.1.1 African trypanosomiasis

Wise direct human interventions led by 2009 to 26% smaller fatalities of 0.09 million residents parasitized by African trypanosomes. Such results instead provided a positive note, beyond the doom and gloom of usual ill-health, unanticipated results of past human imprudent mismanagements of different terrestrial herbivore populations in North America, Asia, and other regions of Africa (Wright, 2017), like ubiquitous decimations of marine copepods (Table 1.2).

Table 1.2

Indeed, one of our last examples of future needed continuations of required medical and ecological consiliences in Section 6.1.6 is the ill-fated introduction to Ethiopia and Eritrea (Italian Somaliland) during 1887 by the Italian army of the rinderpest virus—a relative of measles—within contaminated cows, imported in turn from India. Briefly, an epizootic of viral-killed dead cows along the East African coast had spread to South Africa by 1897 and remained in German East Africa at the end of WWI during 1917 (Curson, 1919). Today other past air-borne measle virus aerosols (Furuse et al., 2010) have also impacted humans in both private physician offices (Bloch et al., 1985) and on public cruise lines (Filia et al., 2015).

On the slopes of Mount Kilimanjaro and over the surrounding lands of the Maasai in Tanganyika (Tanzania) near Ngorongoro Crater, an Austrian traveler Dr. Oscar Baumann described the human starvation consequences: Large numbers of the woeful creatures who now populate Masailand congregated around the thorn fence of our camp. There were skeleton like women with the madness of starvation in their sunken eyes, children looking more like frogs than human beings, ‘warriors’ who could hardly crawl on all fours, and apathetic, languishing elders. … They were refugees from the Serengeti, where the famine had depopulated entire districts, and came as beggars to their tribesmen at Mutyek who had barely enough to feed themselves. Swarms of vultures followed them from high, awaiting their certain victims (Baumann, 1894). Then, those Maasai lost >90% of their cattle herds due to rinderpest during the early 1890s, when ~67% of their tribes also died at that time from lack of food.

Concurrently, a series of trypanosomiasis epidemics (Fig. 6.3), due to the more potent T. brucei rhodesiense (now Zimbabwe) parasites, also killed 250,000 human residents of Uganda during 1900–20 (Fevre et al., 2004), or a mean 1259 deaths year−1. The expanded populations of tsetse vectors Glossina pallidipes and G. swynnertoni were living in the dry thorn bush of the Acacia- and Combretum-dominated woodlands and savannahs of East Africa from Somalia to Tanzania. This African marginal habitat—instead of pastures, from a human point of view—was analogous to the drought-resistant, almost impenetrable chaparral habitat of southern California.

In Gambia, Senegal, and the Democratic Republic of Congo (DRC), more human deaths from sleeping sickness were then also caused by another set of less potent but still pathogenic T. brucei parasites (Fig. 6.3). This toxicity of the protozoan subspecies T. brucei gambienses led to presentment of a different, more rapid case of human sleeping sickness in the Gambia colony by May 1901 (Forde, 1902). Following the first diagnosis of malaria but after no response to antimalarial quinine treatments, further examination yielded occurrence of this additional trypanosome in the patient’s blood along coastal northwest Africa (Dutton, 1902).

More antecedent expansion of tsetse fly habitat had occurred when morbid rinderpest-impacted cattle left behind uncropped plant habitats during human transfers of 19th-century bovine herds across the Sahel from Somalia. Infected and dying cows arrived at both Burkino Faso and the Senegal River, with dead ones drifting downstream in 1891. Other diseased cattle finally reached coastal Dakar, Senegal, in 1892 (Sunseri, 2018) to begin parasite transmissions to adjacent Gambian human residents via presumably comingled tsetse fly bites (Selby et al., 2013).

Yet, in South America, where even fossil tsetse flies were rare and no live ones evidently occur there now, more parasitic infections still stemmed from other vectors. The Spaniards had imported diseased horses throughout the 15th–16th centuries, infected by other sleeping sickness trypanosomes, to their Argentine, Bolivian, Chilean, Ecuadorian, Paraguayan, Peruvian, Uruguayan, and Venezuelan colonies. Consequently, equines became reservoirs of protozoan-mediated heart failures of both European invaders and resident Amerindians, in addition to other earlier ill-health microbial arrivals from Beringia.

Rather than just disease transmissions of T. cruzi via bites of South American assassin bug carriers, however, transfers of additional trypanosomiasis sources of Trypanosoma evansi occurred (Desquesnes et al., 2013; Greif et al., 2017) in exotic and mundane fashions, caused by other blood meals of (1) South American vampire bats, Desmodus rotundus, and (2) horse flies, Tabanus triangulum and Stomoxys calcitrans (Kruger and Krolow, 2015).

One hundred years later during 1990 in the homeland of T. evansi (Desquesnes et al., 2013), total incidence of these fatalities among all sub-Saharan countries had increased to a ~10-fold larger amount of 12,756 African trypanosomiasis victims during that year. But, given the changed regional African population bases over this century, without extensive public health efforts those mortalities could have been much worse. During 1990, 16% of the annual total population loss due to human trypanosomiasis reflected regional deaths in Uganda of 2066 fatalities year−1, remaining close to the mortality rate in the 1900–20 epidemic there (Fevre et al., 2004).

Similar wise remedial health efforts altered the initial course of increasing fatalities due to another version of sleeping sickness in the South American CONE program of Argentina, Bolivia, Brazil, Chile, Paraguay, Peru, and Uruguay, whereby spraying the long-lasting pyrethroid insecticide, the annual incidences of trypanosomiasis fell by 94% from 1991 to 2000. Unfortunately, like recently evolved drug resistances of other microbiota to attempted antimalarial controls of Plasmodium spp. and difficult curtailment of mosquito carriers, the Triatoma spp. assassin bugs have also developed more resilient forms to deal with past insecticides used to eradicate these trypanosome hosts (Lardeux et al., 2010; Gurevitz et al., 2012).

Moreover, in 1990 about 59% of the total sleeping sickness cases represented 7515 deaths that year in the Congo Basin of the DRC. The tsetse flies Glossina palpalis and Glossina caligna there (Fig. 6.3) had instead favored nearby aquatic, rather than brush habitats of mangrove forests and river banks. These flies, when present, could have been in closer contact with HAB sources of aerosol allergens to perhaps force binary selections at the cellular level of either antiallergen, or antiparasite, cytokine components of resident human immune systems in different amounts along each African coast. Yet dinoflagellates were not usually the dominant phytoplankton along the West African coastline, except for occasional seasonal outbursts in the Gulf of Guinea, while tsetse flies did not occur in Madagascar.

Furthermore, during 1965–2005 the mean prevalence of asthma among school children was 9.8% (Table 1.4) along parts of West Africa. There, trypanosome parasitisms, vectored by G. palpalis and G. calignea, were 3.7-fold greater than in Uganda. Along East Africa, humans were bitten instead by G. pallidipes and G. swynnertoni. By contrast, the intervening coastal upwelling ecosystems of the Canary and Benguela Currents mainly supported diatom productivity off northwest and southwest Africa. Without nearshore phytoplankton aerosols of HAB origins, school children in Dakar, Senegal had annual asthma incidences of just 3.0% during 2012 (Hooper et al., 2016) and 3.2% earlier in Cape Town, South Africa, during 1979 (Ehrlich et al., 1995).

In contrast, asthmatic children had a sevenfold greater mean of 20.2% of young residents (Table 1.4) living between Durban, South Africa, and Nairobi, Kenya, next to a downwelling marine ecosystem (Walsh et al., 2017) of the nutrient-poor Agulhas Current (AC), in which diazotrophs and dinoflagellates were abundant. Accordingly, the AC had instead favored release of windblown dinoflagellate HAB aerosols to unfortunately divert production of coastal human cytokines away from dealing with parasites. Rather than attempting to just kill both fungal predators and viral, bacterial, and protozoan parasite invaders, which had entered human tissues and elicited a repel boarders response, upon bites of adjacent land mosquito, tsetse fly, and assassin bug winged carriers, the addition of marine allergens would have also required synthesis of antiallergen chemicals by our immune systems (Berger, 2000).

Away from those shorelines and coastal mangroves of West Africa, uneaten grasslands and open woodlands of East Africa were no longer also grazed by rinderpest-infected cattle imports of the 19th century. Nevertheless, other plants of the dominant thorn bush habitat of Acacia spp. trees and shrubs continued to be available as substrates to house different inland tsetse fly populations of G. pallidipes and G. swynnertoni. While these obligate tsetse predators continued to harvest blood meals from human, they also transferred their parasites T. brucei brucei, T. congolense, and T. vivax to surviving cattle and wildlife prey to yield bovine and other mammal versions of animal trypanosomiasis, that is, nagana there and called surra in South America.

Before this African ecological disaster and human loss of life due to starvation, imported infectious diseases of viral and protozoan origins, and HAB exacerbations of bovine and human tuberculosis (TB), the Maasai cattle herds had to also deal with grasslands herbivore competitors, ranging from giraffes (Giraffa camelopardalis) to blue wildebeests (Connochaetes albojubatus). Yet the still much larger toxic responses of those now surviving domestic cattle, compared to mildly afflicted resident wildlife, which still maintained annual blue wildebeest migrations of C. albojubatus, led to the description of a combination of Trypanosoma and Glossima spp. as the best African game wardens (Pearce, 2000). The apparent greater antigenic resistance of the immune system in the native herbivore C. albojubatus to poisons of T. brucei brucei reflected both of their memberships in an African grassland climax community of the Serengeti Plain, like another one of the prior drought-resistant buffalo grass in the xeric Midwestern US plains of Oklahoma (see Section 6.1.2).

1.1.2 American trypanosomiasis

Hopefully, the present African biting fly vector of sleeping sickness will not soon reoccupy its same ~34-million-year-old niche in today’s climate of another 5°C rapid warming period, analogous to the past North American version of ancient tsetse flies (Cockerell, 1907; Meyer, 2003). Those predators had diverged, based on the ribosomal RNA equivalent of a fossil record (Stevens et al., 1999; Kerr, 2006), within the late Eocene of Colorado, after onset of the Paleocene-Eocene Thermal Maximum (PETM) at the beginning of the Eocene 55.5 million years ago.

Exacerbating dinoflagellate HABs (Bujak and Williams, 1980; Hackett et al., 2004; Nosenko and Bhattacharya, 2007; Janouskovec et al., 2016) were also present. They rode global reversing water currents (Nunes and Norris, 2006) in plankton forms and presumed air currents in aerosol stages, with expansions at times (Brinkhuis and Biffi, 1993) of the spatial domains of subtropical dinoflagellate species and their HAB aerosols during divergent protozoan evolution as very toxic fish predators (Table 1.1).

After separation of the supercontinent Pangaea into Africa, South America, and Euramerica about 100 million years ago in the middle Cretaceous Period, those land trypanosome protozoan parasites diverged into T. brucei and T. cruzi (Stevens et al., 1999), when eastern North America was a shallow sea next to Colorado. Upon geographic isolation, these Mesoamerican trypanosomes presumably then evolved to be hosted by tsetse flies Glossina oligocene (Cockerell, 1907) for a while in North America during warmer periods of the PETM and by T. infestans assassin insects during additional climate changes of the South American continent (Chagas, 1909; Adler, 1959; Medawar, 1967).

Subsequently based on mitochondrial genotype discrete typing units of T. cruzi, this species diverged further within South America during the Miocene epoch of 3–15 million years ago (Machado and Ayala, 2001) into seven genotypes: TcI, TcII, TcIII, TcIV, TcV, TcVI, and Tcbat (Zingales, 2018). The last genotype, Tcbat, was hosted by South American bats (Anez et al., 2009; Marcili et al., 2009), which constituted about 40% of the mammals on that continent.

Similar to monarch butterflies Danaus plexippus, one of those mammals—the overwintering migratory Brazilian free-tailed bat Tadarida brasiliensis—flew south each year over distances of >1800 km from Texas during October–November, returning in March–April at speeds of ~45 m s−1. As a nocturnal in-flight insectivore, feeding instead on mosquitoes and the moth stages of agricultural pests, corn-ear worm Helicoverpa zea and army worm Spodoptera frugiperda (McCraken et al., 2008), these bats presumably did not eat many diurnal cotraveling monarch butterflies en route.

As indices of both the relative age of those genotype origins of T. cruzi and initial human immigrations from North America, the genetic TcI variants of Mesoamerican protozoans mainly occurred within the United States (Roellig et al., 2008; Bern et al., 2011), Mexico (Bosseno et al., 2002; Espinosa et al., 2010; Monteon et al., 2016), Columbia (Vallejo et al., 2009), Venezuela (Anez et al., 2004), and French Guiana (Peneau et al., 2016). When the Central American Seaway was open ~50 million years ago between North and South America, respective TcI and TcII genotypes of T. cruzi had begun to diverge (Briones et al., 1999).

After closure of the Seaway ~3–4 million years ago (Simpson, 1980; Baskin and Thomas, 2007; Montes et al., 2015; Coates and Stallard, 2013) with the emergence of the Isthmus of Panama, some North American large saber-toothed cats Smilodon gracilis and wild horses Equus caballus moved south. Relict TcI genotypes were carried along (Barnabe et al., 2001) in these infected large mammals, including humans and other trypanosome hosts, as part of the Great American Biotic Interchange (GABI).

Other South American mammal TcII victims, like nine-banded armadillos Dasypus novemcinctus, their ground sloth relatives, and common opossums Didelphis marsupialis, instead emigrated north (Baskin and Thomas, 2007). Similarly, during recent follow-ons of GABI, select infected TcI and TcII sets of South American mammals are repeating some of those prior migrations, albeit in now perhaps mainly unidirectional windblown aerosol and microbial parasite transfers from ongoing biotic reservoirs, south of the Gulf of Mexico (GOM) (Roellig et al., 2010) to north of that inland Sea.

Today, in both Chile and Brazil, TcI tracers had later evolved from those found in human skeletal records into more T. cruzi genomes (TcII, TCIII, and TcIV–TcV hybrids) and most of today’s mammals and marsupials, including vampire bats in Uruguay and Argentina. These different terrestrial protozoan genotypes were obtuse records, like those of marine nitrogen isotope tracers in more human skeletons of extant exacerbating single-cell dinoflagellate killers, unless viewed all together in a larger holistic context.

Like mosquitoes, tsetse and horse flies, and some bats, the local kissing bugs unfortunately drew blood protein meals from most mammals and marsupials, including incidental Homo sapiens victims of parasitic sleeping sickness with its associated central nervous system (CNS) failures and cardiomyopathies. Because of inefficient binary immune systems, human residents and travelers in both the Americas and globally were also subjects of malaria and TB diseases, hemorrhagic fevers, fungal predators, and pulmonary allergen attacks, compounded by windblown HABs, desert dust storms, coal smoke emissions, and radionuclide triggers of lung and thyroid cancers.

They all provided dimly seen biochemical data on multiple migrations of ancestral T. cruzi and T. evansi parasites to and from South America (Hotez, 2012), past areas of unrecognized marine allergen exacerbations. Yet the disparate data sets followed along the same seasonal migratory paths of monsoon winds, airborne HAB aerosols, legacy pesticides, monarch butterflies, Brazilian bats, bomb test radionuclide signatures, anthropogenic dust releases, and smoke plumes from agricultural biomass burnings, next to varying epicenters of ill humans at different distances from the surrounding seas over multiple timescales, from seasons to millennia.

For example, 4500-year-old mummies recovered from Peruacu Valley in Minas Gerais State (Lima et al., 2002) and today’s mammal residents (Lima et al., 2014) in Monte Alegre, along the Amazon River in northern Para State, had the same ancestral genotype TcI, presumably reflecting different southward immigrations from Mesoamerica. In the same state, next to Belem at the mouth of the Amazon River, the dominant ancestral lineage was also still that of TcI (Roman et al., 2018), whereas in nearby seaside Piaui and Paraiba States, both TcI and TcII occurred in wildlife (Herrera et al., 2005) and humans (Barnabe et al., 2011), and in adjacent Pernambuco State, TcII prevailed (de Oilveira et al., 2017). Finally, this other earlier ancestral TcII genotype also extended south, from Rio de Janeiro (Lisboa et al., 2015) to the borders with Bolivia, Paraguay, Argentina, and Uruguay (dos Santos Lima et al., 2014; de Oilveira et al., 2017; Roman et al., 2018).

Consequently, possible equatorward dispersions of at least TcII past Guatemala (Iwagami et al., 2007; Pennington et al., 2017) and Columbia (Messenger et al., 2016) to Mexico and Louisiana along the GOM evidently instead reflected more recent human emigrations to North America from Paraguayan (Acosta et al., 2017) and Bolivian (Bern et al., 2009; Messenger et al., 2015) epicenters. As much as 80% infestation rates of Chagas disease occurred among mammals (Chapman et al., 1984) in the Grand Chaco region of western Paraguay, adjacent to other arid Chaco areas of Bolivia and Argentina (Acosta et al., 2017).

Farther poleward, the regional assassin bugs T. infestans instead hosted Chilean populations of T. cruzi, with divergence again to a distinct TcIII genetic signature in the absence of any TcII lineage (Venegas et al., 2011). More details of joint Brazilian public health consequences of (1) multiple TcI–TcII lineages of T. cruzi causes of trypanosomiasis and (2) coccidioidomycosis attacks by xeric fungi also of Chaco origins, exacerbated by both (3) desert dust and (4) seaside HAB allergens, together with additional impacts of (5) mercury neurotoxic, (6) pesticide, and (7) radionuclide poisons will be discussed in Section 2.4.2.4.

TcI and TcII lineages were both toxic protozoan genotypes of T. cruzi to humans, with evolutionary divergence ~63 million years ago in South America (Briones et al., 1999). They each evoked Th1 parasite antigen-specific cytokine (Kumar and Tarleton, 2001) responses in mice, instead of allergen-focused T cell Th2 helpers of the human immune systems, elicited instead by HAB, smoke, and silicon dust allergens. The Ld50 of cultured T. cruzi cells to mice was ~10 TcI invading trypomastigotes per mouse (Henriques et al., 2014). Furthermore, after secretion of additional extracellular vesicles by the more virulent TcI trypomastigotes of T. cruzi, experimental laboratory victims in the form of green monkey cultured cells had greater infectivity than those of the TcII lineage (Ribeiro et al., 2018).

As a reflection of windblown monsoonal, poleward transports of smoke (Yokelson et al., 2009), desert dusts (Fig. 2.10), homeward-bound monarch butterflies (D. plexippus), marine pools of organic mercury toxins (Fig. 1.6), and HAB allergens (Figs. 1.2, 2.10, and 2.13), as well as additional human immigrations, the South American diagnostic TcII indices were found in Argentina, Paraguay, Bolivia, Brazil (Lima et al., 2014), Columbia (Messenger et al., 2016), and very recently in Veracruz and Yucatan, Mexico, as well as in New Orleans, Louisiana. The more toxic TcI genotypes were mainly restricted to the east coasts of South America within both fossil and present human forms, providing direct temporal corroboration of the evolutionary sequence of those protozoan variants.

After multiple human crossings of the Bering land bridge before 15,000 BCE (see Section 2.4.1.1.1) DNA tracers of trypanosome parasites were also exhumed from seaside Chinchorro human mummies, who lived near Arica, Chile, close to today’s border with adjacent Peru in ~7020 BCE (Aufderheide et al., 2003). Subsequent emigrating humans about 1150 years ago (Turpin et al., 1986) would have later also encountered TcI genotypes of T. cruzi in rock caves along the Texas–Mexican Rio Grande border of Coahuila State, with diagnostic gastrointestinal lesions of megacolon, due to this trypanosome (Reinhard et al., 2003).

Upon further parasite divergence, Paraguay, Bolivia, Argentina, and Amazonia (Lima et al., 2008) became epicenters of TcII. By contrast, the Amazon region lacked TcIII but also housed TcI and the divergent hybrid TcV and TcVI genotypes (Lima et al., 2014). Similarly, north of Buenos Aires in Chaco Province near the border with Paraguay, the predominant genotypes of dogs and cats were again TcV and TcVI (Enriquez et al., 2012).

Yet even farther south along the Brazilian coast in Rio de Janeiro, the original genotype TcI of T. cruzi was maintained, while inland due west of Recife the northeast Brazilian seaside State of Piaui, the other major genotype TcII was instead obtained from Triatoma brasiliensis and wildlife (Herrera et al., 2005). In nearby Paraiba State, both TcI and TcII were found in T. cruzi (Barnabe et al., 2011), with the former older and more toxic.

Reflecting the earlier timing of different human emigrations from North America, divergence to other T. cruzi genotypes would have depended upon evolutionary pressures within different habitats and thus ecological niches of North and South America. Accordingly, 12 species of triatomine carriers of sleeping sickness of three major genotypes, Tcbat, TcI, and TcII, were probably present in California and the American southwestern states during the early Holocene of ~10,000 years ago, when equatorward-migrating humans began contacts with those protozoan causes of American trypanosomiasis, carrying mainly the TcI genotype (Roelling et al., 2008; Bern et al., 2011).

This genotype was the most toxic trypanosome to humans in Venezuela (Carrasco et al., 2012), where coastal interactions with nearshore Caribbean HABs (Walsh et al., 2011) and their aerosols would have again diverted some of the binary chemical syntheses by humans to Th2 cytokines, for dealing with additional allergen complications. Perhaps in parallel coevolution of human prey and trypanosome predator, T. cruzi opted for the fittest poison, when and where human immune systems were already distracted.

The first human migrants to South America, who became subsequent victims there of T. cruzi, would thus have initially encountered this genotype as well, before trypanosome genetic divergences into other lineages. Recall that within the rib of a human mummy in Minas Gerais State of Brazil at ~600 km inland from the Atlantic seashore of adjacent Bahia State (Lima et al., 2008; Reinhard and Araujo, 2016) next to the Brazil western boundary Current, the genotype was indeed that of TcI ~5750 years ago.

Furthermore, then and now the subtropical Brazil Current hosted both toxic dinoflagellate HABs (Walsh et al., 2017) and Trichodesmium spp. diazotroph precursors (Fig. 2.17). Later, Charles Darwin had written: I collected a little packet of this brown-colored fine dust … From the direction of the wind whenever it has fallen, … we may be sure that it all comes from Africa … It has often fallen on ships … even more than a thousand miles from the coast of Africa and at points sixteen hundred miles distant in a north and south direction. On March 18, 1832, he continued not far from the Abrolhos Islets (~13°S, 38°W, close to the Brazil coast) … my attention was called to a reddish-brown appearance in the sea … these are small bundles of Trichodesmium erythareum … found in the Red Sea (Montagne, 1844). In almost every long voyage some account is given … They appear especially common near Australia; and off Cape Leeuwin (~35°S, 115°W, at the West Australian coast) … Captain Cook, in his third voyage, remarks that sailors … gave the name of sea-sawdust (Darwin, 1846).

Similarly, nearshore Karenia brevis sources of allergens within the northern GOM were abundant off both northwest Florida and West Texas (Walsh et al., 2006), with a mean asthma rate of 9.6% for school children (Table 1.4) between Texas and North Carolina during 2003 (Akinbami et al., 2009), requiring increased syntheses of Th2 cytokines by asthmatic humans in each region. Yet, among 72% of the potential triatomine predator species found elsewhere in the Southern United States, only a few assassin bugs were noted from Louisiana to Florida (Bern et al. 2011).

Whereas in Texas, when Triatoma gerstaeckeri, Triatoma leticularia, Triatoma indictiva, Triatoma protacta, and Triatoma sanguisuga were all present to elicit competing human Th1 cytokine responses to internal parasites, not enough of this former proinflammatory repellant of T. cruzi (Nardy et al., 2015; Morrot et al., 2016) was evidently synthesized by Texas residents. During 1984–2006, four of the six North American human victims of Chagas disease were living in Texas–Louisiana, that is, 67%, and another one downstream by air in Tennessee along a marine HAB glide path (Fig. 2.10). But no people died in Florida, with instead the last victim killed by trypanosomes in California (Schiffler et al., 1984; Dorn et al., 2007; Bern et al., 2011).

Within 48 of the 254 Texas counties during the same time period of 1993–2007, the T. cruzi–infected dog sentinels of Chagas disease, dying from myocarditis, were mainly coastal ones, verified by serology and histopathology records. They also exhibited breathing difficulties within ~425 km inland of the West Texas shelf (Kjos et al., 2008), that is, about half way to the New Mexico border. Dogs ate assassin bugs and suffered from canine allergic bronchitis, similar to asthma, so that the Texas ones would have been subjected to windblown imports of both trypanosome hosts along butterfly/bat land migration routes and K. brevis imports from the GOM (Fig. 2.10). There, diatoms were no longer the dominant phytoplankton west of the Mississippi River delta (Walsh et al., 2015).

By 1958, T. cruzi had infected raccoons Procyon lotor in Laurel, Maryland (Walton et al., 1958) to the northeast of Washington, DC, after presumed windblown transport of the T. protacta carriers of sleeping sickness along the same multiyear eastern return migration pathway of monarch butterflies (Brower, 1995). Moreover in 2017, Chagas disease had also become a life-threatening, reportable public health concern in Arizona, Arkansas, Louisiana, Mississippi, Tennessee, and Texas, like previous surveillances of blood donor screening in Massachusetts (Bennett et al., 2018).

Those western populations of monarch butterflies also migrated north to California, over which state the T. protacta carriers of American trypanosomiasis were already present at the turn of the last century, that is, after annual renewal of windblown Mexican sources of sand allergens, as well as associated airborne fungal and T. cruzi predators (Fig. 2.10). Yet no cases of human trypanosomiasis had been reported by 1967 after a 25-year study of Griffith Park in Los Angeles (Wood and Wood, 1967), until finally one case during 1984 (Schiffler et al., 1984) as a result of both HAB absences and wildfires. No populations of HAB dinoflagellate Ostreopsis and Karenia spp. asthma triggers lived in the upwelling eastern boundary currrents (EBCs), with observed pulmonary indices of only 3.0%–6.4% asthmatic school children off Oregon and southern California during 1995–2008 (Table 1.4).

Thus human victims of sleeping sickness there would have been able to devote most of their immune responses to ejection of protozoan parasites rather than additionally coping with marine allergens. The frequent wildfires in the chaparral habitats of initial wood rat prey of trypanosome nymphs around Los Angeles would have also required 7 years of normal rainfall to regrow (Wood and Wood, 1967) before the next set of rodent nests and their contained wood rat prey would be available to feed local assassin bug juveniles, let alone more blood meals for the flying adults preying upon humans instead of wood rats.

Are the many protozoan, bacterial, and viral parasites of humans today, together with their unicellular HAB allergen exacerbants of infectious diseases, simple reflections of retrograde evolution, in which multicellular organisms are no longer fit, compared to their single-cell parasitic competitors and marine poison sources? Clearly, burnt wood rat nests and starvation of assassin nymphs to prevent trypanosomiasis during deadly and costly wildfires in California’s draught-prone chaparral canyons and xeric forests, let alone destruction of adjacent human houses and cities, would no more be feasible solutions for pending ecomedical crises than cessation of building seaside structures in hurricane-prone areas of the back end plate of this book. Indeed, assassin bugs live in other ecosystems, from coastal deserts to tropical jungles, which may contain even more dangerous microbial competitors for humans.

Unlike more diverse potential prey of other mammals in subtropical South America, at least in California large nests of the initial wood rat prey Neotoma fuscipes provided beginning blood meals of the young wingless nymph stages of the assassin bug carrier Triatoma protracta of American trypanosomiasis. Like other assassin bug carriers, this disease was also caused by the protozoan T. cruzi upon passage to humans during bites of the flying adult assassin bug on the lips, mouth, and eyes of sleeping humans, while next obtaining more blood meals. Where seaside HABs were also present to elicit human immune synthesis of instead Th2 cytokines to deal with inhaled allergens (Berger, 2000), less Th1 cytokine responses to remove internal parasites may have occurred (Shirtcliffe et al., 2002; Fekih et al., 2010; Bragina et al., 2014, 2016).

By 2006, human cases of trypanosomiasis had also reached New Orleans, Louisiana (Dorn et al., 2007), and Veracruz, Mexico, but with the unfortunate diagnostic genotype TcII of T. cruzi origins in Bolivia (Bern et al., 2009); Paraguay, and Brazil (Sangenis et al., 2015), South America, found for the first times recently in both southern US (Herrera et al., 2015) and northwest Mexican (Ramos-Ligonio et al., 2012) regions. Were these apparent round trips of protozoan parasites, trypanosome carriers, and cotraveling butterfly and bat tracers of insect migrations from North to South America and back again over different seasonal, decadal, and millennial timescales the unwanted interhemispheric harbingers of more tropical disease relocations during future climate changes?

Will they be accompanied by greater wind-borne influxes of HAB, dichlorodiphenyldichloroethane (DDT), mercury neurotoxins, and endocrine disruptors during more future return trips, skirting the nearshore northern GOM depocenters of unwise legacy chemicals left behind there on that sea floor, as well as on other global ones? Like mosquitoes and tsetse flies, those triatomines also bit their sleeping victims for an obligatory blood meal. But passages of their T. cruzi parasites within triatomine feces left at the wound site made by the bite (Bern et al., 2011) did not occur until spread by the victim while scratching. This assassin insect was thus known as the kissing bug, since human lips and eyes were favorite targets, before entrance of fecal T. cruzi parasites into humans (Bern et al., 2011; Telleria and Tibayrenc, 2017).

The first known infestations of humans by T. cruzi in South America about 4000–5000 years ago were found by measuring that protozoan’s DNA within human mummies in the Atacama Desert of Chile (Guhl et al., 1995), compared to 450 years ago in the Minas Gerais State of Brazil (Lima et al., 2008). Subsequent trypanosomiasis events occurred during later colonial times of European discoverers, or invaders, depending upon whose point of view prevailed during composing of such histories.

Darwin also described the predatory behavior of presumably Patagonian T. infestans hosts of T. cruzi parasites during a visit to the Andean foothills of Mendoza, Argentina: At night I experienced an attack (for it deserves no less a name) of the Benchuca, a species of Reduvius, the great black bug of the Pampas. It is most disgusting to feel soft wingless insects, [the young nymphs of the assassin bugs are wingless, but still feed on mammal blood found in usually wood rat nests as prefered prey, while the adults fly like mosquito and tseste fly vectors of other protozoan parasites] about an inch long, crawling over one’s body.

Before sucking they are quite thin, but afterwards they become round and bloated with blood, and in this state are easily crushed. One which I caught at Iquique (for they are found in Chile and Peru) was very empty. When placed on a table, and though surrounded by people, if a finger was presented, the bold insect would immediately protrude its sucker, make a charge, and if allowed, draw blood. No pain was caused by the wound. It was curious to watch its body during the act of sucking, as in less than ten minutes it changed from being as flat as a wafer to a globular form. This one feast, for which the benchuca was indebted to one of the officers, kept it fat during four whole months; but, after the first fortnight, it was quite ready to have another suck (Darwin, 1839).

It is still unknown what actually killed him, despite about 45 recent diagnoses (Colp, 1977) and descriptions of Darwin’s morbidities over the next 40 years before his death, including those reminiscent of lingering chronic sleeping sickness (Adler, 1959) due to at least T. brucei gambiense in West Africa. Yet he evidently did not say that nymphs of the Argentine assassin T. infestans, hosts of Chagas disease, actually bit him, and their Peruvian adult counterparts feasted on a ship’s officer’s finger, not on Darwin, as a source of liquid food. However, the saliva of the blood-feeding assassin bug was an anesthetic to keep the human and other mammals unware of the initial bites, such that Darwin could have slept through the initial feeding of the Argentine assassin nymphs.

Thus he may have instead also died of heart disease—as either a natural fate of 19th-century living or a contributory factor of end-stage trypanosomiasis, since waiting on the Plymouth quay for the Beagle to depart in 1831, he wrote at the age of 22: I was also troubled with palpitation and pain around my heart, and like many a young ignorant man, especially one with a smattering of medical knowledge, I was convinced that I had heart disease. I did not consult any doctor, as I was fully convinced I would hear a verdict that I was not fit for the voyage and I was resolved go at all hazards (Darwin, 1839). Of course, this was a valid concern on his part, but he made a commendable decision and went on to live until an age of 73.

However, additional physical causes of Darwin’s subsequent long sickness in England might also have been brucellosis (Simpson, 1958), lactose intolerance (Campbell and Matthews, 2005), Crohn’s disease (Orrego and Quintana, 2007), and other gastrointestinal disorders, besides malign DNA mutations due to inbreeding, that is, consanguinity of the Darwins and Wedgwoods (Hayman, 2013). Inevitable psychosomatic mental afflictions of hypochondria, anxiety state, panic and bereavement syndromes, as well as chronic depression, were also advanced as more fatal causes (Hubble, 1943; Woodruff, 1965; Colp, 1977; Bernstein, 1984; Bowlby, 1990; Barloon and Noyes, 1997).

I believe that Darwin was organically ill (the case for his having Chagas’ disease is clearly a strong one) but was also the victim of neurosis; and that the neurotic element in his illness by the very obscurity of its origins [not described until Chagas (1909)]; by his being ‘genuinely’ ill, that is to say and having nothing to show for it – surely a great embassment to a man whose whole intellectual life was a marshalling and assay of hard evidence … If this interpretation represents any large part of the truth the physicians who inclined to think Dawin a hypochondriac cannot be held blameless, in spite of the fact that the diagnosis of his ailment, if it was indeed Chagas’ Disease, was entirely byond their competence.

(Medawar, 1967).

In any event, the reality of physical health afflictions due to South American terrestrial protozoan parasites, first described by Darwin, not believed by some and perhaps now exacerbated by asthma-inducing coastal HABs, eventually also spread to North America. By 2004 [World Health Organization (WHO), 2008], American trypanosomiasis, or Chagas disease, had fivefold more malign ill-health impacts in both Americas from T. cruzi than those caused in both hemispheres by malaria parasites (Plasmodium spp.).

By contrast, the saliva of other nonhematophagous reduviid assassin predators consisted of a venomous poison, like modified saliva toxins of snake bites (Table 1.1), to instead liquefy the insides of those insect prey to be later sucked out (Evangelin et al., 2014). Instead of the acute toxicity of Australian brown snakes (Table 1.1), however, this invertebrate assassin bug poison of Rhynocoris marginatus amounted to a mean LD50 of only ~850 mg kg−1 against the agricultural pest, Oriental leafworm moth Spodoptera litura (Sahayaraj and Muthukumar, 2011).

Although no Triatoma spp. assassin bugs survived in the Florissant insect fossil beds of Colorado about 34 million years ago (Myer, 2003), they now occupy most southwestern US states, transported north by both parasitized Latin American human emigrants and seasonal American Monsoon tailwinds, like Aedes mosquitoes (Fig. 2.16) and monarch butterflies, when they were not actively flying. Also around Los Angeles, whenever the local adult stages of assassin bugs were capable of winged dispersion flights (Wood and Wood, 1967), regular northward winds occurred on that western side of the Rocky Mountains.

They were associated with seasonal surface reversals of the southward-flowing California Current to become the northward Davidson Current and would have also airlifted this insect plague to Oregon and other points north. Fortunately, Karenia HABs were absent from both currents so as to not further complicate seaside human immune system responses there. Yet perhaps equally malign public health problems for tourists and residents were induced instead by fungal attacks of Californian coccidioidomycosis and dangers of amnesic shellfish poisonings (ASP) caused by marine diatom domoic acids of nearshore waters (see Sections 1.2.2 and 1.10.5.2).

Once relocated in North American sylvatic and domestic habitats, there were also enough diverse regional mammal protein reservoirs of wood rats, raccoons, opossums, armadillos, bats, cows, dogs, and unfortunate humans to provide blood meals for now 11 dominant species of dispersed terrestrial triatomines. Like plentiful food supplies in South America for T. infestans, regional eradication of another widespread parasitic disease of humans may now be unlikely, with T. gerstaeckeri as the dominant US assassin bug carrier of T. cruzi (Bern et al., 2011).

Moreover, apparent dispersion and exacerbation of internal lung diseases of bacterially mediated TB (Fig. 2.11) and another protozoan-caused malaria (Figs. 2.12 and 2.15) occurrences across North America were compounded by external factors of smoke, HAB, and mineral aerosol allergens, which impacted asthma and other pulmonary severities (Fig. 2.9). Human residents of the US Southwestern regions were not usually affected by windblown particle transports, except perhaps by silicosis, or dust pneumonia, during prior dust bowls of Section 6.1.2 and by recently increased high-speed car wrecks during desert dust storms.

Yet their spatial patterns of the resultant intensities of infectious diseases inside them (trypanosomiasis, as well as aspergillosis, coccidioidomycosis, hemorrhagic fevers, histoplasmosis, malaria, pneumonia, and TB), all from locally inhaled aerosols of dinoflagellate HAB asthma triggers and fungal spores or transmissions from insect bites, did still partly depend upon airborne allergens surrounding them, once a disease vector was present.

These allergenic stimuli invoked additional Th2 cytokine rather than just Th1 parasite responses of their binary immune systems. Thus I hypothesized that today’s realized human victims of Chagas disease in North America were basically a repetition of prior GABI microbial events. Again, first epicenters had reoccurred in Texas, California, and Mexico, amounting in 2005 to ~1,100,000 victims of Chagas disease in Mexico and another 300,000 infected individuals at wind-guided entry points in the United States. Earlier triatomine carries had been reported within South Texas in the 1930s, followed there by Chagas disease events during the 1940s and 1950s (Hotez, 2018).

During annual migrations of butterflies and bats, together with more episodic transfers of agricultural, wildfire, and urban heating smokes, coal ashes, desert dusts, radionuclides, HAB, and chemical pollutant aerosol plumes, most of these poleward monsoon imports to coastal eastern North America, had prevailed each year. By 2017, they now included Chagas infections, which had then also spread to a reportable disease stage, eliciting Th1 cytokine responses (Nardy et al., 2015; Morrot et al., 2016), within six Midwestern US states of Arizona, Arkansas, Louisiana, Mississippi, Tennessee, and Texas (Bennett et al., 2018). Those last events were perhaps part of global expansion of this type of human sleeping sickness during 2004–14.

The North American Monsoon winds on the eastern side of the Rocky Mountains usually began in July (Adams and Comrie, 1997), with seasonal maxima of summer–fall precipitation in northeastern Mexico and Texas until mid-September. Yet some simulated forward air mass HYSPLIT trajectories of 87.1% PM2.5 sizes of smoke from seasonal agricultural biomass burnings on the Yucatan Peninsula during mainly May 22–29, 2006, followed similar paths of other Mesoamerican aerosol dispersions. They exhibited 5-day transits from above the eastern Mexican coastline, across Texas and Oklahoma to Illinois, Kentucky, and Tennessee, then reaching Washington, DC, at an altitude of ~250 m (Yokelson et al., 2009).

Like these spatial patterns of (1) reported smoke trajectories in 2006, (2) TB and (3) malaria occurrences (Figs. 2.11 and 2.12) among humans of the United States during 2014, carried together with the other wind-borne (4) dipterid invasions of mosquito hosts of these diseases and that of (5) yellow fever from Aedes aegypti, they all followed the same paths in 2016 (Fig. 2.16A). Moreover, their poleward penetrations of North America also mimicked the similar distributions of monarch butterflies D. plexippus during multiyear return migrations at the seasonal end of the North American Monsoon, from Mexico to eastern Canada (Brower, 1995). There, they finished grazing upon milkweed Asclepias spp. and began the reverse migration to overwinter once more in Mexico, like the return of free-tailed bats Ta. brasiliensis to South America.

Without a cross-generational road map from butterfly elders to lead migratory American insect swarms over long distances of more than one annual cycle, like seasonal migratory patterns of African elephant and wildebeest herds, how did the monarch butterflies navigate back home to their green fields of milkweeds? The simple answer may have been to fly aloft during the poleward American monsoons, which also transported HAB allergens, sea sprays, infected mosquito carriers (Figs. 2.10, 2.13, 2.14, and 2.16), and more toxic organic mercury compounds (Fig. 1.6) onshore and inland. However, D. plexippus butterflies also used a UV-light magnetic compass (Guerra et al., 2014), like that of fruit flies Drosophila melanogaster (Qin et al., 2016), to tell which way was south during overwintering migrations.

Given the converse north–south alignment of the Indian subcontinent in relation to other seasonal monsoon winds, moreover, those migratory butterflies exhibited instead an east–west migratory pattern under typical wind velocities of ~10 m s−1, compared to usual butterfly speeds of ~4 m s−1, that is, 10-fold less than that of bats. During April–June premonsoon periods of India, other Danaine milkweed herbivores Tirumala dravidarum (Dakhan dark blue tiger) and Euploea core (Indian common crow) butterflies move eastward toward the Bay of Bengal and the Eastern Ghats. During the October–November postmonsoon periods, they return to the Western Ghats (Kunte, 2005) and the southwest Kerala coast. There, large seasonal HABs of Karenia spp. routinely occurred (Fig. 2.21), causing pulmonary hospitalizations, while perhaps no longer rare, cryptic cases of human trypanosomiasis, due to T. evansi, also recently emerged along northwest Gujarat State (Bharodiya et al., 2018) (see Section 2.7.5).

Finally, this same microbial cause of animal and now evidently human sleeping sickness, that is, T. evansi, presumably carried to Uruguay during colonial times by infected horses of Spanish conquistadors and now transmitted there by vampire bats D. rotundus, was recently isolated from an infected dog (Greif et al., 2017). This animal lived at a distance of ~450 km inland from the Atlantic seaside near Montevideo, where very toxic HABs, including Ostreopsis spp., thrived on the Brazilian shelf (Walsh et al., 2017), near the mouth of the Rio de la Plata (Fig. 2.17). Furthermore, much closer to the sea off Vietnam near the Mekong River Delta, where colonial diazotrophs Trichodesmium also fueled more very toxic HABs of Ostreopsis siamensis (Schmidt, 1901), a first case of human trypanosomiasis caused by T. evansi was recently presented there in 2015 (Chau et al., 2016).

Accordingly, my overall hypothesis of this book was that each of the North American, Indian, South American, and Asian terrestrial evolutionary infection performance stages of Earth’s ever changing poison play at local ecological theaters (Hutchinson, 1965), discussed thus far, included marine plankton. They were essential, even if unrecognized players (actors) on a ~70% water-covered planet of dominant regional monsoon winds, transporting intercontinental dust aerosol allergens, insect carriers of infectious diseases, fungal predators, and HAB triggers of exacerbating asthma attacks.

Indeed, as an example of planetary serendipity, illustrated first here in the Americas and from a pragmatic human actuarial point of view, those regional dinoflagellate HABs have served in the past as counterbalances to other land microbial poisoners. When HABs and other inhaled allergens were present, requiring human syntheses of Th2 cytokines by their binary immune systems, less energies and time would have been devoted to biochemically repelling internal parasites, with greater malign results of more widespread and more fatal infectious diseases.

Stepping way outside the box, one might even consequently infer that HABs have waited and watched over decades, if not millennia, for them in their own time frame, while aerial imports of parasite demands on the human immune systems of North America have increased far inland away from the ancestral GOM. Wind-borne protozoan trypanosomiasis and malaria infections, bacterial TB and pneumonia mortalities, together with fungal invasions and viral hemorrhagic fevers have been the foci of instead Th1 cytokine syntheses. By borrowing unicellular competition strategies of earlier evolved coastal marine ecosystems, now operant as the smaller residual seas of the saltwater legacy of each human body, perhaps we can use extant biological warfare weapons of microbes to continue our competitions with now drug-resistant viral, bacterial, and protozoan sources of pathogenic toxins.

Those parasitic predators are still pitted in an external world against a contemporary declining poleward amount of HAB allergens outside of the GOM. In some regions, however, these biotic allergens were nevertheless supplemented by mineral ones of Midwestern US drought, desert, and coal-fired power plant fly ash sources of <8 μm sizes (Figs. 1.7 and 2.10). They also elicited additional human demands for more Th2 cytokine interventions. The same pattern of ecomedical synergy in different physical habitats will emerge here later in the upcoming discussions of (1) the American dust bowl, (2) Asian desert dust and HAB allergens, (3) regional European silico-TB, (4) African and Indian human trypanosomiasis, and (5) global trophic cascades due to overfishing in Chapter 6, Future numerical consiliences, with perhaps again emergences of no longer ignored ancient marine fungal diseases.

Hopefully, we slow growing humans can learn to leverage present dichotomies of marine and land poisoners to thwart future increased death threats from quickly dividing terrestrial microbial parasites, without foolishly setting marine cats to catch land rats. Recall, for example, that importations of Herpestid mongoose to kill rats and snakes in the West Indies, Hawaii, and Okinawa had the unanticipated results of the destruction of local ground-based fauna. Furthermore, note here the consequences of unwise imports of some cattle to Africa and horses to South America.

1.2 Fungal parasites

With an evolutionary history of ~1.0–2.5 billion years (Bengtson et al., 2017), the fungus has basically always been among us from