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ISSN: 2766-2276
Biology Group. 2024 June 14;5(6):584-587. doi: 10.37871/jbres1930.

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open access journal Short Communication

Return to a Warmer Climate of the Middle Pliocene will Boost Bacterial, Viral and Protozoan Parasite Pathogen Induced Diseases

Kevin Roe*

Retired, United States Patent and Trademark Office, San Jose, California, USA
*Corresponding authors: Kevin Roe, MPH Program Director, United States Patent and Trademark Office, San Jose, California, USA E-mail:
Received: 11 June 2024 | Accepted: 12 June 2024 | Published: 14 June 2024
How to cite this article: Roe K. Return to a Warmer Climate of the Middle Pliocene will Boost Bacterial, Viral and Protozoan Parasite Pathogen Induced Diseases. J Biomed Res Environ Sci. 2024 Jun 14; 5(6): 584-587. doi: 10.37871/jbres1757, Article ID: jbres1757
Copyright:© 2024 Roe K. Distributed under Creative Commons CC-BY 4.0.
Keywords
  • Pliocene
  • Climate
  • Bacteria
  • Viruses
  • Protozoan parasites
  • Vectors

A return to the climate of the middle Pliocene is probable within this century and the increased temperatures, particularly at higher latitudes, will boost the spread of several bacterial, viral and protozoan parasite pathogens which cause severe and/or lethal diseases. The warmer climate effects on the spread and evolution of some fungal pathogens may also increase their virulence, although probable, this is less certain. The increase in the range and pathogen populations in the various hosts and vectors during a return to the middle Pliocene epoch will also increase the probability that several pathogens will evolve more immuno-evasive genetic strains which will be more dangerous for humans and animals. There could also be severe impacts on livestock and agricultural food chains.

The middle of the Pliocene epoch occured between 3.3 and 3.0 million years ago and had an average global temperature 2 to 3 degrees Celsius higher than the average of the 19th century taken as a baseline.1 These temperatures are now expected to be reached or surpassed before the year 2100, [1]. The global continental geography and tropical temperatures in the middle Pliocene were approximately the same as today [1]. However, the middle Pliocene sea level was approximately 25 meters higher and temperatures in the high latitudes above 70 degrees were between 10 to 20 degrees Celsius warmer than the baseline temperatures.1 This also raises the important question of what global impacts a return to a climate of the middle Pliocene will have on human and animal diseases caused by various pathogens, including viruses, fungi, bacteria and protozoan parasites. Furthermore, several pathogen carrying vectors (e.g., moquitoes, fleas, ticks, other insects, and plausibly bats) are likely to thrive in a warmer climate.

Bacterial disease consequences

Even before climate warming, several tropical diseases have significantly afflicted the global human population [2-6]. Several bacterial pathogens cause dangerous diseases, including Vibrio cholerae (cholera, potentially lethal), Mycobacterium ulcerans (buruli ulcer, affecting bones or skin), Mycobacterium leprae (leprosy), Mycobacterium tuberculosis (tuberculosis), Chlamydia trachomatis (causes trachoma, permanent blindness), Borrelia burgdorferi (causes Lyme disease) [2,3].

Protozoan parasite consequences

Several protozoan parasites cause dangerous diseases, including Trypanosoma cruzi (causes American trypanosomiasis (Chagas disease)), Leishmania amazonensis, L. donovani, L. infantum and L. major (cause potentially lethal leishmaniasis), and Trypanosoma brucei (Human African Trypanosomiasis (HAT), also called sleeping sickness), and Plasmodium falciparum, P. vivax, P. ovale, P. malariae and P. knowlesi (all can cause malaria and are spread by Anopheles mosquitoes) [3-6].

Viral consequences

Viral pathogens, several hosted in nonhuman mammals (e.g., bats, pigs) and/or transmitted by Aedes aegypti or Culex mosquitoes, can spread dangerous diseases, including dengue virus-2 (dengue fever), chikungunya virus (chikungunya), West Nile virus (West Nile fever), Rift Valley virus (Rift Valley fever) and Zika virus (Zika), Japanese encephalitis virus (encephalitis), yellow fever virus (yellow fever), Ebola virus (Ebola disease) and Nipah virus (Nipah disease) [3,6-9]. Many of these pathogens use regulatory RNA and/or proteins to evade or manipulate the innate and adaptive immune defenses of the vectors and/or hosts [3-6]. Acute or chronic infections by several of these pathogens can also cause severe cardiovascular diseases, respiratory diseases, neurological disorders, encephalitis, or renal disorders (e.g., Plasmodium malaria, Zika virus, dengue virus, Nipah virus, Ebola virus).

The return to a warmer middle Pliocene climate should substantially boost the geographical range, populations and faster reproduction of several bacterial and viral pathogens and protozoan parasites that already cause diseases. One reason is because many pathogens spread more easily and/or reproduce more easily in warmer climates. Studies at moderately higher temperatures confirm faster replications, mutations and transmissions of West Nile virus by Culex mosquitoes [8] and enhanced transmission of dengue fever virus by Aedes mosquitoes [9].

Vector consequences

Furthermore, mosquitoes and other insects can thrive in warmer climates, and mosquitoes and other insects act as vectors in the transmission of several viral, bacterial or protozoan parasite pathogens causing severe diseases [6,8,9]. And mosquitoes act as vectors in the transmission of some protozoan parasites, including Plasmodium protozoan parasite species causing malaria.6 The increase in these global vector and host populations of bacterial and viral pathogens and protozoan parasites will also increase the probability these pathogens will evolve new genetic strains which will be more immuno-evasive and immuno-manipulative in overcoming vector and human immune systems, and possibly less responsive to currently available medical treatments [8,9]. Several of these pathogens already inflict extensive mortality rates and/or inflict substantial organ damage and suffering during infections, in some cases despite timely medical treatments [3,4,6,8,9].

Fungal consequences

There are also fungal pathogens that may be able to evolve and thrive in a warmer middle Pliocene climate. There are several prevalent fungal pathogens, including Crytococcus neoformans and C. gatti (which cause cryptococcosis, frequently lethal) [3,10]. Coccidioides immitis and Coccidioides posadasii cause pulmonary coccidioidomycosis (Valley fever), and coccidioidomycosis is found in warm and dry climates of semi-deserts [11]. Several serious fungal pathogens are found in tropical and sub-tropical regions, including Paracoccidioides brasiliensis and Paracoccidioides lutziiM, which cause paracoccidioidomycosis, which can infect the pulmonary systems of people working outdoors [11]. Talaromyces marneffei, which causes talaromycosis that mainly affects immunocompromised individuals, is also found in tropical and sub-tropical regions [11]. Histoplasma capsulatum, which causes histoplasmosis that can severely affect immunocomprised individuals, occurs under variable conditions ranging from tropical to temperate climates [11].

Candida fungal species can also be dangerous and even fatal for humans, and they have already been evolving [12]. At the end of the 20th century, four species of the Candida genus composed most of the Candida fungal infections in humans, including Candida albicans, C. glabrata, C. parapsilosis, and C. tropicalis. However, a more dangerous pathogenic member of the Candida genus has become increasingly prevalent and resistant to most conventional anti-fungal medicines and disinfectants [12]. Candida auris infections are now causing an increasing percentage of Candida fungal infections. and have been reported to cause serious invasive infections with high mortality rates [12].

Table 1 tabulates several pathogens that may thrive in a warmer middle Pliocene climate, but this table is not comprehensive.

Table 1: Pathogens which will probably thrive in a warmer middle Pliocene climate.
Disease Pathogen Comments
Cholera Vibrio cholerae Bacteria, usually ingested
Trachoma Chlamydia trachomatis Causes blindness
Lyme disease Borrelia burgdorferi Bacteria spread by tick bites
Cryptococcosis Cryptococcus neoformans Fungal pathogen can be fatal
Leishmaniasis Leishmania amazonensis Lethal if visceral
Leishmaniasis Leishmania donovani Lethal if visceral
Leishmaniasis Leishmania infantum Lethal if visceral
Leishmaniasis Leishmania major Non-lethal, cutaneous
Trypanosomiasis Trypanosoma brucei Sleeping sickness
Tuberculosis (TB) Mycobacterium tuberculosis Kills 1.5 million individuals per year
Leprosy Mycobacterium leprae Bacteria controllable by drugs
Chikungunya Chikungunya virus Fatal if untreated
Dengue fever Dengue virus-2 390 million cases yearly, some fatal
Zika Zika virus Fatal if untreated
Japanese encephalitis Japanese encephalitis virus Fatal if untreated
Yellow fever Yellow fever virus Fatal if untreated
West Nile fever West Nile virus CNS cases can be fatal
Rift Valley fever Rift Valley virus Mosquitoes infect humans/animals
Malaria Plasmodium sp. Protozoan spread by mosquitoes
References [4-12]. 
CNS = Central Nervous System.

A return to the climate of the middle Pliocene epoch is virtually certain before the end of this century and the increased temperatures, particularly at higher latitudes, will be favorable for spreading several bacterial, viral and protozoan parasite pathogens which cause severe and/or lethal diseases. The warmer climate effects on the spread and evolution of some fungal pathogens may also increase their virulence, but this is uncertain. The increase in the range and pathogen populations in the various hosts and vectors during a return to the middle Pliocent climate will also increase the probability that several pathogens will evolve more immuno-evasive and/or immuno-manipulative genetic strains which will be more dangerous for humans and animals. There could also be severe impacts on livestock and agricultural food chains. Therefore, it would be preferable to develop new treatments for these pathogens before they cause widespread and uncontrollable disease outbreaks.

There are no acknowledgments.

Data Availability Statement

Not applicable.

Conflict of Interests

The author declares they have no conflicts of interest.

Funding statement

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Author Contribution

KR: Conceptualization, Writing-original draft, Writing-review & editing. No other author contributed to this paper.

Permission to Reproduce

Not applicable.

  1. Robinson MM, Dowsett HJ, Chandler MA. Pliocene Role in assessing future climate impacts. Eos Trans. 2008;89(49):501-502. doi: 10.1029/2008EO490001.
  2. Kaur H, Lynn AM. Mapping the FtsQBL divisome components in bacterial NTD pathogens as potential drug targets. Front Genet. 2023 Jan 4;13:1010870. doi: 10.3389/fgene.2022.1010870. PMID: 36685953; PMCID: PMC9846249.
  3. Roe K. Pathogen regulatory RNA usage enables chronic infections, T-cell exhaustion and accelerated T-cell exhaustion. Mol Cell Biochem. 2023 Nov;478(11):2505-2516. doi: 10.1007/s11010-023-04680-9. Epub 2023 Mar 21. PMID: 36941498; PMCID: PMC10027582.
  4. Henriquez-Figuereo A, Morán-Serradilla C, Angulo-Elizari E, Sanmartín C, Plano D. Small molecules containing chalcogen elements (S, Se, Te) as new warhead to fight neglected tropical diseases. Eur J Med Chem. 2023 Jan 15;246:115002. doi: 10.1016/j.ejmech.2022.115002. Epub 2022 Dec 5. PMID: 36493616.
  5. Pérez-Molina JA, Molina I. Chagas disease. Lancet. 2018 Jan 6;391(10115):82-94. doi: 10.1016/S0140-6736(17)31612-4. Epub 2017 Jun 30. PMID: 28673423.
  6. Bhattacharjee S, Ghosh D, Saha R, Sarkar R, Kumar S, Khokhar M, Pandey RK. Mechanism of Immune Evasion in Mosquito-Borne Diseases. Pathogens. 2023 Apr 23;12(5):635. doi: 10.3390/pathogens12050635. PMID: 37242305; PMCID: PMC10222277.
  7. Leggewie M, Scherer C, Altinli M, Gestuveo RJ, Sreenu VB, Fuss J, Vazeille M, Mousson L, Badusche M, Kohl A, Failloux AB, Schnettler E. The Aedes aegypti RNA interference response against Zika virus in the context of co-infection with dengue and chikungunya viruses. PLoS Negl Trop Dis. 2023 Jul 13;17(7):e0011456. doi: 10.1371/journal.pntd.0011456. PMID: 37440582; PMCID: PMC10343070.
  8. Fay RL, Ngo KA, Kuo L, Willsey GG, Kramer LD, Ciota AT. Experimental Evolution of West Nile Virus at Higher Temperatures Facilitates Broad Adaptation and Increased Genetic Diversity. Viruses. 2021 Sep 22;13(10):1889. doi: 10.3390/v13101889. PMID: 34696323; PMCID: PMC8540194.
  9. Liu Z, Zhang Q, Li L, He J, Guo J, Wang Z, Huang Y, Xi Z, Yuan F, Li Y, Li T. The effect of temperature on dengue virus transmission by Aedes mosquitoes. Front Cell Infect Microbiol. 2023 Sep 21;13:1242173. doi: 10.3389/fcimb.2023.1242173. Erratum in: Front Cell Infect Microbiol. 2023 Oct 24;13:1320461. PMID: 37808907; PMCID: PMC10552155.
  10. Xue X, Deng H, Zhao L, Zang X, Asuquo IP, Meng M, Ma X, Qin C, Meng Y, Wu C, Gao J, Pan L. Cryptococcosis caused by cryptococcus gattii: 2 case reports and literature review. Medicine (Baltimore). 2020 Dec 11;99(50):e23213. doi: 10.1097/MD.0000000000023213. PMID: 33327239; PMCID: PMC7738107.
  11. Salzer HJF, Burchard G, Cornely OA, Lange C, Rolling T, Schmiedel S, Libman M, Capone D, Le T, Dalcolmo MP, Heyckendorf J. Diagnosis and Management of Systemic Endemic Mycoses Causing Pulmonary Disease. Respiration. 2018;96(3):283-301. doi: 10.1159/000489501. Epub 2018 Jun 28. PMID: 29953992.
  12. Roe K. Treatment alternatives for multidrug-resistant fungal pathogens. Drug Discov Today. 2023 Jun;28(6):103596. doi: 10.1016/j.drudis.2023.103596. Epub 2023 Apr 20. PMID: 37086779.

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