the most dangerous animals on Earth. Two points in the P. falciparum life cycle require the parasite to contact the host cell, invade it, and ultimately take control of it. The parasitic cells contain receptors that recognize and bind surface protein on both hepatocytes for the exoerythrocytic cycle and red blood cells in the erythrocytic cycle. This ensures that the parasite invades the correct cell type required for completing the life cycle. Human cells seem to exert little to no control of P. falciparum cells. In fact, humans generate antibodies that prevent the immune system from keeping the parasites from invading erythrocytes (Guevara Patiño et al. 1997). It is like a wrestler tying his wrists together to prevent him from putting his opponent in an arm bar. The only real attempt from the human body to control the invader is to release TNF after monocytes or macrophages bind the parasite, triggering a raging fever and debilitating body aches. This relationship between P. falciparum and humans takes place in the common medium of the human bloodstream interstitial space around hepatocytes, and within human cells. The parasites thrive in each of these chemical environments as do human cells in the absence of the parasite. P. falciparum individuals are so adept at thriving in these vertebrate environments that they trigger the production of antibodies discussed above that prevent human cells from blocking the erythrocytic invasion (Guevara Patiño et al. 1997). The chemical environment changes dramatically once the immune system reacts to the presence of the parasite. Human cells and Plasmodium cells struggle to thrive under the conditions created by TNF. While the body may kill the parasites and prevent further cycles, it does so at the expense of its own flourishing. 2. Original design interface Most readers of Genesis 1, if believing it to be historical narrative, cannot reconcile a relationship like this with a creation that God would declare “very good.” While both members of the symbiotic relationship have the six characteristics of life, they do not seem to be experiencing the flourishing encompassed in nephesh life. It seems that the death God declared would come as soon as Adam and Eve ate of the tree of life has distorted the design and purpose of this relationship. Research indicates that each of the species of Plasmodium may have moved into humans independently (Prugnolle et al. 2011). Plasmodium falciparum seems to have originated in gorillas, and switched hosts when Anopheles transmitted them to humans. It is interesting that P. falciparum demonstrates an ability to take control of cells in human systems and can thrive in the chemical environment within human cells. This indicates that the design in these symbionts is robust enough to use receptors different than those they were specifically designed to interface with. It seems the parasite can be used in a variety of engineered systems with varying levels of success. In fact, Plasmodium species are notorious for host switching, sometimes contributing to terrible pathology in the new hosts. These new hosts, including humans with P. falciparum seem to be unable to control the parasite because they were not designed to interface with them. It is quite possible that no organism was designed to interface with Plasmodium spp. Most research indicates that all Plasmodium spp. and similar parasites in other genera originated from coccidians that completed the entire life cycle within a single host. Coccidians are the largest subclass of Apicomplexan protists and are obligate intracellular parasites of animal intestinal tracts (Marugan-Hernandez et al. 2021). This ancestor likely evaded host immune response or was held in check by host cell control. It is likely that this ancestor and its vertebrate host had a well-developed interface like those seen in the mutualistic relationships discussed previously. As death entered creation, interface components broke down and symbionts entered foreign systems. B. Schistosomiasis Schistosoma mansoni, and other species of blood fluke flatworms in this genus, cause a disease known as schistosomiasis. Like malaria, schistosomiasis has been known for as long as humans have been leaving records. One major difference between the two is the large size of Schistosoma spp. when compared to Plasmodium spp. Both Schistosoma larva and adult, and the durability of the eggs, mean the parasite leaves more lasting evidence behind. In fact, at least 50 records of this disease exist in Egyptian papyri, and Egyptian mummies often contain calcified eggs of the worms (Di Bella et al. 2018). Physicians in Napoleon’s army recorded pathology of schistosomiasis, and within 50 years, Theodor Bilharz discovered evidence of the worm responsible for infecting more than a fourth of all people in Egypt (Di Bella et al. 2018). English surgeons found the parasite in an ape dying in the London Zoo and by World War I both disease and the blood fluke were well known across Europe (Roberts et al. 2012). Schistosomian blood flukes are some of the most feared parasites in the world, with more than 800 million people at risk. It is likely that more than 200 million people are currently infected with schistosomiasis, with 125 million symptomatic, and 20 million with severe disease (Di Bella et al. 2018). The most common sign of schistosomiasis is bloody urine (most common with Schistosoma haematobium) or bloody diarrhea. During the acute phase of infections, the patient suffers from fever, fatigue, headache, malaise, muscle aches, lymphadenopathy (swollen lymph nodes), and gastrointestinal discomfort. If the disease moves to the chronic phase, hosts suffer from bloody urination or diarrhea with abdominal pain and lethargy. In some S. mansoni and S. japonicum infections, eggs block the hepatic portal system and cause ascites, which is a build-up of fluid in the belly. The pathology of Schistosoma spp. is uniquely caused primarily by eggs. While adult worms in the veins present plenty of antigen to the immune system, the release of eggs triggers the immune response and pathology associated with the disease. One response is the production of various white blood cells that include eosinophils, neutrophils, and macrophages. These contribute to the formation of an aggregation of macrophages, called granulomas, around the eggs (Roberts et al. 2012). The formation of granulomas contributes to the release of TNF that causes the pathology of the acute phase. The pathology of the chronic phase is usually the result of the granulomas lodging in vessels or triggering the production of fibroblasts. In heavy infections, with massive fibroblast development, the intestinal wall and/or bladder wall become ulcerated (Roberts et al. 2012). This ulceration can lead to genital and kidney involvement, and even urinary tract blockages, secondary bacterial infections, bladder cancer, and bladder calcification. This is another parasite that is both common and devastating. There is little doubt that something has gone wrong with original Schistosoma relationships as death entered creation. HENNIGAN, GULIUZZA, INGLE, and LANSDELL Interface systems model in key global symbiotic relationships 2023 ICC 236
RkJQdWJsaXNoZXIy MTM4ODY=