Posted by Delight
(here)
Posted by ByTheNorthernSea
(here)
Since one of it's functions is to kill parasites, are we again perhaps looking at Ivermectin as a possible method to combat the parasites in the 'vaccines' (someone else speculated this too in a post I read a couple of days ago - it may have been Bill), as well as being an effective COVID treatment?
Maybe - this perhaps a is a long shot - that's why the authorities are waging such an outright war on IM...they knew a while ago that it has the potential to cripple their plans through limiting the parasite damage from the 'vaccines', which they obviously couldn't allow?
I think this is the case... and we are not alone.
Clin Microbiol Rev. 2011 Oct; 24(4): 655–681.
doi: 10.1128/CMR.00005-11
PMCID: PMC3194829
PMID: 21976603
Trypanosoma cruzi and Chagas' Disease in the United States
Caryn Bern,1,* Sonia Kjos,2 Michael J. Yabsley,3 and Susan P. Montgomery1
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This article has been cited by other articles in PMC.
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Abstract
Summary: Chagas' disease is caused by the protozoan parasite Trypanosoma cruzi and causes potentially life-threatening disease of the heart and gastrointestinal tract. The southern half of the United States contains enzootic cycles of T. cruzi, involving 11 recognized triatomine vector species. The greatest vector diversity and density occur in the western United States, where woodrats are the most common reservoir; other rodents, raccoons, skunks, and coyotes are also infected with T. cruzi. In the eastern United States, the prevalence of T. cruzi is highest in raccoons, opossums, armadillos, and skunks. A total of 7 autochthonous vector-borne human infections have been reported in Texas, California, Tennessee, and Louisiana; many others are thought to go unrecognized. Nevertheless, most T. cruzi-infected individuals in the United States are immigrants from areas of endemicity in Latin America. Seven transfusion-associated and 6 organ donor-derived T. cruzi infections have been documented in the United States and Canada. As improved control of vector- and blood-borne T. cruzi transmission decreases the burden in countries where the disease is historically endemic and imported Chagas' disease is increasingly recognized outside Latin America, the United States can play an important role in addressing the altered epidemiology of Chagas' disease in the 21st century.
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INTRODUCTION
Chagas' disease is caused by the protozoan parasite Trypanosoma cruzi (234). World Health Organization disease burden estimates place Chagas' disease first among parasitic diseases in the Americas, accounting for nearly 5 times as many disability-adjusted life years lost as malaria (343). An estimated 8 million people are currently infected, and 20 to 30% of these will develop symptomatic, potentially life-threatening Chagas' disease (Table 1) (214). T. cruzi is carried in the guts of hematophagous triatomine bugs; transmission occurs when infected bug feces contaminate the bite site or intact mucous membranes. T. cruzi can also be transmitted through transfusion, through transplant, and congenitally (177, 234).
Table 1.
Countries where Chagas' disease is endemic and estimates of the seroprevalence and number of infected inhabitants
Region Country where Chagas' disease is endemica Estimated seroprevalence (%)b Estimated no. of infected individualsb
North America United States NDA 300,167c
Mexico 1.03 1,100,000
Central America Belize 0.74 2,000
Costa Rica 0.53 23,000
El Salvador 3.37 232,000
Honduras 3.05 220,000
Guatemala 1.98 250,000
Nicaragua 1.14 58,600
Panama 0.01 21,000
South America Argentina 4.13 1,600,000
Bolivia 6.75 620,000
Brazil 1.02 1,900,000
Chile 0.99 160,200
Colombia 0.96 436,000
Ecuador 1.74 230,000
Guyana 1.29 18,000
Suriname NDA NDA
French Guiana NDA NDA
Paraguay 2.54 150,000
Peru 0.69 192,000
Uruguay 0.66 21,700
Venezuela 1.16 310,000
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aVector-borne T. cruzi transmission occurs, or occurred until recently, in parts of these countries.
bDisease burden estimates are for the year 2005, based on references 29 and 214. NDA, No data available.
cThe number for the United States reflects the estimated number of infected immigrants from countries in Latin America where the disease is endemic. No estimate of the number of locally acquired infections is currently available.
Historically, transmission and morbidity were concentrated in rural areas of Latin America where poor housing conditions favor vector infestation. However, in the last several decades, successful vector control programs have substantially decreased transmission in rural areas, and migration has brought infected individuals to cities both within and outside Latin America (87, 111, 196). Since 1991, several subregional initiatives have made major advances in decreasing vector infestation in human dwellings and extending screening of the blood supply for T. cruzi (87, 269). In 2007, control efforts in Latin America were formally joined by an initiative to address the “globalization” of Chagas' disease, recognizing the increasing presence of imported cases in Europe, North America, and Japan and the potential for local transmission through nonvectorial routes (344). The United States occupies an ambiguous position in this new initiative. While the United States has never participated in Latin American Chagas' disease control programs, it cannot be classified as an area where the disease is “not endemic” in the same sense as Europe or Japan. The southern tier of states from Georgia to California contains established enzootic cycles of T. cruzi, involving several triatomine vector species and mammalian hosts such as raccoons, opossums, and domestic dogs (26, 151, 345). Nevertheless, most T. cruzi-infected individuals in the United States are immigrants from areas of endemicity in Latin America (29).
This article will present an overview of clinical and epidemiological aspects of Chagas' disease, with a focus on data and issues specific to T. cruzi and Chagas' disease in the United States. Topics to be covered include vector biology and ecology, animal reservoirs, T. cruzi strain typing, human Chagas' disease, and future research needed for control of Chagas' disease in the United States.
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TRYPANOSOMA CRUZI LIFE CYCLE AND TRANSMISSION
Life Cycle
Nearly all the salient features of the T. cruzi life cycle were described by Carlos Chagas, the scientist who discovered the organism, in 1909 (62). T. cruzi is a kinetoplastid protozoan which infects vertebrate and invertebrate hosts during defined stages in its life cycle (234, 292). The triatomine vector ingests circulating trypomastigotes when it takes a blood meal from an infected mammalian host. In the midgut of the vector, trypomastigotes transform through an intermediate form sometimes called a spheromastigote to epimastigotes, the main replicating stage in the invertebrate host. Epimastigotes migrate to the hindgut and differentiate into infective metacyclic trypomastigotes, which are excreted with the feces of the vector. Metacyclic trypomastigotes enter through the bite wound or intact mucous membrane of the mammalian host and invade many types of nucleated cells through a lysosome-mediated mechanism (50). In the cytoplasm, trypomastigotes differentiate into the intracellular amastigote form, which replicates with a doubling time of about 12 h over a period of 4 to 5 days. At the end of this period, the amastigotes transform into trypomastigotes, the host cell ruptures, and the trypomastigotes are released into the circulation. The circulating parasites can then invade new cells and initiate new replicative cycles, and they are available to infect vectors that feed on the host. In the absence of successful antitrypanosomal treatment, the infection lasts for the lifetime of the mammalian host.
Transmission Routes
Vector-borne transmission.
The vector-borne transmission route, occurring exclusively in the Americas, is still the predominant mechanism for new human infections. The feces of infected bugs contain metacyclic trypomastigotes that can enter the human body through the bite wound or through intact conjunctiva or other mucous membranes.
Congenital transmission.
Between 1 and 10% of infants of T. cruzi-infected mothers are born with congenital Chagas' disease (14, 24, 289). Congenital transmission can occur from women themselves infected congenitally, perpetuating the disease in the absence of the vector (263). Factors reported to increase risk include higher maternal parasitemia level, less robust anti-T. cruzi immune responses, younger maternal age, HIV and, in an animal model, parasite strain (9, 32, 34, 107, 289).
Blood-borne transmission.
Transfusional T. cruzi transmission was postulated in 1936 and first documented in 1952 (109, 307). The risk of T. cruzi transmission per infected unit transfused is estimated to be 10 to 25%; platelet transfusions are thought to pose a higher risk than other components such as packed red cells (31, 308). In 1991, the prevalence of T. cruzi infection in donated blood units ranged from 1 to 60% in Latin American cities (268). Since then, blood donation screening has become accepted as an important pillar of the Chagas' disease control initiatives (220, 269). Serological screening of blood components for T. cruzi is now compulsory in all but one of the countries in Latin America where the disease is endemic, and the prevalence of infection in screened donors has decreased substantially (196, 269). Nevertheless, Chagas' disease screening coverage by country was estimated to vary from 25% to 100% in 2002, and the risk of transmission, though much decreased, has not been eliminated (269). The residual risk in Latin America where screening has been implemented is estimated to be 1:200,000 units (269, 308).
Organ-derived transmission.
Uninfected recipients who receive an organ from a T. cruzi-infected donor may develop acute T. cruzi infection. However, transmission is not universal; in a series of 16 uninfected recipients of kidneys from infected donors, only 3 (19%) acquired T. cruzi infection (238). Nineteen instances of transmission by organ transplantation have been documented in the literature (13 kidney, 1 kidney and pancreas, 3 liver, and 2 heart transplants) (16, 61, 66, 79, 99, 101, 157, 238, 279). The risk from heart transplantation is thought to be higher than that from kidney or liver transplantation (65). One case of transmission through unrelated cord blood transplantation has been reported (104).
Oral transmission.
Recently, increasing attention has focused on the oral route of T. cruzi transmission; several outbreaks attributed to contaminated fruit or sugar cane juice have been reported from Brazil and Venezuela (28, 82, 208). Most outbreaks are small, often affecting family groups in the Amazon region, where the palm fruit açaí is a dietary staple that appears to be particularly vulnerable to contamination, perhaps from infected vectors living in the trees themselves (74, 208). The largest reported outbreak to date led to more than 100 infections among students and staff at a school in Caracas; locally prepared guava juice was implicated (82).
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TRIATOMINE VECTOR BIOLOGY AND ECOLOGY
Background
The epidemiology of vector-borne T. cruzi is closely linked to the biological and ecological characteristics of local vectors and mammalian reservoir hosts. Triatomines of both sexes must take blood meals to develop through their nymphal stages to adults, and females require a blood meal to lay eggs. Thus, nymphs and adults of either sex may be infected with T. cruzi, but infection rates increase with increasing vector stage and age. Most domestic triatomine species feed nocturnally and are able to complete their blood meal without waking the host (169). The major Latin American vectors defecate during or immediately after taking a blood meal.
T. cruzi infection is transmitted to wild mammals by sylvatic triatomine species; these bugs often colonize the nests of rodent or marsupial reservoir hosts (169, 311). Sylvatic triatomine adults may fly into human dwellings because of attraction by light and cause sporadic human infections (74). Domestic transmission cycles occur where vectors have become adapted to living in human dwellings and nearby animal enclosures; domestic mammals such as dogs, cats, and guinea pigs play important roles as triatomine blood meal sources and T. cruzi reservoir hosts (69, 124, 131). Some triatomine species can infest both domestic and sylvatic sites and may play a bridging role (192).
There are more than 130 triatomine species in the Americas, many of which can be infected by and transmit T. cruzi (169, 311). However, a small number of highly domiciliated vectors are of disproportionate importance in the human epidemiology of disease (Table 2) (311). The domestic environment provides abundant blood meal sources, and poor quality housing with adobe or unfinished brick walls provides crevices and other diurnal hiding places for triatomines (170, 201). Thatch roofs provide an attractive habitat for some species (117). In communities where the disease is endemic, 25 to 100% of houses may be infested, and a house and its immediate surroundings may support large colonies of juvenile and adult bugs (170, 201, 230).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3194829/
Good find, Delight. I am trying to get a photo of one.