Toxoplasmosis and Effects on Abortion, And Fetal Abnormalities
Toxoplasmosis and Effects on Abortion, And Fetal Abnormalities
The placenta is an immune-privileged organ that may tolerate antigen exposure without eliciting a strong inflammatory response that could result in an abortion. After that, the pregnancy can progress normally. Th1 answers, characterized by interferon-, are essential for suppressing intracellular infections. Therefore, the maternal immune system finds a catch-22 when intracellular parasites invade the placenta. The pro-inflammatory response required to eradicate the virus carries the danger of causing an abortion. Toxoplasma is a potent parasite that causes lifetime infections and is a leading cause of abortions in people and animals. This paper speculates that the pregnancy outcome may be affected by the Toxoplasma strain and the effectors of the parasite, both of which can modify the signaling pathways of the host cell.
Fetuses infected with the protozoan parasite Toxoplasma gondii can develop a disorder known as toxoplasmosis, sometimes called congenital toxoplasmosis. This disease is transmitted from mother to child in the womb. A miscarriage or a stillbirth might happen as a result. A child with this illness may also have significant and progressively deteriorating difficulties in their vision, hearing, motor skills, cognitive ability, and other areas of development. The parasite Toxoplasma gondii is blamed for many pregnancies ending in miscarriage (Arranz-Solís et al., 2021). Most abortions happen in the first trimester of pregnancy or during the early stages of acute sickness. This research aimed to determine if women who had an abortion were more likely to be infected with toxoplasmosis.
To make matters worse, the toxoplasmosis-causing Toxoplasma gondii is an obligate intracellular pathogen that infects nearly every animal species with a thermoregulatory system. Transferring Toxoplasma from one host to another requires the development of tissue cysts that are infectious when ingested. This means the parasite is incentivized to ensure that the host organism lives during the infection. The parasite does this by stimulating an immune response powerful enough to limit parasite reproduction. Toxoplasma, on the other hand, uses a unique set of effectors to evade the immune response and ensure that the parasite population does not decrease to zero.
Type II strains are the most common cause of infection in both animal and human hosts. However, all four clonal lineages of Toxoplasma may be found throughout Europe and North America. It has been established, however, that the bulk of the South American isolates identified is genetically distinct from the strains seen in North America and Europe. Certain sorts of isolates have been labeled as atypical strains. Birth abnormalities apart, type II strains are the most common in Europe and North America, where the great majority of investigations of this kind have been undertaken (Olariu et al., 2019). Although most studies have not shown a connection between type XII strains (the most frequent non-type II strains in North America) and severe congenital toxoplasmosis, a few studies have found such a connection. When the condition was visible at birth, a link was found. In addition, illnesses and miscarriages are linked to nonclonal variants of the parasite Toxoplasma in South American nations (Arranz-Solís et al., 2021). Frequent strains in a given place and a preference for symptomatic infections over asymptomatic ones, from which there are generally fewer samples available, are two possible factors that might have a big influence.
Vertical transmission of T. gondii from mother to fetus might cause miscarriage, stillbirth, or other complications depending on the gestational age of the mother and the fetus at the time of infection. Longer pregnancies are associated with a lower rate of fetal mortality. Fetal immune systems are not completely developed until beyond the first trimester of pregnancy; hence when vertical transmission occurs, it nearly invariably ends in fetal death or abortion. Increased vertical transmission rates during the second trimester of pregnancy are associated with an increased risk of premature birth and serious birth abnormalities, including hydrocephalus, microcephaly, and mental retardation.
Fetal infection is most frequent during the third trimester of pregnancy. Most infants with this syndrome may appear healthy immediately following birth, but they may have neurological, ophthalmological, or auditory problems down the road (Kheirandish et al., 2019). These effects were mostly documented in pregnant women, although comparable results have been seen in other species. This may be because certain animals are more susceptible to or resistant to the toxin. Toxoplasmosis in pregnant ewes can present clinically in two ways: a late, normal abortion around one month after infections, or an early abortion during the acute stage of the disease, within the first two weeks after infection. Both types of abortions have been recorded. Likewise, the duration of the pregnancy, the particular strain of the parasite, and the host species all have significant roles in determining the outcome of a parasitic infection during pregnancy. The next paragraphs will elaborate on these topics.
It is unlikely that every Toxoplasma strain can strike a happy medium between triggering an immune response and avoiding mortality in every animal species. The evolution of unique strains of Toxoplasma likely occurred so that the parasite could strike the optimal balance in a wide variety of host animals. Therefore, it is possible that a mismatch between the species of the host and the strain of Toxoplasma is to blame for the virulence of Toxoplasma, which ultimately results in the death of its host. Likewise, when certain host genetic backgrounds are infected with particular parasite strains, the host may develop immune-related diseases due to the parasite’s production of a strong immune response. Abortions can occur in people and animals when the protozoan parasite toxoplasma invades the placenta, infects the fetus, and causes the fetus to miscarry (El Bissati et al., 2018). Some data suggest that particular strains of Toxoplasma, when combined with a susceptible host, might induce pregnancy difficulties. Fetal mortality and pregnancy termination might arise from exposure to an immune-evading strain that grows easily in the placenta and is transmitted to the fetus. Contrarily, a strain that elicits a strong immunological response is more likely to cause an inflated inflammatory response in the placenta. This might disrupt pregnancy, resulting in the mother’s incapacity to provide adequate care for her developing kid. In this opinion post, we focus on parasite effectors and host immune genes to address the various variables that might affect the outcome of pregnancy in a host infected with Toxoplasma.
A month after contracting Toxoplasma, most pregnant ewes will give birth to a stillborn child. The underlying mechanisms are linked to the death of the fetal organs, caused by the damage to those organs caused by the parasite’s multiplication in the placenta and, after crossing the placental barrier, in the fetus. In contrast to this late “classical” abortion, a variant known as “early abortion” has been recorded and is known to exist. Abortions that occur during the acute phase of the disease are also classified as “sterile” since they are linked to hypoxic damage to the fetus rather than the parasite itself (Kheirandish et al., 2019). Abortions have been connected to the condition, although it is unknown what causes them during the acute phase. Regardless of gestational age and at doses as low as 50 oocysts, M4 type II oocysts caused abortions during the first two weeks after oral infection. This was a shocking discovery.
Since toxoplasma infections have been connected to spontaneous abortions in pregnant women, humans can likely experience abortions soon after catching the infection, as was seen in sheep. A few case-control studies have examined the prevalence of toxoplasma seropositivity in women who have had spontaneous abortions with women who have had healthy pregnancies (Khan, & Khan, 2018). Similar to human pregnancy terminations, the causes of most animal abortions are unknown. However, because there are no detectable antibodies or parasites during the acute phase of the illness, early miscarriages that occur at this period are likely misdiagnosed in the field. Therefore, more study is needed to understand the reasons behind these abortions better.
While much remains unknown, new research has shed light on how specific Toxoplasma effectors can determine the outcome of an infection in a pregnant woman. The presence of several Toxoplasma-carrying genes may increase one’s chance of either an early or late miscarriage. Parasite clearance may be aided by Toxoplasma gene products that enhance inflammation in the host, but these same products also have the potential to trigger spontaneous miscarriages. However, Toxoplasma virulence factors that play a role in the evasion of the host immune system and dissemination increase the risk of late-term (classical) miscarriage due to vertical transmission of the parasite and fetal harm produced by replicating parasites (El Bissati et al., 2018). Predicting the most likely result of a pregnancy might be aided by the fact that each strain has a potentially distinct phenotype due to a unique polymorphism or mix of active versions of such components. Thus, serotyping methods could help researchers investigate the link between certain strains and abortions. In a similar line, serotyping in cases of unexplained abortions would allow scientists to determine if particular strains of Toxoplasma are responsible, as these cases are sometimes not explored further. Finally, more study is needed to determine the function that particular parasite components and strains play in the transmission of the parasite vertically and the termination of a pregnancy.
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