Brain infections and early development
palsy, are thought to be caused to virus-induced apoptosis of neural stem cells which are differentiating, leading to damage in regions of the brain, such as those related to motor function.
The Zika virus was first discovered in 1947 in a monkey in the Zika forest in Uganda, and shortly after was found present in mosquitoes and humans in Nigeria. Before the Zika epidemic in Brazil in 2015, the virus was generally considered benign, as it only caused very mild symptoms in adults such as rashes or fevers. However, following the outbreak, a rising trend in babies born with microcephaly – a birth defect where the baby has a smaller head than normal often causing an underdeveloped brain – was noticed, leading to congenital Zika syndrome (CZS) being recognized. The mechanism in which Zika harms neurodevelopment is its disruption of neural progenitor cells which are multipotent stem cells that play a very important role in the embryonic development of the brain. Zika virus can infect these cells in embryos causing NPC death and reducing cell growth and division (also known as proliferation). Furthermore, the effects of congenital Zika infection go beyond just microcephaly. In many cases, babies born without clear signs of CZS can go on to have developmental delays and defects due to Zika exposure in the womb, including ones affecting motor skills, regulation of mood, and executive function. In addition, secondary microcephaly may occur, where the baby’s head size is normal at birth, but then fails to grow at a normal rate, resulting in a similar condition to standard microcephaly. A further study has found that even in babies born without any brain defects, in those that were exposed to CZS, long-term immune system issues were a possibility, altering the balance of T-cells produced, which changed how their bodies responded to childhood vaccines, increasing the risk of other infections such as tetanus or diphtheria. Toxoplasmosis is a parasitic disease caused by the parasite Toxoplasma gondii and was discovered in 1908, with its full life cycle discovered in 1970. The parasite is typically obtained by consuming improperly cooked or raw meat or through exposure to cat faeces. The severity of the effects of the parasite is dependent on when the infection occurs. Infections that occur in the first trimester are the most severe, being most likely to lead to miscarriages or the greatest neurological disorders. Infections that occur later in pregnancy give the foetus a higher chance of survival but still carry the risk of problems arising in the baby after birth. There are 3 classic signs of congenital toxoplasmosis in a baby: hydrocephalus, a build-up of cerebrospinal fluid in the brain which risks causing brain damage; intracranial calcifications, symptoms of which include movement disorders and cognitive impairment; and chorioretinitis. The mechanism in which toxoplasmosis harms brain development is through the formation of cysts in neural tissue. Many babies born with congenital toxoplasmosis may appear asymptomatic, but the cysts can cause symptoms months or years later, which results in the disease being hard to diagnose in many cases. One real-world example that highlights the potentially widespread and severe effects of brain infections in early development on a large scale was the 2015/16 epidemic of the Zika virus in Brazil. During this period, many pregnant women were infected with the virus, resulting in approximately 3500 babies being born with CZS; throughout the outbreak, it was noticed that there was a significant increase in the number of infants born with microcephaly. In February 2016, the WHO declared the epidemic a ‘public health emergency of international concern’ because of how severe the outbreak was. The most-affected zone was northeastern Brazil, with hospitals reporting 20x the number of microcephaly cases compared to standard levels. This particular epidemic also illustrated how the
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