Malaria is a disease transmitted by mosquitoes that affects around 230 million people worldwide. The common symptoms of malaria consist of fever, chills, body aches, nausea, vomiting, and headaches. Without treatment, the infection can significantly worsen, causing seizures, comas, and death. This illness is particularly detrimental towards rural and underdeveloped countries where there are low funds and a lack of infrastructure to take the proper measures.
Vecteezy, “Malaria Infographic”
Testing for Malaria
Currently, there are rapid diagnostic tests (RDTs) for malaria, but it comes with several drawbacks. It cannot detect malaria in its early stages, determine its severity, and occasionally give false positive and negative results. In Nanyang Technological University, Singapore, a team led by Dr. Quan wanted to create a test for malaria that was both accurate and inexpensive to produce.
For RDTs, malaria-infected blood is examined under a microscope by an expert. Both factors are uncommon in rural locations, significantly delaying the diagnosis. The image below displays the only available RDT for malaria in the US.
CDC, “BinaxNOW Malaria Test”
The new test kit from Nanyang Technological University does not rely as heavily on laboratory equipment as it only needs water and a blood sample. Requiring a mere ten microliters of blood or less than one drop, the kit mixes this with water which releases the malaria parasites. Malaria parasites digest blood to grow and proliferate, creating hemozoin as a by-product. The kit proceeds to pump blood through an area of chemical patches that light up hemozoin. A light detector called the Raman spectrometer records the frequency and strength of these flashes of light to determine the presence of malaria as well as its severity.
Nanyang Technological University, “Malaria Test Kit”
In order to confirm the accuracy of this new test, the research team added early-stage malaria-infected blood into the kit. They found that the test detected these early-stage parasites, making them more sensitive than RDTs available in the United States. Due to the test’s sensitivity, it can quantify the number of parasites in the blood sample. Physicians can utilize this test to track how well the patient is fighting against malaria.
Dr. Quan and his team hope to cooperate with an industry partner in order to continue conducting more trials and further improve this testing kit. It is estimated that the test would cost about $1 for the US to manufacture, meaning it could be utilized in the field on a large scale. In the future, these test kits will pave way for underserved populations to gain easier access to important public health resources.
Kyle Phong, Youth Medical Journal 2021
Center for Disease Control and Prevention, “Malaria”, 30 June 2021
You’ve probably heard the term “yellow fever” being thrown around the internet. Urban Dictionary defines this term as males having preference over women with Asian descent but in this article, we will not be diving into this internet slang. Instead, we will be diving into the topic of a very serious infectious tropical disease commonly known as yellow fever.
Yellow fever, also known as bunyavirus infection, is a viral infection that can affect the liver, kidneys, and the gastrointestinal tract which is a tract from the mouth to the anus. Mosquitos are the most common carrier of this yellow fever disease and typically located near the Carribean Islands and Africa. In this article, we will be diving into all there is to know about the yellow fever disease. From all the symptoms to even the causes and treatment for this disease.
CAUSES OF YELLOW FEVER
A human is able to contract the yellow fever infection when they have been bitten by a mosquito that also carries the disease. This mosquito is known to be called the Aedes Aegypti Mosquito and is known to do really well in human habitations. A simple bite from the mosquito can be extremely harmful and if bitten by one can also contract the yellow fever disease. This mosquito is also known to spread and can carry dengue fever, zika fever, mayaro, and many more.
SYMPTOMS OF YELLOW FEVER
Symptoms of yellow fever can impact different parts of the human body, often beginning with severe headaches and delirium. Yellow fever can also impact your eyes causing redness and also causing the eyes to be more sensitive to light. Common symptoms also include muscular problems like aches and seizures and also liver issues like hepatitis, which is inflammation of the liver. There are also many symptoms that affect the stomach like nausea, abdominal pain, and even cause vomiting as well. People with yellow fever may also experience decreased urination as well as bleeding in the mouth and nose. Another symptom of yellow fever is a slower heart rate.
TREATMENT/CURE FOR YELLOW FEVER
Currently, like many other diseases there is no cure for yellow fever because it is an infection that multiplies over time that cannot be killed by anti biotics. However, prevention for yellow fever does exist and those who live in continents that are mostly affected are highly encouraged to take the vaccination in order to prevent contraction of yellow fever. Those who travel to continents with yellow fever are also recommended to take the vaccine as well. However, those who have contracted the disease go through many treatments including oral rehydration therapy. ORT (oral rehydration therapy) involves drinking water with sugar and salt in order to treat dehydration, this can also be given by a nasogastric tube.
Like many other diseases, yellow fever is very complicated and harmful to human beings. Symptoms of yellow fever range from delirium and weak eyesight, to bleeding and hepatitis. The cause of all these symptoms come from a small mosquito known as the Aedes Aegypti Mosquito which is known to be very common for carrying the Yellow Fever disease. Being bitten by one of these mosquitoes can cause yellow fever but thankfully, there are medical interventions that can help prevent someone from contracting this disease. Overall, yellow fever is very harmful and those who live or plan on moving to places with higher risk of yellow fever should proceed with caution. Diseases like yellow fever aren’t curable and can cause many complications. Thankfully, with the help of prevention vaccines that are available to many of us and to those who live in countries that are affected by this disease, many of us can stay safe from the yellow fever mosquito and live a life that is yellow fever free.
Mary Mai, Youth Medical Journal 2021
“Delirium.” Mayo Clinic. Mayo Foundation for Medical Education and Research, 01 Sept. 2020. Web. 01 July 2021.
“Gastrointestinal Tract.” Encyclopædia Britannica. Encyclopædia Britannica, Inc. Web. 01 July 2021.
“Yellow Fever.” NORD (National Organization for Rare Disorders). Web. 01 July 2021.
“Yellow Fever: Causes, Symptoms, And Treatment.” Netmeds. Web. 01 July 2021.”Yellow Fever: Symptoms and Treatment.” WebMD. WebMD. Web. 01 July 2021.
Most people are born with 46 chromosomes. What are chromosomes? In very simple terms they are structures inside the nucleus of a cell made up of DNA and other proteins. They are typically genetic material and hence they provide a child with genetic and hereditary characteristics. Going back to the first sentence: most people are born with 46 chromosomes. People with Down Syndrome [DS], however, are born with one extra chromosome. This explains why the syndrome is also more commonly called trisomy 21–because in this condition, one is born with an extra copy of their 21st chromosome. The effects of this are commonly a lag in both physical and mental developments. However, the range of these lags or delays can differ from patient to patient and the ability to live with ease also depends. According to the World Health Organization, the predictable incidence of DS is between 1 in 1,000 to 1 in 1,100 live births all over the world.
The scope of this article covers the causes of the syndrome, effects, types and finally some lesser-known facts about Down Syndrome!
Causes of Down Syndrome
As mentioned previously, parents pass on their genes to the child through chromosomes. There is a lot of process and details within this procedure but to understand the causes of the syndrome, it will suffice to know what is mentioned above. Each cell in the child is supposed to have 46 chromosomes, (23 pairs) which are half from the mother and half from the father.
In situations where the child goes on to develop Down Syndrome, one chromosome cannot separate fully, resulting in 3 copies of the 21st chromosome instead of 2.
Symptoms of Down Syndrome
The presence of DS in people typically causes slowed mental and physical development. As mentioned above, this lag or delay in development varies from person to person depending on several factors including the type of DS diagnosed in them (which is discussed in greater detail shortly). Some featured symptoms are (keep in mind that even these differ vastly):
Upward slanting eyelids (palpebral fissures)
Unusually shaped or small ears
Poor muscle tone
Broad, short hands with a single crease in the palm
Relatively short fingers and small hands and feet
Tiny white spots on the coloured part (iris) of the eye called Brushfield’s spots
Some other symptoms are cognitive disabilities such as slowed learning and memory.
Types of Down Syndrome
There are 3 types of DS: Trisomy 21, mosaicism and translocation. Out of these, the first is the most common. The name is very self-explanatory; trisomy 21 refers to the fact that there is an extra copy of the 21st chromosome in every cell of the body. Mosaicism is very similar, however, it’s different in that not all cells have an extra copy of the 21st chromosome; only some do. Hence there are also lesser symptoms and of lesser intensity in this form. In the 3rd mention form translocation, there are three 21 chromosomes, but one of the 21 chromosomes is attached to another chromosome. Out of these three given types of Down Syndrome, trisomy-21 is the most prevalent: about 95% of people with DS have this type. 2% of people with DS have mosaic DS and 3% of people with DS have the translocation type.
Other than the main differences between these 3 types, some other differences that the type of DS can have an influence on are the severity of the symptoms. As mentioned above, every individual’s symptoms vary vastly.
The exact cause of the extra chromosome that triggers Down syndrome is unknown.
One in every 691 babies in the U.S. is born with Down syndrome, making it the most common chromosomal condition.
There are more than 400,000 people living with Down syndrome in the U.S.
In 1983, the average life expectancy of a person with Down syndrome was a mere 25-years-old. Today, it is 60.
Children and adults with Down syndrome share some common features, but naturally, the individuals will more closely resemble their immediate family members.
Since the 1970s, public schools have been required by law to provide free and appropriate education to children with Down syndrome.
The likelihood of giving birth to a child with Down syndrome increases with maternal age, however, 80% of babies with Down syndrome are born to women under 35 years of age because this age group gives birth most frequently.
Roughly 25% of families in the U.S. are affected by Down syndrome.
While behaviour, mental ability, and physical development vary from person to person, many individuals with Down syndrome grow up to hold jobs, live independently, and enjoy normal recreational activities.
One of the most common types of dementia in the UK, Alzheimer’s disease (AD) is a physical disease that affects the brain. It is estimated that in 2040 there will be over 1.5 million people with dementia in the UK at the current rate of prevalence. Despite the alarmingly high figures, research is being undertaken to tackle this with 126 different agents currently being assessed to treat Alzheimer’s. Recently, the FDA approved a new drug, aducanumab, for clinical use in Alzheimer’s patients after reviewing evidence on its effectiveness in slowing the progression of symptoms in people with early-stage AD.
What we know:
The effect of Alzheimer’s on the brain
In order to understand how aducanumab treats Alzheimer’s, we must understand the effect AD has on the brain. AD is a neurodegenerative disease. During Alzheimer’s, vital communication between neurons is disrupted as many neurons stop functioning, which results in cell death and leads to shrinking of the brain. This process is known as cerebral atrophy. AD disrupts important processes in neural networks such as communication, metabolism, and repair. As these neurons die, a person suffering from AD will begin to lose the ability to think, remember, make decisions and function independently. This is due to pathological changes and damage to multiple brain structures such the cerebrum, cortex and hippocampus.
The exact cause of AD is still unknown. Many scientists believe that two proteins called ‘beta-amyloid’ and ‘tau’ play a huge role in the toxic changes that occur in the brain. Both of these proteins form the buildup of two abnormal pathologies. The first pathologies are plaques (composed of beta-amyloid) which build up slowly in the neurons and are found scattered between nerve cells. The second pathologies are neurofibrillary tangles formed inside cells which result from the accumulation of abnormal tau. But it is important to note that these are not the only factors which contribute to AD. Furthermore, it is due to the lack of universal acceptance of the amyloid hypothesis that aducanumab has been so heavily criticised, which is explored in further detail below.  
What are the current treatment options for AD?
At the moment, treatment for AD revolves around helping patients maintain mental function, slow down progression of symptoms, and manage and ease behavioural symptoms. There are several pharmaceuticals available which can help manage symptoms of Alzheimer’s. Acetylcholinesterase inhibitors are the main drugs used to treat AD in the UK. These include donepezil, galantamine, and rivastigmine. These work by preventing the enzyme acetylcholinesterase from breaking down acetylcholine, a critical neurotransmitter. Levels of acetylcholine are very low in patients with AD due to nerve cell death. By preventing breakdown of this vital chemical, acetylcholine levels will increase, leading to reduction in some symptoms of AD. 
The last approved drug was memantine in 2004, which is an oral medication. Unlike the cholinesterase inhibitors which are considered ‘symptomatic’ treatment, memantine is considered a ‘neuroprotective’ drug as it may slow the underlying progression of AD. In AD, too much glutamate leaks out of damaged brain cells, and these high concentrations can result in over-excitation of nerve cells, which leads to cell death.  Memantine protects the nerve cells by dampening the excitatory effect of the neurotransmitter glutamate. 
What is aducanumab (aduhelm)?
It is an antibody infusion targeting amyloid beta protein (Aß), a defining feature of the biology of AD. Current drugs aim at suppressing cognitive symptoms whereas aducanumab is aiming to tackle the underlying cause of AD, which is to both stop and cure it. Aducanumab is aiming to do this by targeting amyloid, clumps researchers believe are responsible for brain cell death.
The antibody will preferentially bind to aggregated amyloid-beta. This will reduce the presence of amyloid plaques in hopes to slow AD progression. These plaques are also responsible for the inability to perform simple tasks and memory loss.
Back in March 2015, an early-stage clinical trial provided evidence that aducanumab drastically reduced beta-amyloid plaques in the brain. However there were some flaws within this trial such as small testing groups but also the assumption that beta-amyloid oligomers decreased. The latest updates have found that the intermediate deposits, ‘beta-amyloid oligomers’ may be the real culprit and not the end state ‘beta-amyloid plaques’.  Four years later and Biogen announced that the development of aducanumab will be discontinued. That is until a couple months later the announcement that the FDA would now be considering it for marketing approval.
The FDA granting accelerated approval is under much speculation. As mentioned earlier, the amyloid hypothesis has influenced a large proportion of Alzheimer’s disease research. The amyloid hypothesis is still doubted by many professionals with its more recent ‘failed’ drug trials adding further doubt. The FDA’s ignorance towards data from the trial which showed no slowing in disease progression is alarming considering the “FDA’s own advisory committee last November voted 8 to 1 against approving the drug, citing “lack of strong evidence that the drug works.” In fact, a member of the of the FDA’s expert panel for nervous system therapies has even gone as far to resign over the FDA ruling, STAT reported.
Even if we were to ignore the lack of data proving any clinical benefits of aducanumab on declining disease progression, the question of whether there is a connection between plaque reduction and cognitive improvement still remains uncertain. Some believe beta-amyloid may not be the underlying cause of the disease at all and hence aducanumab may not be the answer.
Furthermore, we need to be realistic. Professor John Hardy of neuroscience at University College London, said: “We have to be clear that, at best, this is a drug with marginal benefit which will help only very carefully selected patients.” It is likely that aducanumab will be better for those with mild AD and cognitive impairment, as opposed to those with advanced AD.
It’s Future and the Challenges that lie ahead
The potential side effects are another reason to approach aducanumab treatment with caution. Patients undergoing aducanumab treatment will need continual monitoring due to its main side effect, amyloid-related imaging abnormalities (ARIA). ARIA-E refers to cerebral edema or brain swelling, whereas ARIA-H refers to cerebral microhemorrhages or micro bleeds in the brain.
While many have heavily criticised the approval, others are praising it with caution under the acknowledgement that it is far from a cure. The accelerated approval of aducanumab (as opposed to standard approval) is paving a new path for other treatments of neurodegenerative diseases. The ‘accelerated approval’ pathway is used for treatments that are “reasonably likely” but not certain to help patients. Furthermore, the revival of aducanumab is also bringing more interest towards research for treatments of neurodegenerative diseases. As Mario Carrillo, chief science officer at the nonprofit Alzheimer’s Association, has said: “History has shown us that approvals of the first drug in a new category invigorates [sic] the field”.
In order for us to ensure aducanumab could truly be the way forward for AD treatment, companies marketing the drug, Biogen and Eisai, should verify its clinical benefits with further study. While the amyloid hypothesis may be doubtful, there is no reason to give up in this direction of treatment yet.
Uncertainty still remains over aducanumab’s future impact; it is yet to be available in the UK and Europe. Nevertheless aducanumab is providing a spark of hope for our endless search for treatments of AD, as it is the first treatment in a very long time. With dementia research having been chronically underfunded in the UK, the need for new life-changing treatments is only increasing.
As it stands currently, aducanumab is not exactly a cure for Alzheimer’s and there are still many more obstacles we will have to overcome. However, it undoubtedly is a remarkable moment and marks a great milestone in dementia research.
Jack, Clifford R., et al. “NIA-AA Research Framework: Toward a Biological Definition of Alzheimer’s Disease.” Alzheimer’s & Dementia, vol. 14, no. 4, 2018, pp. 535–62. Crossref, doi:10.1016/j.jalz.2018.02.018.
Sevigny, Jeff, et al. “The Antibody Aducanumab Reduces Aβ Plaques in Alzheimer’s Disease.” Nature, vol. 537, no. 7618, 2016, pp. 50–56. Crossref, doi:10.1038/nature19323.
Sabbagh, Marwan Noel, and Jeffrey Cummings. “Open Peer Commentary to ‘Failure to Demonstrate Efficacy of Aducanumab: An Analysis of the EMERGE and ENGAGE Trials as Reported by Biogen December 2019.’” Alzheimer’s & Dementia, vol. 17, no. 4, 2020, pp. 702–03. Crossref, doi:10.1002/alz.12235.
The plague is a disease that is caused by the bacterium Yersinia Pestis. The Black Death, one of the most notable pandemics in history, was a result of the transmission of Y. pestis from rats and fleas to humans, making it a zoonotic disease (Frey, “Plague). This transmission often occurred through flea bites or contact with the body fluid of an infected animal. The plague takes on three different forms depending on the affected area of the body: bubonic (affecting lymph nodes), pneumonic (affecting the lungs), and septicemic (affecting the blood). The Black Death is characterized by both the swelling of lymph nodes, which turn black as a result of bubonic plague, and the blackening of skin, resulting from septicemic plague (Frey, “Plague). An estimated 75 to 200 million lives were lost before the end of the Black Death (Frey, “Bubonic Plague”). Today, the number of fatalities resulting from (and cases of) the plague are not even remotely close to the numbers seen during the Black Death; the recorded numbers are not zero, however.
Plague in the modern day
Cases of the plague, although much less frequent, still exist today. A majority of the present day cases of the plague occur in developing countries. In fact, the plague is still endemic to (regularly found in) Madagascar, Peru, and the Democratic Republic of the Congo (Frey, “Bubonic Plague). Madagascar reports more plague cases than any other single country, averaging 200 to 400 cases every year (Hardman).
A portion also occurs in the United States. The Centers for Disease Control and Prevention (CDC) reports between 1 to 17 cases of the plague each year in the United States (with an average of 7 reported cases per year). Plague in the United States occurs in western, rural areas; northern New Mexico, northern Arizona, southern Colorado, California, southern Oregon, and western Nevadea are the most affected regions. 80% of these U.S. cases are in bubonic form (“Plague in the United States”).
Figure 1: This figure shows a world map of plague cases reported to the World Health Organization (WHO) by country between 2000 and 2009 (Centers for Disease Control and Prevention)
There are about 5,000 cases of the plague reported to the World Health Organization (WHO) each year worldwide, and 95% of these cases occur in Africa. Interestingly, the only two continents that are plague-free are Australia and Antarctica (Frey, “Plague”).
More “recent” plague outbreaks include an outbreak of pneumonic plague in Surat, India in 1994, where 876 cases of infections, including 52 deaths, were reported to the WHO (Frey, “Plague”). The most recent outbreak in Madagascar occurred in 2017 and resulted in 2,575 confirmed or probable cases of bubonic and pneumonic plague, including 221 deaths (World Health Organization 2017). Even more recently, the WHO began reporting on an ongoing outbreak of suspected pneumonic plague in the Dominican Republic of Congo in January of 2020. As of May 2021, there are a total of 564 suspected pneumonic plague cases, including 43 deaths (World Health Organization 2021).
Today, the plague is treatable with antibiotics. 80% to 90% of patients with bubonic plague that received rapid diagnosis and appropriate treatment will survive; the survival rates for septicemic plague and pneumonic plague are lower in comparison at 75% and 50%, respectively (Frey, “Bubonic Plague”). If left untreated however, each form of the plague is still fatal a majority of the time. Bubonic plague has a mortality rate of 60% to 70% in untreated cases, while untreated septicemic and pneumonic plague both have a mortality rate of 100%. Pneumonic plague, specifically, is 100% fatal if left untreated for 48 hours (Frey, “Bubonic Plague”).
Streptomycin, an antibiotic discovered in the 1940s, is one of the first-line treatments for plague (Hardman). Gentamicin, chloramphenicol, and tetracycline are alternatives that can also be administered. It is important that the administration of antibiotics is started as soon as possible (Cua).
Some scientists have also considered the association between climate and plague. The conditions following warmer weather in the spring and wet weather in the summer are beneficial for fleas and bacteria, which play key parts in the spread of plague (Hardman). Additionally, outbreaks of plague among local animals (called epizootics) most commonly occur after wet winters and cool summers; these epizootics could also affect humans (Frey, “Plague”). In the case of the plague outbreak in Surat, India, rainfall also influenced the spread of plague, as flooding increased contact with drowned, infected animals that were not disposed of (Frey, “Plague”). Similarly to other climate sensitive and infectious diseases, the effects of global warming may increase the number of outbreaks of plague in animals and, in turn, in human populations (Hardman).
Lastly, the animal reservoirs of the plague (the host animal populations that infectious diseases survive off of) make the disease impossible to eradicate (Frey, “Plague”). Rats play a large role in the spread of the plague. Controlling that spread—considering their sheer numbers and the scope of human capabilities—proves to be near impossible. Surveillance of animal populations and careful reporting of plague cases, however, is still important in preventing plague (Frey, “Plague”).
The plague is an infectious disease that is well known due to its connection to the Black Death, one of the most notable epidemics in history. While the occurrence of the plague has changed since medieval times, the high mortality rates of untreated plague cases have remained and are currently affecting different regions of the world. Considering its connections to climate change and recent developments, the plague is not a disease of the past, but rather, one that is still relevant to the modern world.
Michelle Li, Youth Medical Journal 2021
Centers for Disease Control and Prevention. “World Plague Map – 2000 to 2009 – CDC.” Wikimedia Commons, commons.wikimedia.org/wiki/File:World_Plague_Map_-_2000_to_2009_-_CDC.jpg. Accessed 30 June 2021. Map.
Cua, Arnold, and Rebecca J. Frey. “Plague.” The Gale Encyclopedia of Medicine, edited by Jacqueline L. Longe, 6th ed., vol. 7, Gale, 2020, pp. 4067-71. Gale Health and Wellness, link.gale.com/apps/doc/CX7986601475/HWRC?u=mlin_m_newtnsh&sid=bookmark-HWRC&xid=851c3f42. Accessed 1 July 2021.
Frey, Rebecca J., PhD. “Bubonic Plague.” The Gale Encyclopedia of Emerging Diseases, edited by Deirdre S. Hiam, Gale, 2018, pp. 45-52. Gale Health and Wellness, link.gale.com/apps/doc/CX3664800021/HWRC?u=mlin_m_newtnsh&sid=bookmark-HWRC&xid=0a3632e4. Accessed 1 July 2021.
—. “Plague.” The Gale Encyclopedia of Public Health, edited by Brigham Narins, 2nd ed., vol. 2, Gale, 2020, pp. 847-51. Gale Health and Wellness, link.gale.com/apps/doc/CX7947900220/HWRC?u=mlin_m_newtnsh&sid=bookmark-HWRC&xid=d93f373c. Accessed 1 July 2021.
Hardman, Lizabeth. “Plague Today and Tomorrow.” Plague, Lucent Books, 2010, pp. 74-87. Diseases & Disorders. Gale Health and Wellness, link.gale.com/apps/doc/CX1334700011/HWRC?u=mlin_m_newtnsh&sid=bookmark-HWRC&xid=8b9c5d6d. Accessed 1 July 2021.
World Health Organization. Weekly Bulletin on Outbreaks and Other Emergencies. 15 Dec. 2017. World Health Organization, apps.who.int/iris/bitstream/handle/10665/259709/OEW50-1015122017.pdf;jsessionid=9E1F0CC89024B909F1E30F0B1064B43A?sequence=1. Accessed 30 June 2021.
—. Weekly Bulletin on Outbreaks and Other Emergencies. 27 June 2021. World Health Organization, apps.who.int/iris/bitstream/handle/10665/342077/OEW26-2127062021.pdf. Accessed 30 June 2021.
During an epidemic, scientists tend to search for sources of the outbreak. If the outbreak has foreign origins, scientists often enlist the help of anthropologists to study local practices and customs since cultural awareness is necessary for any public health campaign or outbreak control. However, the role of anthropologists seems to extend further than that. Anthropologists identify ‘risky behaviours’ present within a society which may escalate an outbreak. Yet, these ‘risky behaviours’ always tend to be rooted in cultural contexts. Scholars tend to ignore socioeconomic factors, such as overcrowding, poverty, etc., which may have a greater hand to play in the proliferation of a disease through a population. This instinctive ignorance lets slip the presence of racism and Eurocentric bias in the subconscious beings of scientists and researchers.
Ebola and Africa [1980s]
The Ebola Virus Disease (EVD), a rare and fatal disease, was first discovered in 1976 in the Democratic Republic of Congo (DRC) (Centers for Disease Control and Prevention , 2021). After an incident on a shipping boat in 1989, Western media’s interest in the virus erupted. Due to its foreign origins, media and Western society linked the source of the outbreak to practices in African culture (Jones, 2011).
The Ebola virus is a zoonotic disease meaning that the virus had been transferred from animals — specifically nonhuman primates (monkeys, gorillas, and chimpanzees) — to people. Thus, enlightened with this information, scholars proposed the Bushmeat Hypothesis: “hunting, slaughtering, and eating infected gorilla or monkey meat is the primary cause of the virus’s entrance to a new population (Jones, 2011).
This argument became one of the dominant explanations of the Ebola outbreaks as it provided a correlation between cultural practice and a viral outbreak. However, doing so overshadowed other arguments which may have been greater factors at play; factors such as overcrowding, poor sanitation, and inadequate provision of healthcare, exacerbated by a legacy of colonialism were responsible for much of Ebola’s spread. However, cultural factors were emphasised more than sociopolitical and economic factors. Africans were presumed to have beliefs rooted in witchcraft and superstitions which may have hindered efforts by doctors and scientists to control the outbreak (Jones, 2011). Disputing this notion was a Harvard professor and a medical anthropologist, Paul Farmer, who was at the forefront of the Ebola epidemic control. The failure to control the outbreak did not occur due to local customs and traditions but rather due to distrust in the healthcare system and the government.
“People fled the medical system, not because of superstitions, but mostly when the medical system was unable to rescue or treat its patients as constituted.”
(Paul Farmer in an interview with Ashish Jha on Lessons from Ebola)
Due to the lack of adequate hospital infrastructure, doctors had implemented a disease control paradigm that concentrated its efforts on isolating suspected cases and confirmed cases without providing actual care (unlike the current COVID-19 care centres). This approach was rendered ineffective. Distrust in the healthcare system further grew and people started turning to traditional healing systems as a desperate resort.
The erroneous depictions of the Western media and the presumptions of Western society of the Ebola outbreak reveal the lingering presence of racism in our society and the remnants of colonialism. Additionally, it affirms the presence of bias in biomedical research.
AIDS as a Haitian Disease [the 1980s]
It is the 1980s. Haiti, a Caribbean country, has been receiving widespread publicity as the possible birthplace for AIDS. Acquired Immunodeficiency Virus (AIDS) is a chronic and fatal condition caused by the human immunodeficiency virus (HIV); HIV is a sexually transmitted infection (STI) that weakens one’s immune system. A severely damaged immune system progresses into AIDS as it is unable to protect the body from infections or cancers that a person with a healthy immune system wouldn’t normally acquire (Mayo Clinic, 2020). Upon the emergence of an AIDS epidemic, scientists begin investigating the sources of the outbreak. In an eruption of imagination, Western society and media speculated that voodoo rites, sacrificial practices, the eating of cats, and ritualized homosexuality, were the causes of the epidemic – “a rich panoply of exotica” (Farmer & Kim, Anthropology, Accountability, and the Prevention of AIDS, 1991). The speculations gave rise to stereotypes that were enforced time and time again by the U.S. press. Also notable was the media representation of Haitian-Americans: black, poor, immigrants, and associated with cult-like religious practices. As media sensationalized and misrepresented the Haitian-American community, incidents of harassment began to propagate. People of Haitian origin bore the stigma of a fatal condition. The statement of one Haitian-American physician mirrors this sentiment:
“After all the wild theories of voodoo rites and genetic predisposition were aired and dispelled, and the slip-shod scientific investigation was brought to light, the public perception of the problem remained the same that if Haitians have AIDS, it is very simple because they are Haitians (Farmer & Kim, Anthropology, Accountability, and the Prevention of AIDS, 1991).”
However, none of the speculations and gossip surrounding the epidemic had any epidemiological research to back them up. As a matter of fact, declarations of plausible theories of the sources of the outbreak by scientific researchers had slowly begun unravelling the lies illustrated by the press. On December 1, 1982, the following statement was made:
“Homosexuals in New York take vacations in Haiti, and we suspect that this may be an epidemic Haitian virus that was brought back to the homosexual population in the United States.”
(Dr. Bruce Chabner of the National Cancer Institute, 1982)
At the 1988 conferences of the American Anthropological Association, researchers congregated to discuss “Ethical Considerations in Anthropological Research.” The focal point of the meetings was the failure to lighten the burden of stigma on the Haitian-American community, aggravated by the spread of misinformation. Further addressed was the economic damage of Haitian businesses, which were boycotted by tourists and investors, and the rise in unemployment within the Haitian-American community. Nevertheless, in February 1990, the Food and Drug Administration (FDA) ruled that no person of Haitian origin will be allowed to donate blood (Farmer & Kim, Anthropology, Accountability, and the Prevention of AIDS, 1991). The incessant discrimination against the community, not only resulted in economic damage but also a decline in the mental and emotional health of members of the ethnicity. All this, due to the deep-rooted racism in a system that embraced popular societal opinion rather than verified scientific research.
SARS – CoV – 2 (COVID-19) Pandemic : Hate Crimes Against South East Asians
SARS-CoV-2, colloquially known as COVID-19, originated in Wuhan, the capital city of the Hubei province, China. The virus evidently has zoonotic origins (similarly to Ebola) with genetic similarities to bat genomes. The COVID-19 virus first caused a viral outbreak in the Hubei province region, soon spread to surrounding provinces and all over China. In China, it has declared an epidemic. Subsequently, the virus infiltrated borders and crossed seas through international travel and infected millions of people; On March 11, 2020, the World Health Organization (WHO) had declared the COVID-19 viral outbreak, a pandemic (World Health Organization, 2020).
Proclaimed as a zoonotic disease, researchers began investigating the source of the animal-to-human transfer and traced it back to the Wuhan Southern China Seafood Market where wild animals were being sold. The bushmeat theory, first proposed during the Ebola outbreak, found new ground almost 40 years later in the SARS-CoV-2 epidemic. However, the magnitude of this viral outbreak significantly surpassed the Ebola epidemic; millions, if not billions, of lives, have been affected around the world; trillions of dollars are being spent on reviving an economy that has seen its deepest slump since the Great Depression. Now, at a very vulnerable state, with dear lives lost, people need someone to take blame and responsibility. Hate incidents and crimes against the Chinese and Asian communities increased. The pandemic had given rise to stigma and discrimination. News media picked up on this sentiment and began referring to the SARS-CoV-2 virus as the “Chinese virus,” or the “Wuhan virus.” Associations of such may have provoked people to detest a community that was struggling with an outbreak, too (Xu, et al., 2021).
“Pandemics do not materialise in isolation. They are part and parcel of capitalism and colonisation. The countries that struggled to contain and control major epidemics in the recent past, from Haiti to Sierra, had deficient public health systems prior to these crises, partially as a result of their colonial histories. Moreover, products of capitalism – from war to migration to mass production and increased travel – contribute massively to the proliferation of diseases.”
(Edna Bonhomme, Postdoctoral Fellow at the Max Planck Institute for the History of Science in Berlin, on the topic of COVID-19 and Inequality (Bonhomme, 2020))
In the three occurrences discussed above, there seems to also be three recurrent themes. Firstly, the sudden media interest in the three cases amplified the racialization of these epidemics. Arguably, the media played the biggest role in the dramatization of the epidemic’s events. Unexpectedly, scholars often also shared the view proposed by the popular press. The prejudices and biases present in these scholars subconsciously affected their judgements in an epidemic control centre or a research centre, thus adversely influencing the healthcare quality available in these countries. Additionally, in the media frenzy, the western way of living was enforced as the norm, painting foreign cultures as exotic. This is where the remnants of colonialism become apparent once again. Lastly, through analysis of media reports and scholarly articles or journals, one can understand that some researchers subliminally undermine indigenous knowledge and accept biomedical research as the divine truth.
Media Manipulation: Sensationalism
Western media portrayals in each of the three case studies seem to have subconsciously depicted Western ways of living as norms by contrasting them with the ways of living of other ethnic communities. This juxtaposition depicts the complex and vibrant cultures of various ethnic groups around the world as simply exotic. Exotic, meaning interesting, different, and ‘other’. The exoticization of an ethnic community and its practices alienates its members, thus leaving them more susceptible to racial discrimination. This dramatization is not only demeaning for an ethnic community but also an exploitation of the credibility the masses of people associate with news media reporting.
Systematic Racism, Stigma, & Discrimination
The existence of systematic racism, ingrained within institutions — in the laws, policies, and decisions — are mainly what hinders the provision of healthcare in epidemic control centres; it is what distorts epidemiological research. The erroneous conclusions of such scientific and anthropological research attribute the causes of an epidemic to local practices, traditions, and customs of an ethnic community while hardly considering sociopolitical or economic factors. This, in addition to media sensationalism, places a degrading spotlight on a community that may be suffering as well. Stemming from such situations is stigma and racial discrimination. At a moment when people are at their most vulnerable state, systematic racism and media sensationalism give rise to hate crimes as currently seen occurring against the South East Asian community due to the COVID-19 pandemic.
Worth Found in Indigenous Knowledge
When planning epidemic centre controls in different countries, scientists and anthropologists often study the local practices, customs, and traditions — indigenous knowledge. However, the lens with which this body of knowledge is viewed indicates that scholars believe indigenous knowledge serves to hinder the provision of healthcare rather than aid its use. Subliminally, all scholars undermine indigenous knowledge and regard it as ‘backwards’. Associated with many of these communities is a cumulative body of knowledge and know-how honed through years of observations, experiments, and reflections. Although these practices have been developed through years of observations, it is not possible to ascertain their reliability or accuracy since they have not been assessed by the wider intellectual community as of now due to there being notions that indigenous knowledge is retrogressive and anti-development. If we aspire to put in the effort to inspect the accuracy of indigenous knowledge, we may be able to verify that the majority of their claims may be accurate and, in fact, useful in developing future theories or innovations, instead of labelling them as regressive.
In conclusion, the notion that any ethnic community’s customs or traditions hamper epidemic control efforts should be challenged. Publishing unverified scientific information that may be linking the source and spread of an outbreak to an ethnic community can prove to be very degrading and even detrimental for members of a community, leaving them predisposed to scorn and resentment. Although our world has come a long way from its colonizing history, the legacy and remnants of it can still be seen today in the form of the exoticization of ethnic practices through systematic racism.
Xu, J., Sun, G., Cao, W., Fan, W., Zhihao Pan, Z. Y., & Li, H. (2021). Stigma, Discrimination, and Hate Crimes in Chinese-Speaking World amid Covid-19 Pandemic. Asian Journal of Criminology, 16(1 ), 51-74.
In today’s digital age, many swap their jump ropes and exercise shoes for the newest iPad or cellular device. While some argue that this is simply an inevitable product of our developing society, others emphasize the health risks this new lifestyle poses.
As sedentarism sweeps through today’s world, we must be cognizant of the damage we are doing to our minds and bodies. Not only does physical inactivity deplete your brain of crucial hormones needed for well-being, therefore increasing the risk of mental illness, but it also wreaks havoc on your physical health and is an increasingly large cause of mortality. Fortunately, it is not too late to fix your lifestyle and put a stop to the harm inactivity is inflicting on your body.
The notion that a sedentary lifestyle poses risks for one’s physical health is widely accepted, however the mental and emotional drawbacks of inactivity are often overlooked. In a number of studies, researchers have identified a link between brain health and physical activity levels, specifically with depression and anxiety. In fact, sedentary adolescents have ~10% higher chance of developing depressive symptoms before they become adults (Thomas 1). This increased risk can be chalked up to an absence of feel-good hormones, such as serotonin, that one would typically receive during exercise. Regular physical activity has been shown to increase serotonin levels within the brain, and because many mental illnesses stem from a serotonin deficit, exercise is thought to be among the most effective methods to combat these mental disorders. Therefore, when one completely cuts physical activity out of their daily life, they are losing an essential part of brain hormone stabilization. Additionally, lack of activity is often synonymous with staying indoors, meaning less exposure to sunlight and nature, which is also important in boosting serotonin and is needed to get adequate levels of vitamin D. In fact, conditions like seasonal affective disorder (SAD) and vitamin D deficiency both have substantial impacts on one’s psyche, and both arise specifically as a result of lack of sunlight. Consequently, there is a higher prevalence of the condition in sedentary individuals (Danahy 1).
When one becomes sedentary, their physical health will inevitably decline. In fact, according to a study conducted by the Lancet, those who are in the worst shape as determined by a treadmill test, had a 500% higher chance of premature death than those who are more fit. As the body adapts to reflect its sedentary lifestyle, changes can be seen in a multitude of ways. The first, more surface-level changes can be seen with weight gain and muscle decomposition, as well as increased fatigue, breathlessness, and even bone brittleness. One may also suffer insomnia and sleep deprivation, which, if continued long-term, can heighten the risk of developing more severe health conditions such as diabetes and heart disease (Csatari 1). Not only that, but one may suffer high blood sugar because exercise is needed to regulate glucose and since cardio-respiratory fitness worsens without activity. On top of these already striking concerns, inactive individuals run the risk of heart damage, with lower levels of HDL cholesterol a.k.a “the good cholesterol” and an 18% increased risk of total heart failure (ahajournals.org). And, although there are no controlled studies determining the impact of sedentarism on cancer, independent stories lead scientists to believe that the two are linked. All of these factors come together to increase the risk of premature death by 5 times.
So, what can be done? While the solution seems simple, many lack the motivation or time to fit exercise into their daily routines. For those individuals, it may be beneficial to look for simple yet effective ways to get moving, such as biking rather than driving to work, or opting for a standing desk. One might also consider taking up more “fun” forms of exercise such as dancing, trampolining, or joining a recreational youth or adult sports team. Health experts recommend at least 30 minutes of physical activity a day, so even taking a walk around the neighborhood for half an hour each morning has the potential to substantially boost one’s physical and mental health.
Florido, Roberta, et al. “Six-Year Changes in Physical Activity and the Risk of Incident Heart Failure.” Circulation, vol. 137, no. 20, 2018, pp. 2142–51. Crossref, doi:10.1161/circulationaha.117.030226.
NIH (National Institutes of Health) have revealed that up to 23.5 million American citizens have an autoimmune disease and the prevalence is increasing. 80-100 various autoimmune diseases have been identified by scientists who also assume that at least 40 other diseases could potentially have an autoimmune basis.
Classifications of Autoimmune Diseases
No tissue or organ is exempt from autoimmune diseases: these diseases can affect various organs and organ systems, varying greatly among the individuals who have them, in terms of severity and responsiveness to therapy.
Autoimmune diseases can be either localized or systemic:
– Systemic autoimmune diseases affect many organs and tissues simultaneously. Examples of systemic autoimmune diseases include scleroderma (affecting the skin, intestines, and less commonly lungs and kidneys) and Sjogren’s Syndrome (affecting salivary glands, tear glands, and joints.)
– Localised autoimmune diseases are organ-specific and remain in only a certain part of the body, but often can develop into systemic diseases. Examples of localized autoimmune diseases include Hashimoto’s disease (affecting the thyroid) and Discoid Lupus Erythematosus (affecting the skin). Discoid LE is an example of a localized disease that can progress into Systemic LE, affecting various organs such as the kidneys.
In the UK alone, the incidence of various autoimmune diseases is increasing at ranges between 3% and 9% year on year. This includes:
• 7.0% increase per year of rheumatic diseases such as rheumatoid arthritis
• 6.3% increase of endocrinological conditions such as type 1 diabetes
• 3.7% increase of neurological such as Multiple Sclerosis (MS)
• 4–9% increase per year of coeliac disease
In the United States of America, the prevalence of autoimmunity is also rising. According to researchers at the Allergy and Immunology section at Yale School of Medicine, in the last 25 years, there has been a 44% increase in ANA antibodies (antinuclear antibodies), which are antibodies that target themselves, with over 41 million people affected. These ANA antibodies presage autoimmune diseases such as lupus and autoimmune arthritis.
Image 1 – ANA antibodies with fluorescent dye
Costs for hospitals to aid affected individuals continue to rise as the incidence of these diseases increases. Direct and indirect costs for just three autoimmune diseases alone (type 1 diabetes, rheumatoid arthritis, and multiple sclerosis) currently add up to more than £13 billion per year in the UK. The costs are significantly high due to the absence of treatments that cure autoimmune diseases and the likelihood for patients to develop major secondary diseases. Treatment of autoimmune disease focuses on controlling the autoimmune reaction with immunosuppressants: Corticosteroids are often used to control inflammation and suppress the immune response. Another medication such as pain medication is often prescribed to suppress symptoms of the disease.
Causes and Possible Reasons for Increasing Cases
The immune system is exceedingly complex, and research has revealed some potential triggers for excess immune responses.
Genetics, and Environmental Factors
The most simple theory is that as a result of a mutation, an individual inherited a faulty allele (a version of a gene, which codes for a specific protein). Hence, the protein does not form correctly and fails to function effectively. E.g., In Type I Diabetes mellitus, a mutation in particular protein results in the destruction of beta cells in the Islets of Langerhans, as the cells are wrongfully targeted and destroyed, which results in the inability to produce insulin.
Another genetic-related theory is that a certain genetic background makes an individual more likely to have a sensitive immune system, which, upon an encounter with a certain trigger (such as an infection or climate), sets off an autoimmune disease. Chilblain Lupus Erythematosus is an example of a disease that can be inherited but may only be expressed when an affected individual inhabits a colder climate.
Smoking and Drugs
Certain substances, particularly blood pressure medications or antibiotics, can trigger the onset of drug-induced lupus, which is a more benign form of the disease but can still greatly affect an individual’s daily activities. Statins can trigger the onset of statin-induced myopathy, which causes muscle weakness.
Weight and Obesity
Being overweight or obese raises the risk of developing autoimmune diseases such as rheumatoid arthritis or psoriatic arthritis. The greater fat content and greater weight put stress on the joints, particularly the knees, and intruding fat tissues encourage further inflammation. The increasing global epidemic of obesity can contribute to the rising incidence of autoimmune diseases.
Research Advances to Lower Number of Cases
Knowledge about various autoimmune diseases and new therapies can be gained from clinical research studies, conducted with volunteers who undergo various medical tests. Clinical trials for autoimmune diseases include studying “the Pathogenesis of Chronic Inflammatory Rheumatic Diseases’” and studying “Patients Undergoing Therapy for Immune-Mediated Inflammatory Skin Conditions.” The purpose of these clinical research trials can enable various worldwide healthcare professionals to assess the safety and effectiveness of current and future therapies and to study how the onset and severity of the diseases can be dependent on inherited or acquired traits.
Researchers in laboratories investigate the molecular mechanisms of the immune response to understand the disease progression further whilst uncovering new treatment approaches. This information can enable patients’ risk for certain diseases to be recognized earlier and to provide appropriate treatments.
This involves linking both laboratory and clinical research as materials and information are exchanged and shared between these two disciplines. For example, demographic data and medical data from clinical trials can be studied together with blood samples and tissue samples to understand the diseases’ pathogenesis and progression to better target treatments.
Swetha Babu, Youth Medical Journal 2021
The increasing prevalence of autoimmune diseases and immune-related diseases continues to exert pressure on hospitals and to increase the costs for hospital treatments, due to the chronic nature of the diseases and the regular requirement for medication.
The ultimate goal of early diagnosis and therapy is prevention – before autoimmune diseases become a clinical problem.
Swetha Babu, Youth Medical Journal 2021
Lovell, D., Huang, B., Chen, C., Angeles-Han, S., Simon, T., Brunner, H. (2021) Prevalence of autoimmune diseases and other associated conditions in children and young adults with juvenile idiopathic arthritis. National Centre for Biotechnology Information. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7978075/
Motor neurone disease is the condition where messages from the motor neurones, which help carry electrical impulses from stimuli and sensory neurones, begin to stop reaching the muscles, preventing response. Stimuli include anything from sound, touch, smell, and even taste, which then allow an appropriate response, such as moving your hand away from a boiling object. In motor neurone disease (or MND), muscles, which are effectors in the stimuli-response cycle, meaning they put the response into action, begin to stiffen and waste away. Behavior and mental ability can also be affected. The disease is very uncommon, affecting roughly 5000 in the UK at any time, and can cause different symptoms in each patient.
The causes of motor neurone disease are currently unknown. There is no clear hereditary link, although you are more likely to suffer from MND if a close relative has had the disease. MND is much more common in those over 50 and with other conditions, such as specific types of dementia.
Weakness in the legs and ankles as well as trouble climbing stairs and more frequent trips and falls
Speech difficulty, including slurring as well as trouble swallowing and inability to express yourself through gestures and body language
Difficulty gripping items such as pens, opening jars, and often dropping things
Muscle cramps and tingling
Weight loss due to muscle decay, which can cause thinning of arms and legs in particular
Inability to control laughter or tears in inappropriate situations
Changes to saliva consistency or volume
Weakened coughing, causing difficulty as unable to remove saliva
Difficulty breathing, leading to fatigue
Amyotrophic lateral sclerosis (ALS)- the most common form of MND that causes muscle wastage
Bulbar onset MND or Progressive bulbar palsy (PBP)- less common than ALS and affects the muscles in the face, throat, and speech, causing slurring and difficulty swallowing
Progressive muscular atrophy (PMA)- affects a very minute proportion and causes problems with the hands and grip
Primary lateral sclerosis (PLS)- highly uncommon and causes muscle stiffness and selected speech problems and is not usually life-shortening due to very slow progression
What can Motor Neurone Disease be Misdiagnosed as?
Motor Neurone Disease can sometimes present very similarly to Kennedy’s Disease or SBMA. Kennedy’s disease also affects the motor neurones and can cause muscle weakness and wastage, although additional hormonal problems may contribute. These two diseases are often confused at diagnosis, however, those with Kennedy’s disease usually live a normal lifespan. Problems with inflammation of the spinal cord, nerve damage, and muscle damage can also mimic MND, as well as strokes. It is vital to contact a GP as soon as symptoms of MND are observed for diagnostic tests
How is it Diagnosed?
Blood and urine tests can show rises in creatinine kinase, which is produced due to muscle wastage
MRIs can prove that symptoms are not caused by another condition such as a stroke
Electromyography (EMG) and nerve conduction study (NCS) to show how electrical impulses and nerve function is working
Muscle biopsies to disprove other muscular conditions
Spinal taps and lumbar punctures can also rule out other conditions
Although there is no way to treat the disease itself, there are ways that patients’ quality of life can be improved and day to day actions facilitated. Riluzole is a drug that has been proven to slightly slow down the progression of motor neurone disease, despite it still not being a cure. Specialized clinics with nurses and occupational therapists can help motor neurone disease sufferers. Regular physiotherapy can also help to combat muscle weakness, stiffness, and pain. In a more holistic approach, speech therapists and dieticians can also be involved in patient care to offer advice.
Emotional support can also be vital for those with motor neurone disease and carers can be one way to allow sufferers to remain living independently. Joining groups and forums, such as the one run by the “Motor Neurone Disease Association”, can help to have advice and support from others who also have the disease. Organizations such as this can also offer financial support for those with motor neurone disease and advise as to where sufferers can seek professional help from hospitals who have expertise in motor neurone disease.
The black fungus infection of India, also known as “mucormycosis,” is a very rare infection. It isn’t contagious and doesn’t spread from one person to another. It is caused by exposure to “mucor” that is found in soil, plants, manure, and decaying fruits or vegetables. It affects the sinuses in the brain and causes severe damage in immunocompromised and diabetic patients. Diabetes not only increases a person’s risk for COVID-19 but can also provide conditions in which fungal infection can occur. Mucormycosis begins as a skin infection, but it later progresses to the eyes, lungs, jaws, face, and even to the brain. Dr. Hemant Thacker explains that “One of the ways mucormycosis travels is by invading the blood vessels.” Mucormycosis also blocks blood flow which kills infected tissue, once it dies or becomes necrotic, the tissue has a black discoloration. Thus the term “black fungus” has spread.
Fatality Rates + Process of Attack
Doctors currently believe that the mortality rate of the black fungus is 50%, which may be triggered by the steroids used to treat COVID-19. While steroids help to fight against COVID-19, they also happen to make the body less immune and spike up blood sugar levels. For example, dexamethasone, a drug used to treat COVID-19 suppresses the immunity of an individual, providing a greater leeway for the fungal infection to prevail. Since there is a drop in immunity when a body gets attacked by COVID-19, patients are becoming far more susceptible to this deadly disease. Dr. VP Pandey, head of the hospital at Maharaja Yeshwantrao Hospital, says that “The black fungus infection has now become more challenging than Covid-19. If patients are not treated in time and properly, then the mortality rate can go up to 94%. The cost of treatment is expensive, and the drugs are in short supply.”
Symptoms + Treatment
Dr. Anita Mathew, an Infectious disease specialist from Fortis Hospital explains that some of the common symptoms of mucormycosis include sinusitis (nasal blockage or congestion), pain on the cheekbone, facial pain, numbness or swelling, black discoloration over the nose, loosening of teeth (jaw involvement), blurred or double vision with pain, chest pain, or severe respiratory problems. Mucormycosis is treated with anti-fungal medicines, such as Amphotericin B, taken intravenously. Demand for Amphotericin B is rising continuously every day in India. Other medications like posaconazole or isavuconazole (anti-fungal medicines) can also be taken either intravenously or by mouth. Another potential treatment is to have surgery in order to remove the necrotic tissue. The disease itself is pretty rare and, according to the San Francisco Bay Area, during 1992-1993, the number of mucormycosis cases was around 1.7 cases per 1 million people. However, due to the prevalence of COVID in India, the risk of getting diagnosed with this disease is on the rise. Even though mucormycosis is a rare disease, please do not disregard it as it could have serious consequences. Additionally, many doctors believe that the most effective way to combat mucormycosis is to wear a mask while venturing out especially to gardens or dusty areas (where chances of inhaling mucor are on the rise). Also, diabetic and immunocompromised individuals should take efforts to control glucose levels. And most importantly, if ANY of the symptoms written above persist, please call your local doctor immediately to get help.