Coronavirus Disease 2019: Covid-19 Pandemic, States of Confusion and Disorderliness of the Public Health Policy-making Process
By Francis Sarr
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About this ebook
Francis Sarr
Francis Sarr, Associate Professor of Community Health Education and Fellow of the West African College of Nursing, is the Acting Dean of the School of Graduate Studies and Research at the University of The Gambia.
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Coronavirus Disease 2019 - Francis Sarr
Chapter 1: Origin of Confusion and disorderliness: Coronavirus disease 2019 (COVID-19)
The pandemic exposed the fragility of public health systems and produced much confusion and disorderliness in public health policy. This is a novel virus that the world has a great deal to learn about. Governments and health care personnel struggled to understand how it is transmitted, what therapies to use and development of effective vaccines, amongst other things. Adding to the confusion are causes such as misinformation coming from some religious and political leaders, and conspiracy theorists.
Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Coronaviruses are a family of viruses that can cause illnesses such as the common cold, severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) (Ceylan et al., 2020). Those coronaviruses are different from SARS-CoV-2 because the virus started with an animal population and was transmitted to a human and now can go from human to human. This is why the virus is called ‘novel’.
Figure 1 presents a picture of the Covid-19 coronavirus.
Figure 1: Covid-19 Coronavirus
Source: Bis Research. Com (2020)
Our immune systems have never seen this particular strain of virus before. For this reason, we haven't developed immunity. SARS-CoV-2 is more contagious than the viruses that cause influenza and common cold because it is new to humans. Also, there is a lot not yet known about COVID-19, and it is unclear how it will act in the future (WHO, 2020a). Bis Research, a market intelligence company, explains the difference in the origin of the COVID-19 pandemic and other previous pandemics (Bis Research, 2020):
"In light of the ongoing COVID-19 (coronavirus) pandemic, it is imperative to understand the origin of this virus. Previously, such pandemics were often a result of the spread of viruses such as H1N1, H5N1, and Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV), among others. The majority of pandemics that occurred in the recent past have been known to have spread through cross-species transmission of microorganisms. It is said that during this transmission, the pathogen evolves; the entire procedure of evolution can be categorized into five stages.
•Stage 1 refers to the animal microbes that are not present in a healthy human body.
•Stage 2 refers to the disease-causing pathogens that have evolved, and now have the potential to transmit the disease in the human body. This stage includes pathogens that spread diseases such as Nipah, Rabies, and other viruses.
•The secondary transmission of virus in humans referred to as the stage 3.
•Stage 4 signifies the complete transmission of these pathogens along with their evolution in terms of animal genetics undergoing the complete sequence of human to human transmission.
•Lastly, stage 5 is limited to pathogens that spread diseases exclusively to humans, for instance, HIV and smallpox" (BisResearch, 2020).
The drivers of zoonotic disease (illness caused by germs that are passed between animals and people) are rather complicated, singly and collectively. Some of these drivers are food insecurity for workers in a logging or mining camp in Africa, resulting in increased hunting and consumption of bushmeat. Although we may understand some of these drivers in isolation or in their simpler, worldly fundamental interaction with each other, the complex ways in which they change over time, such as in lengthy intervals as with HIV, and how they interact are not well comprehended. Constant with the coexistence of humans on the planet are the demands that the drivers present for when, how, and where zoonotic diseases will emerge (National Academy of Sciences 2009).
Timothy Sly, Epidemiologist and professor at Ryerson University, Toronto, also compared the COVID-19 pandemic to past pandemics in terms of spread, deadliness, treatment and knowledge about the virus as follows:
The degree of spread (global) is similar to the 1918, 1957, 1968, and 2009 influenza pandemics, although this one is almost certainly much faster than 1918 [the Spanish Flu], due to rapid airflight to global destinations. The lethality (in terms of the case fatality rate) of the Coronavirus is about ten times more than 1957, 1968, and 2009, and about half that of the 1918 pandemic, but because the population is greater than 100 years ago, we may see more deaths for the same global incidence rate
"Treatment remains only supportive (ventilators, corticosteroids) perhaps later we may see antivirals. We do have genetic sequencing now, allowing early testing and possibly more candidates for vaccine development based in genetics. Also greater understanding of viral pathology [study of the causes and effects of disease or injury], cytokine responses [Cytokines are a diverse family of intercellular signalling molecules that regulate inflammation and immune responses]. (During 1918, not everyone was convinced it was caused by a virus. Many thought a bacterium was to blame which caused the pneumonia, hence Pfeiffer’s bacillus, later known as Haemophilus influenzae was isolated as the scapegoat.). The age distribution of serious cases is also different to influenza pandemics" (Sly 2020).
As indicated, the disease was first identified in 2019 in Wuhan, the capital of China's Hubei province, and has since spread globally, resulting in the ongoing coronavirus pandemic (Hui et al., 2020; WHO 2020a). In late December 2019, Li Wenliang, MD, an ophthalmologist at Wuhan Central Hospital sent a message to a group of medical school alumni warning them about a mysterious new illness that looked very much like the severe acute respiratory syndrome (SARS).
Ankel (2020) reported that authorities in Wuhan, China, tried to silence Li Wenliang by forcing him to sign a letter admitting to spreading rumours
and making false comments’’ about the outbreak. LiWenliang's subsequent death of the same virus, on February 7th 2020, sparked anger with many people across China, as they took to social media calling for freedom of speech and the end of state censorship. However, China later declared the doctor a
martyr," the highest honour the Communist Party can bestow on a citizen. The country also observed a three-minute silence to honour Li and other coronavirus victims.
Health care workers in other countries had also been infected and many had died during the pandemic. In Spain, for example, healthcare workers in the country had by February 25th, 2020, accounted for more than 13% of the country’s Covid-19 cases, and doctors struggled to cope as 514 died from the coronavirus in a day (The Guardian, 2020).
The following sections cover COVID-19’s terminology, signs and symptoms, causes and spread, affected populations, mortality, pathophysiology, diagnosis, prevention, management including treatments, prognosis, reinfections and chronic conditions of the disease, history, epidemiology, misinformation, scams, myths and conspiracies, and research on vaccines and treatments. The COVID-19 pandemic is an evolving situation and the following descriptions on this unprecedented health crisis covers only information available at the time of writing.
Terminology
The World Health Organization (WHO) announced in February 2020 that COVID-19 is the official name of the disease. The WHO chief Tedros Adhanom Ghebreyesus explained that CO stands for corona, VI for virus and D for disease, while 19 is for the year that the outbreak was first identified; 31 December 2019. The reason for this name was to avoid mentioning a specific geographical location (i.e. China), animal species, or group of people, in line with international recommendations for naming viruses aimed at preventing stigmatisation.
Although the disease is named COVID-19, the virus that causes it is called severe acute respiratory syndrome coronavirus 2 or SARS-CoV-2. The virus was at the beginning cited as the 2019 novel coronavirus or 2019-nCoV. In addition, the WHO used the COVID-19 virus
and the virus responsible for COVID-19
in public communications. Coronaviruses were named in 1968 for their appearance in electron micrographs which was reminiscent of the solar corona, corona meaning crown in Latin as shown in Figure 1.
Signs and symptoms
The signs and symptoms include fever, dry cough, fatigue, chills, headache, and shortness of breath which often indicates pneumonia. About 70% of those infected developed a fever (CNN, 2020e). A study reported by David Alson (2020) showed that most patients in New York hospitals did not have fever (CNN, 2020e). There may be muscle pain, sputum production, diarrhoea, sore throat, loss of sense of smell, taste, appetite, and abdominal pain. Also, there may be neurological symptoms, gastrointestinal (GI) symptoms, or both. These may occur with or without respiratory symptoms. Less common symptoms include sneezing, runny nose, nausea, vomiting and diarrhoea.
A study has suggested a 9-day period between when a person is infected and when he/she develops symptoms. Recently, a study found that on average, the time from exposure to symptom onset (known as the incubation period) is about five to six days. However, studies have shown that symptoms could happen as soon as three days after exposure to as long as 13 days later. These findings go on to reinforce the US Center for Disease Control and Prevention (CDC) recommendation of self-quarantine and monitoring of symptoms for 7 to 14 days post-exposure.
While the majority of cases result in mild symptoms, some progress to pneumonia and potentially multi-organ failure and death.
There could be several reasons why there is such a wide range in severity of symptoms for COVID-19 infections. These include: (1) differences in people’s immune response (2) either a crossover sensitivity from another viral agent, or genetically-based (3) more than one distinct strain of the virus, promoting differing immune responses and (4) initial viral dose, whether virus was inhaled into upper respiratory tract or lower respiratory tract. The majority of the signs and symptoms, namely, fever, lung congestion, all the elements of inflammation, are not due directly to the virus, but are effects of the immune response itself. This is also the case with novel influenza virus such as H5 or H7.
Causes and spread
The disease is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), as indicated. Also, as mentioned, scientists say the virus originated from human impact on the environment that might have driven the spread of the virus from animal to human. However, there remains some uncertainty regarding the mechanism of spread of the virus. It is primarily spread between people during close contact and via respiratory droplets from coughs and sneezes. Infectious viral particles can float or drift around in the air for up to three hours. Another person can breathe in these viral particles and become infected with the coronavirus. This is why people are asked to wear face masks in public.
Experts do not know when people are most infectious. However, a recent study suggests that new mutations could make COVID-19 more infectious. Evidence suggested that the D614G strain of the COVID-19 virus may spread more easily than the original strain. This is because infected individuals with this strain seem to have more virus in their upper respiratory tracts, and thus may be more likely to transmit infection to others. To date, the mutated strain has not appeared to cause more severe COVID-19 disease. Studies published between 25/11/2020 and 1/12/2020 found no evidence of recurrent mutations associated with increased viral transmission. Mutations identified up to that point, appeared to be evolutionary neutral rather than a result of viral adaptation.
However, new Covid-19 variants like the Delta and Omicron had emerged causing significant outbreaks and governments had introduced or reintroduced strict control measures such as mask and vaccine mandates.
Although new variants are a predictable piece of the evolution of viruses, a new variant can be more aggressive, highly transmissible, vaccine-resistant, able to cause more severe disease, or all of the above, compared with the original strain of the virus.
News about the COVID-19 Delta and Omicron variants was overpowering our daily lives during the pandemic. Delta (B.1.617.2) was the variant that was mostly reported about by late 2020. It had a number of offshoots, such as Delta AY.4.2, some of which were said to have mutations new to Delta but that were found in other variants (When a virus is circulating widely and causing several infections, the possibility of the virus mutating increases. The more chances a virus has to spread, the more chances it has to undergo changes).
Delta was first identified in India in late 2020, and quickly spread throughout the world, becoming the predominant strain of the coronavirus, up until Omicron replaced it in mid-December 2021. However, the Delta variant nevertheless endured, causing much concern because evidence had shown the variant to be more infectious and to spread more quickly than other variants, even in people who were vaccinated.
It had been estimated that Delta caused more than twice as many infections as previous variants, such as the Alpha variant. Also, reports had shown that Delta might cause more severe disease than other variants in people who were not vaccinated. However, although no vaccine was thought to be 100% effective against Delta, vaccines were considered highly effective against severe illness, hospitalizations, and death from Delta.
The Omicron variant of COVID-19 had caused even more concern than the Delta variant because it had several mutations that might have an impact on how it behaved. There was ample doubt concerning Omicron and a lot of research was underway to evaluate its transmissibility, severity and reinfection risk. Reports had suggested that the Omicron variant had by that time it was identified in Botswana and South Africa in late November 2021 spread to many countries around the world, probably in most countries, even if it had not been noticed yet.
Although research was continuing to determine the severity of Omicron, early reports had suggested that Omicron might be less severe than the Delta variant, but more data was required. Research was also on-going on any potential impact the Omicron variant had on the effectiveness of COVID-19 vaccines. Some reports had suggested that there might be a small reduction in the effectiveness of vaccines against severe illness and death, and a decline in preventing mild disease and infection. But, other reports had indicated that available vaccines appeared to offer significant protection against severe disease and death. Thus, it was also important to be vaccinated to protect against the other widely circulating variants, such as the Delta variation.
Each means of spreading the virus is examined further in the sections below.
i. Close contacts and gatherings
By July 7th 2020, scientists had warned that airborne threats of the virus were under-emphasized. The virus appeared to be most infectious when people are in contact at close range, especially indoors, where infected people release virus-carrying respiratory micro-droplets into the air. This includes contact within one metre for one minute or longer without face-to-face contact. It also includes a person who has been within 2 metres of someone who has tested positive for COVID-19 for more than 15 minutes. Reports suggest that some COVID-19 patients infect many others, whereas most don’t spread the virus at all.
Four out of five people who are infected got it from people who did not know they were infected. A person with COVID-19 may be contagious 48 to 72 hours before starting to experience symptoms. Actually, people without symptoms are more probable to spread the illness, because they are unlikely to act in ways that can prevent spread.
The virus is three times more contagious than the ordinary flu. It is most contagious when people are symptomatic, but substantial transmission occurs from asymptomatic individuals. A report from the US on June 25th 2020, says that half of new cases registered in the country were under the age of 35 years and were asymptomatic. Also, on July 10th 2020, Dr Fauci said that 40% to 45% of those infected in the US were asymptomatic (CNN 2020e).
Reports suggest that super-spreading
events of the virus or clusters have occurred in the COVID-19 pandemic in various places, such as aboard ships and at nursing homes, meatpacking plants, ski resorts, churches, restaurants, hospitals, and prisons. Sometimes a single person infects dozens of people, whereas other clusters unfold across several generations of spread, in multiple venues. The disease spreads faster where people are close together or travel between areas. A lab simulation shows that droplets from a cough can travel as far as 12 feet more than the recommended 6 feet for social distancing between one person to another for COVID-19, and those droplets could remain in the air for about ten minutes. This is different if an individual wears a mask. Research suggests the virus can be spread through breathing and talking (Devor 2020)
As mentioned, the degree of spread (global) is similar to the 1918, 1957, 1968, and 2009 influenza pandemics, although COVID-19 is almost surely quicker than the 1918 Spanish Flu because of rapid air-flight to world destinations (Sly 2020).
A recent study that compared the quantity of coronavirus in the nose, throat, and lungs of symptomatic and asymptomatic adults infected with SARS-CoV-2 (the COVID-19 coronavirus) found that both groups of patients had corresponding amounts of virus in their bodies throughout the infection (WHO 2020j).
The virus may be shed in saliva and semen. But it is uncertain if it is shed in vaginal fluids. The virus can be transmitted through kissing. However, transmission of the virus during vaginal or anal intercourse or oral sex, seems to be extremely remote at this time.
ii. Surfaces
Touching a contaminated surface and then touching the face can cause infection. A study investigating the rate of decay of the virus found no viable viruses after four hours on copper, 24 hours on cardboard, 72 hours on stainless steel, and 72 hours on plastic. Estimation of the rate of decay with a Bayesian regression model suggests that the virus may remain viable up to 18 hours on copper, 55 hours on cardboard, 90 hours on stainless steel, and over 100 hours on plastic (Raj 2020). However, according to a report from the U.S. Center for Disease Control and Prevention (CDC), surface exposure is not a particularly effective way for the virus to infect its host (CDC 2021). The agency maintains that person to person contact is the most reliable way for the virus to spread. Unfortunately, COVID-19’s incubation period differs from similar respiratory illnesses caused by other coronaviruses studied in the past. For a start, carriers are the most contagious while symptoms are still mild or before they even begin (asymptomatic). During this window, infected individuals shed a considerable amount of viral debris often giving the virus to three people before recovery.
iii. Mother to child
An observational study of nine people found no vertical transmission from mother to the newborn. Another study also showed that there is no evidence for intrauterine transmission of COVID-19 infection from infected mothers to their foetuses but, infected pregnant women may be at increased risk of pulmonary complications.
iv. Gastrointestinal tract
The virus has been found in the faeces of as many as 53% of hospitalised people and more positive anal swabs have been found than positive oral swabs in the later stages of infection. The virus was found in faeces from one to twelve days, and 17% of patients continued to present the virus in faeces after no longer presenting them in respiratory samples, indicating that the viral gastrointestinal infection and the potential faecal-oral transmission can last even after viral clearance in the respiratory tract.
Re-occurrence of the virus has also been detected through anal swabs suggesting a shift from more oral positive during the early stages of the disease to more anal positive during later periods.
Affected populations
The elderly are more vulnerable. In the US, for example, people aged 20-44 make up 20% of hospitalization, and 54% of cases between 18-49 years old. Children are less vulnerable but they can infect older people. However, during the crisis, the CDC investigated 85 cases of an illness children had that might have been linked to COVID-19 (CNN 2020e). A study reported by CNN also showed that nearly 25% of children in ICU had multiple organ failure (CNN 2020e). Data from Italy showed more men died than women. This has been attributed to women having two x chromosomes that help the immune system fight the virus, whereas men have only one x chromosome. However, women are more infected than men partly because women are more on the front-line in the fight against the virus, such as nurses (CNN 2020e). A study suggests that people with certain enzymes were more vulnerable as the enzymes helped the virus to enter the cells. The enzymes are more in men than women (CNN 2020e).
For example, inherent health conditions reported among adult patients with severe COVID-19 include hypertension, diabetes, cardiovascular disease, chronic respiratory disease, chronic kidney disease, immune compromised status, cancer, smoking and obesity. Also pre-existing medical conditions have been recommended as a risk factor for severe disease and ICU admission in children and adolescents. A European multi-centre cohort study shows that the most frequent conditions given were chronic pulmonary disease, malignancy, neurological disorders, congenital heart disease, chromosomal abnormalities and chronic kidney disease. In other studies analogous co-morbidities in hospitalised and ICU patients were found. More data is required to understand how pre-existing conditions can influence the course of COVID-19 in children and adolescents.
Mortality
Although cases represent the disease burden for a country, it is also important to estimate the death rate of COVID-19. Furthermore, differences in mortality between groups of people and countries are important proxy indicators of relative risk of death that guide policy decisions regarding scarce medical resource allocations. For example, in the US, compared with 5—17-year-olds, the rate of death was 45 times higher in 30—39-year-olds and 7,900 times higher in 85+-year-olds (CDC, 2020). Also, it is important to show the time trend of the dynamic development of the epidemiological picture around the world, not just the cumulative. There have been several reports on COVID-19 cases, deaths and time trends of cases and deaths since the crisis started in 2019. For example, WHO (2020d) reported on the number of COVID-19 cases and deaths, as well as the time trend of cases and deaths by WHO region as shown in Figure 2 and in Africa as detailed in Figure 3.
Figure 2: Number of COVID-19 cases reported weekly by WHO Region, and global deaths, 30 December 2019 through 11 October 2020 (WHO, 2020)
The figure above shows the time trend in COVID-19 cases and deaths reported globally. As of March 2020, there was a sharp increase in the number of deaths. Within a span of three months, the deaths increased from less than 5,000 to over 50,000 in April, eventually dropping to less than 40,000 deaths between May to June 2020. A slight increase was seen between June and August 2020. As of October 11, about one million deaths were reported globally, with over half of these deaths reported in the Americas (WHO, 2020).
Figure 3: Number of COVID-19 cases and deaths reported weekly by the WHO African Region, as of 11 October 2020 (WHO, 2020)
In the initial stage of the pandemic, the African continent had seen a slow but steady increase in the number of deaths. The peak was seen in July and August 2020, reaching over 2,500 deaths, following the surge in cases in the preceding months. As of September 28, the total deaths were about 1,000 with South Africa accounting for the majority of the cases in the region (74%) (WHO, 2020).
Pathophysiology
Pathophysiology means the disordered physiological processes associated with a disease. The pathophysiology of the COVID-19 disease has been characterised by the lungs being the organs most affected by COVID-19 because the virus accesses host cells via the enzyme ACE2, which is most abundant in the type II alveolar cells of the lungs. The virus uses a special surface glycoprotein called a spike
(peplomer) to connect to ACE2 and enter the host cell. The density of ACE2 in each tissue correlates with the severity of the disease in that tissue and some have suggested that decreasing ACE2 activity might be protective, though another view is that increasing ACE2 using angiotensin II receptor blocker medications could be protective and that these hypotheses need to be tested. As the alveolar disease progresses, respiratory failure might develop and death may follow. Figure 4 presents an overview of the COVID-19 disease pathophysiology.
Figure 4: Pathophysiology of COVID-19 disease
Source: Parasher (2020)
The virus also affects gastrointestinal organs as ACE2 is abundantly expressed in the glandular cells of gastric, duodenal and rectal epithelium as well as endothelial cells and enterocytes of the small intestine.
Diagnosis
The standard method of diagnosis is by reverse transcription polymerase chain reaction (RT-PCR) from a nasopharyngeal swab, as shown in Figure 5. While the test is typically conducted on respiratory samples obtained by a nasopharyngeal swab, a nasal swab or sputum sample may also be used. Results are mostly available within a few hours to two days. Although blood tests can be used for diagnosing COVID-19, these require two blood samples taken two weeks apart and the results have little prompt value.
Figure 5: Diagnostic testing for COVID-19 from a nasopharyngeal swab
Source: Medicins Sans Frontières (2020)
The infection can also be diagnosed from a combination of symptoms, risk factors and a chest CT scan showing features of pneumonia. As of March 19th 2020, there were no antibody tests though efforts to develop them were ongoing. By June 14th, 2020, the US Federal Drug Agency (FDA) was validating antibody tests.
The FDA approved the first point-of-care test on March 21st, 2020, for use at the end of that month. The FDA also authorised COVID-19 tests on June 9th, 2020 that also look for mutations of the virus. As indicated, a recent study suggests that mutations could make COVID-19 more infectious. By end of November 2020, there was a Covid Rapid Test App that could tell one if his/her symptoms corresponded with COVID-19, or if he/she has
