Monkeypox virus particle, colored transmission electron micrograph (TEM). Monkeypox is a poxvirus that was identified in Cynomolgus monkeys in 1958 and then in humans in 1970. The virus consists of a DNA (deoxyribonucleic acid) core in a protein coat, or capsid, surrounded by an envelope. The proteins allow the particles to enter and leave host cells. The virus reproduces by entering cells and hijacking their biochemical machinery, producing many copies of itself. Monkeypox is zoonotic, passing from animals (such as rodents) to humans and vice versa. Human infections are often caused by animal bites or from direct contact with infected bodily fluids. There is no proven safe treatment or vaccine for monkeypox (as of 2008). Magnification: x125,000 when printed 10 centimeters tall.


Monkeypox virus is an orthopoxvirus that causes a disease with symptoms similar, but less severe, to smallpox. While smallpox was eradicated in 1980, MONKEYPOX occurs in Central and West African countries. Two distinct clades are identified: the West African clade and the Congo Basin clade, also known as the Central African clade.



It is one of the viral zoonotic diseases that originate in tropical rainforests of Central and West Africa (World Health Organization, 2020). While the disease has a significant fatality rate of 10%, as you note, I believe that it is one of the least known diseases. Still, it is pretty insightful to know that it closely resembles smallpox, which has since been eradicated (World Health Organization, 2020). You have used the disease outbreak incidence in Nigeria to exemplify how stigma by healthcare professionals and community members can derail efforts to combat health crises and how effective health communication can reduce this stigma.

When facts-based information about a disease, including its causes, transmission, safety, preventive measures, and cure, is made available to healthcare professionals, patients, their families, and the community, fear, and panic associated with ignorance and uncertainty are alleviated. Consequently, little room is left for stigma to thrive and bar healthcare professionals from extending the proper care to patients, patients seeking care, and family members and the community supporting them.

Currently, there are no proven treatments specifically for monkeypox. Instead, cases of monkeypox can be treated with medical countermeasures designed for the closely related smallpox virus. There are currently three smallpox vaccines that could be used in the US, 2 of which are licensed for smallpox, and the other could be used for smallpox under an investigational new drug (IND) protocol. The two licensed vaccines for smallpox are JYNNEOSTM (also known as Immune or Imvanex) and ACAM2000®, of which JYNNEOSTM is also approved for monkeypox.



Clinical Criteria

  • New rash (any of the following)
    • Macular
    • Papular
    • Vesicular
    • Pustular
    • Generalized or localized
    • Discrete or confluent
  • Fever (either of the following)
    • Subjective
    • The measured temperature of ≥100.4° F [>38° C]
  • Other signs and symptoms:
    • Chills and sweats
    • New lymphadenopathy (periauricular, axillary, cervical, or inguinal)

Epidemiologic Criteria

Within 21 days of illness onset:

  • Report having had contact with a person or people who have a similar-appearing rash or received a diagnosis of confirmed or probable monkeypox OR
  • Is a man who regularly has close or intimate in-person contact with other men, including through an online website, digital application (“app”), or social event (e.g., a bar or party) OR
  • Traveled to a country with confirmed cases of monkeypox AND at least one of the above criteria OR
  • Traveled to a country where MPXV is endemic OR
  • Contact with a dead or live wild animal or exotic pet that is an African endemic species or used a product derived from such animals (e.g., game meat, creams, lotions, powders, etc.)

Exclusion Criteria

A case may be excluded as a possible, probable, or confirmed monkeypox case if:

  • An alternative diagnosis* can fully explain the illness OR
  • An individual with symptoms consistent with monkeypox but who does not develop a rash within five days of illness onset OR
  • A case where specimens do not demonstrate the presence of orthopoxvirus or monkeypox virus or antibodies to orthopoxvirus as described in the laboratory criteria

†Categorization may change as the investigation continues (e.g., a patient may go from PUI to probable)

* The rash associated with monkeypox can be confused with other diseases that are more commonly encountered in clinical practice (e.g., secondary syphilis, herpes, chancroid, and varicella-zoster). Historically, sporadic reports of patients co-infected with monkeypox virus and other infectious agents (e.g., varicella-zoster, syphilis).


Guidelines to diagnose:

Person Under Investigation

Persons under investigation (PUI) are individuals who are reported as suspicious but have not been tested in an LRN laboratory. This includes cases on which health departments have been consulted because of clinician concerns.

Possible Case

Meets one of the epidemiologic criteria AND has a fever or new rash AND at least one other sign or symptom with onset 21 days after last exposure meeting epidemiologic criteria

Probable Cause

Meets one of the epidemiologic criteria AND has a new rash with or without fever AND at least one other sign or symptom with onset 21 days after last exposure meeting epidemiologic criteria


Demonstration of detectable levels of anti-orthopoxvirus IgM antibody during the period of 4 to 56 days after rash onset

Confirmed Orthopoxvirus Case

Meets possible case definition AND

Demonstration of orthopoxvirus DNA by polymerase chain reaction testing of a clinical specimen OR demonstration of the presence of orthopoxvirus using immunohistochemical or electron microscopy testing methods

Confirmed Monkeypox Case

Meets possible case definition AND

Demonstration of monkeypox virus DNA presence by polymerase chain reaction testing or Next-Generation sequencing of a clinical specimen OR isolation of monkeypox virus in culture from a clinical sample.

Recommendations for Clinicians

Human-to-human transmission is limited, with the longest documented chain of information being six generations. The last person infected in this chain was six links away from the original sick person. It can be transmitted through contact with bodily fluids, skin lesions, or internal mucosal surfaces, such as mouth or throat, respiratory droplets, and contaminated objects.

Detection of viral DNA by polymerase chain reaction (PCR) is the preferred laboratory test for monkeypox. The best diagnostic specimens are directly from the rash – skin, fluid, crusts, or biopsy where feasible. Antigen and antibody detection methods may not be helpful as they do not distinguish between orthopoxviruses.

1-monkeypox-virus-particle-tem-hazel-appleton-centre-for-infectionshealth-protection-agency.jpg (836×900)

Fig: The monkeypox virus, shown in a colored electron micrograph, typically spreads by skin-to-skin contact or respiratory droplets.



  1. CDC. (2022)
  2. The Johns Hopkins Center for Health Security. (2022)
  3. WHO. (2022).




OMICRON- The Third Wave

OMICRON- The Third Wave

  1. On 26 November 2021, WHO designated the variant B.1.1.529 a variant of concern, named Omicron, on the advice of WHO’s Technical Advisory Group on Virus Evolution (TAG-VE).  This decision was based on the evidence presented to the TAG-VE that Omicron has several mutations that may have an impact on how it behaves, for example, on how easily it spreads or the severity of illness it causes. Here is a summary of what is currently known.Introduction
  1. Current knowledge about Omicron

            Researchers in South Africa and around the world are conducting studies to better understand many aspects of Omicron and will continue to share the findings of these studies as they become available.


It is not yet clear whether Omicron is more transmissible (e.g., more easily spread from person to person) compared to other variants, including Delta. The number of people testing positive has risen in areas of South Africa affected by this variant, but epidemiologic studies are underway to understand if it is because of Omicron or other factors.

2.2. Severity of disease
It is not yet clear whether infection with Omicron causes more severe disease compared to infections with other variants, including Delta.  Preliminary data suggests that there are increasing rates of hospitalization in South Africa, but this may be due to increasing overall numbers of people becoming infected, rather than a result of specific infection with Omicron.  There is currently no information to suggest that symptoms associated with Omicron are different from those from other variants.  Initial reported infections were among university students—younger individuals who tend to have more mild disease—but understanding the level of severity of the Omicron variant will take days to several weeks.  All variants of COVID-19, including the Delta variant that is dominant worldwide, can cause severe disease or death, in particular for the most vulnerable people, and thus prevention is always key.

III. Effectiveness of prior SARS-CoV-2 infection

Preliminary evidence suggests there may be an increased risk of reinfection with Omicron (Ie , people who have previously had COVID-19 could become re infected more easily with Omicron), as compared to other variants of concern, but information is limited. More information on this will become available in the coming days and weeks.

3.1.Effectiveness of vaccines
WHO is working with technical partners to understand the potential impact of this variant on our existing countermeasures, including vaccines. Vaccines remain critical to reducing severe disease and death, including against the dominant circulating variant, Delta. Current vaccines remain effective against severe disease and death.

3.2.Effectiveness of current tests
The widely used PCR tests continue to detect infection, including infection with Omicron, as we have seen with other variants as well. Studies are ongoing to determine whether there is any impact on other types of tests, including rapid antigen detection tests.

3.3.Effectiveness of current treatments
Corticosteroids and IL6 Receptor Blockers will still be effective for managing patients with severe COVID-19. Other treatments will be assessed to see if they are still as effective given the changes to parts of the virus in the Omicron variant.

  1. Studies underway

            At the present time, WHO is coordinating with a large number of researchers around the world to better understand Omicron. Studies currently underway or underway shortly include assessments of transmissibility, severity of infection (including symptoms), performance of vaccines and diagnostic tests, and effectiveness of treatments.

WHO encourages countries to contribute the collection and sharing of hospitalized patient data through the WHO COVID-19 Clinical Data Platform to rapidly describe clinical characteristics and patient outcomes.

More information will emerge in the coming days and weeks. WHO’s TAG-VE will continue to monitor and evaluate the data as it becomes available and assess how mutations in Omicron alter the behavior of the virus.

  1. Recommended actions for countries

As Omicron has been designated a Variant of Concern, there are several actions WHO recommends countries to undertake, including enhancing surveillance and sequencing of cases;  sharing genome sequences on publicly available databases, such as GISAID; reporting initial cases or clusters to WHO; performing field investigations and laboratory assessments to better understand if Omicron has different transmission or disease characteristics, or impacts effectiveness of vaccines, therapeutics, diagnostics or public health and social measures.  More detail in the announcement from 26 November.

Countries should continue to implement the effective public health measures to reduce COVID-19 circulation overall, using a risk analysis and science-based approach. They should increase some public health and medical capacities to manage an increase in cases.  WHO is providing countries with support and guidance for both readiness and response.

In addition, it is vitally important that inequities in access to COVID-19 vaccines are urgently addressed to ensure that vulnerable groups everywhere, including health workers and older persons, receive their first and second doses, alongside equitable access to treatment and diagnostics.

  1. Recommended actions for people

The most effective steps individuals can take to reduce the spread of the COVID-19 virus is to keep a physical distance of at least 1 meter from others; wear a well-fitting mask; open windows to improve ventilation; avoid poorly ventilated or crowded spaces; keep hands clean; cough or sneeze into a bent elbow or tissue; and get vaccinated when it’s their turn.

WHO will continue to provide updates as more information becomes available, including following meetings of the TAG-VE. In addition, information will be available on WHO’s digital and social media platforms.

VII. Omicron COVID Variant Symptoms

Symptoms for the new COVID Variant “Omicron” are given below.

Note: Symptoms are classified in most common symptoms, less common symptoms & serious symptoms.

Most common symptoms

Most common symptoms for the new COVID Variant “Omicron” are fever, cough, tiredness, loss of taste or smell.

Less common symptoms

Less common symptoms for the new COVID Variant “Omicron” are sore throat, headache, aches, pains, diarrhea, a rash on skin, discoloration of fingers or toes

red or irritated eyes.

Serious symptoms

Serious symptoms for the new COVID Variant “Omicron” are difficulty breathing or shortness of breath, loss of speech or mobility, or confusion or chest pain.

Note: If anyone has any of these symptoms then he/she should urgently take the COVID test.

After the detection of a new variant of COVID, the WHO has advised the country and every individual to follow the SOPs (Standard Operating Protocols).

Source: Update on Omicron (

Brain Transplant

Parkinson’s disease

Parkinson’s disease is a progressive disease that affects motor function in patients. In the beginning, the symptoms can go unnoticed since it starts with tremors on the hand, slowed movement, and stiffness as it progresses. Dopamine is a neurotransmitter that is responsible for coordinating muscle movements in the body. Produced in the substantia nigra, dopamine production may reduce when the cells of the substantia nigra die after the onset of PD (Brooks,2016). According to Zeng et al. (2018), PD first affects the olfactory bulbs and vagus nerve’s dorsal motor nucleus and later moves to substantia nigra. In the later stages of the disease, the brain cortex becomes affected. As the disease progresses, other brain areas and the nervous system become affected, resulting in impairments to the cognitive neuropsychological, and motor systems.

Epidemiology –

Continued loss of neurons that produce dopamine results in the development of PD. Although the cause is not well understood, various factors could result in the development of PD. Genetic factors are considered to cause about 15% of PD cases (Tysnes & Storstein, 2017).

Researchers argue that various genetic mutations can result in the development of the disease, and these mutations are associated with a family history of the disease. The other causes include environmental factors. For instance, continued exposure to some toxins increases PD risk (Zeng et al., 2018). Other environmental factors include exposure to certain metals, herbicides and pesticides, and head injury. Other causes include the presence of Lewis Bodies, which is believed to cause PD.

Risk Factors

Age is one of the risk factors for PD. For instance, Parkinson’s Disease is common among older adults above 60 years and less common among young adults. However, the disease could begin in middle life. The other risk factor is a family history of PD. Hereditary factors mean that the risk of developing PD is high when one has a close relative to the disease. However, the risk is low if only one family member has the disease. The sex of an individual is also a risk factor since PD is common among males than females. Lastly, getting exposed to various forms of toxins such as pesticides and herbicides, heavy metals could result in developing the disease (Emamzadeh & Surguchov, 2018). Lastly, head injuries may also lead to PD.

Conditions Associated with PD

The condition is linked to various health conditions and complications. For instance, individuals with PD are likely to develop cardiovascular disease. Studies show that those with PD are likely to develop cardiovascular disease, with a 50 percent chance of dying from the complication. This is because cardiovascular disease can result in heart attacks or stroke. Also, gastrointestinal illness is common among people with PD. This is because PD could start in the nervous system, which controls the gastrointestinal system. In this case, early symptoms of PD could include constipation and dysregulation of the gut bacteria.

The other associated condition is skin cancer. Persons living with PD have a lower risk of developing cancer. However, malignant melanoma is common among people with Parkinson’s disease. Also, genitourinary dysfunction is joint among people with PD, which includes complications associated with the urinary system or sex organs. In this case, sexual dysfunction and urinary incontinence are joint. Lastly, diabetes is associated with PD since individuals living with diabetes type 2 have an increased risk of developing PD. Estimates show that about 10 to 30 percent of people with PD have diabetes, while about 80 percent of people with PD establish low glucose tolerance, indicating pre-diabetes.

Physical exam for PD involves visual observation, auscultation, and palpation of the patient. In this case, a neurologist conducts the physical exam to determine the presence or absence of PD. The physician also assesses the patient for balance impairments, episodes of freezing, and tremor symptoms. The neurologist examines gait to determine abnormalities such as spastic, steppage, waddling, or propulsive gait. Also, gait observation looks for the initiation, arm swing, turning to assess balance, or hesitancy associated with postural instability. In addition, step strength/size looks whether the patient has a shuffling gait or festinate gait, which helps maintain balance. The neurologist also checks posture to determine trunk flexion, stooped or rounded shoulders, and involuntary forward head craning.

Differential Diagnosis

Dementia with Lewis Bodies (DLB). This is a common cause of dementia and is characterized by parkinsonism, visual hallucinations, and cognitive impairments. In this case, Lewis Bodies is a common pathology in dementia with Lewis bodies and PD (Stoker & Greenland, 2018). The diagnostic criteria for PD and DLB provide that if cognitive impairment happens during the first year of parkinsonism, DLB is diagnosed. However, when cognitive impairment develops after PD is established, the diagnosis becomes PD with dementia.

Fluctuation in cognition and visual hallucinations are critical in the diagnosis of DLB.

Progressive Supranuclear Palsy (PSP). This neurodegenerative disease is characterized by difficulties walking, visual impairment/blurred vision, and instability. Postural instability is typical in both PD and PSP. However, this symptom marks disease progression in PD, while in PSP, it could occur earlier, and the patient falls frequently. Abnormal eye movement reduced verbal fluency, and executive function is also standard in PSP (Stoker & Greenland, 2018). Neuroimaging can help differentiate PSP from PD, but the reduced response to levodopa, eye movement problems, and frequent early falls happens in PSP than in PD.

Multiple system atrophy (MSA). This condition is characterized by its effect on autonomic functions such as breathing, motor control, the functioning of the bladder, and blood pressure. The disease shares most PD symptoms, including reduced balance, muscle rigidity, and reduced movements. It is also associated with tremors, although this is rare in MSA. Other symptoms associated with MSA include sleep disorders, erectile dysfunction, dysarthria, unsteady gait, dysphagia, and visual disturbances. However, MSA is considered to progress rapidly and is less responsive to levodopa and autonomic problems in the early stages of the disease. This differentiates MSA from PD.

Diagnostic Tests

There is no specific test for diagnosing PD. However, neurologists can use the patient’s medical history and a review of the signs and symptoms, and a physical exam to diagnose the condition. Also, a DAT scan can be ordered to help support the diagnosis. Other Imaging tests include MRI, PET scans, and CT, which help rule out other conditions but not necessary to diagnose PD (Tynes & Storstein, 2017). Also, blood and urine tests can be ordered to rule out other conditions. In most cases, analyzing PD could take time, which means that follow-up appointments may be necessary to ensure an accurate diagnosis. In most cases, neuro- examination and physical examination are critical in PD diagnosis.


Various forms of treatment are used to help manage the condition, but PD cannot be cured. In this case, therapy helps control the symptoms to allow the patient to reduce tremors, enhance walking and movement, and substitute dopamine. Carbidopa-levodopa, commonly called Levodopa, is the widely used medication since it shows the best results (Emamzadeh & Surguchov, 2018). The dosage should be between 300 to 600mg/day taken 3 or 4 times a day. The medication enters the brain and converts into dopamine. Carbidopa is a substance that helps ensure that levodopa enters the brain since dopamine cannot pass through the brain.

 The other medication is Duopa. This drug contains carbidopa and levodopa, but it is administered through a tube for patients with advanced PD. Duopa should be administered through intrajejunal infusion with a maximum dose of 2000mg daily over 16 hours. Other medication includes dopamine agonists such as Ropinirole (9mg/day), apomorphine (3- 6mg/day), and Mirapex (initial dose of 0.125smg/daily 2hours before bed). This is a group of drugs that are not converted into dopamine but work by mimicking the effects of dopamine in the brain. Also, MAO B inhibitors are used to help inhibit dopamine metabolizing enzymes from ensuring dopamine breakdown does not take place (Emamzadeh & Surguchov, 2018). Example include Selegiline (10 mg/day taken at a dose of 5mg twice)

In terms of education, patients must ensure that they adhere to the doses given to ensure they get the desired outcome from the treatment. Also, working together with the doctor is crucial to ensure that the best treatment plan is achieved to get the most significant benefits by reducing symptoms and side effects. In addition, the doctor may recommend lifestyle changes to

Help promote a healthy lifestyle. This could involve eating healthy foods rich in fiber and intake of more fluids to avoid constipation, a common symptom of PD. Also, exercises could be suggested to help maintain flexibility and improve balance. In this case, adherence to the doctor’s instructions is crucial to achieving/reaping the benefits of the treatment plan.


Although PD is not a fatal condition, it is degenerative, which worsens and progresses with time. In most cases, one can live with the disease for ten to twenty years. However, the health status and age of the patient play a crucial role in making accurate estimates. Also, the progression rate differs with patients as the disease could be more aggressive and severe in some patients than others. If left untreated, PD could worsen, resulting in reduced brain functions and, in other cases, early death.


Mitochondrial dysfunction is one of the critical pathogenic pathways established in the initiation of PD (Kouli et al., 2018). In the post-mortem examination of substantial nigra pars compacta of patients who died of PD, it was discovered that PD brains lack mitochondrial complex-1, an essential factor of the electron transport chain (ETC) (Kouli et al., 2018) (Figure 5). This association of MC-1 deficiency in the brain and skeletal muscles of patients with PD is further supported by examining the induced Parkinsonism of MTP, as discussed in the earlier part of this paper.

Postmortem of the brains of patients who abused MTP as a recreational drug revealed loss of dopaminergic neurons in the brain and lower amounts of MC-1 in the brain (Kouli et al., 2018). Involvement of MC-1 in the ETC could lead to the conclusion that loss of ETC regulator in the brain could lead to energy depletion, leading to the energy deprivation of dopaminergic neurons and leading to their deaths (Kouli et al., 2018) (Figure 5). Another supporting information for the MC-1 involvement in the initiation of PD is the association of MC-1 to PNK1 and parkin, as discussed earlier in the proposed single gene mutation factor for the initiation of PD (Kouli et al., 2018). Both PNK1 and parkin are involved in the pathway focused on the destruction of dysfunctional mitochondria, a process called mitophagy (Kouli et al., 2018). Furthermore, loss-of-function mutation of the regulation pathway of dysfunctional mitochondria could lead to impaired mitochondrial control checking and further contribute to the neuronal deaths in the brain.


The classical manifestation of Parkinson’s disease includes bradykinesia, resting tremor, postural instability, and rigidity (Kouli et al., 2018). Bradykinesia is often characterized as slowness and difficulty maintaining movement and is often influenced by depression and rigidity. With the manifestation of bradykinesia, at times, patients may present with “freezing episodes,” wherein patients would present with a sudden block of movement when challenged and when distractions are offered in a patient’s course (Kouli et al., 2018). In later stages of the diseases, patients could also present with akinesia, or absence of movement due to the loss of the preparatory phase in the initiation of action, still connected with the disinhibition of the basal ganglia circuitry. Rigidity is one of the clinical hallmarks of PD. In Parkinson’s disease, patients may present with increased resistance to movement regardless of velocity, as seen in spasticity.

Resting tremor is the most common manifestation and is often the initial manifestation of PD. The tremor in PD is described as a “pill-rolling” movement with 3-5 Hz frequency, seen in resting position, and is often obliterated with training. This is different from the tremors manifested by basal ganglia affectation, wherein the tremors are not stopped even with movement. Other manifestation of PD tremor includes pronation-supination of the forearm, and tremors of the jaw or tongue.


  1. Brooks, D. J. (2016). Chapter 24 – Imaging of genetic and degenerative disorders primarily causing Parkinsonism. Handbook of Clinical Neurology, 135, 493-505.
  2. Emamzadeh, F. N., & Surguchov, A. (2018). Parkinson’s Disease: Biomarkers, Treatment, and Risk Factors. Frontiers in neuroscience, 12, 612.
  3. Stoker, T. B., & Greenland, J. C. (Eds.). (2018). Parkinson’s Disease: Pathogenesis and Clinical Aspects. Codon Publications.
  4. Tysnes, O. B., & Storstein, A. (2017). Epidemiology of Parkinson’s disease. Journal of neural transmission (Vienna, Austria: 1996), 124(8), 901–905. 017-1686-y
  5. Buono, V. L., Palmeri, R., Stroscio, G., Corallo, F., Lorenzo, G.D., Sorbera, C., Ciurleo, R., Cimino, V., Bramanti, P., Marino, S., Bonanno, L., Lo Buono, V., & Di Lorenzo, G. (2020). The effect on deep brain stimulation of subthalamic nucleus and dopaminergic treatment in Parkinson’s disease. Medicine, 99(32), 1-5.
  6. Dahodwala, N., Siderowf, A., Xie, M., Noll, E., Stern, M., & Mandell, D. (2009). Racial differences in the diagnosis of Parkinson’s disease. Movement Disorders24(8), 1200-1205.
  7. Deep Brain Stimulation. Retrieved 9 November 2020, from
  8. Giannoccaro, M., La Morgia, C., Rizzo, G., & Carelli, V. (2017). M mitochondrial DNA and primary mitochondrial dysfunction in P Parkinson’s disease. Movement Disorders32(3), 346- 363.

COVID-19 Vaccine Side Effects.

Sometimes the remedy is worse than the disease.”

“Francis Bacon”


Coronavirus disease (COVID-19) is an infectious disease caused by a newly discovered coronavirus. Most people infected with the COVID-19 virus will experience mild to moderate respiratory illness and recover without requiring special treatment.  Older people, and those with underlying medical problems like cardiovascular disease, diabetes, chronic respiratory disease, and cancer are more likely to develop serious illness. The best way to prevent and slow down transmission is to be well informed about the COVID-19 virus, the disease it causes and how it spreads. Protect yourself and others from infection by washing your hands or using an alcohol based rub frequently and not touching your face. The COVID-19 virus spreads primarily through droplets of saliva or discharge from the nose when an infected person coughs or sneezes, so it’s important that you also practice respiratory etiquette (for example, by coughing into a flexed elbow).

COVID-19 Vaccine Side Effects.

Some people may experience side effects after the vaccine. These are usually mild and are much less serious than developing coronavirus or complications associated with coronavirus. Any side effects usually go away within a few days.  Most side effects are a sign your immune system is responding well to the vaccine, and are nothing to worry about. The most common side effects that have been reported are soreness at the site of the injection, mild fever, chills, headaches, fatigue and muscle aches. These do not tend to last long and are a sign that your immune system is reacting well to the vaccine.

1.The most common reported side effect following vaccination is pain at the injection site.

2.If you have a history of severe allergic reactions to vaccines, your doctor may advise you not to get the COVID-19 vaccine.

Common side effects.

Some of the common side effects of the coronavirus vaccine may include:

tenderness, swelling and/or redness at the injection site


muscle ache

feeling tired

fever (temperature above 37.8°C).

A less common side effect is swelling of the glands. This starts a few days after the vaccine and may last for up to 2 weeks. This is to be expected and is a sign of the immune system responding to the vaccine.

Fever after the coronavirus vaccine.

It’s quite common to develop a fever after a vaccination. This normally happens within 48 hours of the vaccination and usually goes away within 48 hours.

You do not need to self-isolate or book a test unless you have other coronavirus symptoms or:

you have been told by NHS Test and Protect, or your occupational health team, that you are a close contact of someone who has tested positive for coronavirus.

you live with someone who has recently tested positive for coronavirus

you live with someone who has symptoms of coronavirus.

If the fever starts more than 48 hours after the vaccination or lasts longer than 48 hours, you should self-isolate.