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Corona Virus by Dr Anurag Yadav
1. COVID 19 (CORONA VIRUS)
DR ANMOL MANASWINI
DR ANURAG YADAV
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By Dr Anmol Manaswini @SRRITCD
2. Things to be dealt!!!
Introduction
Pathogenesis
Clinical Features
Diagnosis
Management
Prevention
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By Dr Anmol Manaswini @SRRITCD
3. Introduction
• Corona viruses are important human and
animal pathogens.
• At the end of 2019, a novel coronavirus was
identified as the cause of a cluster of
pneumonia cases in Wuhan, a city in the
Hubei Province of China.
• It rapidly spread, resulting in an epidemic
throughout China, followed by a global
pandemic.
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By Dr Anmol Manaswini @SRRITCD
4. • In February 2020, the World Health
Organization designated the disease COVID-19
• The virus that causes COVID-19 is designated
severe acute respiratory syndrome
coronavirus 2 (SARS-CoV-2); previously, it was
referred to as 2019-nCoV.
• Understanding of COVID-19 is evolving
everyday
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By Dr Anmol Manaswini @SRRITCD
5. Corona Virus
Single Stranded RNA
Non segmented
Protein Envelope (Capsid)
Crown Shaped Virions
<100nm
Largest among RNA Viruses
CORONA VIRUS (CoV)
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By Dr Anmol Manaswini @SRRITCD
8. EPIDEMIOLOGY
• Globally, over 50 million confirmed cases of
COVID-19 have been reported.
• Cases have been reported in all continents,
except for Antarctica.
• The reported case counts underestimate the
overall burden of COVID-19, as only a fraction of
acute infections are diagnosed and reported
• The rate of prior exposure to SARS-CoV-2, as
reflected by seropositivity, exceeds the incidence
of reported cases by approximately 10-fold or
more
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By Dr Anmol Manaswini @SRRITCD
9. Next generation Sequencing (NGS) revealed that bats are the
primary source of the CORONA virus as there was 98% homology
between bats and Human viruses 10
By Dr Anmol Manaswini @SRRITCD
10. CORONA VIRUSES ARE ZOONOTIC
Dromedary Camels
Civet Cats
Bats
Pangolins
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By Dr Anmol Manaswini @SRRITCD
12. Transmission
Person to person
Direct transmission
(via droplet)
Indirect
transmission
(via fomites)
Vertical
transmission
Breast feeding
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By Dr Anmol Manaswini @SRRITCD
17. Period of Infectivity- Highest is 2 days prior to onset of symptoms
and until 7 days after development of symptoms
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By Dr Anmol Manaswini @SRRITCD
20. Immunity following infection
Humoral immunity
• Detectable neutralizing antibodies depending on
severity
• These antibodies decline over a period of few
months
Cell mediated immunity
• Studies have also identified SARS-CoV-2-specific
CD4 and CD8 T cell responses
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By Dr Anmol Manaswini @SRRITCD
21. High risk factors for severe disease
• Age > 60yrs
• Cardiovascular disease
• Diabetes mellitus
• Hypertension
• Chronic lung disease
• Chronic kidney disease
• Cancer
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By Dr Anmol Manaswini @SRRITCD
22. Symptoms
• Fever
• Dry cough
• Dyspnea
• Myalgia/fatigue
• Sputum production
• Sore throat
• Headache
• Diarrhoea
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By Dr Anmol Manaswini @SRRITCD
23. Other Symptoms
• Conjunctival congestion
• Anosmia
• Dysguesia
• Hemoptysis
• Nausea
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By Dr Anmol Manaswini @SRRITCD
25. 26
• Fever
• Cough
• Sore throat
• Nasal congestion
• Malaise
• Headache
Uncomplicated
• Signs of Pneumonia
• But No signs of Severe Pneumonia
Mild Pneumonia
• Fever with suspected respiratory
infection plus one of the following
• RR>30/min
• Respiratory distress
• SpO2 <90% on Room air
Severe
Pneumonia
No signs of Dehydration Sepsis
or SOB
By Dr Anmol Manaswini @SRRITCD
26. Acute Respiratory Distress Syndrome
(ARDS)
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Definition
• Onset: new or worsening respiratory symptoms within one week of known clinical
insult.
• Chest imaging (radiograph, CT scan, or lung ultrasound): bilateral opacities, not fully
explained by effusions, lobar or lung collapse, or nodules.
• Origin of oedema: respiratory failure not fully explained by cardiac failure or fluid
overload. Need objective assessment (e.g. echocardiography) to exclude hydrostatic
cause of oedema if no risk factor present
Oxygenation
(adults)
• Mild ARDS: 200 mmHg < PaO2/FiO2 ≤ 300 mmHg (with PEEP or CPAP
≥5 cm H2O, or non-ventilated)
• Moderate ARDS: 100 mmHg < PaO2/FiO2 ≤200 mmHg with PEEP ≥5
cm H2O, or non-ventilated)
• Severe ARDS: PaO2/FiO2 ≤ 100 mmHg with PEEP ≥5 cm H2O, or non-
ventilated)
• When PaO2 is not available,SpO2/FiO2 ≤315 suggests ARDS (including
in non-ventilated patients)
By Dr Anmol Manaswini @SRRITCD
27. Sepsis
• life-threatening organ dysfunction
caused by a dysregulated host
response to suspected or proven
infection, with organ dysfunction
• altered mental status
• difficult or fast breathing
• low oxygen saturation
• reduced urine output
• fast heart rate
• weak pulse
• cold extremities or low blood
pressure
• skin mottling
• laboratory evidence of
Coagulopathy, thrombocytopenia,
acidosis, high lactate or
hyperbilirubinemia
Septic shock
• persisting hypotension
despite volume
resuscitation
• requiring vasopressors to
maintain MAP ≥65
mmHg
• serum lactate level
< 2 mmol/Ls
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By Dr Anmol Manaswini @SRRITCD
28. Complications
Short term
• ARDS
• Cardiac
• Acute liver injuery
• AKI
• DIC
• Pancreatic injury
• Septic shock
• Secondary infection
• Neurological
complication
Long term
• End stage pulmonary
fibrosis
• Rhabdomyolysis
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By Dr Anmol Manaswini @SRRITCD
32. Laboratory features associated with
severe COVID-19
Abnormality Possible threshold
Elevations in:
•D-dimer >1000 ng/mL (normal range: <500 ng/mL)
•CRP >100 mg/L (normal range: <8.0 mg/L)
•LDH
>245 units/L (normal range: 110 to 210
units/L)
•Troponin
>2× the upper limit of normal (normal
range for troponin T high sensitivity:
females 0 to 9 ng/L; males 0 to 14 ng/L)
•Ferritin
>500 mcg/L (normal range: females 10 to
200 mcg/L; males 30 to 300 mcg/L)
•CPK
>2× the upper limit of normal (normal
range: 40 to 150 units/L)
Decrease in:
•Absolute lymphocyte count <800/microL 33
By Dr Anmol Manaswini @SRRITCD
33. IMAGING FINDINGS
• Chest radiographs
– normal in early or mild disease
– 20 percent did not have any
abnormalities on chest radiograph at
any point during the illness
–consolidation and ground-glass
opacities, with bilateral, peripheral,
and lower lung zone distributions
– peak in severity at 10 to 12 days after
symptom onset 34
By Dr Anmol Manaswini @SRRITCD
34. • Chest CT
• Typical appearance—
– Peripheral, bilateral, GGO with or without
consolidation or visible intralobular lines ("crazy-
paving")
– Multifocal GGO of rounded morphology with or
without consolidation or visible intralobular lines
("crazy-paving")
– Reverse halo sign or other findings of organizing
pneumonia (seen later in the disease)
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By Dr Anmol Manaswini @SRRITCD
35. Indeterminate appearance
• Absence of typical features AND
• Presence of:
– Multifocal, diffuse, perihilar, or unilateral GGO
with or without consolidation lacking a specific
distribution and are non-rounded or non-
peripheral.
– Few very small GGO with a non-rounded and non-
peripheral distribution.
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By Dr Anmol Manaswini @SRRITCD
36. • Atypical appearance
Absence of typical or indeterminate features AND
• Presence of:
– Isolated lobar or segmental consolidation without
GGO
– Discrete small nodules (centrilobular, "tree-in-bud")
– Lung cavitation
– Smooth interlobular septal thickening with pleural
effusion
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By Dr Anmol Manaswini @SRRITCD
42. Serologic Testing
• Currently approved tests
to detect antibodies to
the spike and
nucleocapsid proteins
• Rapid lateral flow assays
detect IgM and IgG
produced during infection
• Seroconversion in 7 days
in 50% patients
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By Dr Anmol Manaswini @SRRITCD
43. Management
• Supportive measures
• Immunomodulator drugs
• Non Invasive or invasive ventilator support
• Convalescent plasma therapy
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By Dr Anmol Manaswini @SRRITCD
50. Monoclonal antibody treatment
• Bamlanivimab is a neutralizing monoclonal antibody
that is derived from human convalescent plasma and
targets the SARS-CoV-2 spike protein
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By Dr Anmol Manaswini @SRRITCD
51. • In November 2020 bamlanivimab received
emergency use authorization (EUA) from the
US Food and Drug Administration (FDA) for
the treatment of adult non-
hospitalized COVID-19 patients with mild to
moderate illness
– not requiring supplemental oxygen
OR
– if on chronic supplemental oxygen, without an
increased oxygen requirement
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By Dr Anmol Manaswini @SRRITCD
54. Convalescent plasma
• Obtained from individuals who have
recovered from COVID-19 is a potential option
for therapy of SARS-CoV-2 infection in
hospitalized patients
• Neutralizing antibodies are thought to be the
main active component(Passive immunity)
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By Dr Anmol Manaswini @SRRITCD
55. • Although convalescent plasma improved the rate
of nasopharyngeal viral RNA clearance at 72
hours compared with standard treatment alone,
there were no statistically significant differences
in the overall rates of clinical improvement by 28
days.
• It is possible that convalescent plasma provides
clinical benefit when
– it contains high neutralizing antibody titers
– is given early in the course of disease (ie, in patients
who do not require mechanical intubation)
– may be of particular interest for individuals with
deficits in antibody production (eg, those receiving
anti-CD20 therapies)
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By Dr Anmol Manaswini @SRRITCD
56. Follow up
• For most patients, outpatient based visits are
scheduled on days 4, 7, and 10 (following the
onset of clinical illness)
• Increased frequency of follow up in :
– Patients aged ≥65 years
– Any patient with moderate dyspnea at the time of
initial evaluation
– Patients who we feel may not reliably report a
deterioration in symptoms
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By Dr Anmol Manaswini @SRRITCD
57. Recovery
• According to the WHO
Severity of disease Recovery time
Mild 2 weeks
Severe 3-6 weeks
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By Dr Anmol Manaswini @SRRITCD
58. Reinfection
• CDC suggests that the possibility of reinfection
be investigated in patients who:
– Have a repeat positive NAAT ≥90 days after the
initial infection, regardless of symptoms
or
– Have a repeat positive NAAT 45 to 89 days after
the initial infection AND have symptoms
consistent with COVID-19 (with no alternative
explanation or in the setting of recent exposure)
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By Dr Anmol Manaswini @SRRITCD
59. Vaccination
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• The Covid-19 vaccine AZD1222 developed by
Swedish-British pharma major AstraZeneca and the
University of Oxford could come as better news than
that of the vaccines developed by Pfizer-
BioNTech and Moderna, despite both of them having
earlier reported much higher protection
• The 70% overall efficacy of up to 95 per cent.
By Dr Anmol Manaswini @SRRITCD
Whether COVID-19 virus is transmitted directly from bats or through some other mechanism (eg, through an intermediate host) is unknown
Corona Viruses are a large family of viruses that causes illnesses ranging from the common cold to more severe respiratory diseases
The name "coronavirus" is derived from the Latin corona, meaning crown or halo, which refers to the characteristic appearance of the virus particles (virions): they have a fringe reminiscent of a royal crown or of the solar corona.
Electronic Microscopic Image of Corona Virus
On the surface of the envelope are club shaped projections thatresemble a “Solar Corona”
Bats are hosts to the largest number of viral serological Corona virus
Cell-mediated immunity – Studies have also identified SARS-CoV-2-specific CD4 and CD8 T cell responses in patients who had recovered from COVID-19 and in individuals who had received an investigational SARS-CoV-2 vaccine,
Routine screening CT for diagnosis or exclusion of COVID-19 is currently not recommended by most professional organizations or the US Centers for Disease Control and Prevention
Therapeutic targets of the currently considered drugs for repurposing against COVID-19. 1. Coronaviruses suppress the antiviral immunity, hence maintaining an antiviral state with interferons. 2. Virus enters the cell by fusion of the viral spike proteins with cellular ACE2 receptor, followed by ACE2 downregulation. Angiotensin receptor blockers (ARBs), Angiotensin-converting enzyme inhibitors (ACEIs) and statins increase ACE2 expression, hence may have efficacy in this condition. 3. Fusion is followed by endocytosis of the virus, where low endosomal pH helps in lysis of the viral structural proteins. Disruption of this acidic environment by diprotic bases like chloroquine and hydroxychloroquine may produce an antiviral effect. 4, 5. Release of nucleic acid (NA) into the cytoplasm and translation of the viral proteins using host ribosomes, 6. Proteolysis by viral main protease enzyme makes functional proteins e.g. RNA dependent RNA polymerase (RDRP). Thus, inhibition of the main protease enzyme by inhibitors like lopinavir, ritonavir and darunavir, may have efficacy against the virus. 7. RDRP is essential for replication and transcription of the virus. RDRP inhibitors, remdesivir, favipiravir, ribavirin and arbidol may be effective against coronaviruses. 7, 8. Subsequent translation and proteolysis into structural proteins followed by packaging makes intact virions, which get exocytosed (9) from the cell
Schematic diagram of the renin-angiotensin system and the proposed therapeutic treatment for COVID-19 targeting SARS-CoV-2 viral entry mechanism. (Left) The receptor-binding domain (RBD) of the spike protein from SARS-CoV-2 binds to ACE2, allowing host cell entry and infection. TMPRSS2 indicates transmembrane protease serine 2. (Middle) The physiological role of ACE2 in renin-angiotensin system and its protective effect on organs. The protease renin, an enzyme produced by the juxtaglomerular cells of the kidney, cleaves angiotensinogen (a precursor of angiotensin produced by the liver) to generate angiotensin I. ACE plays an important role in converting angiotensin I into angiotensin II. Angiotensin II may exert some biological functions through angiotensin II receptor type 1 and 2 receptors (AT1R and AT2R), leading to potent vasoconstriction in several organs. Activation of AT1R increases the transmembrane proteinase (ADAM17) activity. Furthermore, tumor necrosis factor-α (TNF-α) activation of its tumor necrosis factor receptor (TNFR) represents another pathway increasing ADAM17 activity. TNF-α along with cytokines released due to SARS-CoV-2 infection can lead to a cytokine storm. ADAM17 cleaves the extracellular juxta-membrane region of ACE2, whether such ACE2 cleavage contributes to SARS pathogenesis is not known yet. ACE2 hydrolyzes Angiotensin II to the vasodilator Angiotensin 1–7, which binds the Mas receptor and plays a protective role in several organs. The balance between ACE/Ang II/AT1R and ACE2/Ang 1–7/MasR is vital for maintaining normal health. (Right) According to recent studies, increasing of hrsACE2 at tissue sites can effectively compete with the endogenous ACE2 and limits SARS-CoV-2 entrance into the host cells and decreases angiotensin II levels.1,4 Significantly, hrsACE2 injection did not reduce the generation of anti-SARS-CoV-2 IgA and IgG antibodies
Most participants in all groups had a decline in viral levels by day 11, although the intermediate antibody dose was associated with a larger reduction in viral load than placebo