Pathophysiology of Corona Virus

PATHOPHYSIOLOGY: Corona virus also known as COVID-19. This virus infects the lungs and the major symptoms are fever and dry cough. The outbreak of this respiratory disease started in Wuhan (China) in December 2019. The causative organism was discovered in January 2020 and was named as NOVEL- BETA CORONA VIRUS. COVID-19 has rapidly spread throughout the world with the symptoms ranging from mild- moderate respiratory disorders to severe pneumonia. COVID-19 has been represented as global public health concern and WHO declares public health emergency. The percentage of death in China reported 2684 cases i.e. 2.84% on January 25^th 2020. Reports of infected patients with corona virus showed increased Leukocyte count, increased levels of plasma pro-inflammatory cytokines and respiratory findings. One of the patients reported with dry cough, body temperature of 102.2⁰F and coarse breathing sound of lungs on the 5^th day. The patient sputum reports showed positive real time PCR (Polymerase Chain Reaction) results which confirmed the infection. Powerful lab experiences showed Leukopenia furthermore leucocyte lowers going from 2.91×10ᶺ9 cells/l consisting of which 70% have always been immune cells. Furthermore, a cost epithetical 16.16mg/l was noted above the normal range (0-10 mg/l). High ESR and D-dimer was also observed. Corona virus infects the upper respiratory tract and gastrointestinal tract. There are 5 different strains of corona viruses that can infect humans. The most popular human corona virus is SARS-CoV which causes Severe Acute Respiratory Syndrome which leads to both upper and lower respiratory tract infections and can also cause Gastroenteritis. Lungs are mostly affected organs from Corona virus since the virus access into the host through the enzyme called ACE-2 (Angiotensin-converting Enzyme 2) which is present in type-2 alveolar cells of the lungs. The virus containing a glycoprotein called “Spike” joins to the ACE-2 and enters the host cell. The density of ACE-2 enzymes in each tissue determines the severity of disease i.e. increase in ACE-2 increases the severity and decrease in ACE-2 enzymes reduces the risk of the disease. The virus also affects the gastrointestinal tract and organs as ACE-2 is widely distributed in Glandular cells of gastric, duodenal and rectal epithelium as well as in endothelial cells. ACE-2 is also present in brain and it is not sure that if the virus can infect the brain directly by crossing the blood brain barriers that separates the systemic circulation and general circulation. Common neurological symptoms may include headache, nausea and vomiting, loss of smell. 12% of infected patients have seen with acute myocardial injury when admitted in Wuhan, China. This cardiac injury is more frequent in severe cases of the disease this may be related to ACE-2 receptors present in the heart tissues which are involved in the function of heart. 31% of patients with thrombosis and 25% of patients with thromboembolism is seen in ICU patients with COVID-19 infection due to poor prognosis. Due to the blood vessel dysfunction and clot formation which leads to pulmonary embolism and ischemic events within the brain have been represented as complications leading to the deaths in patients with SARS-CoV-2. Another common cause of the death is due to the kidney injury since the COVID-19 directly infects the kidney cells. Lymphocytes containing inflammatory infiltrates and diffused alveolar damage is seen in the report of the dead patients with COVID-19. Since the ACE-2 expressing epithelial cells can be turned into a particular direction in response to SARS-CoV-2 on the respiratory tract, the patients with severe infection of COVID19 infection have the symptoms of systemic Hyperinflammation. The clinical reports shows the elevated levels of Intraleukin-2 (IL-2), Intraleukin-7 (IL-7), Intraleukin-6 (IL-6), (GM-CSF) Granulocyte Macrophage- colony stimulating factor, Macrophage inflammatory protein 1-α (MIP 1-α),  Tumour Necrosis Factor-α (TNF-α) indicative of Cytokine Release Syndrome (CRS), Interferon-ϒ inducible protein- 10 (IP-10) and Monocyte chemoattractant protein-1 (MCP-1) suggests underlying immunopathology. People with COVID-19 and ARDS (Acute respiratory Distress Syndrome) have classical serum biomarkers (CRS) and increased levels of C-reactive protein (CRP), Lactate dehydrogenase (LDH), Ferritin and D-dimer. Systemic inflammation resulting in vasodilation, allowing inflammatory monocytic and lymphocytic infiltration of the Lungs and Heart.

The World Health Organisation (WHO) has introduced some of the tests and protocols for the diagnosis of COVID-19. rRT-PCR (real-time reverse transcription polymerase chain reaction) is the standard method of diagnosis. The test is done by the respiratory samples obtained by the nasopharyngeal swabs and sputum. Results are usually seen within few hours to two days. In April 4^th 2020 the antibody test was produced but it is not widely used. The Chinese testing have shown the accuracy of 60% to 70%. Zhongnan Hospital of Wuhan University in China has released diagnostic guidelines for detecting infections based upon clinical features and epidemiological risks. This involved identifying the people who had atleast two symptoms i.e. fever, reduced lymphocyte count, normal or reduced white blood cell count, imaging features of pneumonia apart from the travel history to Wuhan or have been in contact with another infected person. Along with laboratory testing chest CT-scan is also helpful in the diagnosis of the patients with severe symptoms of COVID-19 but it is not recommended in the routine screening.

The following data reveals the pathological findings during the Autopsy.

• Macroscopy: Lung consolidation, pericarditis, pulmonary oedema is seen.
• Bronchoalveolar lavage plasmocytosis.
• Microvesicular steatosis is seen in liver.
• Blood shows disseminated intravascular coagulation.
• Different types of viral pneumonia can be observed.
  • Minor pneumonia: minor serous and fibrin exudation.
  • Mild pneumonia: pneumocyte hyperplasia, pulmonary oedema, interstitial inflammation with lymphocytic infilteration and multinucleated giant cell formation.
  • Severe pneumonia: diffused alveolar damage and diffuse alveolar exudates, it is the main cause of Acute Respiratory Distress Syndrome (ARDS) severe hypoxemia.

Prevention: The preventative measures to be taken to avoid and reduce the chances of infection since there is no medication known to be effective at preventing COVID-19, it includes washing hands often with soap and water for atleast 20 seconds, maintain personal hygiene, avoid social gatherings, use mask while going out, cover your mouth with handkerchief while choughing or sneezing, promote social distancing, practise good respiratory hygiene and avoid touching nose, mouth or eyes with unwashed hands. Use hand sanitizers containing 60% of alcohol if the soap and ware is not readily available.