This document summarizes the pathogenesis and morphological features of SARS-CoV-2 in various organs. It begins with an introduction and timeline of the virus. It then discusses the mode of transmission and laboratory handling guidelines. The pathogenesis involves the virus binding to ACE2 receptors in lungs and other organs. This causes cytokine release syndrome and acute respiratory distress syndrome seen in lungs. Effects in other organs like heart, gastrointestinal tract, and kidney are also discussed based on autopsy findings like thrombi, inflammation and necrosis. Long term sequelae could include altered lipid metabolism and cardiovascular complications.

1. Pathogenesis andmorphological features of various
organs in sars-cov-19
Presentor :Dr Rashmi Budha
Moderator: Dr Netra M Sajjan

2. • Introduction
• Timeline
• Mode of Transmission
• Handling of specimens and laboratory guidelines
• Pathogenesis
• Pathophysiology & Morphology of various organs in COVID-19
• First Autopsy in Karnataka
• Updates and Conclusion

3. CORONAVIRUS
• Coronaviruses (CoV) are a large family of viruses that cause
illness ranging from the common cold to more severe diseases
such as Middle East Respiratory Syndrome (MERS-CoV) and
Severe Acute Respiratory Syndrome (SARS-CoV).
• A novel coronavirus (nCoV) is a new strain that has not been
previously identified in humans.

4. STATS
As on January 1st 2021:
TOTAL CASES:
• Worldwide- 8,43,56,081
• India- 1,03,03,409
• Karnataka- 9,20,373
DEATH:
• Worldwide- 18,34,502
• India- 1,49,205
• Karnataka- 12,096

5. TIMELINE
• November 2019- Dr Li Winliang first noticed cases of pneumonia
which was unresponsive to routine line of management in Wuhan,
China.
• December 31, 2019- China informs WHO about the same.
• January 07, 2020- Airborne spread was confirmed.
• January 09,2020- First Death reported in China.
• January 12, 2020- Genetic Sequence done.
• January 13, 2020- First death from imported Virus.

6. INDIA:
• January 30, 2020
- First case in Kerala.
- WHO declared it as Public Health Emergency of
International Concern.
• February 3, 2020- Two more cases detected.
• March 11, 2020- Declared as a pandemic by WHO.
• March 24, 2020- Nation wide lockdown.

7. Mode of transmission
• The spread occurs chiefly via the respiratory route.
• It is transmitted through large droplets or aerosols and less
commonly by contact with infected surfaces or fomites.
• Human-to-human transmission has been described with an
incubation span ranging between 2 to 10 days.

8. • In view of the repeated exposure to potentially infectious patients
and specimens, health care and laboratory personnel are highly
susceptible to infection with COVID-19.

10. Why is handling of specimens important in
laboratory?
• The reported detection rate of COVID-19 virus in different clinical
samples is variable.
Sputum was 72% infective;
Bronchoalveolar lavage 93%;
Nasal swab 63%;
Pharyngeal swab 32%,
Fibrobronchoscopic brush sample 46%,
Stool samples 10.1%,
Serum 2.8%,
Conjunctival swab 1.1% ,
Urine 0.8%.

11. Guidelines for laboratories
• In brief, we’ll be dealing with the guidelines given for Pathology
sections.
Hematology Section:
• Use of hematology analyzers should be encouraged during
COVID-19.
• Manual preparation of blood smears should be discouraged.
• If EDTA vial needs to be opened for making smears, they should be
opened in a BSC and with all safety precautions.

12. • The smears should be left to dry naturally without blowing air or
drying under the fan thus preventing aerosol formation.
• Subsequently, the working surface should be properly disinfected as
other surfaces.
• Two tubes of 1% Hypochlorite solution should be run before
shutting down the hematology analyzer.

13. Histopathology Laboratory:
• Histopathology specimens should be properly fixed in 10% buffered
formalin or Glutaraldehyde.
• Formalin inactivates the virus in a contact time of 24 hours if
specimens are kept at a temperature of 37°C.
• Glutaraldehyde fixation requires 2 days for inactivating the virus.

14. • Larger specimens should be sliced and then dipped in formalin.
• The level of formalin should be in the formalin: tissue ratio of at
least 10:1.
• Paraffin-embedded blocks carry a low risk of infectivity. Filing of
paraffin blocks and glass slides should be done with caution.

15. Cytopathology laboratory:
• The number of fine needle aspiration cytology (FNAC) should
be restricted to bare minimum and should be advised only if it
truly alters the medical management of the patient.
• Drying of the smears by shaking or blowing of air should not
be done as it can lead to generation of aerosol and small
droplets.

16. • Cytology samples should preferably be fixed in alcohol-based
fixatives (with alcohol concentration more than 70%) or
formalin.
• The fixatives used for the high-risk cases should be discarded
daily.

17. PATHOGENESIS
• SARS-CoV-2 is structurally similar to the original SARS
virus responsible for the 2002–2003 outbreak.
• Studies have shown that both of these viruses share a
similar spike glycoprotein structure in the receptor-
binding domain (RBD) that is responsible for their
affinity for the ACE2.
• The affinity between the RBD on viral cells to host ACE2
cells is crucial in pathogenicity.

19. • The virion infects the cell by attaching its glycoprotein into host cell
receptors, leading to fusion and insertion of viral replication
components into the host.
• This interaction between the virions and the ACE2 is strongly linked
to the severe ARDS and pneumonias.
• The surge of ICU cases and respiratory failure all over the country
has demonstrated that lung-related mortality is a key feature of
SARS-COV-2.

21. Viral load density in COVID-19

22. PATHOPHYSIOLOGY
• Understanding the role of ACE-2 and pathogenesis of SARS paves
the way for explaining why SARS-CoV-2 is so destructive to the
lungs.
• Zhao et al. studied healthy pulmonary parenchyma from eight
donors and found that ACE2 is expressed in 83% of type II alveolar
epithelial cells.
• Gene ontology analysis has revealed that these type II alveolar cells
also contain genes that somehow promote viral replication and
ensure its survival. Though evidence on this phenomenon is
inconclusive.

24. CYTOKINE-RELEASE SYNDROME
• Cytokine-release syndrome (CRS) is a dysregulated pro-
inflammatory condition where a positive cycle of cytokine release is
established leading to systemic shock and multisystem organ failure.
• As a response to bacterial and viral infections, the mechanisms
discussed in the immunology section allow cell messengers of the
innate immunity release cytokines that recruit monocytes and
lymphocytes and reinforce the response to eradicate the infection.

25. • Failure to eradicate the infection leads to a sustained
inflammatory state, where the cytokines exert a positive
feedback on the immune cells, which further secrete cytokines,
thus creating a cycle.
• The prolonged immune response then becomes detrimental to
the host as systemic vasodilation develops leading to shock
and organ failure.

27. Effect of COVID-19 on various organs
• Angiotensin-Converting Enzyme 2 (ACE2) is expressed
in different tissues including lung, gastrointestinal tract,
vessels, brain, liver, kidney, spleen, and skin.
• This may lead to possible short-term and long-term
involvement of multiple human organs.

28. LUNGS
GROSS:
• Increase in lung weight
• Copious amounts of gray-white
viscous fluid
• Vascular engorgement
• Consolidation
• Edema
• Pleurisy
• Mildly erythematous trachea
• Presence of white mucous in lungs
• Pink froth in airways with dark-
colored hemorrhage.
Acute respiratory distress syndrome (ARDS) and pneumonia are usually the
clinical diagnosis of infected cases.

29. Gross pathology, lung
parenchyma:
(a) This right lung alone
weighed 1100 g and
showed diffuse
consolidation.
(b) A pattern of patchy
areas of gray–white
consolidation was also
frequently seen.

30. Tracheobronchial
inflammation in COVID-
19.
(a), (b) are gross
photographs of trachea and
main stem bronchus
showing circumscribed
white patches of 2.0–3.0
mm in diameter.

31. • MICROSCOPY:
 Diffuse alveolar damage (DAD)
 Infiltration of lymphocytes in interstitial regions
 Giant pneumocytes adjacent to multinucleated giant cells
 Hyperplasia of pneumocytes
 Intra-alveolar fibrin deposition
 Exudate formation, lymphocytic inflammation, loose connective
tissue within the alveolar ducts and bronchioles
 Intra-alveolar fibrin surrounded by fibroblasts
 Viral particles within pneumocytes
 Hyaline membrane formation

32. Patterns of acute respiratory
distress syndrome.
(a)A combination of hyaline
membranes, type 2 cell hyperplasia,
and interstitial fibroblastic
proliferation is shown.
(b) Type 2 pneumocyte hyperplasia
without fibroblastic proliferation.
(c) Pneumocytes were enlarged and
atypical.
(d) Some pneumocytes showing
multinucleated syncytial features
and/or basophilic intracytoplasmic
inclusions.

33. Vascular injury in COVID-19
lung.
(a) A gross image showing
multiple thrombi.
(b) In addition to large thrombi,
smaller caliber arteries showing
fibrin thrombi.
(c) Thrombi were seen in small
arteries, including precapillary
channels.
(d) In some cases, thrombi were
predominantly composed of
platelets, and were also seen in
the capillary bed.

34. HAPPY HYPOXICS!!
• Among the many surprises of the novel coronavirus, some
patients seem to defy the basic physiology of hypoxia as they
can be well observed generally, and to describe themselves as
comfortable with no signs of distress.
• For such patients, SpO2 and SaO2 have been reported as low
as 62% and 69%, respectively. Clinicians call them happy
hypoxics.

35. HEART
• There is an increased risk of cardiovascular involvement
during respiratory viral infections.
• In the context of COVID-19, it has become apparent that
cardiovascular complication is a major cause of death,
particularly in individuals having comorbidities.

37. • GROSS:
– Cardiomegaly and right ventricular dilation were prominent in
some patients.
– Autopsies showed firm myocardium with red-brown appearance
without injury.

38. •Right coronary artery
thrombosis
•A heart showing
extreme right ventricular
dilatation, with
straightening of the
interventricular septum.

39. • MICROSCOPY:
– Dispersed area of myocyte necrosis near to lymphocytes in
few cases (suggesting microvascular blood supply failure in
heart).
– Infiltration of mononuclear leukocytes in interstitial areas
was also reported by one study

40. Cardiac myocytes showing focal, atypical myocyte degeneration
( arrows)

41. Complications..

42. Possible Sequelae…
• After the SARS-CoV experience
that occurred 12 years ago,
many patients who survived
infection had altered lipid
metabolism resulting in
hyperlipidemia, a state known to
increase the risk of
atherosclerosis and myocardial
infarction

43. VASCULAR SYSTEM
• Autopsy findings revealed accumulation of inflammatory cells and
endothelial and inflammatory cell death, which are the features of
endotheliitis.
• There are a few possible mechanisms through which the vascular
system is damaged in the setting of COVID-19.
– One possibility is that the damage caused by the virus in the
lungs can result in hypoxia of the blood vessels and resulting
vascular injury.

44. – Another possibility is that many ACE2 receptors in the
vascular systems are prone to an increased risk of SARS-
CoV-2 infection.
– Lastly, since COVID-19 affects many different organ
systems and promotes an inflammatory state, the
vasculature can get damaged as a direct consequence of this
state.

45. • Damage to the vasculature caused by any of these
three mechanisms can lead to abnormal activation of
the coagulation cascade.
• Many COVID-19 patients have an increased D-dimer
level, indicative of increased clot formation.

46. • A hypercoagulable state, indicated by an increased levels
of D-dimer and fibrinogen, is common during COVID-19.
• In such a state, patients are at an increased risk of
pulmonary embolism, deep vein thrombosis, stroke, and
disseminated intravascular coagulation.

47. Multisystem microscopic thromboses were common including in the
intracardiac arteries and arterioles

48. GASTROINTESTINAL TRACT
• COVID-19 infection may also affect Gastrointestinal
(GI) tract since ACE2 is abundantly present in the
enterocytes.
• SARS-CoV-2 has been found in stool specimen and
diarrhea was reported in several infected cases.

49. • Morphological features:
Lymphocytes in the esophageal squamous epithelium, and
lamina propria of the stomach, duodenum, and rectum.
Interstitial edema.
Viral nucleocapsid protein was seen in glandular epithelial
cell of stomach, duodenum, and rectum, but not in the
esophageal epithelium.

50. The intestine with
normal color,
alternating
segmental dilatation
and stenosis in an 85-
year-old
man with COVID-19
autopsy.

51. • As ACE2 is highly distributed in glandular
epithelial cell , it is worth mentioning that there
are evidences suggesting that SARS-CoV-2 may
cause acute and chronic sialadenitis in infected
cases.

52. LIVER
• High level of hepatic enzymes, such as alanine
aminotransferase(ALT), aspartate aminotransferase
(AST), and lactate dehydrogenase(LDH) in infected
cases suggests involvement of liver tissue.
• GROSS:
– Autopsy samples showed dark red liver with
hepatomegaly.

53. • Microscopy:
– Hepatocyte degeneration with lobular focal
necrosis
– Congestion of hepatic sinuses with microthrombus
– Fibrosis of portal tract, proliferation of portal vein
branches
– Mononuclear leukocyte and neutrophil infiltration
within the portal area

54. • Sonzogni et al. found alteration of vascular structure, both
acute (thrombosis, luminal ectasia) and chronic (fibrous
thickening of vascular wall or phlebosclerosis, and abnormal
asset of portal intrahepatic system).

55. (C) Mild sinusoidal
dilatation with increased
lymphocytic infiltration.
(D) Higher power view
showing
sinusoidal lymphocytes.
(E) Focal hepatic
necrosis in periportal
zone.
(F) Focal centrilobular
hepatic necrosis.

56. • Atypical arrangement of intrahepatic blood vessels was
also observed with CD34 staining, decorating a peri-
portal network of sinusoidal vessels, which may show
increased arterial pressure.
• Also, biopsy findings of patients with Covid-19 revealed
moderate microvascular steatosis and mild lobular and
portal activity.

57. KIDNEY
• Multiple mechanisms leading to the development of renal
manifestations have been proposed, including volume
depletion effects, systemic inflammation, hemodynamic
disturbances, direct viral invasion, and rhabdomyolysis, among
others.
• Histopathologic findings of biopsy samples showed proximal
acute tubule injury (ATI) in renal tissues.

58. Morphological features:
• Luminal brush border sloughing
• Vacuole degeneration, tubular necrosis
• Infiltration of lymphocytes (mainly CD8+T cells) and CD68+
macrophages in the tubulointerstitial and sub-capsular area
• Interstitial fibrosis in cortical parenchyma

59. • Strong complement membrane attack complex (MAC)
deposition in tubules
• Mild focal tubular atrophy
• Hypertrophy and hyperplasia of glomerular epithelial cells
• Hemosiderin granules in tubular epithelium
• Podocyte vacuolation were reported.

60. (A) Epithelium of proximal
convoluted tubules shows
decreased/ loss of the brush border.
(B)Tubular epithelial cells show
vacuolar degeneration (arrows),
leading to collection of necrotic
debris in the lumen (asterisks).
Blocked peritubular capillaries due
to erythrocytic aggregates
(arrowheads).
(C,D) Inflammatory cells
(arrowhead) infiltrate the tubules
and arcuate artery (arrows),
Bacterial foci (asterisks) is also
observed.

61. (E,F) Tubular deposition of
hemosiderin granules, calcium
deposits (arrowhead) and
pigmented cast (arrow).
(G,H) Glomeruli show
ischaemic contraction
(arrows) and fibrin thrombi
(arrowhead).
Bowman’s space show
presence of leaked
accumulated plasma.

62. SKIN
• COVID-19 also causes skin tissue alterations.
• Skin macroscopic manifestations can be divided into:
 Viral exanthems
– Morbilliform rash
– Petechial rash co-existing with thrombocytopenia
– Erythematous-to-purpuric coalescing macules
– Widespread urticaria
– Varicella-like vesicles

63. • Vasculopathy-related skin manifestations
– Peripheral cyanosis with bullae
– Dry gangrene
– Transient unilateral livedo reticularis
– Red papules on fingers resembling chilblains

64. Chilblain lesions on toes and heel

65. (a) Papular lesions on heel (b) Same lesions a week later

66. Acral lesion with crust Erythematous lesions.

67. (a, b) Morbilliform eruption observed
on the trunk and neck. These
manifestations are primarily seen on
the skin of the trunk
Erythematous-violaceous lesions
in the toe.

68. (A)Arrow showing telangiectatic blood
vessels in early exanthematous rash.
(B) Epidermis (arrow) showing groups of
Langerhans cells in the later phase of
exanthematous rash.
Superficial dermis also shows
perivascularinfiltration of
lymphocytes.
(C) An intraepidermal group of
Langerhans cell seen in a papulo-
vescicular rash.
(D)Maculo-papular erruption.
(E) Capillary thrombosis (arrow) along
with diffuse haemorrhage in an
exanthemous

69. MICROSCOPY:
• Superficial and deep perivascular dermatitis
• Blood vessels surrounded by lymphocytes
• Focal acantholytic suprabasal clefts
• Dyskeratotic and ballooning herpes-like keratinocytes
• Necrosis of keratinocytes
• Mucin deposition in the dermis and hypodermis
• Nests of langerhans cells within the epidermis

70. • Moreover, thrombus formation and extravasation of
erythrocyte in mid-dermis blood vessels was found.
• Also, swollen thrombosed blood vessels in the
dermis with the presence of eosinophils, neutrophils
and nuclear debris was visualized.

71. SPLEEN AND LYMPH NODES
• Studies showed that viral nucleocapsid protein (NP)
could be seen in splenic tissue.
• Viral NP+ Cells were distributed in both red
(primarily) and white pulp.
• NP antigen was also found in macrophages within the
lymph nodes.

72. • GROSS:
– Congestion and hemorrhagic appearance were visualized in
the spleen
– Diminished spleen size and reduced spleen weights
• In microscopic examination of vessels, splenic infarction due
to arterial thrombosis, CD20+B cells surrounding splenic
artery, and proliferation of fibrotic tissues in sinuses were seen.

73. MICROSCOPY:
• Reduction of cell composition
• Atrophy of white pulp
• Neutrophil and plasma cell infiltration
• Reduction or absence of lymph follicles
• Increase in red pulp to white pulp proportion
• Reduction of T and B cells due to necrosis and apoptosis
• Atrophy of corpuscles in the spleen of infected cases.

74. Lymph nodes with
preserved architecture.

75. The subcapsular and intraparenchymal sinuses contain large transformed cells
with prominent nucleoli and amphophilic cytoplasm.

76. NERVOUS SYSTEM
• It is important to know that patients may present with neurological
symptoms as the first or only sign of the SARS-CoV-2 infection.
• Viral particles of SARS-CoV-2 were also found in the frontal lobe
of the brain and brain capillary endothelial cells.
• Also, microglia and type I astrocytes, infected by murine
coronavirus (MHV-A59), can produce pro-inflammatory
cytokines.

77. • GROSS:
– Mild hypoxic manifestations were present in several autopsies.
• MICROSCOPY:
• Hemorrhagic white matter lesions with axonal injuries
• white blood cells such as macrophages
• Perivascular acute disseminated encephalomyelitis (ADEM)-like
appearance
• Neocortical microscopic infarcts

78. ENDOCRINE SYSTEM
MECHANISMS OF INCREASED COVID-19
SEVERITY IN DIABETIC PATIENTS
• In general, diabetic patients are more susceptible to infection due
to dysfunctional immune responses such as decreased neutrophil
chemotaxis and decreased phagocytosis by the innate immune
cells.
• Immune cell function, like killing via respiratory burst, is also
inhibited by hyperglycemia seen in diabetic patients.

79. • Diabetic patients have decreased proportions of CD4+,CD8+, and
anti-inflammatory regulatory T cells, and also have a higher
proportion of pro-inflammatory immune cells (eg, Th17 cells).
• This altered immune landscape may allow inflammatory cascades
to go unchecked in diabetic patients.

80. • There is also evidence that patients with hypertension
and diabetes have a delayed clearance of viral load,
prolonging infections.
• With respect to SARS-CoV-2 specifically, it is
theorized that diabetes increases the risk of infection
due to up-regulation of angiotensin-converting
enzyme 2 (ACE2), which the virus uses to infect
cells.

81. • The effects of diabetes on ACE2 are two fold.
• While acute hyperglycemia has been shown to up-regulate
ACE2, there is evidence that chronic hyperglycemia down-
regulates ACE2 expression.
• This effect of ACE2 down-regulation may, however, increase
the inflammatory damage caused by COVID-19, as ACE2 is
protective against inflammation.

82. OTHER ENDOCRINE DISEASES
Adrenal Insufficiency
• SARS-CoV employs an immunoevasive technique wherein it knocks down
the host cortisol stress response.
• It does so by mimicking amino acid sequences of host adrenocorticotrophic
hormone (ACTH).
• Because SARS-CoV-2 is related to SARS-CoV, it is theorized that COVID-19
may affect the hypothalamic–pituitary–adrenal (HPA) axis.
• There are currently prospective studies underway to analyze this.

83. THYROID GLAND

84. Subacute Thyroiditis
• Subacute thyroiditis is an inflammatory thyroid
disease, which is generally precipitated by a viral
infection of the upper respiratory tract.

86. OPHTHALMOLOGY
• The most common, and only, ophthalmic manifestation of the
SARS-CoV-2 virus reported is conjunctivitis.
• Conjunctivitis can present as a first, or only, sign of infection
from SARS-CoV-2.
• All the reports of conjunctivitis associated with SARS-CoV-2
have been “bilateral, mild, follicular conjunctivitis without
corneal involvement” with some exceptions.

87. BLOOD
• Although leukopenia and lymphocytopenia occurred in infected
cases, blood flow cytometry detected high levels of T-helper 17 and
CD8+T cells.
• Other flow cytometric analyses revealed that monocytes count did
not change in patients; however, they were larger in comparison to
normal monocytes.
• Autopsy findings of bone marrow showed reactive left-shifted
myelopoiesis and hyperplasia of CD8+T cells.

88. Peripheral Smear findings
• Peripheral blood films showing large
granular lymphocytes.
• Round to indented nuclei, condensed
chromatin, prominent nucleoli in a few,
along with abundant pale blue cytoplasm.
• Distinct variable sized azurophilic
granules are present (long black arrow).
• Cytoplasmic pod formation (long green
arrows) and apoptotic lymphocytes (long
red arrow) are highlighted. Giemsa
×200–400.

89. • Peripheral blood films showing
various neutrophils with C-
shaped, fetus-like COVID nuclei
(black arrowheads) with aberrant
nuclear projections (blue
arrowhead).
• Toxic granulations and
vacuolations (yellow arrowhead),
ring nuclei (red arrowheads) and
elongated nucleoplasm (green
arrowheads) are highlighted.

90. • Peripheral blood films
showing activated
monocytes with
prominent cytoplasmic
vacuolisation and a few
granules (small red
arrow).
• Nuclear blebbing (small
green arrow) is also
seen.

91. CYTOLOGY
Pleural fluid Characteristics
Parameter Results
Appearance Turbid
Color Orange
pH 7.5
Total Protein 60 g/dl
Lactate dehydrogenase 1185 U/L
Glucose 6.8 mmol/L
WBC count 2450/mcl (45% lymphocytes, 41%
neutrophils and 9% eosinophils)
Microbiology Negative
Cytology Few mesothelial cells, numerous
inflammatory cells, mainly lymphocytes

92. • The most common pleural change in COVID 19 patients is pleural
thickening while pleural effusion is extremely uncommon.
• Our patient had an exudative effusion with high LDH and normal
pleural fluid PH and glucose.
• As all relevant pleural fluid microbiology was negative and the
patient improved on the COVID 19 guideline based treatment, they
attributed the pleural effusion to be secondary to SARS Cov-2 and
highlight that the effusion in COVID 19 has a high pleural LDH

93. BAL FLUID CYTOLOGY
(A) Many clusters of
activated plasma cells
(B) Alveolar macrophage
intranuclear cytopathic
inclusion SARS-CoV-2
infection
(C,D) Groups of polyclonal
CD138- positive plasma
cells

95. MENTAL HEALTH MANIFESTATIONS IN
COVID-19
• One unexplored visible impact of COVID-19 is on the
mental health of people- patients, their loved ones, and
the general public under nationwide lockdowns.
• Everyone is affected, whether directly or indirectly,
highlighting the massive impact the pandemic has had
socially, economically, and psychologically.

96. Populations Affected
• Patients with COVID-19
• Patients with mental illness
• Health-care workers
• The general population

97. RECENT FINDINGS…
• In Karnataka, the first autopsy on a deceased who was
SARS-CoV-2 positive was conducted by Dr Dinesh
Rao, Professor and Head of the Department, Dept of
Forensic Medicine of BGS Global College,
Bengaluru.
• The following gross and microscopic features was
noted.

102. Dr Dinesh Rao Concluded that:
• Live virus in nose and oropharynx present 18hrs after
death.
• Virus absent over the skin surface of face, neck,
trachea, bronchi and lung surface 18hrs after death.

103. Updates
• First reported in the UK in September, the new variant of the
coronavirus SARS-CoV-2 that causes COVID-19 is believed
to be 71% more transmittable than other variants.
• It is termed as B.1.1.7.
• Another new variant is said to discovered in South Africa,
currently termed as 501.V2.
• It is associated with a higher viral load, meaning a higher
concentration of viral particles in patients’ bodies, possibly
contributing to higher levels of transmission.

104. • The variants reported by South Africa and the UK
share a common change in the spike protein that may
make them more infectious.
• But they are different variants, and sequence analysis
revealed that they originated separately, the World
Health Organization said.

105. CONCLUSION

106. REFERENCES
• Misra V, Agrawal R, Kumar H, Kar A, Kini U, Poojary A, et al. Guidelines
for various laboratory sections in view of COVID-19: Recommendations
from the Indian Association of Pathologists and Microbiologists. Indian
J Pathol Microbiol 2020;63:350-7.
• Sigaroodia AP, Bashasha D, Fateh F, Abolghasemi H. Laboratory findings
in COVID-19 diagnosis and prognosis. Clinica Chimica Acta 510 (2020)
475–482.
• Singh S, Madan J, Nath D, Tiwari N. Peripheral Blood Smear
Morphology- A Red Flag in COVID-19. International Journal of TROPICAL
DISEASE & Health 41(8): 54-58, 2020.
• Singh A, et al. Morphology of COVID-19–affected cells in peripheral
blood film. BMJ Case Rep 2020.

107. • Tian S et al. Pathological study of the 2019 novel coronavirus
disease (COVID-19) through postmortem core biopsies. Modern
Pathology, 2020.
• M. Tabary, et al. Pathologic features of COVID-19: A concise
review. Pathology - Research and Practice 216 (2020) 153097.
• Deshmukh V, Motwani R, Kumar A, et al. J Clin Pathol Epub.
• Su S et al. Involvement of digestive system in COVID-19:
manifestations, pathology, management and challenges Ther
Adv Gastroenterol 2020, Vol. 13: 1–12.
• Bradley BT et al, Histopathology and ultrastructural findings of
fatal COVID-19 infections in Washington State: a case series.
Lancet 2020; 396: 320–32