Diagnostic Imaging of Novel Coronavirus Pneumonia
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About this ebook
This book presents radiological findings in patients with 2019 Novel Coronavirus Pneumonia (COVID-19). It starts with a general review of COVID-19 Pneumonia discovery, including etiology characteristics, transmission routes and pathogenic mechanisms. In the following chapters, details in clinical classification, imaging manifestations in different groups, and imaging features of family aggregated coronavirus pneumonia are introduced. In addition, key points in differential diagnosis of COVID-19 Pneumonia are summarized in the last chapter. The book provides a valuable reference source for radiologists and doctors working in the area of COVID-19 Pneumonia.
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Diagnostic Imaging of Novel Coronavirus Pneumonia - Minming Zhang
© Henan Science and Technology Press 2020
M. Zhang, B. Lin (eds.)Diagnostic Imaging of Novel Coronavirus Pneumoniahttps://doi.org/10.1007/978-981-15-5992-1_1
1. Overview of the COVID-19
Yuantong Gao¹, Liya Wang², ³, Bin Lin⁴ , Hui Mao⁵ and Minming Zhang⁴
(1)
Department of Radiology, the Third Affiliated Hospital of Wenzhou Medical University, Ruian, China
(2)
Department of Radiology, Southern Medical University Affiliated Longhua People’s Hospital, Shenzhen, Guangdong, China
(3)
Department of Radiology, the Third School of Clinical Medicine Southern Medical University, Shenzhen, Guangdong, China
(4)
Department of Radiology, the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
(5)
Department of Radiology and Imaging Sciences, Emory University School of Medicine, Atlanta, GA, USA
Bin Lin
Email: zjdxlinbin@zju.edu.cn
Hui Mao
Email: hmao@emory.edu
Minming Zhang (Corresponding author)
Email: zhangminming@zju.edu.cn
1.1 Identification and Nomenclature of COVID-19
The novel coronavirus that caused pandemic in 2020 started from a number of cases of unexplained pneumonia in the city of Wuhan, Hubei Province, China, in December of 2019. Unlike the other human coronavirus previously reported, this new strain of coronavirus is much more contagious and rapidly spread in the city of Wuhan and subsequently various regions of China from the epicenter of Wuhan. Within several weeks, many countries of Asia, Europe, North America, and Oceania reported the confirmed cases with the worldwide total number quickly rising to over 5.35 million and more than 343,000 deaths on May 24, 2020. The World Health Organization (WHO) initially named this novel coronavirus as 2019 Novel Coronavirus
(2019-nCoV) on January 12, 2020. National Health Commission of China named the pneumonia caused by 2019-nCoV as Novel Coronavirus Pneumonia (NCP) on January 20, 2020. In the meantime, National Health Commission of China issued an announcement to include this disease in the category B infectious diseases as stipulated in the Law of the People’s Republic of China on the Prevention and Treatment of Infectious Diseases, but to manage this disease according to Class A infectious diseases. On February 11, 2020, Tedros Adhanom Ghebreyesus, director general of WHO, announced the revised name of the pneumonia caused by novel coronavirus as Coronavirus Disease 2019
(COVID-19). At the same time, the International Committee for Virus Classification named the novel coronavirus Severe Acute Respiratory Syndrome Coronavirus 2
(SARS-CoV-2). Given the high incidence of SARS-CoV-2 infection and the rapid increase of the cases globally, WHO officially declared on March 11, 2020 in Geneva that the COVID-19 caused by SARS-CoV-2 has the characteristics of a global pandemic. At present, the origin of SARS-CoV-2 is still under investigation.
1.2 Etiological Characteristics
The coronavirus is named after its coronal-like spinous spike glycoproteins protruding from the viral envelope, which can be seen under the electron microscope as shown in Fig. 1.1. The first coronavirus was isolated from poultry in 1937. Until 1965, the coronavirus was first found in human. It is now known that the parasitic hosts of coronaviruses include bats, camels, birds, mice, hedgehogs, dogs, cats, and other mammals, as well as humans [1].
../images/499836_1_En_1_Chapter/499836_1_En_1_Fig1_HTML.pngFig. 1.1
Electron microscope images of 2019-nCoV. Photo source: National Resource Bank of Pathogenic Microorganisms (Institute for Virus Disease Prevention and Control, Chinese Center for Disease Control and Prevention)
Based on the genetic characteristics, different coronaviruses can be divided into four genera: α, β, γ, and δ. SARS-CoV-2 belongs to the β coronavirus. The enveloped viral particles are round or oval in shape. It is often pleomorphic with a diameter of 60–140 nm. The genetic characteristics of SARS-CoV-2 infecting humans are significantly different from severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV), previously discovered in humans and unlike any known coronaviruses [1, 2]. Current studies have shown that SARS-CoV-2 has more than 85% homology with bat-SL-CoVZC45. When isolated and cultured in vitro, SARS-CoV-2 can be found in human respiratory epithelial cells in about 96 h. Based on the prior knowledge on SARS-CoV and MERS-CoV, SARS-CoV-2 is considered to be sensitive to ultraviolet and heat. It is reported that exposure to 56 °C for 30 min or chemicals such as ether, 75% ethanol, peracetic acid, chloroform, and chlorine-containing disinfectant can effectively disinfect the SARS-CoV-2 [3].
1.3 Epidemiological Characteristics
1.3.1 Sources of Infection
The source of infection is mainly the symptomatic patients carrying SARS-CoV-2. Asymptomatic patients can be the source of infection; however, whether and how transmission of the virus from asymptomatic patients to the general population is still under investigation. Worth noting, there is still no confirmed report whether the virus can be transmitted from the animals to human or vice versa.
SARS-CoV-2 is highly contagious with a strong infectious power measured by the transmission efficiency. Epidemiology commonly uses the basic reproduction number (R0) to describe the infectious ability and transmission efficiency of a pathogen. R0 is the average number of cases that an infected person or the host of virus can cause during his/her infectious period without the external intervention and immunity for all. The pathogen with a higher R0 is more contagious. According to the report from WHO [4], SARS-CoV-2 has an R0 between 2.0 and 3.5 in the early stage of disease prevalence. Several other studies estimated the R0 of SARS-CoV-2 between 3.8 and 4.7, or possibly even higher, reaching 5.7. By comparison, the R0 of SARS is 2.0–3.5 and MERS is less than 1.0 [5, 6].
1.3.2 Routes of Transmission
SARS-CoV-2 is primarily transmitted between people through respiratory droplets and contact routes. Individuals in close contact with infected person or virus carriers may inhale droplets containing the virus. Contact routes mean that the droplets emitted by patients with confirmed infection (including asymptomatic infection) are deposited on the surface, then touched by healthy individuals, and transferred to the mucous membrane of the mouth, nose, eyes, and so on. Therefore, the incidence of infection in persons with the household or the cluster in close contact is significantly higher. Wearing masks, washing hands frequently, and ventilating with constant fresh air are conducive to cutting off the transmission routes.
Aerosol transmission is considered to be a special type of droplet transmission, which means that the droplets containing viruses form aerosols under certain conditions, then suspend in the air for an extended period of time. Aerosol transmission may spread the virus to distant areas with the movement of the airflow. The possibility of aerosol transmission exists only when exposed to high concentrations of aerosols for a long time in a relatively closed environment.
As SARS-CoV-2 can be isolated in the feces, contact routes caused by fecal pollution may also contribute to the infection and disease spread [7].
1.3.3 Susceptible Population
It is reported that the probability of SARS-CoV-2 infection can be related to the amount of virus exposure [8]. The risk of getting infected increases as a person is exposed to a large number of viruses, even if their immune system is normal. However, immunocompromised and immunocompetent individuals are considered to be vulnerable to COVID-19.
Existing reports have shown that the age of COVID-19 patients is mainly 30–70 years old. Most of the critically ill patients are the elderly, obese, and those with underlying diseases [9]. The high-risk groups of severe illness and death are those over 60 years old and those with pre-existing diseases, such as hypertension, diabetes, chronic respiratory disease, and cancer. A small number of young and middle-aged patients were found to suffer from fulminant multiple system organ failure due to the strong inflammatory response (cytokine storm syndrome, CSS). Their prognosis is very poor. Cases of infection in children are relatively rare and mild.
1.4 Pathological Characteristics
The correlation between imaging findings and pathology is the base of radiological diagnosis. Every sign of imaging has its pathological basis. While there has been a significant amount of reports from COVID-19 research since the start of the pandemic, the report on pathological findings is still limited. Thus, the pathological characteristics of COVID-19 presented in this chapter are based on existing histopathological data collected from autopsy or biopsy.
1.4.1 The Specimen
Based on the chest X-ray computer tomography (CT) imaging descriptions and the autopsy report [10–12], COVID-19 is generally manifestation of interstitial pneumonia in the early stage, acute exudative pneumonia in the progressive stage, and focal pulmonary consolidation in the later stage. In the severe stage, interstitial pneumonia causes the lung lesions mixed with extravasated blood congestion, hemorrhage, and inflammatory exudation. The lung tissue loses its inherent spongy function and texture, appearing as a wet lung with bronze color. The severely infected lung becomes rigid, containing with white plaque or large consolidation found in the tissue section. A large amount of thick secretion and dark red liquid overflowing, and fiber streak-like changes can be seen in the tissue sections [12].
1.4.2 Histopathology and Stage
In the progress stage of COVID-19, the main involvement is pulmonary alveoli, which becomes inflamed and infiltrated with serous fluid, red blood cells, and macrophage. They are condensed and coagulated into a layer of red stained fibrin like membrane, i.e., the hyaline membrane attached to the inner surface of alveoli. In the severe stage, the epithelial cells in reactive hyperplasia alveolus become swelled or degenerated, necrotic, and eventually falling off. The pathological changes from acute exudative pneumonia to desquamation pneumonia involve proliferation of local fibroblasts. The reticular fibers are found proliferated and broke like glomerular hyperplasia. The fibrin deposition resulted from alveolar exudation exhibits the pattern as in the organizing pneumonia. Simultaneously, hypersecretion of mucus in goblet cells of the respiratory tract, mucoprotein dilution, disintegration of degradation system, and massive phlegm thrombus take places.
In early stage, the COVID-19 exhibited the general characteristics, which are similar with highly pathogenic viral pneumonia, such as exudation and consolidation. The details included proteinaceous exudate with globules, focal hyperplasia of pneumocytes with only patchy inflammatory cellular infiltration, and multinucleated giant cells. The exudate cells found were mainly monocytes and macrophages, some moderate multinucleated giant cells, a few lymphocytes, eosinophils, and neutrophils. The lymphocytes were mainly CD4 positive T cells. Type II alveolar epithelial cells were found proliferated significantly, which is not as obvious as in SARS [13]. Hyaline membranes were not prominent (Fig. 1.2).
../images/499836_1_En_1_Chapter/499836_1_En_1_Fig2_HTML.pngFig. 1.2
The appearance of histological changes revealed in the early stage of COVID-19 involving focal proteinaceous exudates in alveolar spaces (a), scattered protein globules (b), granuloma-like nodules consisted of fibrin (c), inflammatory cells, and multinucleated giant cells inside the airspaces (d) [11]
These pathological changes may present as single or multiple ground glass opacity (GGO) lesions in CT images as shown in Fig. 1.3.
../images/499836_1_En_1_Chapter/499836_1_En_1_Fig3_HTML.pngFig. 1.3
The CT images from different patients with COVID-19 showed single GGO lesion (a) and multiple GGO lesions (b) separately
In the later stage, substances in alveoli may disappear by liquefaction, absorption, and can be discharged from coughing. Pulmonary fibrosis can also be observed. If there is a secondary bacterial infection following COVID-19, neutrophil infiltration in alveoli and interstitium can be found. Reactive hyperplasia can be seen in the bronchial and alveolar epithelium with cytoplasmic bisexuality, nuclear enlargement, prominent nucleoli, and even formation of multinuclear giant cells. The post-mortem examination presented scattered oval protein globules in the local alveolar cavity, which may indicate disintegrating hemoglobin. Myozyme and myoglobin were found increased in some patients. The increased troponin was also reported in a case. In severe COVID-19 patients, D-dimer is typically increased likely due to the destruction of red blood cell membrane caused by hemolysis, and gradually reduced