Acta Scientific Microbiology (ISSN: 2581-3226)

Review Article Volume 4 Issue 5

Coronavirus Disease 2019: A Review of Transmission, Clinical Manifestations, Laboratory, and Radiologic Findings

Sabah Mohamed Alharazy*

Independent Researcher, United Kingdom

*Corresponding Author: Sabah Mohamed Alharazy, Independent Researcher, United Kingdom.

Received: March 01, 2021; Published: April 27, 2021

Abstract

  Coronavirus Disease 2019 (COVID-19) is a highly transmissible and pathogenic viral infection caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). It has been confirmed that COVID-19 is transmitted from person to person through infected droplets or direct contact. The symptoms of COVID-19 range from asymptomatic or mild infection to critical illness. Symptoms may include fever, cough, fatigue, dyspnea, myalgia, headache, sore throat, nasal congestion, loss of smell or taste. Gastrointestinal symptoms, such as nausea, vomiting, anorexia, and diarrhea can also occur. Ground-glass opacity (GGO) with or without consolidation is the hallmark of this disease in Chest Computed Tomography. Many laboratory parameters are affected in COVID-19 patients, some of which are associated with disease severity and poor prognosis, such as severe lymphopenia, abnormal coagulation parameters, and elevated levels of D-dimer, ferritin, and C-reactive protein (CRP). This review summarizes the current understanding of transmission, common clinical features, common laboratory as well as radiologic findings of COVID-19 infection.

Keywords: Coronavirus Disease 2019 (COVID-19); Severe Acute Respiratory Syndrome Coronavirus-2; Transmission; Clinical Features; Laboratory Parameters; Radiologic Findings

Introduction

  Coronavirus Disease 2019 (COVID-19) is caused by the virus known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [1], which was first reported in Wuhan, China, at the end of 2019 [2] and has since spread widely throughout the world. As of 14 December 2020, COVID-19 affects 218 countries and territories across the world and 2 international conveyances. The total confirmed cases of COVID-19 are 72,654,602, with a total reported death of 1,619,028. Approximately 50,871,457 individuals have now recovered from this virus worldwide [3]. This review provides the current understanding of the mode of transmission, as well as the common clinical manifestations, laboratory, and radiologic findings of this disease.

Modes of COVID-19 transmission

  Thirty human single-rooted mandibular premolar teeth extracted for periodontal reasons or due to orthodontic treatment, were collected from the outpatient clinic of Oral Surgery Department, Faculty of Dentistry, Cairo University. Criteria for teeth selection included straight roots with single root canals and completely formed apices. Teeth with open apices, visible cracks and root resorption were excluded. The selected teeth were thoroughly washed under running water and immersed in 5.25% NaOCl solution for 15 minutes to disinfect the teeth and remove any soft deposits on the root surface. The remaining hard deposits were removed from the root surface using curettes and finally teeth were stored in saline solution till the time of use.

Aim of the Study

  COVID-19 infection is mainly transmitted through respiratory droplets of infected individuals. The modes of transmission of COVID-19 infection are included in table 1 [4-6].

Modes of COVID-19 transmission

The properties of this Mode

Respiratory droplet transmission

Respiratory droplet transmission is the predominant mode of transmission of COVID-19 infection.

The transmission of the virus occurs when the virus spreads from infected individuals while sneezing, coughing or talking without covering the mouth or nose.

Individuals who are in close contact with an infected person may become infected when these infectious respiratory droplets get into their mouth, nose, or eyes.

Respiratory droplets are generally > 5-10 μm in diameter.

“Close contact" is described in various ways:

The WHO described it as within 1 metre.

The U.S. CDC describes it as "within 6 feet (1.8 m) of the infected person of 15 minutes or more over a 24-hour period starting from 2 days’ prior illness onset (or, for asymptomatic patients, 2 days before to test specimen collection) until the time the patient is isolated.

The ECDC suggests that close proximity is typically less than 1 meter (3.3 ft) apart.

The Australian Health Department describes close contact as sharing an enclosed space for a longer duration such as more than two hours. This occurs in the timeline beginning from 48 hours’ prior symptoms onset in the confirmed or probable case. It also defines close contact as face-to-face contact in any setting with a confirmed or probable case, for 15 minutes or more. This is accumulated over the course of a week. It begins from 48 hours’ prior the symptoms onset in the confirmed or probable case [74].

airborne transmission/ Aerosol transmission

Airborne transmission is not a common mode of transmission of COVID-19 infection, it remains controversial outside medical facilities.

The transmission of the virus occurs by aerosols, the dissemination of a droplet nuclei that capable of being suspended in the air over long distances and for longer periods of time.

Aerosols or droplet nuclei refer to droplets with a diameter of ≤ 5μm.

Airborne transmission can occur in healthcare settings, with certain aerosol-generating medical procedures performed on COVID-19 patients.

Outside of medical facilities, it occurs in enclosed space, crowded and poorly ventilated areas where infected people spend a long time with others.

According to US. CDC, in some cases, there is evidence that individuals with COVID-19 appear to have spread the infection to others who were more than 6 feet away.

This form of transmissions occurred within the confined areas, that under ventilated where infected person could have breathed heavily, for example when singing or exercising.

Physical intimacy

 

It carries a substantial risk of transmission due to close proximity.

The virus spreads through saliva and mucus, and kissing.

Vertical transmission (mother to child)

 

Intrauterine transmission has been reported in a few cases but is generally rare.

There is insufficient evidence to ensure the vertical transmission of COVID- 19 through breast feeding, as no viable breast milk virus has been reported in the studies.

WHO recommends that mothers with suspected or confirmed COVID-19 should be advised to start or continue breastfeeding.

 

Bloodborne transmission

The role of bloodborne transmission remains unclear, and low plasma and serum viral titers indicate that there may be a low risk of transmission via this route.

Fecal/urine-oral transmission

No significant evidence of COVID-19 virus transmission through feces and urine.

 

Fomite transmission.

Fomite transmission is considered a likely mode of transmission for COVID-19 infection.

Despite consistent evidence of surface contamination by SARS-CoV-2 and the survival of the virus on certain surfaces, no specific reports have explicitly shown fomite transmission. People who have made contact with infectious surfaces also have close contact with an infectious individual, making it difficult to distinguish between respiratory droplets and fomite transmission.

Food and water

 

No significant evidence of COVID-19 virus transmission through food and water.

 

Animal-to-human transmission

Evidence shows that humans infected with COVID-19 may be able to infect other mammals. However, the risk of transmission of COVID-19 from animals to humans is considered to be low.

Abbreviation

WHO: World Health Organization; CDC: Centres for Disease Control and Prevention; ECDC: European Center for Disease Prevention and Control.

Table 1 adapted from: World Health Organization (WHO) 2020: Transmission of SARS-CoV-2: implications for infection prevention precautions.[4]; European Center for Disease Prevention and Control (ECDC) 2020: "Q and A on COVID-19: Basic facts" [5]. Centers for Disease Control and Prevention (CDC 2020) How COVID-19 Spreads [6].

Table 1: Modes of COVID-19 transmission [4-6].

Incubation period of COVID-19

  The incubation period is important for understanding the nature of the spread of the COVID-19 epidemic as well as the effective length of the quarantine period. This is defined as the time between the date of infection and the onset of the disease. The WHO estimated the median incubation period of this infection to be between 5 to 6 days but may be up to 14 days [4,7]. However, a large cross-sectional study including 1,084 cases with confirmed COVID-19 from Wuhan found an incubation period of more than 14 days in 5% (95th percentile, 16.32) to 10% of cases (90th percentile, 14.28) and more than 20 days (99th percentile, 20.31) in 1% of cases [8]. The median of the incubation period was 7.76 days, while the mean was 8.29 days [8]. The study used a renewal process (renewal theory in probability) [8].

Clinical manifestations of COVID 19 infection

  COVID 19 infection has a wide range of clinical manifestations, ranging from asymptomatic or mild manifestations to critical illness [9,10]. The majority of COVID-19 infections are not severe [7,11-13]. Evidence of COVID-19 transmission from asymptomatic and presymptomatic patients has been reported [4,5]. However, the exact proportion of the transmission due to pre-symptomatic or asymptomatic infection compared to symptomatic infection remains unclear [14].

  COVID-19 is most commonly associated with respiratory symptoms, but it can also cause several extra-pulmonary manifestations [15]. The COVID-19 associated symptoms and their frequency are summarized in table 2 based on the study of 1,099 patients from China [16] and the WHO-China Joint Mission report of 55,924 patients with COVID-19 [7]. Symptoms were also summarized from Surveillance data of 1,320,488 patients from the United States [17] and meta-analysis including 24,410 patients with COVID-19 from 9 countries (China, the United Kingdom, the United States, Singapore, Italy, Australia, Japan, Korea, and the Netherlands) [18]. Of note, the accurate frequency of COVID-19 associated symptoms remains unknown.

Study

Guan et al study [16]

WHO-China Joint Mission [7]

Stokes EK, study [17]

A systematic review and meta-analysis [18]

Patients no

 

1,099

 

55,924

1,320,488

24,410

Median/mean age (years)

47 years

51 years

48 years

49 years

Symptoms (%)

 

 

 

 

Fever

88.7%

87.9%

43.1%

78%

Cough

67.8%

67.7%

50.3%

57%

Fatigue

38.1%

38.1%

NA

31%

Dyspnea

18.7%

18.6%

28.5%

23%

Sputum production

33.7%

33.4%

 

NA

Myalgia or arthralgia

14.9%

14.8%

36.1%

17%

Rigors

11.5%

11.4%

NA

18%

Headache

13.6%

13.6%

34.4%

13%

Sore throat

13.9%

13.9%

20%

12 %

Nasal congestion and/or Rhinorrhea

4.8%

4.8%

6.1%

5%

Conjunctival congestion/conjunctivitis

0.8%

0.8%

NA

2%

Haemoptysis

0.9%

0.9%

NA

2%

Nausea and vomiting

5%

5%

11.5%

10%

Diarrhea

3.8%

3.7%

19.3%

10%

loss of smell or taste.

NA

NA

8%

NA

NA; not available

Table 2: Clinical Manifestations of COVID 19 infection [7,16-18].

Laboratory features of COVID-19

  The most-reported laboratory findings in the first large study of 1,099 COVID-19 patients from China were lymphopenia (83.2%), leukopenia (33.7%), and thrombocytopenia (36.2%) [16]. Most of the patients (60.7%) had an elevated level of C-reactive protein (CRP) [16]. Increased levels of alanine aminotransferase, aspartate aminotransferase, creatine kinase, and D-dimer were less common. These findings are more prominent in patients with severe disease than in patients with non-severe disease (96.1% versus 80.4% for lymphopenia, 57.7% versus 31.6% for thrombocytopenia, and 61.1% versus 28.1% for leukopenia) [16].

  Leukopenia appears to be inconsistent, as several studies have shown that patients with COVID-19 infection have varying white blood cell counts [11,20,21]. In a study of 41 patients with COVID-19 infection, 45.0% of patients had normal leukocyte counts (white blood cell count: 4000-10000 per µL), 25% had leukopenia (white blood cell count ˂ 4000 per µL) with the majority (63.0%) had lymphopenia while 30.0% had leukocytosis (>10000 per µL) [20]. Patients with severe disease were found to have leukocytosis (2.0-folds increase) than those with non-severe disease [20]. Similarly, in a study of 140 patients with COVID-19 infection, most of the patients (68.1%) had normal leukocyte counts, 19.6% had leukopenia with 75.4% of the patients had lymphopenia and 12.3% had leucocytosis [46]. Notably, leukocytosis was significantly found in severe compared to non-severe patients [46]. It was also reported that non-survivors were more likely to develop leucocytosis [11].

  Lymphopenia is a common reported haematologic finding in COVID-19 patients [11,16,20,21]. It is also more prominent among patients with severe compared to non‐severe COVID-19 disease [16,21,33]. Furthermore, severe lymphopenia has been associated with critical illness and mortality in COVID-19 [13,33]. Among 24 critically ill patients with confirmed COVID-19 who were admitted to ICUs in the Seattle region, lymphopenia was reported in 75% of patients on admission [13]. In another study of 1,045 hospitalized COVID-19 patients from France, lymphopenia was observed in 60.9% of patients and a lymphocyte count < 1,000 per µL (OR: 1.4; 95% CrI: 1.1-2.0) was associated with the development of severe disease [33]. A systematic review and meta-analysis of 24 studies involving 3,099 patients, found that lymphopenia with the cut-off point at ≤ 1100 per µL was associated with the threefold risk of poor outcome in COVID-19 patients [47]. The correlation appeared greater in younger patients compared to older patients [47]. Because the lymphocytes have ACE2 receptors on their surface, the SARS‐CoV‐2 can directly infect these cells and causing their lysis [48]. Other potential explanations for lymphopenia in COVID‐19, including lymphocyte apoptosis induced by a cytokine storm [48]. Atrophy of lymphoid organs, including the spleen, and further impairs the turnover of lymphocytes [48]. Inhibiting the proliferation of lymphocytes by coexisting lactic acidosis, which may be more common among cancer patients at increased risk for complications from COVID-19 [48].

  Neutrophilia (increased neutrophil counts) and increased NLR (neutrophil to lymphocyte) ratio were also reported in COVID-19 patients [11]. NLR is determined by dividing the absolute neutrophil count by the absolute lymphocyte count and used as a measure of systemic inflammation and infection [49]. Additionally, elevated NLR is a risk factor of mortality in malignancy, acute coronary syndrome, intracerebral hemorrhage, polymyositis, and dermatomyositis [11,49].

  Thrombocytopenia (low platelet count) is also frequently present in COVID-19 and has been associated with poor outcomes [12]. The possible mechanism of thrombocytopenia in COVID-19 includes purely consumptive, in particular, endothelial damage, platelet aggregate formation in the lungs, marrow suppression, and immune clearance [50,51]. The incidence of thrombocytopenia varies with the severity of the disease [12,16,50,51]. Mild thrombocytopenia (a platelet count of 100-150 ×109/L) was detected in 5-41.7% of patients with COVID-19 infection, [12,16,50,51] and in 58-95% of patients with severe disease [16,52,53]; on average, patients with severe disease had a platelet count of only 23 ×109/L to 31 ×109/L lower than those with the non-severe disease [54,55]. A meta‐analysis of 9 studies including 1,779 COVID-19 patients suggested that thrombocytopenia is significantly associated with a threefold increased risk of severe disease and also with the risk of mortality [54]. A further systematic review and meta-analysis of 24 studies involving 5,637 COVID-19 patients suggested that the weighted incidence of thrombocytopenia was 12.4% and was associated with the severity and outcome of COVID-19 [56].

  Many studies have shown that several inflammatory parameters and cytokines were significantly elevated in severe patients with COVID-19 or those admitted to the ICU [11,20,41]. Among the inflammatory parameters, CRP, erythrocyte sedimentation rate (ESR), procalcitonin (PCT), and ferritin were commonly elevated in the COVID-19 infection, but with varying values.

  CRP is one of the most distinctive acute phase reactants that can increase rapidly following inflammation, cell damage, or tissue injury. Elevated CRP level is associated with a poor prognosis of COVID-19 infection. Among 78 patients with COVID-19 infection, the CRP was significantly elevated in the progression group compared to the improvement/stabilization group (38.9 versus 10.6 mg/L, P = 0.024) [57]. Another study of 298 patients with COVID-19, found that admission CRP level correlated with the severity of disease and predicted an adverse outcome [58]. With a cut-off value of 41.3, CRP demonstrated a sensitivity of 65%, specificity of 83.7%, for discrimination of disease severity, with the area under the curve (AUC) of the receiver-operating characteristic (ROC) of 0.783. More notably, the positive predictive value (PPV) was 81.6%, indicating that 81.6% of COVID-19 patients will develop severe disease. CRP was also a good independent predictor of adverse outcomes with an AUC of 0.833, a sensitivity of 90.5%, a specificity of 77.6%, PPV of 61.3%, and negative predictive value (NPV) of 95.4% [58].

  ESR is another measure of acute-phase reactants that reflects an inflammatory condition but lacks specificity such as CRP [59]. Marked ESR increases (>100 mm/hr) are commonly associated with certain infection (33%), neoplasm (17%), and end-stage renal disease (17%) [59]. A high level of ESR is also found in severe COVID-19 patients [21] .

  Many studies have shown that elevated PCT levels are significantly associated with the severity of COVID-19 infection [11,16,20,46,60]. A meta-analysis also showed that increased PCT level was associated with an approximately 5-fold higher risk of severe COVID-19 infection (OR 4.76) [61]. Additionally, serial PCT measurements may be contributed to predicting progression towards a more severe form of the disease [60]. A study in 95 patients with COVID-19 infection showed that the PCT level was decreased during recovery in discharged patients and there was a significant difference between the levels within 3 days of admission and 7 days before hospital discharge, while the PCT level increased as the disease progressed in non-survivor cases [60]. Of note, a substantial increase in PCT levels may indicate bacterial coinfection in COVID-19 patients who have developed severe form of disease. A study of 41 patients with COVID-19, showed that increased PCT levels were 25% versus 0% in ICU patients compared to non-ICU patients, respectively. All patients in the ICU had secondary infections [20].

  Ferritin level was reported to be significantly higher in COVID-19 patients with severe/critical disease and was the last laboratory value to return to normal [62]. On the other hand, hs-CRP returned to normal levels at least 5 days before ferritin [62]. It also reported the increase in ferritin level is associated with the worsening of the COVID‐19 infection [31]. A systematic review and meta-analysis of 52 studies involving 10,614 confirmed COVID‐19 patients showed a significant increase in ferritin levels in severe patients compared to non-severe patients and a significant increase in ferritin levels in non-survivors compared to survivors [63]. In patients with one or more comorbidities, including diabetes, thrombotic complications, and cancer, ferritin levels were also significantly higher [63]. Ferritin is thus associated with poor prognosis and could predict worsening of COVID‐19 patients [63].

  Increased lactate dehydrogenase level (LDH) was also a common laboratory finding among COVID-19 patients [21]. Among 99 patients with COVID-19 infection, 76% showed elevated LDH levels [21]. Elevated LDH levels are commonly observed in COVID-19 patients with severe disease compared to those with non-severe disease, and they are also associated with an increased risk of death [64]. A pooled analysis of 9 studies, including 1,532 patients with COVID-19, showed that increased LDH levels were associated with an approximately 6-fold increase in the probability of having severe disease and an approximately 16-fold increase in odds of mortality [64]. In another retrospective study of 191 patients with COVID‐19, non‐survivors, as compared with survivors, had significantly higher levels of LDH, PCT, serum ferritin, and IL‐6 [31]. It has also been shown that an increase or decrease in LDH is considered to be an indicator of radiographic progression or improvement as an increase in LDH at a cut-off value of 62.5 U/L significantly predicted progression of CT chest image while LDH at a cut-off value of 48.5 U/L predicted an improvement in CT chest image [65].

  Increased levels of numerous inflammatory cytokines; prominent among them are IL-6, IL-2, IL-7, IL-10, granulocyte-colony stimulating factor, interferon-γ (IFN-γ)-inducible protein, monocyte chemoattractant protein, macrophage inflammatory protein 1α, and TNF-α were detected in many critical COVID-19 patients admitted to the ICU, which suggested that a cytokine storm occurred and contributed to the severity and prognosis of the disease [20,21].

  In a retrospective study of 54 patients with critical or severe COVID-19 infection, inflammatory cytokines including IL-1, soluble IL-2 receptor [sIL-2R], IL-6, IL-8, IL-10, and TNF-α were evaluated in 47 patients within 24 hours of admission [62].The study found that the levels of IL-6 and sIL-2R in critically ill patients were significantly higher than those with severe disease, whereas the levels of IL-10 and TNF-α levels did not differ significantly between the two groups [62].

  Elevated D-dimer and other coagulation parameters abnormalities such as prothrombin time (PT), activated partial thromboplastin time (aPTT) international normalized ratio (INR), thrombin time (TT), fibrinogen degradation products, in COVID-19 patients have been associated with a higher risk of ARDS, ICU admission or death [20,21,31,66,67]. A study of 1,561 patients with COVID-19 infection in China showed that patients with severe COVID-19 have significantly abnormal coagulation parameters including PT, aPTT, INR, TT, fibrinogen degradation products, D-dimer [68]. Besides, a meta-analysis including the previous study and other 12 studies involving a total of 2,574 patients with COVID-19 infection showed that the odds ratio of severe COVID-19 was associated with D-dimer level higher than 0.5 μg/ml on admission [68]. Furthermore, elevated D-dimer level greater than 1 μg/mL in COVID-19 patients, on admission was associated with increased mortality [31,66].

  High levels of creatine Kinase, alanine aminotransferase, aspartate aminotransferase, total bilirubin, urea, creatinine and decreased levels of albumin have also been observed in COVID-19 patients [16,26].

  Notably, none of the previous laboratory features are specific to COVID-19. Thus the diagnosis should be confirmed by molecular and serological investigations of SARS-CoV-2, while initial treatment would be focused on the clinical and epidemiological evaluation of the risk of COVID-19 infection [19].

Radiologic findings

  Chest computed tomography (CT) abnormalities of COVID-19 are usually ground-glass opacity (GGO) with or without consolidation combined with bilateral, multilobe, peripheral, posterior, and diffuse or lower involvement of the lung [24,69].

  Typical patterns of GGOs in COVID-19 include crazy-paved, rounded, or linear morphology [24]. A crazy-paving pattern is defined as an inter- and intralobular septal thickening superimposed on diffuse GGO [24]. Solid pulmonary nodules, cavitation, and mediastinal/hilar lymph node enlargement are not usually observed in COVID-19 [69]. Pleural effusions are unusual [69]. Linear consolidations and other signs indicating organizing pneumonia such as the reverse halo sign (i.e., areas of GGO surrounded by a complete or almost complete ring of consolidation) are also seen several days after the onset of disease [69]. A literature review of COVID-19 infection in neonates and children has shown that the GGO was less frequent at hospital admission (32.7%) but, it was more frequent in patients admitted to the Pediatric Intensive Care Unit (PICU) for respiratory failure [44].

  According to the Fleischner Society for thoracic radiology, indications of chest CT imaging in COVID-19 include patients with moderate/severe symptoms irrespective of RT-PCR test results, evidence of deterioration of respiratory status as indicated by hypoxemia [70]. Normal chest CT scans have been observed in many patients with COVID-19 infection at an early stage of infection [69]. In the previous study of 1,099 patients with COVID-19 infection from China, no radiographic or CT abnormality was reported in 17.9% (157 of 877) patients with non-severe disease and in 2.9% (5 of 173) patients with severe disease [16]. On the other hand, abnormal chest CT findings may develop in asymptomatic patients [69]. A study of 295 confirmed cases with COVID-19 showed that 49 cases had an initial negative CT scan and 15/49 developed findings after 3-6 days, while 34/49 CT scans remained negative [71]. Of note, CT imaging is not routinely recommended as a COVID-19 screening test in asymptomatic individuals, and patients with mild COVID-19 symptoms unless they are at risk of disease progression [70]. Impotently, COVID-19 testing is essential to confirm any suspected infection based on imaging findings [70]. Chest CT imaging without confirmation by RT-PCR has limited specificity for the identification of COVID-19 [72]. In a retrospective study of 1,014 suspected COVID-19 cases in China, chest CT findings were compared with RT-PCR. Of the total patients, 59% (601/1014) had positive RT-PCR results, and 88% (888/1,014) had a positive chest CT scan. Based on positive RT-PCR results, chest CT imaging had higher sensitivity of 97% (580/601) and a specificity of only 25% (105/413). The PPV, NPV and accuracy were 65% (580/888) 83% (105/126), and 68% respectively [72].

  CT abnormalities of COVID-19 pneumonia vary over time, with different presentations depending on the stage and severity of the lung infection. Pan et al. classified the evolution of lung features into four stages based on time during recovery from COVID-19 (Table 3) [24].

Stage

Time of onset

Main CT imaging features

Early stage

0-4 days after the onset of initial symptoms

Normal CT findings or mainly GGO.

Distribution: subpleurally in the lower lobes unilaterally or bilaterally.

Progressive stage

5-8 days after symptomatic presentation

Diffuse GGO, crazy-paving appearance, and consolidation.

Distribution: bilateral multilobe.

Peak stage

9-13 days after symptomatic presentation

Diffuse GGO, crazy-paving appearance, consolidation, and residual parenchymal bands.

Late stage

≥14 days after symptomatic presentation

Gradual absorption of consolidation and ground-GGO, disappearance of crazy-paving pattern due to recovery, whereas signs of fibrosis (including parenchymal bands, architectural distortion, and traction bronchiectasis) may appear.

Table 3: Chest CT Evaluation in COVID-19 [24].

  The extent of CT abnormalities has been visually quantified. Each of the five lung lobes was visually graded from 0 to 5 as follows: 0, no involvement; 1, < 5% involvement; 2, 25% involvement; 3, 26%-49% involvement; 4, 50%-75% involvement; and 5, > 75% involvements [24].

Based on the total CT score, the absorption stage was extended for 26 days from the onset of the initial symptoms [24].

  Initial CXR may be normal [70] and may lack the sensitivity to identify some of the lung abnormalities frequently observed in mild or early COVID-19 pneumonia that are otherwise recognized by chest CT [16,19,70]. Similar to CT, the most widely reported CXR findings in COVID-19 include GGOs and lung consolidation [21,26,70,73]. CXR findings are likely to peak at 6 - 12 days of symptoms onset of COVID-19 pneumonia [73]. CXR may be preferred over CT when access to CT is limited unless features of respiratory worsening indicate the use of CT [70]. To reduce the risk of cross-infection of COVID-19 from moving patients, some centers request only the anterior-posterior CXR (usually bedside) to be performed [70,73].

Conclusion

  The COVID-19 pandemic continues to spread worldwide at an alarming rate. This review tried to discuss the current literature on the transmission, clinical features, common laboratory as well as radiologic findings of COVID-19 infection.

  Human-to-human transmission occurs mainly through the respiratory route. Other modes of transmission have also been described, such as contact with contaminated fomites due to the persistence of the virus on the surface for a certain time.

  The symptoms of COVID-19 range from asymptomatic or mild infection to critical illness. COVID-19 is most commonly associated with respiratory symptoms, but it can also cause several extra-pulmonary manifestations. The proportion of the transmission of the disease from presymptomatic and asymptomatic individuals compared with transmission from symptomatic patients remains unclear.

  Many non-specific laboratory parameters are affected in COVID-19 patients, some of which are associated with disease severity and poor prognosis, such as severe lymphopenia, abnormal coagulation parameters, and elevated levels of D-dimer, ferritin, and CRP. Typical CT features of COVID-19 pneumonia include multiple GGO with or without consolidation. Less typical features are also described. CT abnormalities vary over time, with different presentations based on the stage and severity of the lung infection.

Financial Support

None.

Declaration of Competing Interest

None.

References

  1. Gorbalenya A E., et al. “The species Severe acute respiratory syndrome-related coronavirus: classifying 2019-nCoV and naming it SARS-CoV-2”. Nature Microbiology4 (2020): 536.
  2. Lu H., et al. “Outbreak of pneumonia of unknown etiology in Wuhan, China: The mystery and the miracle”. Journal of Medical Virology4 (2020): 92.
  3. “Coronavirus Update (Live): COVID-19 Virus Pandemic”. Worldometer (2020).
  4. World Health Organization. “Transmission of SARS-CoV-2: implications for infection prevention precautions. Scientific brief, 09 July 2020”. WHO (2020): 1-10.
  5. European Centre for Disease Prevention and Control. “Questions and answers on COVID-19: Basic facts”. ECDC (2020).
  6. Centers for Disease Control and Prevention. “How COVID-19 Spreads | CDC”. CDC (2020).
  7. World Health Organization. “Report of the WHO-China Joint Mission on Coronavirus Disease 2019 (COVID-19)”. WHO (2020): 16-24.
  8. Qin J., et al. “Estimation of incubation period distribution of COVID-19 using disease onset forward time: A novel cross-sectional and forward follow-up study”. Science Advances33 (2020): eabc1202.
  9. da Rosa Mesquita R., et al. “Clinical manifestations of COVID-19 in the general population: systematic review”. Wiener klinische Wochenschrift (2020).
  10. Center for Disease Control. “Coronavirus (COVID-19) frequently asked questions | CDC”. CDC (2020).
  11. Wang D., et al. “Clinical Characteristics of 138 Hospitalized Patients with 2019 Novel Coronavirus-Infected Pneumonia in Wuhan, China”. JAMA - Journal of the American Medical Association 11 (2020): 1061-1069.
  12. Yang X., et al. “Thrombocytopenia and its association with mortality in patients with COVID-19”. Journal of Thrombosis and Haemostasis 6 (2020): 1469-1472.
  13. Bhatraju PK., et al. “Covid-19 in Critically Ill Patients in the Seattle Region — Case Series”. New England Journal of Medicine 21 (2020): 2012-2022.
  14. Liu Y., et al. “Viral dynamics in mild and severe cases of COVID-19”. The Lancet Infectious Diseases6 (2020): 656-657.
  15. Gupta A., et al. “Extrapulmonary manifestations of COVID-19”. Nature Medicine7 (2020): 1017-1032.
  16. Guan W., et al. “Clinical Characteristics of Coronavirus Disease 2019 in China”. New England Journal of Medicine18 (2020): 1708-1720.
  17. Stokes EK., et al. “Coronavirus Disease 2019 Case Surveillance — United States, January 22-May 30, 2020”. MMWR Morbidity and Mortality Weekly Report 24 (2020): 759-765.
  18. Grant MC., et al. “The prevalence of symptoms in 24,410 adults infected by the novel coronavirus (SARS-CoV-2; COVID-19): A systematic review and meta-analysis of 148 studies from 9 countries”. Hirst JA, editor. PLOS ONE6 (2020): e0234765.
  19. Wong CKH., et al. “Clinical presentations, laboratory and radiological findings, and treatments for 11,028 COVID-19 patients: a systematic review and meta-analysis”. Scientific Reports 1 (2020): 19765.
  20. Huang C., et al. “Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China”. The Lancet10223 (2020): 497-506.
  21. Chen N., et al. “Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study”. The Lancet10223 (2020): 507-513.
  22. Richardson S., et al. “Presenting Characteristics, Comorbidities, and Outcomes Among 5700 Patients Hospitalized With COVID-19 in the New York City Area”. JAMA20 (2020): 2052.
  23. Yang BY., et al. “Clinical Characteristics of Patients With Coronavirus Disease 2019 (COVID-19) Receiving Emergency Medical Services in King County, Washington”. JAMA Network Open 7 (2020): e2014549.
  24. Pan F., et al. “Time Course of Lung Changes at Chest CT during Recovery from Coronavirus Disease 2019 (COVID-19)”. Radiology 3 (2020): 715-721.
  25. Liu K., et al. “Clinical characteristics of novel coronavirus cases in tertiary hospitals in Hubei Province”. Chinese Medical Journal9 (2020): 1025-1031.
  26. Zhang G., et al. “Clinical features and short-term outcomes of 221 patients with COVID-19 in Wuhan, China”. Journal of Clinical Virology 127 (2020): 104364.
  27. Chen J., et al. “Clinical progression of patients with COVID-19 in Shanghai, China”. Journal of Infection5 (2020): e1-6.
  28. Li R., et al. “Substantial undocumented infection facilitates the rapid dissemination of novel coronavirus (SARS-CoV-2)”. Science6490 (2020): 489-493.
  29. Norman DC and Yoshikawa TT. “Fever in the elderly”. Infectious disease clinics of North America 1 (2021): 93-99.
  30. Arons MM., et al. “Presymptomatic SARS-CoV-2 Infections and Transmission in a Skilled Nursing Facility”. New England Journal of Medicine 22 (2020): 2081-2090.
  31. Zhou F., et al. “Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study”. The Lancet10229 (2020): 1054-1062.
  32. Liang W., et al. “Development and validation of a clinical risk score to predict the occurrence of critical illness in hospitalized patients with COVID-19”. JAMA Internal Medicine 8 (2020): 1081-1089.
  33. Kaeuffer C., et al. “Clinical characteristics and risk factors associated with severe COVID-19: prospective analysis of 1,045 hospitalised cases in North-Eastern France, March 2020”. Euro surveillance : bulletin Europeen sur les maladies transmissibles = European Communicable Disease Bulletin48 (2020): 2000895.
  34. Pan L., et al. “Clinical characteristics of COVID-19 patients with digestive symptoms in Hubei, China: A descriptive, cross-sectional, multicenter study”American Journal of Gastroenterology5 (2020): 766-773.
  35. Goyal P., et al. “Clinical Characteristics of Covid-19 in New York City”. New England Journal of Medicine 24 (2020): 2372-2374.
  36. Cheung KS., et al. “Gastrointestinal Manifestations of SARS-CoV-2 Infection and Virus Load in Fecal Samples From a Hong Kong Cohort: Systematic Review and Meta-analysis”. Gastroenterology1 (2020): 81-95.
  37. Tong JY., et al. “The Prevalence of Olfactory and Gustatory Dysfunction in COVID-19 Patients: A Systematic Review and Meta-analysis”. Otolaryngology-Head and Neck Surgery1 (2020): 3-11.
  38. Giacomelli A., et al. “Self-reported olfactory and taste disorders in patients with severe acute respiratory coronavirus 2 infection: A cross-sectional study”. Clinical Infectious Diseases. Oxford University Press 71 (2020): 889-890.
  39. Yang X., et al. “Clinical course and outcomes of critically ill patients with SARS-CoV-2 pneumonia in Wuhan, China: a single-centered, retrospective, observational study”. The Lancet Respiratory Medicine 5 (2020): 475-481.
  40. Lechien JR., et al. “Loss of Smell and Taste in 2013 European Patients With Mild to Moderate COVID-19”. Annals of Internal Medicine NLM (Medline) 173 (2020): 672-675.
  41. Wu C., et al. “Analysis of therapeutic targets for SARS-CoV-2 and discovery of potential drugs by computational methods”. Acta Pharmaceutica Sinica B 5 (2020): 766-788.
  42. Centers for Disease Control and Prevention. “COVID-19 in children and teens”. CDC (2020).
  43. Viner RM., et al. “Systematic review of reviews of symptoms and signs of COVID-19 in children and adolescents”. Archives of Disease in Childhood (2020): archdischild-2020-320972.
  44. Di Nardo M., et al. “A literature review of 2019 novel coronavirus (SARS-CoV2) infection in neonates and children”. Pediatric Research (2020): 1-8.
  45. Liguoro I., et al. “SARS-COV-2 infection in children and newborns: a systematic review”. European Journal of Pediatrics 7 (2020): 1029-1046.
  46. Zhang J jin., et al. “Clinical characteristics of 140 patients infected with SARS-CoV-2 in Wuhan, China”. Allergy: European Journal of Allergy and Clinical Immunology 7 (2020): 1730-1741.
  47. Huang I and Pranata R. “Lymphopenia in severe coronavirus disease-2019 (COVID-19): Systematic review and meta-analysis”. Journal of Intensive Care. BioMed Central Ltd. 8 (2020): 36.
  48. Terpos E., et al. “Hematological findings and complications of COVID-19”. American Journal of Hematology. Wiley-Liss Inc 95 (2020): 834-847.
  49. Liu Y., et al. “Neutrophil-to-lymphocyte ratio as an independent risk factor for mortality in hospitalized patients with COVID-19”. Journal of Infection 1 (2020): e6-12.
  50. Zhang Y., et al. “Mechanisms involved in the development of thrombocytopenia in patients with COVID-19”. Thrombosis Research 193 (2020): 110-115.
  51. Wool GD and Miller JL. “The Impact of COVID-19 Disease on Platelets and Coagulation”. Pathobiology 1 (2021): 15-27.
  52. Levi M., et al. “Coagulation abnormalities and thrombosis in patients with COVID-19”. The Lancet Haematology. Elsevier Ltd 7 (2020): e438-40.
  53. Thachil J. “What do monitoring platelet counts in COVID-19 teach us?”. Journal of Thrombosis and Haemostasis : JTH8 (2020): 2071-2072.
  54. Lippi G., et al. “Thrombocytopenia is associated with severe coronavirus disease 2019 (COVID-19) infections: A meta-analysis”. Clinica Chimica Acta 506 (2020): 145-148.
  55. Henry BM., et al. “Hematologic, biochemical and immune biomarker abnormalities associated with severe illness and mortality in coronavirus disease 2019 (COVID-19): a meta-analysis”Clinical Chemistry and Laboratory Medicine (CCLM)7 (2020): 1021-1028.
  56. Zong X., et al. “Thrombocytopenia Is Associated with COVID-19 Severity and Outcome: An Updated Meta-Analysis of 5637 Patients with Multiple Outcomes”. Laboratory Medicine 1 (2021): 10-15.
  57. Liu W., et al. “Analysis of factors associated with disease outcomes in hospitalized patients with 2019 novel coronavirus disease”. Chinese Medical Journal 9 (2020): 1032-1038.
  58. Luo X., et al. “Prognostic Value of C-Reactive Protein in Patients With Coronavirus 2019”. Clinical Infectious Diseases : An Official Publication of the Infectious Diseases Society of America 16 (2020): 2174-2179.
  59. Fincher RME and Page MI. “Clinical Significance of Extreme Elevation of the Erythrocyte Sedimentation Rate”. Archives of Internal Medicine 8 (1986): 1581-1583.
  60. Hu R., et al. “Procalcitonin levels in COVID-19 patients”. International Journal of Antimicrobial Agents2 (2020).
  61. Lippi G and Plebani M. “Procalcitonin in patients with severe coronavirus disease 2019 (COVID-19): A meta-analysis”. Clinica Chimica Acta 505 (2020): 190-191.
  62. Li Y., et al. “Retrospective analysis of laboratory testing in 54 patients with severe- or critical-type 2019 novel coronavirus pneumonia”. Laboratory Investigation 6 (2020): 794-800.
  63. Cheng L., et al. “Ferritin in the coronavirus disease 2019 (COVID-19): A systematic review and meta-analysis”. Journal of Clinical Laboratory Analysis. John Wiley and Sons Inc 34 (2020).
  64. Henry BM., et al. “Lactate dehydrogenase levels predict coronavirus disease 2019 (COVID-19) severity and mortality: A pooled analysis”. American Journal of Emergency Medicine9 (2020): 1722-1726.
  65. Wu M-Y., et al. “Clinical evaluation of potential usefulness of serum lactate dehydrogenase (LDH) in 2019 novel coronavirus (COVID-19) pneumonia”. Respiratory Research1 (2020): 171.
  66. Tang N., et al. “Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia”. Journal of Thrombosis and Haemostasis4 (2020): 844-847.
  67. Wu C., et al. “Risk Factors Associated With Acute Respiratory Distress Syndrome and Death in Patients With Coronavirus Disease 2019 Pneumonia in Wuhan, China”. JAMA Internal Medicine 7 (2020): 934-943.
  68. Yu HH., et al. “D-dimer level is associated with the severity of COVID-19”. Thrombosis Research 195 (2020): 219-225.
  69. Ng M-Y., et al. “Imaging Profile of the COVID-19 Infection: Radiologic Findings and Literature Review”. Radiology: Cardiothoracic Imaging 1 (2020): e200034.
  70. Rubin GD., et al. “The role of chest imaging in patient management during the covid-19 pandemic: A multinational consensus statement from the fleischner society”. Radiology1 (2020): 172-180.
  71. Ling Z., et al. “Asymptomatic SARS-CoV-2 infected patients with persistent negative CT findings”. European Journal of Radiology. Elsevier Ireland Ltd 126 (2020).
  72. Ai T., et al. “Correlation of Chest CT and RT-PCR Testing for Coronavirus Disease 2019 (COVID-19) in China: A Report of 1014 Cases”. Radiology 2 (2020): E32-40.
  73. Jacobi A., et al. “Portable chest X-ray in coronavirus disease-19 (COVID-19): A pictorial review”. Clinical Imaging. Elsevier Inc 64 (2020): 35-42.
  74. “Quarantine for coronavirus (COVID-19)”. Australian Government Department of Health (2020).

Citation

Citation: Sabah Mohamed Alharazy. “Minimum Inhibitory Concentration and Susceptibility Patterns of Organisms to Fosfomycin as Determined by BD Phoenix M50”. Acta Scientific Microbiology 4.5 (2021): 19-22.

Copyright

Copyright: © 2021 Sabah Mohamed Alharazy. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.




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