An Overview on Covid-19, With Homoeopathic Approach

An Overview on Covid-19, With Homoeopathic Approach

Coronavirus infection in humans is commonly associated with mild to severe respiratory diseases, with high fever, severe inflammation, cough, and internal organ dysfunction that can even lead to death (1). Most of the identified coronaviruses cause the common cold in humans.

However, this changed when SARS-CoV was identified, paving the way for severe forms of the disease in humans (2). Our previous experience with the outbreaks of other coronaviruses, like SARS and MERS, suggests that the mode of transmission in COVID-19 as mainly human-to- human transmission via direct contact, droplets, and fomites (25). Recent studies have demonstrated that the virus could remain viable for hours in aerosols and up to days on surfaces; thus, aerosol and fomite contamination could play potent roles in the transmission of SARS- CoV-2 (25).

The immune response against coronavirus is vital to control and get rid of the infection. However, maladjusted immune responses may contribute to the immunopathology of the disease, resulting in impairment of pulmonary gas exchange. Understanding the interaction between CoVs and host innate immune systems could enlighten our understanding of the lung
inflammation associated with this infection (24).

SARS is a viral respiratory disease caused by a formerly unrecognized animal CoV that originated from the wet markets in southern China after adapting to the human host, thereby enabling transmission between humans (9). The SARS outbreak reported in 2002 to 2003 had 8,098 confirmed cases with 774 total deaths (9.6%) (3). The outbreak severely affected the Asia
Pacific region, especially mainland China (94). Even though the case fatality rate (CFR) of SARS-CoV-2 (COVID-19) is lower than that of SARS-CoV, there exists a severe concern linked to this outbreak due to its epidemiological similarity to influenza viruses (95, 27). This can fail the public health system, resulting in a pandemic (6).

MERS is another respiratory disease that was first reported in Saudi Arabia during the year 2012.
The disease was found to have a CFR of around 35% (7). The analysis of available data sets suggests that the incubation period of SARS-CoV-2, SARS-CoV, and MERS-CoV is in almost the same range.


The longest predicted incubation time of SARS-CoV-2 is 14 days. Hence, suspected individuals are isolated for 14 days to avoid the risk of further spread (8). Even though a high similarity has been reported between the genome sequence of the new coronavirus (SARS-CoV-2) and SARS- like CoVs, the comparative analysis recognized a furin-like cleavage site in the SARS-CoV-2 S protein that is missing from other SARS-like CoVs (9). The furin-like cleavage site is expected to play a role in the life cycle of the virus and disease pathogenicity and might even act as a therapeutic target for furin inhibitors. The highly contagious nature of SARS-CoV-2 compared to that of its predecessors might be the result of a stabilizing mutation that occurred in the
endosome-associated-protein-like domain of nsp2 protein.

Similarly, the destabilizing mutation near the phosphatase domain of nsp3 proteins in SARS- CoV-2 could indicate a potential mechanism that differentiates it from other CoVs (10). Even though the CFR reported for COVID-19 is meager compared to those of the previous SARS and MERS outbreaks, it has caused more deaths than SARS and MERS combined (11). Possibly
related to the viral pathogenesis is the recent finding of an 832-nucleotide (nt) deletion in ORF8, which appears to reduce the replicative fitness of the virus and leads to attenuated phenotypes of SARS-CoV-2 (25).

Coronavirus is the most prominent example of a virus that has crossed the species barrier twice from wild animals to humans during SARS and MERS outbreaks .The possibility of crossing the species barrier for the third time has also been suspected in the case of SARS-CoV-2 (COVID- 19). Bats are recognized as a possible natural reservoir host of both SARS-CoV and MERS-CoV
infection. In contrast, the possible intermediary host is the palm civet for SARS-CoV and the dromedary camel for MERS-CoV infection (12).

Bats are considered the ancestral hosts for both SARS and MERS (103). Bats are also considered the reservoir host of human coronaviruses like HCoV-229E and HCoV-NL63 (14). In the case of COVID-19, there are two possibilities for primary transmission: it can be transmitted either through intermediate hosts, similar to that of SARS and MERS, or directly from bats (13).


The disease caused by SARS-CoV-2 is also named severe specific contagious pneumonia (SSCP), Wuhan pneumonia, and, recently, COVID-19 (15). Compared to SARS-CoV, SARS- CoV-2 has less severe pathogenesis but has superior transmission capability, as evidenced by the rapidly increasing number of COVID-19 cases (16).
The incubation period of SARS-CoV-2 in familial clusters was found to be 3 to 6 days (15). The mean incubation period of COVID-19 was found to be 6.4 days, ranging from 2.1 to 11.1 days (13). Among an early affected group of 425 patients, 59 years was the median age, of which more males were affected (14). Similar to SARS and MERS, the severity of this nCoV is high in
age groups above 50 years (2, 15). Symptoms of COVID-19 include fever, cough, myalgia or fatigue, and, less commonly, headache, hemoptysis, and diarrhea (116, 282). Compared to the SARS-CoV-2-infected patients in Wuhan during the initial stages of the outbreak, only mild symptoms were noticed in those patients that are infected by human-to-human transmission (20).

The initial trends suggested that the mortality associated with COVID-19 was less than that of previous outbreaks of SARS (11). The updates obtained from countries like China, Japan, Thailand, and South Korea indicated that the COVID-19 patients had relatively mild manifestations compared to those with SARS and MERS (4). Regardless of the coronavirus type, immune cells, like mast cells, that are present in the submucosa of the respiratory tract and nasal cavity are considered the primary barrier against this virus (9). Advanced in-depth analysis of the genome has identified 380 amino acid substitutions between the amino acid sequences of SARS- CoV-2 and the SARS/SARS-like coronaviruses.

These differences in the amino acid sequences might have contributed to the difference in the pathogenic divergence of SARS-CoV-2 (16). Further research is required to evaluate the possible differences in tropism, pathogenesis, and transmission of this novel agent associated with this change in the amino acid sequence. With the current outbreak of COVID-19, there is an expectancy of a significant increase in the number of published studies about this emerging coronavirus, as occurred with SARS and MERS (17).

SARS-CoV-2 invades the lung parenchyma, resulting in severe interstitial inflammation of the lungs. This is evident on computed tomography (CT) images as ground-glass opacity in the lungs. This lesion initially involves a single lobe but later expands to multiple lung lobes (18).

The histological assessment of lung biopsy samples obtained from COVID-19-infected patients revealed diffuse alveolar damage, cellular fibromyxoid exudates, hyaline membrane formation, and desquamation of pneumocytes, indicative of acute respiratory distress syndrome (19). It was also found that the SARS-CoV-2-infected patients often have lymphocytopenia with or without leukocyte abnormalities. The degree of lymphocytopenia gives an idea about disease prognosis, as it is found to be positively correlated with disease severity (28).

Pregnant women are considered to have a higher risk of getting infected by COVID-19. The coronaviruses can cause
adverse outcomes for the fetus, such as intrauterine growth restriction, spontaneous abortion, preterm delivery, and perinatal death.

Nevertheless, the possibility of intrauterine maternal-fetal transmission (vertical transmission) of CoVs is low and was not seen during either the SARS- or MERS-CoV outbreak (20). However, there has been concern regarding the impact of SARS-CoV-2/COVID-19 on pregnancy.

Researchers have mentioned the probability of in utero transmission of novel SARS-CoV-2 from COVID-19-infected mothers to their neonates in China based upon the rise in IgM and IgG antibody levels and cytokine values in the blood obtained from newborn infants immediately postbirth; however, RT-PCR failed to confirm the presence of SARS-CoV-2 genetic material in
the infants (23). Recent studies show that at least in some cases, preterm delivery and its consequences are associated with the virus. Nonetheless, some cases have raised doubts for the likelihood of vertical transmission (23,24).

COVID-19 infection was associated with pneumonia, and some developed acute respiratory distress syndrome (ARDS). The blood biochemistry indexes, such as albumin, lactate dehydrogenase, C-reactive protein, lymphocytes (percent), and neutrophils (percent) give an idea about the disease severity in COVID-19 infection (31). During COVID-19, patients may present leukocytosis, leukopenia with lymphopenia (24), hypoalbuminemia, and an increase of lactate dehydrogenase, aspartate transaminase, alanine aminotransferase, bilirubin, and, especially, D- dimer (24).

Middle-aged and elderly patients with primary chronic diseases, especially high blood pressure and diabetes, were found to be more susceptible to respiratory failure and, therefore, had poorer prognoses. Providing respiratory support at early stages improved the disease prognosis and facilitated recovery (28). The ARDS in COVID-19 is due to the occurrence of cytokine storms that results in exaggerated immune response, immune regulatory network imbalance, and, finally, multiple-organ failure (32-33). In addition to the exaggerated inflammatory response seen in patients with COVID-19 pneumonia, the bile duct epithelial cell- derived hepatocytes upregulate ACE2 expression in liver tissue by compensatory proliferation
that might result in hepatic tissue injury Coronavirus infections in humans typically range from mild to severe respiratory diseases, often accompanied by high fever, inflammation, cough, and potential organ complications leading to fatal outcomes.

While most coronaviruses cause common cold symptoms, this perception changed with the identification of SARS-CoV, indicating more severe human diseases. Past experiences with SARS and MERS suggest that COVID-19 primarily spreads through human-to- human contact via direct contact, droplets, and surfaces. Recent studies revealed the virus’s viability in aerosols and on surfaces, highlighting their potential roles in transmission.

Understanding the immune response against coronaviruses is crucial for managing infections. However, imbalanced immune responses can contribute to the disease’s immune-related pathology, impacting lung function adversely. Studying how CoVs interact with the host’s innate immune systems can shed light on the lung inflammation linked with these infections.
SARS, originating from wet markets in southern China, caused a severe outbreak in 2002-2003, with a high mortality rate. MERS, reported in Saudi Arabia in 2012, exhibited a high case fatality rate. Both SARS-CoV and MERS-CoV share similarities in their incubation periods.

Despite differences in fatality rates, COVID-19 raises concerns due to its resemblance to influenza viruses, potentially leading to a pandemic, despite a lower CFR than SARS-CoV. The genetic analysis of SARS-CoV-2 reveals distinctive features in its spike protein, potentially influencing its infectivity and pathogenicity. Mutations within SARS-CoV-2’s proteins suggest differences from other CoVs, potentially affecting its behavior and clinical outcomes. Despite a lower CFR compared to SARS and MERS, COVID-19 has caused more deaths due to its widespread nature.

Coronaviruses like SARS and MERS crossed the species barrier from animals to humans, and similar concerns exist for SARS-CoV-2. Bats are considered natural reservoir hosts for various coronaviruses, and intermediary hosts like palm civets and dromedary camels were implicated in the transmission to humans for SARS and MERS, respectively. The possibility of SARS-CoV- 2’s transmission directly from bats or through intermediate hosts remains under scrutiny The plasticity in coronaviruses, their adaptive mutations, and their ability to jump between species raise concerns about interspecies transmissions, with bats identified as a primary reservoir host. While the pathogenesis of many bat coronaviruses remains unknown, evidence
points to the potential for cross-species transmission.

The pathology of SARS-CoV-2, causing COVID-19, showcases less severe symptoms than SARS-CoV but exhibits higher transmissibility. The incubation period, clinical symptoms, and severity, especially in older age groups, align with previous CoV outbreaks. Lung lesions in COVID-19 patients, observed via CT scans, resemble acute respiratory distress syndrome
(ARDS), indicating severe lung inflammation. The virus also impacts blood chemistry indexes, affecting various organs and potentially leading to multiple-organ failure.

Pregnant women infected with COVID-19 face risks, although evidence of intrauterine transmission remains limited. However, concerns persist regarding the impact of COVID-19 on pregnancy outcomes, indicating a need for further research and monitoring. Understanding the genetic variations between SARS-CoV-2 and other coronaviruses provides insights into the differences in their pathogenicity and transmission. With ongoing research and increasing studies on COVID-19, further understanding and strategies for managing this novel coronavirus are expected to evolve.

According to Calvin B. Knerr(34)
Suffocation (See Asphyxia, Asthma, Dyspnœa.) :- Agar., Anan., Arum-d., Arum-m.,
Arund., Atrop-s., Aur., Bell., Calc-s., Camph., Cedr., Cham., Chlor., Coff., Cub., Cupr-a.,
Dros., Ferr-m., Guai., Hydr-ac., KALI-I., LACH., Lact., Laur., Meli., MEPH., Nat-m.,
Nux-m., Nux-v., Spong., Stram., Tab., Tarent., Vesp., Zing.
Air :-
 Open, better in, worse by motion :- Ip.
 Doors, wants, and windows open, particularly at night :- SULPH.
 Fanned, has to be :- Cann-i.

 Fanned, wants to be, in pneumonia :- CARB-V., Kali-n.
 Live, as if she could not, for want of :- Apis.

Bronchi :-
 Acute inflammation :- Cact.
 Secretion, from, in bronchitis :- Hippoz.

Chest :-
 Gnawing pain :- Mosch.
 Moving chest, on (cyanosis) :- Lach.
 Mucus, from accumulation of :- Coc-c., Ip.
 Mucus, from accumulation of, also in throat :- Coc-c.
 Mucus, could not raise (bronchitis) :- Cina.
 Mucus, by rattling of, threatened :- Hep.
 Pain :- Spong.
 Pressure :- Kali-c.
 Pressure, with, on lungs :- Ptel.
 Pulsation, with, while coughing, or as soon as he begins to talk :- Manc.
 Rattling in pneumonia :- ANT-T.
 Sticking and burning behind sternum :- Phos.
 Tightness across upper part (dilatation of heart) :- Tab.
 Croup :- Brom., Kaol.
 Alternating with free intervals :- Lyc.
 Croupy, choking :- Ail.
 Membranous, with :- Phos.
 Spasmodic :- BELL.
 Stage, resembling last :- SAMB.
 Tough mucus, causing strangulation :- Kali-bi.
Lungs :-
 Threatening paralysis, with long-lasting attacks :- LACH.
 Pneumonia, in :- Ant-t.
 Sudden, in epidemic pneumonia :- Cupr.
Air :-
 Capacity diminished :- Arg-n.
 Cold, seems (valvular insufficiency) :- Lith-c.
 Could not get air deep enough, as if she :- Caps.

 Could not breathe, as if there were none and he :- Kali-c.
 Could not get enough, as if he, inspires forcibly :- Brom.
 Could not expand, as if, painful on deep inspiration :- Chr-ac.
 Could not fill completely :- Chlor.
 Fill, has to, but has no power to eject :- Med.
 Fill, vainly endeavors to, by full inspirations and utmost enlargement of
chest :- Coca.
 Fill, cannot :- Phos.
 Freely in, passes, but cannot exhale :- Chlor.
 Impervious, left, later affects right (bronchial catarrh) :- Lach.
 Inflate lower lobes, could only, when sitting up :- Calen.
 Inspiration, feeling of air escaping into pleural cavity at each :- Chlor.
 Mucous membrane very sensitive, any change sets patient
coughing (whooping cough) :- Cor-r.
 Stuck together, as though air cells were :- Ail.
 Upper part impervious, except on full inspiration, when there is a
prolonged paroxysm of coughing (chronic coughing) :- Lyc.

Dyspnœa (difficult, labored breathing) :- Abies-c., Acet-ac., Æsc., Æth., Aloe, Alumn., Aml-
ns., Amyg., Ant-c., Ant-s-aur., Ant-t., Apis, Arn., ARS., Ars-met., Ars-s-f., Arum-
d., Arund., Asaf., Asc-t., Aspar., Astac., Bell., Benz-ac., Bor., Brom., Cact., Cahin.,
Calad., Calc-p., Camph., Carb-v., CARBN-S., Cedr., Cham., Chel., Chin., Chlf., Chlol.,
Chlor., Cina, Coc-c., Cor-r., Crot-h., Cub., Cupr., CUPR-A., Cupr-ar., Dig., Dulc., Eup-
pur., FERR., Fl-ac., Gels., Glon., Hippoz., Iber., Inul., Iod., Iodof., KALI-AR., Kali-
bi., Kali-br., KALI-C., Kali-i., Kali-ma., Lac-c., LACH., Laur., Lith-c.,
Lob., LYC., Lyss., Merc., Merc-c., Merc-sul., Mosch., Mygal., Naja, NAT-S., Nit-ac., Nux-
m., Nux-v., Œna., Osm., Ph-ac., Phel., PHOS., Phys., Phyt., Plat., Plb., Polyg., Ptel.,
Puls., Sal-ac., Samb., Sec., Sil., Spong., Squil., Sulph., Tab., Verat., Vesp., Zinc.
Auscultation sounds :- 
 Ægophony, right side towards upper part (pleurisy) :- Seneg.
 Ægophony, in pneumonia :- Zinc.
 Amphoric, in tuberculosis :- Nat-ar.
 Apices audibly diseased, one of the :- Tub.
 Bronchial :- Sec.
 Bronchial, at base (phthisis) :- Ars-i.
 Bronchial, in catarrhal pneumonia :- Hyos.
 Bronchial, after coughing and profuse expectoration (bronchial catarrh) :- Hep.
 Bronchial, indistinct, with numerous râles, partly dry, partly moist, with dull
percussion over lower portion of thorax on right side :- Phos.

 Bronchial, in pleuritis :- Cact.
 Bronchial, in pneumonia :- Chel., KALI-I., Lyc., Phos., Sang., Stram.
 Bronchial, from 5th rib downward, in pneumonia :- Sulph.
 Bronchial, on right side, in phthisis :- Iod.
 Bronchial, in right, suprascapular region (phthisis) :- Ars-i.
 Bronchial, in right side (pleuro-pneumonia biliosa) :- Rhus-t.
 Bronchial, strong in front, right side, above and behind (pneumonia) :- Ant-t.
 Bronchial, in tuberculosis :- Ferr-i.
 Bronchial, upper half (asthma) :- Dig.
 Camphoric sounds in right :- Iodof.
 Creaking leathery noise, over middle and lower 3rd of right (pneumonia) :- Iod.
 Crepitant râles (pleuro-pneumonia biliosa) :- Rhus-t.
 Crepitation in bilateral croupous pneumonia :- Kali-i.
 Crepitation, coarse, beneath left clavicle (hæmorrhagic pthisis) :- Ars-i.
 Crepitation, coarse, below border of pectoralis major, and around posteriorly to
back of lung (hæmorrhagic phthisis) :- Ars-i.
 Crepitation, coarse, in phthisis :- Ars-i.
 Crepitation, coarse, posteriorly about centre (phthisis) :- Ars-i.
 Crepitation, dry, over both, veiled by co-existing coarse bronchial râles (measles) :-
 Crepitation, with or without expectoration, and a sensation of heat and sharp pain
during inspiration :- PHOS.
 Crepitation, fine, in broncho-pneumonia :- Lyc.
 Crepitation, with feeble respiration :- Kali-cy.
 Crepitation, in left (pneumonia) :- Ant-t.
 Crepitation, in both lower lobes (pneumonia) :- Sulph.
 Crepitation, before and after menses (phthisis) :- Ars-i.
 Crepitation, in pneumonia :- Elaps., Lyc., Phos.
 Crepitation, posteriorly, in right lung, from forced inspiration (phthisis) :- Ars-i.
 Crepitation in right suprascapular region (phthisis) :- Ars-i.
 Crepitation, but distinct, in upper part of chest, on right side, superiorly and
posteriorly feeble, respiration sharp and expiratory murmur
indistinct (pneumonia) :- Sulph.
 Murmur, in pneumonia :- Ant-t.
 Murmur, lung, expiratory sound long in apex of (incipient phthisis follow
amenorrhœa) :- Sang.
 Murmur, harsh, in left apex (phthisis) :- Ars-i.
 Murmur in apices, rattling, weak, worse in right (consumption) :- Kali-bi.
 Murmur, weak respiratory, in right side, in nipple line in 5th intercostal
space (bronchial catarrh) :- Hep.
 Purring, in bronchial catarrh :- Ant-t.
 Purring, with cough :- Ant-t.
 Râle, consonating, at 4th rib (pneumonia) :- Sulph.
 Râles, subcrepitant, over summit of, right :- Ant-t.

 Râles in base, small crepitant, posteriorly (infantile pneumonia) :- Phos.
 Râles, fine vesicular, at left apex :- Sep.
 Rasping, increasing towards evening (croup) :- Kaol.
 Ronchi, dry (phthisis) :- Ars-i.
 Ronchi, sibilant, wheezing :- Spong.
 Sibilant, at night (hay catarrh) :- Stict.
 Sibilant, all over, especially lower right lobe (pneumonia) :- Sulph.
 Snoring, loud, as if through a tube (bilateral croupous pneumonia) :- Kali-i.
 Vesicular murmur absent in dropsy of chest :- Kali-i.
 Vesicular murmur absent in left :- Elaps.
 Vesicular murmur absent in posterior half of left :- Lach.
 Vesicular murmur absent in pleuritis, with plastic exudation :- Hep.
 Vesicular murmur absent in pneumonia :- Lyc., Squil.
 Vesicular murmur absent at top of right :- Tub.
 Vesicular murmur absent in upper part of superior lobe :- Sulph.
 Vesicular murmur dry in upper part (asthma) :- Arg-n.
 Vesicular murmur feeble :- Dig.
 Vesicular murmur feeble in cardiac dropsy :- Dig.
 Vesicular murmur feeble and obscure :- Gels.
 Vesicular murmur almost inaudible :- Bar-c.
 Vesicular murmur indistinct, especially in lower lobes :- Nat-ar.
 Vesicular murmur indistinct in several places (asthma) :- Arg-n.
 Vesicular breathing, weak (œdema of lungs) :- Ant-t.
 Vocal fremitus increased (pneumonia) :- Sulph.
 Vocal resonance, increased, of right :- Iodof., Tub.


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About the Author:

Dr. Ashok Yadav (Head Of Department, Deprtment Of Practice Of Medicine), Dr Virendra Chauhan
(ASS.PROF. PRACTICE OF MEDICINE) Dr. Mansi Mishra Md(Pgr) Deprtment Of Practice Of
Medicine, Dr. Anandita Debonath Md(Pgr) Deprtment Of Practice Of Medicine

About the author

DR Mansi Mishra