Background

Pneumonia is a severe acute lower respiratory tract infection that impacts the pulmonary parenchyma in one or both lungs. Pneumonia is the sixth leading cause of mortality in the United States and the only infectious condition in the top ten. It is a prevalent and possibly fatal infectious disease with significant morbidity and fatality.  

Viral pneumonia is an infection of the lungs caused by a virus etiology. It is characterized by inflammation of the alveoli, the tiny air sacs in the lungs responsible for facilitating oxygen and carbon dioxide exchange. It commonly affects individuals in vulnerable populations such as infants, the elderly, and those with existing respiratory conditions or compromised immune systems.  

Epidemiology

The most common causes of viral pneumonia among adults are influenza A and B, together responsible for more than half of all such hospitalizations annually in the United States. Other important pathogens include RSV (respiratory syncytial virus), adenovirus, parainfluenza virus, hMPV (human metapneumovirus), and coronaviruses. Influenza is particularly severe among the elderly who represent 63% of hospital admissions and 85% deaths despite making up only 10% of the population.

RSV causes most cases of child viral pneumonitis worldwide but is increasingly seen in older people where it leads to 60 000–160 000 hospitalisations annually amongst those and individuals aged 65 years with 6000-10 000 deaths in the US alone each year. Residents in nursing homes get infected with RSV at a rate of 10% per year while adenovirus accounts for 10% childhood pneumonia. 

Anatomy

Pathophysiology

Three primary causes can lead to viral pneumonia which include direct introduction of viral particles into the lung, contiguous spread from a nearby infection in the upper respiratory tract, and hematogenous dissemination from a distant site. The microscopic pathogenesis of the disease is characterized by the invasion of viral particles that target pneumocytes causing alveolar damage, inflammation, and secondary submucosal edema together with microhemorrhage as well as a cellular immune response.

Mononuclear lymphocytes are attracted and then followed by polymorphonuclear leukocytes while fibrin release also plays a role in the immune reaction;[4] at the same time, CD4 and CD8 cells become activated resulting into increased vascular permeability which leads to more severe edema. If left untreated this can progress towards intra-alveolar organization with clinical symptoms similar to those seen in obliterans disease states. 

Etiology

Viral pneumonia stems from a multitude of DNA and RNA viruses, some of which are known as lung pathogens and have established themselves by causing common clinical and radiographic manifestations. These include families like Coronaviridae (e.g. SARS, MERS, and 2019-nCoV), Adenoviridae, and Orthomyxoviridae (such as the influenza virus). Others such as Paramyxoviridae, Picornaviridae, and Herpesviridae may also be implicated since they cause anything between mild and severe infections.

When it comes to community-acquired viral pneumonia, the most frequently associated pathogens are influenza virus, respiratory syncytial virus, adenovirus, parainfluenza virus, coronavirus, rhinovirus and human metapneumovirus. Depending on the immune status and age of the host, these viruses differ in their means of transmission as well as clinical manifestations severity. Therefore, it is important to understand how different pathogenic mechanisms work if we are to effectively manage this condition through diagnosis, treatment or prevention strategies. 

Genetics

Prognostic Factors

Several factors affect the outlook for viral pneumonia, which include the virulence of viral species, immune competence of the patient, underlying pathology such as diabetes, COPD, diabetes mellitus (DM), dyscrasias, and haematological disorder and whether there is a coexisting bacterial infection or not and if recognized, the progress of infection and specific therapy started where available. Patients who are immunocompromised due to having been infected with HIV have an even worse prognosis than those without any other underlying medical conditions. 

Clinical History

Pathognomonic history cues are not available for diagnosing viral pneumonia compared to bacterial pneumonia. However, some cues hint towards viral pneumonia during differential diagnosis as follows: 

1. Lower temperature 
2. History of HIV 
3. Associated flu symptoms 
4. Collateral gastrointestinal symptoms 
5. Upper respiratory tract infections that can be diagnosed 
6. Progressive onset of symptoms rather than sudden onset 
7. History of neoplasm 
8. Sputum that lacks pus 

Physical Examination

 These findings resemble to those of pyogenic pneumonia and are not specific. In physical examination increased fremitus, bronchial breath, crackles and wheezing may be noticed. Some patients may show mild fever, respiratory failure or multiple organ failure. Other observations may include: 

Chills 

Fever 

Dyspnea and/or tachypnea 

Rhonchi 

Wheezing 

Dullness to percussion 

Pleurisy 

Cough with presence or absence of sputum 

Cyanosis 

Rash 

Pleural friction rub 

Acute respiratory distress 

Age group

Associated comorbidity

1. Secondary multiple organ failure and sepsis 
2. Cardiovascular collapse 
3. Bacterial infections causing empyema, abscess, or pleural effusion 
4. Acute respiratory distress syndrome 

Associated activity

Acuity of presentation

Differential Diagnoses

• Bacterial pneumonia 
• Cytomegalovirus 
• Enteroviruses 
• Fungal pneumonia 
• Heart transplantation 
• Herpes simplex 
• Influenza 
• Lung transplantation 
• Pleural effusion 
• Adenovirus 
• Aspiration pneumonitis and pneumonia 
• Hantavirus pulmonary syndrome 
• Heart- lung transplantation 
• Herpes zoster 
• Respiratory failure 
• Varicella-Zoster virus 
• Pneumococcal infections 
• Respiratory failure 

Laboratory Studies

Imaging Studies

Procedures

Histologic Findings

Staging

Treatment Paradigm

Approach considerations: All the patients suffering from viral pneumonia should be considered for supportive care with oxygen, analgesics, nutrition, antipyretics and rest. 

Supportive care: The patients need oxygen if they have hypoxemia or are unable to breathe adequately, which must be given by the EMTs. Prehospital providers can deliver drugs that help breathing through the airways. Intubation and a breathing machine are required for someone who cannot breathe on their own because of their lungs not working. If a person is in shock without heart failure, then they should be given fluids intravenously such as normal saline solution. In acute care settings this might involve giving medications like acyclovir (Zovirax), putting them on antibiotics if there is an infection and isolating them from others who may become infected while also using mechanical ventilation when necessary due to respiratory failure. 

by Stage

by Modality

Chemotherapy

Radiation Therapy

Surgical Interventions

Hormone Therapy

Immunotherapy

Hyperthermia

Photodynamic Therapy

Stem Cell Transplant

Targeted Therapy

Palliative Care

Use of antiviral agents

• Zanamivir: This drug inhibits a glycoprotein, neuraminidase which is present on the surface of influenza virus and destroys the receptor of infected cell for viral hemagglutinin. This inhibition also causes the release of virus from infected cells and reduces the spread of virus. It is effective in treating infections due to influenza A and B. 
• Oseltamivir:  This drug inhibits a glycoprotein, neuraminidase which is present on the surface of influenza virus and destroys the receptor of infected cell for viral hemagglutinin. This inhibition also causes the release of virus from infected cells and reduces the spread of virus. It is effective in treating infection of influenza A or B. 
• Peramivir:  This drug acts by inhibiting neuraminidase enzyme which releases viral particle from plasma membrane of the infected cells. It is used in treating uncomplicated influenzas in children aged 6 months or above and adults. 
• Acyclovir: It suppresses the activity of HSV-1 and HSV-2. Viral thymidine kinase has an affinity for this and upon phosphorylation, it causes DNA chain termination as DNA polymerase acts on it. For patients who start applying it within 24-48 hours from when they first notice rashes, HSV or VZV lesions disappear quickly with fewer painful sensations. Commencement of medication at first signs of disease is critical. 
• Ganciclovir:  This is a synthetic derivative of guanine which is active against HSV, CMV, HHV-8 and HHV-6. Being an acyclic nucleotide of 2-deoxyguanosine, it inhibits the replication of herpes virus both in vivo and in vitro.  
• Foscarnet: This is an analogue of inorganic pyrophosphate which inhibits the replication of herpesviruses which includes HSV-1, HSV-2 and CMV. It suppresses the replication of virus at phosphate-binding site on DNA polymerases that are virus-specific. 

Use of monoclonal antibodies

premature babies who are at an elevated risk for severe RSV-associated conditions. 

Nirsevimab: It is given as an IM injection each year with an indication to prevent lower respiratory syncytial virus (RSV) disease in neonates and infants born during or entering their first RSV season as well as in those children up to 24 months old still at high risk for serious RSV infection during their second RSV season. 

Use of immune globulins

Immune globulin IV: Anti-idiotypic antibodies neutralize the circulating myelin antibodies in immune globulin IV. They reduce INF-gamma and proinflammatory cytokines; suppress inducer T cells and B cells; block Fc receptors on macrophages; and increase suppressor T cells. This medication also promotes remyelination, obstructs the complement cascade, and may cause an elevation in CSF IgG levels (10%). 

Use of beta-agonists

Albuterol: It is a beta-agonist indicated in the treatment of bronchospasm. It acts on β2 receptors by relaxing bronchial smooth muscles. 

Use of vaccines

• Adjuvanted Respiratory syncytial virus (RSV) vaccine: The vaccine contains a recombinant subunit pre-fusion RSV F glycoprotein antigen (RSVPreF3) in combination with the AS01E adjuvant. It is intended to be used as an active immunization for the prevention of lower respiratory tract disease (LRTD) caused by infection with respiratory syncytial virus (RSV) among people aged 60 years or older. It may also be used in adults aged 50-59 years at high risk of RSV-induced LRTD. 
• Respiratory syncytial virus vaccine: The vaccine consists of a non-distinguished measure of precaution against respiratory syncytial virus in older adults in terms of active immunization to protect their lower respiratory tract from the infection (caused by the virus also known as RSV) using equal quantities of recombinant RSV prefusion F from SGA and SGB. The vaccine contains equal concentrations of RSV prefusion F antigens from RSV subgroup A and B recombinant proteins. It is designated for the active immunization for prevention of lower respiratory tract diseases that result from respiratory syncytial virus (RSV) infection in adults 60 years of age and older. 
• Respiratory syncytial virus vaccine, mRNA: It is ideal for preventing respiratory syncytial virus (RSV) infection-induced lower respiratory tract diseases among individuals who are 60 years old and above by use in bioengineering RSV prefusion F of proteins from subgroups A and B. 

use-of-phases-of-management-in-treating-viral-pneumonia

Oxygen is crucial for patients experiencing hypoxemia or shortness of breath, and emergency medical personnel should administer it to dyspnoeic patients. Prehospital providers can deliver beta-agonist treatments to improve breathing. Respiratory failure patients require endotracheal intubation and ventilator support. Isotonic sodium chloride solution is used for shock without heart failure. Acute care may include oxygen, beta-agonists, dehydration fluids, Acyclovir, respiratory isolation, antibiotics, and mechanical ventilation. 

Medication

Future Trends

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References

Alpha Thalassemia – StatPearls – NCBI Bookshelf (nih.gov)