Influenza, COVID-19 and viral pneumonitis

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Viral pneumonitis ranges from a self-limiting febrile illness to diffuse alveolar injury and multiorgan disease. Presentation alone rarely identifies the virus. The decision model therefore asks four questions: is respiratory support needed, is an organism-specific treatment time-sensitive, is there bacterial or fungal coinfection, and what infection-control or public-health action applies today?

Treatment is unusually volatile. Influenza recommendations respond to circulating susceptibility and COVID-19 eligibility changes with evidence, variants and commissioning. Before each prescription, check same-day NICE, UKHSA, BNF and local policy, including pregnancy, renal function and interactions.

Key points

Influenza and SARS-CoV-2 can produce primary viral pneumonitis, trigger decompensation of chronic disease and permit secondary bacterial pneumonia; RSV and other viruses matter particularly in older or immunocompromised adults.
Use the current local respiratory-virus panel and infection-prevention policy because circulating strains, isolation rules and antiviral eligibility change.
Severe influenza and influenza in clinical-risk groups should receive prompt antiviral treatment under current UKHSA guidance, even when presentation is later than the ideal early window.
Oseltamivir is the usual first-line influenza antiviral for most adults and is preferred for most pregnant patients; adjust for renal function and use current seasonal resistance advice.
For COVID-19, systemic corticosteroids benefit people who require supplemental oxygen because of COVID-19; do not give them solely for COVID-19 in people who do not need oxygen.
COVID antivirals and immunomodulators require current NICE eligibility, interaction and timing checks; they are not interchangeable with influenza antivirals.
Do not prescribe antibacterial therapy for a likely viral pneumonia unless bacterial coinfection is suspected from the clinical, microbiological or radiological picture.
Prescribe oxygen to a target, reassess frequently and combine test results with timing: a negative upper-airway test does not always exclude lower-respiratory infection in an immunocompromised patient.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Seasonal respiratory viruses

Influenza, SARS-CoV-2, respiratory syncytial virus and other viruses spread through respiratory particles and can infect lower airways directly.

Host vulnerability

Older age, pregnancy, immune suppression, obesity and chronic cardiac, respiratory or metabolic disease increase the likelihood of severe lower-respiratory involvement.

Exposure and immunity

Close-contact exposure, outbreaks and waning or absent variant-relevant immunity shape infection risk and clinical severity, whose relevance depends on the complete exposure and clinical history.

Secondary bacterial infection

Viral epithelial damage and altered immune defence permit bacterial superinfection, which may develop during or after initial viral illness.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Respiratory epithelial infection
Virus enters susceptible airway or alveolar cells, replicates and disrupts mucosal and ciliary defence, and the downstream physiological effect determines clinical severity.
2
Innate immune response
Interferon and inflammatory pathways recruit immune cells, causing fever, systemic symptoms and local epithelial injury, which links the underlying lesion to the observed respiratory dysfunction.
3
Alveolar involvement
Diffuse inflammation, oedema and microatelectasis impair ventilation-perfusion matching and oxygen diffusion, contributing to the resulting loss of respiratory reserve.
4
Endothelial and thrombotic effects
Severe viral illness can activate endothelium and coagulation, contributing to microvascular injury and thromboembolism, with effects that increase as the pathological process progresses.
5
Repair or organisation
Most inflammation resolves, but severe injury may progress to ARDS, organising pneumonia or persistent physiological impairment.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Influenza pneumonitisRed flag

Abrupt fever, myalgia, headache and cough progressing to dyspnoea or diffuse infiltrates, with particular concern in pregnancy, older age, immunocompromise and chronic cardiac, neurological or respiratory disease.

COVID-19 pneumonitisRed flag

Fever, cough, breathlessness and hypoxaemia with bilateral peripheral or diffuse opacities; thromboembolism, myocarditis and inflammatory deterioration may complicate the course.

Secondary bacterial pneumoniaRed flag

New focal consolidation, purulent sputum, recurrent fever or deterioration after initial viral improvement suggests bacterial superinfection, including pneumococcus or post-influenza Staphylococcus aureus.

Immunocompromised viral diseaseRed flag

Prolonged shedding, muted fever, lower-airway disease despite a negative nasal sample, mixed infection and antiviral resistance are more likely after transplant, chemotherapy or substantial immunosuppression.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Respiratory viral PCRFirst step
Why
Identify influenza, SARS-CoV-2, RSV or another virus and guide treatment and infection control.
Interpretation and limitations
Sample early using the locally validated platform. A negative upper-airway result may need repeat or lower-respiratory testing when severe lower-airway disease or immunocompromise sustains suspicion.
02
Oxygenation and blood gas
Why
Grade respiratory failure and identify the need for enhanced support.
Interpretation and limitations
Trend saturation against the prescribed target, respiratory effort and FiO2. Hypercapnia, acidosis, exhaustion or a rapidly rising requirement needs critical-care assessment.
03
Chest imaging
Why
Assess pneumonitis extent and identify focal bacterial disease, oedema, embolism or pleural complication.
Interpretation and limitations
Radiographic patterns overlap. CT or CTPA should answer a specific unresolved question and not delay antiviral treatment or stabilisation.
04
Bacterial and inflammatory assessment
Why
Identify coinfection and organ complications without treating every inflammatory rise as bacterial.
Interpretation and limitations
Use sputum/blood cultures, FBC, CRP, renal/liver profile and lactate according to severity. Procalcitonin may inform stewardship locally but cannot independently rule infection in or out.
05
Treatment eligibility screen
Why
Confirm safe access to current antiviral or immunomodulatory treatment.
Interpretation and limitations
Record symptom onset, oxygen requirement, vaccination, pregnancy, immunocompromise, renal/liver function and interacting medicines; check current NICE and UKHSA criteria on the treatment day.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Bacterial pneumonia

Focal consolidation, purulent sputum and microbiological evidence support bacterial infection, but coinfection can accompany confirmed viral disease.

Pulmonary embolism

Sudden deterioration, pleuritic pain or disproportionate hypoxaemia with thrombotic risk warrants probability-led imaging despite viral positivity.

Cardiogenic pulmonary oedema

Orthopnoea, oedema and cardiac congestion suggest hydrostatic fluid, which infection may precipitate, with targeted examination and testing used to resolve the uncertainty.

Drug or inflammatory pneumonitis

Medicine timing, autoimmune features or negative serial virology may support non-infective inflammation with a similar imaging pattern.

Pulmonary tuberculosis

Chronic symptoms, epidemiological risk and upper-zone or cavitating disease require mycobacterial assessment and infection-control measures, while chronology and directed testing distinguish the competing explanation.

Additional chapter-specific clues

Non-infective mimic

Pulmonary oedema, embolism, drug pneumonitis, organising pneumonia and diffuse alveolar haemorrhage can resemble viral pneumonitis and may coexist.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01InitialStabilise, sample and isolateFirst stepSuspected viral pneumonitis with lower-respiratory symptoms.

1Perform ABCDE assessment, prescribe target-based oxygen, obtain viral samples and apply the current local isolation/PPE pathway without delaying emergency support.
2Assess timing and risk factors for influenza or COVID-specific treatment, and search for focal bacterial infection, embolism, myocarditis or decompensated chronic disease.
3EscalationEscalate early for rising oxygen needs, fatigue, shock or altered consciousness; use high-flow, NIV or invasive ventilation only in an appropriate monitored pathway.

02InfluenzaTreat severe and at-risk disease promptlyConfirmed or strongly suspected influenza meeting current UKHSA treatment criteria.

1First lineStart the current first-line antiviral promptly; do not wait for confirmation in severe illness during circulation or a credible outbreak.
2Adjust oseltamivir for renal function and use zanamivir or another current option when resistance, absorption or intolerance requires specialist advice.
3Investigate deterioration or recrudescent fever for bacterial pneumonia, myocarditis, encephalitis or antiviral resistance, particularly in immunocompromised patients.

03COVID-19Match treatment to oxygen and eligibilityConfirmed or strongly suspected COVID-19 requiring clinical treatment.

1Give systemic corticosteroid when supplemental oxygen is required because of COVID-19, unless contraindicated; do not use it for non-hypoxic COVID alone.
2Check current NICE criteria, timing and interactions for antiviral therapy and for tocilizumab, sarilumab or baricitinib in hospitalised inflammatory disease.
3Use standard thromboprophylaxis and organ-support pathways unless contraindicated, while investigating sudden deterioration for pulmonary embolism or secondary infection.

04CoinfectionAdd antibiotics only with evidenceFocal signs, purulence, new consolidation, bacteraemia or deterioration suggests bacterial infection.

1Obtain appropriate cultures and use the current CAP or HAP regimen according to acquisition, severity and resistance risk.
2Reassess at 48 hours and stop or narrow antibacterials when bacterial infection is unsupported; viral PCR positivity does not exclude genuine coinfection.
3Consider post-influenza staphylococcal necrotising pneumonia when shock, haemoptysis, leucopenia or cavitation appears and seek urgent microbiology input.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

First-line antiviral for most people with influenza who meet UKHSA treatment criteria, including most pregnant patients.

Oseltamivir

A typical adult treatment course is 75 mg orally twice daily for 5 days; severe or immunocompromised cases and renal impairment require current UKHSA/BNF adjustment.

Start promptly and do not delay for testing in severe suspected influenza. Adjust for renal function; persistent infection in immunocompromise may need resistance testing and specialist duration.

Reduces mortality in hospitalised patients who need oxygen because of COVID-19.

Dexamethasone for hypoxic COVID-19

6 mg orally or IV once daily for up to 10 days, stopping earlier at discharge, when COVID-19 causes a need for supplemental oxygen.

Do not use solely for COVID-19 without oxygen requirement. Monitor glucose, delirium, secondary infection and gastrointestinal risk; consider pregnancy and existing steroid therapy.

Immunomodulation for selected adults receiving systemic corticosteroids who need supplemental oxygen or mechanical ventilation.

Tocilizumab for eligible COVID-19

Use the current NICE weight-based single IV dose only after same-day eligibility, infection and laboratory checks in a specialist hospital pathway.

Exclude uncontrolled non-COVID infection and review neutrophils, platelets, liver tests and bowel-perforation risk. National criteria and supply arrangements can change.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Acute respiratory distress syndrome

Diffuse alveolar and endothelial injury may produce severe non-cardiogenic oedema, shunt and prolonged ventilation, with severity determined by its extent and the patient's underlying reserve.

Bacterial superinfection

Damaged epithelium and altered immunity permit secondary pneumonia, sepsis, empyema or necrotising infection, particularly when baseline cardiopulmonary reserve is limited.

Thromboembolism

Inflammation, endothelial activation and immobility increase venous and arterial thrombotic events in severe illness, particularly when baseline cardiopulmonary reserve is limited.

Cardiac injury

Systemic stress, myocarditis, ischaemia and arrhythmia can complicate severe viral infection, with severity determined by its extent and the patient's underlying reserve.

Persistent post-viral illness

Breathlessness, fatigue, cognitive symptoms and reduced exercise capacity may continue after acute infection through multiple biological and functional mechanisms.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Trend oxygen delivery, saturation, work of breathing, respiratory rate, haemodynamics and mental state; record the direction of travel rather than one observation.
Monitor renal and liver function for antiviral dosing and inflammatory or drug toxicity; check glucose during corticosteroid therapy.
Repeat microbiological assessment when an immunocompromised patient has persistent viral replication or clinical failure and discuss resistance testing with UKHSA specialists.
Reassess daily for bacterial or fungal coinfection and stop unnecessary antibacterials rather than continuing because CRP remains elevated.
Apply current discharge, isolation and occupational advice from the relevant UK nation and local infection-prevention team.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Timing differs by virus

Influenza antivirals are most effective early but remain indicated in severe or at-risk illness under UKHSA guidance; COVID therapies each have their own timing and severity window.

Steroids are indication-specific

Dexamethasone helps hypoxic COVID-19 but is not routine influenza treatment and can harm when given to non-hypoxic COVID without another indication.

A positive PCR is not the whole diagnosis

Detection may coexist with oedema, embolism or bacterial pneumonia; in prolonged immunocompromised shedding it may not explain every new deterioration.

A negative nose swab can miss the lung

Sampling timing and compartment matter, especially in severe lower-airway disease after transplant; discuss lower-respiratory testing rather than declaring the virus excluded.

Seasonal guidance is live

Resistance patterns, circulation thresholds and commissioned drugs change. A regimen copied from last winter is not a safe substitute for the current UKHSA document.

11Common pitfallsFrequent interpretation and management errors.

01
Giving dexamethasone for uncomplicated COVID-19 without an oxygen requirement.
02
Withholding influenza antivirals from a severely ill patient because symptoms began more than 48 hours ago.
03
Using a viral diagnosis to dismiss new focal bacterial consolidation or shock.
04
Starting antibiotics automatically for every viral pneumonitis without evidence of bacterial coinfection.
05
Failing to recheck current national eligibility and interaction guidance before prescribing COVID therapeutics.