Pneumonia
Influenza
Pneumonia Prevention
Pneumonia Management
OMT & Review
100

Describe the signs, symptoms, and sequelae of viral pneumonia

Signs and symptoms: progressively worsening fever, chills, headache, myalgias, non-productive cough, and dyspnea

Sequelae:

  1. Viral infections predispose secondary bacterial infections through impairment of host immune response and disruption of epithelial barrier integrity, leading to more severe clinical manifestations and increased risk of respiratory failure

  2. Severe cases may require mechanical ventilation and intensive care

  3. Cooperative interplay between viruses and bacteria results in worse outcomes than either infection alone

100

Identify common pathogens, bacterial and viral, for pneumonia.

  1. Viral:

    1. Respiratory syncytial virus (RSV)

    2. Rhinovirus

    3. Influenza A and B

    4. Parainfluenza viruses

    5. Human metapneumovirus

    6. Adenovirus

    7. Coronaviruses

  2. Bacterial:

    1. Streptococcus pneumoniae (most common)

    2. Haemophilus influenzae

    3. Methicillin-susceptible and methicillin-resistant Staphylococcus aureus

    4. Moraxella catarrhalis

100

Outline prevention of viral pneumonia.

  1. Vaccination: recommended against influenza, COVID-19, and Streptococcus pneumoniae

  2. Prophylactic Antiviral Medications: Neuraminidase inhibitors (oseltamivir, zanamivir) can prevent influenza A and B infections when used prophylactically; particularly valuable during outbreaks or for high-risk individuals with known exposures

  3. Infection Control: symptom screening, surveillance testing, transmission-based precautions, universal masking during high transmission periods, adequate ventilation, and vaccination of healthcare personnel

  4. Behavioral Modifications: smoking cessation and limiting excessive alcohol consumption

100

Justify the confirmation and identification of the influenza strain in a public health surveillance program.

Essential for vaccine strain selection, monitoring viral evolution, detecting novel or pandemic threats, and guiding antiviral resistance surveillance

Strain identification enables detection of antigenic drift and emergence of novel variants that may evade existing immunity

100

Outline OMT treatment for the PE findings.

Rib raising:

  1. Can be performed as a multitude of modalities: LVMA (springing), articulatory (ART), soft tissue (ST), myofascial (MFR), lymphatic

  2. Indications: Viscerosomatic (SNS) SD, visceral, improving respiration, rib SD

MFR of the thoracoabdominal diaphragm: Compress to palpate to the layer of the bone and surrounding myofascium anteriorly and posteriorly; utilize the lower costal cage as a lever to move the diaphragm

200

Describe the epidemiology and risk factors of viral pneumonia.

Epidemiology:

  1. Significant cause of community-acquired pneumonia, accounting for 1/3 of cases in adults and up to 66% in hospitalized children, with the highest burden in young children (especially those under 2 years) and older adults

  2. Outpatients and younger adults are more likely to have viral infections, while patients requiring intensive care are more likely to have bacterial etiologies

  3. Viral etiologies account for up to 80% of pneumonia cases in children younger than 2 years, but proportion decreases substantially in older children

  4. Co-infections with multiple viruses occur in 2-33% of pediatric cases

  5. Seasonal patterns are characteristic:

    1. RSV epidemics occur in late autumn every 1-2 years

    2. Rhinovirus peaks in autumn and spring

    3. Influenza predominates in late autumn-early winter

  6. Risk factors:

    1. Age extremes represent the highest risk: infants under 2 years and elderly patients

    2. Immunocompromised hosts: susceptible to more severe disease from community-acquired viral pathogens

    3. The elderly and patients with cancer experience high mortality rates

200

Compare and contrast influenza type A and B.

  1. Influenza A:

    1. Infects multiple species: humans, birds, pigs, and other mammals

    2. Classified into subtypes based on hemagglutinin (HA) and neuraminidase (NA) surface proteins

      1. Current circulating human subtypes: A(H1N1)pdm09 and A(H3N2)

    3. Undergoes both antigenic drift (gradual mutations) and antigenic shift (reassortment creating novel subtypes; responsible for pandemics)

  2. Influenza B:

    1. Primarily infect only humans (lacks the zoonotic reservoir that gives influenza A its pandemic potential)

    2. Divided into two lineages: B/Victoria and B/Yamagata

    3. Undergoes only antigenic drift, causing epidemics every 2-4 years but not pandemics

    4. Demonstrates superior HA activation by a broader panel of proteases; HA shows pronounced adaptation to the cooler temperature (33°C) and mildly acidic pH of human upper airways

    5. Accounts for approximately 25% of the annual influenza disease burden, though this proportion varies by season

  3. Both have clinical presentations that are remarkably similar and generally indistinguishable

    1. Cause acute respiratory illness with fever, cough, myalgia, and headache, with similar duration of illness across age groups

200

Describe the differences between active and inactivated vaccine administration.

  1. Live attenuated vaccine: contain weakened pathogens that undergo limited replication; induce an immune response similar to natural infection and are typically effective after a single dose with longer-lasting protection; elicit both local mucosal immunity (IgA) and systemic responses, including cellular immunity

    1. Contraindicated in immunosuppressed patients due to the risk of serious infections from attenuated organisms

    2. ex) Measles-mumps-rubella (MMR) and Varicella vaccines

    3. Live attenuated influenza vaccine is administered intranasally

  2. Inactivated vaccine: contain non-viable pathogens that cannot replicate; produced by growing pathogens in culture and inactivating them using heat or chemicals; cannot replicate; require multiple doses because the first dose typically primes rather than protects, with protective immunity developing after the second or third dose; protection wanes over time, necessitating periodic booster doses; primarily induce systemic antibody responses (predominantly IgG)

    1. mRNA, adenoviral vector, recombinant, toxoid, and polysaccharide vaccines

    2. Inactivated influenza vaccine is administered intramuscularly

200

Explore antivirals and antibiotics that can be given to a patient that is allergic to penicillin.

  1. Doxycycline is recommended as the first-line alternative

  2. Respiratory fluoroquinolones (levofloxacin or moxifloxacin) are another option but should be reserved for patients with no alternative treatment options

  3. Carbapenems and aztreonam

  4. Non-beta-lactam alternatives: macrolides, quinolones, sulfonamides, vancomycin, and clindamycin

    1. Carry significant risks

  5. Antiviral medications do not cross-react with penicillins and are safe to use in penicillin-allergic patients

200

Identify the top three most common bacterial and viral pathogens that cause acute otitis media in children.

Bacterial: Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis

Viral: Respiratory Syncytial Virus (RSV), Adenovirus, and Influenza viruses

300

Relate the physical exam findings to pathogenesis of viral pneumonia.

  1. Fever: results from systemic inflammatory response triggered by viral infection; viral invasion of the respiratory epithelium activates cytokine release (including interleukin-1 and tumor necrosis factor), which acts on the hypothalamic thermoregulatory center to elevate body temperature

    1. Inflammatory response is typically less pronounced than in bacterial pneumonia, with viral pneumonia often presenting with fever less than 101.3°F

  2. Tachycardia: compensatory response to fever (increasing metabolic demands) and hypoxemia; cardiovascular system increases heart rate to maintain oxygen delivery to tissues when oxygen saturation is compromised

  3. Low oxygen saturation: diffuse alveolar damage with intraalveolar edema, fibrin deposition, inflammatory cell infiltrates, and interstitial inflammation; disrupts normal gas exchange across the alveolar-capillary membrane, resulting in ventilation-perfusion mismatch and hypoxemia

  4. Use of accessory muscles with tachypnea: compensatory effort to maintain adequate ventilation despite impaired gas exchange

  5. Warm and moist skin: peripheral vasodilation associated with fever and increased metabolic state as the body attempts to dissipate excess heat

  6. Abdominal diaphragm bilateral somatic dysfunction in exhalation: viscerosomatic reflexes; inflammatory process in the lungs creates afferent neural signals that can cause diaphragmatic dysfunction due to the increased work of breathing and altered respiratory mechanics

  7. T1-6 bilateral TART changes: viscerosomatic reflexes; inflammatory process in the lungs creates afferent neural signals that can cause reflex muscle spasm and tissue texture changes in the corresponding spinal segments (T1-T6 for upper and mid-lung fields)

300

Outline the features, mode of transmission, and epidemiology for influenza A (H3N2).

Features: Orthomyxovirus, (-) ssRNA, segmented (negative- sense single- stranded RNA), enveloped, linear, helical capsid

Mode of Transmission: Direct person-to-person contact and respiratory droplets

Epidemiology: Most prevalent in winter months; Influenza A (most common) causes world-wide pandemics

300

Discuss potential benefits and limitations of oseltamivir.

  1. Potential benefits:

    1. Symptom reduction: in adults with confirmed influenza, reduces time to first alleviation of symptoms by 16.8 hours), shortening illness from approximately 7 days to 6.3 days; in otherwise healthy children, oseltamivir reduces symptom duration by 29 hours, though it shows no effect in asthmatic children

    2. Prophylaxis: reduces the risk of symptomatic influenza by 3.05% in individuals and by 13.6% in household contacts

  2. Potential limitations:

    1. Gastrointestinal adverse effects: significantly increases nausea and vomiting in adults

    2. Neuropsychiatric events: increase in psychiatric adverse events (delirium and abnormal behavior) during prophylaxis

    3. Limited impact on serious outcomes: evidence for reducing clinically significant complications is limited due to lack of standardized diagnostic definitions and rarity of events

    4. Timing considerations: guidelines traditionally recommend initiation within 48 hours of symptom onset

300

Discuss the complications of concomitant or secondary bacterial pneumonia infection.

  1. Viral infections predispose to bacterial superinfection through multifactorial immune dysregulation

    1. Influenza and other respiratory viruses induce microbiome alterations ("dysbiosis") in both respiratory and gastrointestinal tracts, which disrupts normal host defense and enhances proliferation of pathogenic bacterial species

    2. Immune dysfunction includes suppressed TNFα signaling and reduced expression of innate and adaptive immunity genes

    3. Viral infections directly disrupt epithelial barriers while simultaneously modifying infected cells to enhance bacterial adherence and invasion

  2. Significantly worsens pneumonia severity and outcomes

  3. Failure of debris clearance, inflammation attenuation, and tissue repair pathways can lead to persistent pulmonary sequelae including fibrosis, emphysema, bronchiectasis, and pneumatoceles

300

Characterize Staphylococcus aureus, including structure, physiology, epidemiology, and mode of transmission

Structure/Physiology: Gram + cocci, Clustered, Facultative anaerobe, Catalase +, Coagulase +, Protein A surface protein, Capsule

Epidemiology: Normal human flora on skin and mucosal surfaces

Risk factors: presence of foreign body (catheter, suture), previous surgical procedure, and use of antibiotics that suppresses normal micrbiofloura

Mode of transmission: Person-to-person spread through direct contact or exposure to contaminated fomites, although most infections are with patient's own organisms

400

Diagram and relate the pathogenesis and pathophysiology to the natural history of influenza.

  1. Viral:

    1. Inhaled droplets transmit the virus, which uses Hemagglutinin (HA) to bind to sialic acid receptors on respiratory epithelial cells, entering via endocytosis

    2. Inside the cell, low pH in the endosome triggers membrane fusion

    3. Virus uncoats, releasing its RNA genome into the nucleus for replication and transcription

    4. New virions assemble, budding from the cell membrane, with Neuraminidase (NA) cleaving sialic acid to prevent clumping and allow spread to new cells

    5. Viral replication and the subsequent host immune response (cytokines, cell death/apoptosis) destroy infected epithelial cells, causing inflammation and tissue damage in the airways and alveoli

    6. Host immune response determines disease severity:

      1. In most cases, a balanced innate immune response triggers cellular immunity and recovery through adaptive immune responses; resolution by day 8 in healthy adults

      2. Dysregulated immune responses can lead to cytokine storms, particularly with elevated IL-6, IL-8, and other proinflammatory mediators, resulting in acute lung injury, ARDS, and multiorgan failure

  2. Bacterial: typically occurs within the first 6 days of influenza infection, during periods of high viral shedding; common bacteria include Streptococcus pneumoniae and Haemophilus influenzae

    1. Influenza virus damages the respiratory lining, creating easy entry points for bacteria

    2. Inflammation increases mucus, hindering mucus clearance and trapping bacteria

    3. Viral infection compromises immune cells (neutrophil and macrophage function) and triggers excessive inflammation, creating a permissive environment for bacterial growth and severe tissue damage

400

Explain the virulence factors and pathogenesis for influenza A (H3N2).

Virulence Factors:

Hemagglutinin (H): binds to the monosaccharide sialic acid (present on the surface of its target cells) and facilitates the entry of the viral genome into the target cells by causing the fusion of host endosomal membrane with the viral membrane

Neuraminidase (N): cleaves neuraminic acid from glycoproteins (enables virus to be released from the infected host cell)

M2 protein (proton channel): activated by low pH environment

Antigenic drifts: minor changes in H and N due to random mutation; vary from year to year

Antigenic shift: segmented genome allows for high rates of ressortment when 2 viruses infected same cell; forms new virus


Pathogenesis:

Hemagglutinin (HA) binds to sialic acid receptors on respiratory epithelial cells, entering via endocytosis 

Inside the cell, low pH in the endosome triggers membrane fusion

Virus uncoats, releasing its RNA genome into the nucleus for replication and transcription

New virions assemble, budding from the cell membrane, with Neuraminidase (NA) cleaving sialic acid to prevent clumping and allow spread to new cells 

Viral replication and the subsequent host immune response (cytokines, cell death/apoptosis) destroy infected pithelial cells, causing inflammation and tissue damage in the airways and alveoli

400

Drug chart (spectrum, mechanism of action, resistance, indications, drug interactions, adverse effects/contraindications, ADME) oral oseltamivir.

Drug name & subclass: Neuraminidase Inhibitor (Oseltamivir, zanamivir)

Spectrum: Influenza A and B

Mechanism of Action: Inhibits influenza virus neuraminidase, which cleaves the budding viral progeny from its cellular envelope attachment point (neuraminic acid) just prior to release

Resistance: Hemagglutinin or Neuraminidase mutations; H1N1 is 100% resistant world wide

Drug Interactions: Serotonergic drugs (selective serotonin reuptake inhibitor antidepressants)

Adverse effects/Contraindications: Nausea, abdominal discomfort, emesis, neuropsychiatric events (prophylaxis)

A: oral or IV (prodrug); GI absorption

D: 80% bioavailable

M: liver

E: renal

400

Justify completing a course of antibiotics.

Antibiotics are generally not justified for completing a full course in viral pneumonia unless there is clinical suspicion or evidence of bacterial coinfection

Risks of completing antibiotic courses in viral pneumonia: Clostridioides difficile colitis, organ damage, arrhythmias, drug-drug interactions, allergic reactions, microbiome disruption, and selection for antimicrobial resistance

If bacterial coinfection cannot be definitively excluded and antibiotics were started empirically, a 5-day course represents the minimum recommended duration for community-acquired pneumonia in patients showing clinical improvement, though this may be unnecessary if viral etiology is confirmed without bacterial evidence

400

Characterize Streptococcus pyogenes, including structure, physiology, epidemiology, and mode of transmission.

Structure/Physiology: Gram + cocci, arranged in long chains, Facultative anaerobe, A antigen, M protein

Epidemiology: Typically affects children 2-5 years, patients with soft-tissue infection, and patients with prior streptococcal pharyngitis or soft-tissue infection

Mode of transmission: Transient colonization in upper resp tract and skin surface; Person-to-person spread by resp droplets and through breaks in skin after direct contact with infected person, fomite, or arthropod vector

500

Discuss and justify the expected findings of pneumonia from laboratory tests including: chest x-ray, CBC w/ differential, serum procalcitonin and lactate, sputum cultures, blood cultures, rapid influenza diagnostic test (RIDT), and RT-PCR.

Chest x-ray: bilateral patchy interstitial infiltrates

  1. Bacterial pneumonia typically shows alveolar (lobar) infiltrates

  2. Viral pneumonia more commonly presents with interstitial infiltrates

CBC with Differential: Elevated white blood cell count

Serum procalcitonin and lactate: low/normal procalcitonin (0.07 ng/mL) and low/normal lactate (0.8 mmol/L)

  1. Elevated procalcitonin levels (>0.5 μg/L) suggest bacterial pneumonia

  2. Low procalcitonin levels (<0.1 ng/mL) suggest viral pneumonia

  3. Elevated lactate indicates tissue hypoperfusion and severe disease with organ dysfunction; not specific for pneumonia etiology

    1. Elevation reflects severity rather than causative pathogen

Sputum cultures: collecting a deep cough sample into a sterile container, which is sent to a lab to identify the specific pathogen causing the infection by growing them on a special medium

  1. Gram stain and culture of sputum should be obtained for hospitalized patients

  2. Allows identification of typical bacterial pathogens (Streptococcus pneumoniae, Haemophilus influenzae)

Blood cultures: draw blood, ideally before antibiotics, and placing it in special bottles (aerobic/anaerobic) for lab incubation to grow bacteria; helps identify the germ causing the infection and determines the best antibiotic

Rapid influenza diagnostic test (RIDT) for types A & B: quick, point-of-care tests that detect influenza A and B viral proteins (antigens) in respiratory samples; provide results in under 30 minutes but are less sensitive than molecular tests like PCR

RT-PCR: converting an RNA template into complementary DNA (cDNA) and then using polymerase chain reaction (PCR) to amplify the DNA for detection or analysis; widely used for gene expression analysis and diagnosing RNA viruses; superior sensitivity and specificity

  1. RNA Extraction: RNA is isolated and purified from a biological sample

  2. Reverse Transcription (RT): purified single-stranded RNA (ssRNA) is a fragile template and cannot be amplified by standard PCR; reverse transcriptase is added to synthesize a stable, double-stranded complementary DNA (cDNA) molecule from the RNA template

  3. Polymerase Chain Reaction (PCR) Amplification: newly created cDNA is rapidly copied through a series of temperature cycles

    1. Denaturation: mixture is heated to separate the double-stranded cDNA into single strands

    2. Annealing: mixture is cooled, allowing short DNA fragments called primers to bind (anneal) to specific target sequences on the single strands

    3. Elongation/Extension: DNA polymerase enzyme adds nucleotides to the primers, synthesizing a new, complementary DNA strand for each template

  4. Detection and Analysis: process is repeated for many cycles (typically 35-40), exponentially increasing the amount of target DNA copies

500

Outline the diagnosis, prevention/treatment, and evolutionary history for influenza A (H3N2).

Diagnosis:

Rapid influenza diagnostic tests (RIDTs): detects parts of viral antigens that stimulate an immune response; results in 10-15 min. but not as accurate as other flu tests

Rapid molecular assays (NAAT): detects genetic material of the flu virus; results in 15-20 min. and are more accurate than RIDTs

Reverse transcription polymerase chain reaction (RT-PCR)

Viral culture

Immunofluorescence assays


Prevention

Seasonal flu vaccines are formulated to protect against influenza viruses known to cause epidemics, including: A(H1N1) virus, A(H3N2) virus, B/Victoria lineage virus, influenza B/Yamagata lineage virus

Nasal spray vaccine uses live, temperature- sensitive mutant viruses that replicate in the nose (not the lungs)


Treatment

Zanamivir (inhaled) or Oseltamivir (oral) inhibit influenza virus neuraminidase; only demonstrate efficacy when given within the first 48 hours


Evolutionary History:

Natural reservoir: aquatic birds
Diversified to infect multiple host species, including humans

Influenza A and B viruses diverged approximately 4,000 years ago, while influenza A virus diverged from influenza C virus around 8,000 years ago

Wild aquatic birds maintain all 16 hemagglutinin (H1-16) and 9 neuraminidase (N1-9) subtypes that are enzootic in avian species

In humans, only a limited number of subtypes (H1, H2, H3 with N1, N2) have successfully established sustained transmission

20th century witnessed three major pandemics: the 1918 H1N1, 1957 H2N2, and 1968 H3N2 viruses

Viruses evolve through antigenic drift

500

Outline vaccine chart for influenza (type, indications, contraindications, adverse effects, surveillance and reporting).

Type: 

Egg-based inactivated influenza vaccines (IIV4s): traditional vaccines produced in eggs

Cell culture-based inactivated influenza vaccine (ccIIV4): produced in cell culture rather than eggs

Recombinant influenza vaccine (RIV4): produced using recombinant technology without eggs

Live attenuated influenza vaccine (LAIV4): intranasal spray containing weakened live virus


Indications:

Optimal timing: September or October

Routine annual influenza vaccination for all persons aged ≥6 months who do not have contraindications

LAIV: non-pregnant individuals aged 2-49 years without chronic medical conditions


Contraindications:

History of severe allergic reaction (anaphylaxis) to any vaccine component or previous dose

LAIV:

Concomitant aspirin or salicylate therapy in children/adolescents

Children 2-4 years with asthma/ wheezing history (past 12 months)

Immunocompromised patients

Close contacts of severely immunosuppressed patients

Pregnancy

Active CSF leak or communication between CSF and oropharynx/nasopharynx

Cochlear implants

Recent influenza antiviral use


Adverse Effects:

IIV: injection site reactions including pain, redness, swelling, fever, muscle aches, headache, and fatigue

LAIV: in children, runny nose, wheezing, headache, vomiting, and muscle aches; in adults, runny nose, headache, sore throat, and cough

Serious effects: Guillain-Barré syndrome (GBS) and Anaphylaxis


Surveillance/Reporting:

VAERS: passive surveillance system that collects spontaneous reports of adverse events following vaccination

VSD: provides active surveillance through analysis of large linked databases from healthcare organizations

State and local health departments should be consulted regarding reporting of influenza outbreaks and influenza-related pediatric deaths

500

Drug chart (spectrum, mechanism of action, resistance, indications, drug interactions, adverse effects/contraindications, ADME) Empiric IV levofloxacin.

Spectrum: Broad spectrum (gram negative, atypical, pseudomonas)

Mechanism of Action: Bactericidal; inhibition of topoisomerase II and IV (DNA gyrase)

Resistance: Modification of enzymes

Drug Interactions: Divalent cations (Ca, Fe, Mg) interfere with absorption

Adverse Effects: Tendonitis/tendon rupture, Peripheral neuropathy, CNS issues (impaired memory and attention), Q-T prolongation/ arrhythmia

Contraindication: pregnancy

A: highly bioavailable (but can be IV)

D: widely distributed (can get into CNS)

M: hepatic metabolism

E: renal excretion

500

Explain the pathogenesis of Moraxella catarrhalis and its ability to cause acute otitis media.

Nasopharyngeal Colonization: M. catarrhalis is a common, human-restricted commensal bacterium found in the upper respiratory tract

Viral Trigger: preceding viral upper respiratory tract infection (URI) causes inflammation; leads to swelling and congestion of the Eustachian tubes, which impairs their normal function of drainage and pressure regulation

Adherence: Outer membrane proteins (OMPs), such as the Ubiquitous Surface Proteins (UspA1 and UspA2), facilitate the bacterium's binding to host epithelial cells

Bacterial Migration: Eustachian tube dysfunction creates negative pressure in the middle ear, leading to the aspiration or migration of nasopharyngeal secretions containing M. catarrhalis into the middle ear cavity

Infection and Inflammation: once in the middle ear, the bacteria proliferate and induce a strong local inflammatory response, leading to the accumulation of fluid (middle ear effusion), pressure buildup, and pain

Antibiotic Resistance: M. catarrhalis produce beta-lactamase enzymes, which inactivate common antibiotics like ampicillin and amoxicillin

M
e
n
u