22.2 Bacterial Infections of the Respiratory Tract

Bacterial Pathogens and Diseases of the Respiratory Tract

Bacterial respiratory infections target the upper and lower airways, ranging from localized throat infections to life-threatening lung disease. Understanding how each pathogen colonizes, invades, and evades host defenses helps explain why these infections present differently and require different treatment approaches.

Key Pathogens of Respiratory Infections

Strep Throat

Strep throat is caused by Streptococcus pyogenes (Group A Streptococcus), which invades the pharynx and tonsils. Symptoms include severe sore throat, high fever, swollen cervical lymph nodes, and white patches or streaks of pus on the tonsils. A rapid antigen detection test (RADT) or throat culture confirms the diagnosis.

Treatment is a course of penicillin or amoxicillin. Completing the full antibiotic course is critical not just to clear the infection, but to prevent serious post-infectious complications like rheumatic fever (which can damage heart valves) and post-streptococcal glomerulonephritis (kidney inflammation).

Pneumonia

Several bacterial species commonly cause pneumonia, with Streptococcus pneumoniae being the most frequent in community-acquired cases. Other common causes include Haemophilus influenzae, Staphylococcus aureus, and Klebsiella pneumoniae. These bacteria infect the lower respiratory tract, filling alveoli with fluid and inflammatory cells (a process called consolidation).

Symptoms include productive cough with purulent mucus, pleuritic chest pain, high fever, dyspnea, and fatigue. Treatment depends on the causative organism but typically involves antibiotics such as amoxicillin, azithromycin, or fluoroquinolones, along with supportive care (oxygen therapy, IV fluids) for severe cases.

Tuberculosis (TB)

Mycobacterium tuberculosis is a slow-growing, acid-fast bacterium that primarily affects the lungs but can disseminate to other organs (miliary TB). Most people exposed to M. tuberculosis develop latent TB, where the immune system walls off the bacteria in granulomas without causing symptoms. Only about 5–10% of latently infected individuals progress to active TB disease.

Active TB symptoms include chronic cough lasting more than 3 weeks, fever, drenching night sweats, unintended weight loss, and hemoptysis (coughing up blood). Treatment requires a multi-drug regimen taken for 6–9 months. The standard first-line combination is:

• Isoniazid (INH)
• Rifampin (RIF)
• Pyrazinamide (PZA)
• Ethambutol (EMB)

Multiple drugs are used simultaneously to prevent the emergence of drug-resistant strains. Multi-drug resistant TB (MDR-TB) is a growing global concern.

Bacterial Colonization of the Respiratory Tract

Adherence and Colonization

Bacteria use surface proteins called adhesins to bind specific receptors on respiratory epithelial cells. Without this initial attachment, the mucociliary escalator would sweep them out. The M protein of S. pyogenes mediates adherence to pharyngeal cells, while the pili of S. pneumoniae help it attach to lung epithelium.

Invasion and Spread

Once attached, some pathogens invade epithelial cells or penetrate into subepithelial tissues to cause deeper infection. S. pneumoniae produces pneumolysin, a pore-forming toxin that lyses host cell membranes, destroying tissue and allowing the bacteria to spread into surrounding areas.

Evasion of Host Defenses

Respiratory pathogens have evolved multiple strategies to dodge the immune system:

• Polysaccharide capsules surround the cell wall of S. pneumoniae and H. influenzae, making them slippery targets that resist phagocytosis. The capsule is the major virulence factor for S. pneumoniae, and the pneumococcal vaccine targets capsular polysaccharide antigens.
• M. tuberculosis survives inside macrophages by preventing phagosome-lysosome fusion. The very cells meant to destroy it become its hiding place.

Induction of Host Inflammatory Responses

Bacterial cell wall components like lipoteichoic acid (Gram-positive bacteria) and lipopolysaccharide (Gram-negative bacteria) trigger production of inflammatory cytokines by host immune cells. While inflammation is meant to fight infection, excessive inflammation causes collateral damage: fluid accumulation in the alveoli, tissue destruction, and many of the symptoms patients actually experience (fever, pain, difficulty breathing).

Host Defense Mechanisms and Bacterial Countermeasures

• Mucociliary clearance is the respiratory tract's first line of defense. Goblet cells produce mucus that traps inhaled pathogens, and ciliated epithelial cells beat in coordinated waves to push the mucus (and trapped bacteria) up toward the throat for swallowing or expulsion.
• Alveolar macrophages patrol the alveoli and phagocytose bacteria that reach the lower airways. If macrophages are overwhelmed, they recruit neutrophils and trigger a larger inflammatory response.
• Biofilms are structured bacterial communities encased in a self-produced matrix. Some respiratory pathogens, including H. influenzae and S. pneumoniae, form biofilms on airway surfaces. Biofilm bacteria are significantly more resistant to both immune clearance and antibiotic penetration than free-floating (planktonic) cells.
• Antibiotic resistance complicates treatment of respiratory infections. Resistance mechanisms include beta-lactamase production (which breaks down penicillin-class drugs), altered penicillin-binding proteins, and efflux pumps that expel antibiotics from the bacterial cell.

Diagnostics for Respiratory Pathogens

Culture Methods

Bacterial culture remains the gold standard for identifying the causative pathogen. The general process:

1. Collect a clinical specimen (sputum, bronchoalveolar lavage fluid, or pleural fluid)
2. Inoculate the sample onto selective and differential media
3. Incubate and identify colonies based on morphology, Gram stain, and biochemical tests
4. Perform antibiotic susceptibility testing on the isolate to guide treatment

The main drawback is time. Standard cultures take 24–48 hours for most bacteria, and M. tuberculosis can take weeks to grow.

Serological Tests

Serological tests detect antibodies the patient's immune system has produced against specific bacterial antigens. They're especially useful when direct pathogen detection is difficult or when you need evidence of a recent or past infection.

• The anti-streptolysin O (ASO) test detects antibodies against streptolysin O toxin, confirming recent S. pyogenes infection. This is particularly helpful when diagnosing post-streptococcal complications like rheumatic fever.
• The tuberculin skin test (TST/Mantoux test) detects a delayed-type hypersensitivity response to M. tuberculosis antigens injected intradermally. A positive result indicates exposure but does not distinguish latent from active TB.

Molecular Techniques

Polymerase chain reaction (PCR) amplifies specific bacterial DNA sequences from clinical samples, offering rapid and highly sensitive detection.

• Multiplex PCR assays can detect multiple respiratory pathogens simultaneously (e.g., S. pneumoniae, H. influenzae, Moraxella catarrhalis) from a single sample.
• The GeneXpert MTB/RIF assay is a real-time PCR test that detects M. tuberculosis DNA and rifampin resistance mutations in sputum samples within approximately 2 hours. This is a major advancement over traditional TB culture, which can take weeks.

Molecular methods are faster and more sensitive than culture for many pathogens, though culture is still needed when you want a live isolate for full susceptibility testing.