Chest

Question 1

Nocardia infection (Nocardiosis):

Answer 1

• Nocardia is an aerobic gram positive bacteria found in soil that cause opportunistic infection
• Infections typically occur through inhalation or direct contact with contaminated material. Nocardia infections can affect various organs in the body, and the severity of the infection can range from mild to severe.
• Nocardia can also be seen in underlying pulmonary disease such as silicosis, pulmonary fibrosis, emphysema, alveolar proteinosis

Manifestations:
* Respiratory Infections: secondary to inhalation of the bacteria → pneumonia, lung abscesses (cavitating lesions). Immunocompromised pts more susceptible.
* Cutaneous Infections: Nocardia can also cause skin and soft tissue infections via direct contact with contaminated soil → cellulitis, skin abscesses
* Disseminated Infections: More common in immunocompromised individuals, infections can disseminate to other organs. This can involve the brain, kidneys, joints, and other organs.

Immunocompromised Individuals: People with weakened immune systems, such as those with HIV/AIDS, organ transplant recipients, or individuals receiving immunosuppressive therapy, are at higher risk of developing severe nocardiosis.

**Treatment: **The choice of antibiotics for treating Nocardia infections depends on the specific species of Nocardia, usually trimethoprim

Question 2

Pulmonary actinomycosis

Answer 2

Pulmonary infection of Actinomyces species, which are anaerobic bacteria normally found in the oral cavity, gastrointestinal tract, and female genital tract.
Pulmonary actinomycosis typically occurs when there is an alteration in the integrity of the respiratory mucosa, allowing these bacteria to invade and cause infection.

• Pulmonary actinomycosis most commonly seen with alcoholic men.
• Other risk factors include
• aspiration
• cigarette smoking
• COPD
• DM
• poor oral hygiene
• periodontal disease.

Clinical Presentation:
* Non-specific symptoms, and the clinical course can be slow and insidious.
* Common symptoms include cough, sputum production, chest pain, weight loss, and fatigue

Treatment: prolonged courses of antibiotics; several weeks to months, drainage of abscesses

It’s important to note that pulmonary actinomycosis can mimic other lung diseases, both clinically and radiologically.

Question 3

Allergic Bronchopulmonary Aspergillosis (ABPA):

Answer 3

• Allergic hyperimmune response to fungus aspergillus fumigatus which grows within the lumen of the bronchi, without invasion. The hypersensitivity initially causes bronchospasm and bronchial wall oedema, which is IgE-mediated. Ultimately, there is bronchial wall damage with loss of muscle and bronchial wall cartilage resulting in bronchiectasis (typically central bronchiectasis)
• Classified as an eosinophilic lung disease
• Leads to development of bronchiectasis
• Often occurs in patients with asthma or CF
• Dx: Eosinophilia, High serum IgE, serum Abs to aspergillus on bloods, and intense airway inflammation with eosinophils and formation of mucus plugs which play a primary role in the development of bronchiectasis.
• Colonisation. Fungal hyphae seen on special stains within the mucoinflammatory contents of the dilated segmental bronchi
• Imaging features: bronchiectasis. Mucous plugging, transient or chronic airspace infiltrates (usually due to atelectasis)
• Tx: Corticosteroids are commonly used to reduce inflammation. Antifungal medications, such as itraconazole, may be considered in some cases.
• Allergic bronchopulmonary aspergillosis (ABPA) is classified as a type I (immediate) and type III (delayed or immune complex-mediated) hypersensitivity reaction. It involves an exaggerated immune response to the fungus Aspergillus, particularly to its spores (conidia), which leads to inflammation and allergic manifestations in the respiratory system.
• Type I Hypersensitivity (Immediate Reaction):
• Inhaled Aspergillus spores (conidia) are recognized by the immune system as foreign antigens.
• This recognition stimulates the production of immunoglobulin E (IgE) antibodies against Aspergillus.
• The IgE antibodies attach to mast cells and basophils in the respiratory mucosa.
• Upon subsequent exposure to Aspergillus antigens, the IgE antibodies on the mast cells and basophils bind to the antigens, triggering the release of inflammatory mediators such as histamine.
• Histamine and other mediators cause bronchoconstriction, mucus production, and inflammation, leading to symptoms like wheezing, coughing, and difficulty breathing.
• Type III Hypersensitivity (Immune Complex-Mediated Reaction):
• Chronic exposure to Aspergillus antigens leads to the formation of immune complexes in the lungs.
• These immune complexes deposit in the walls of small blood vessels and airways.
• Activation of the complement system and recruitment of inflammatory cells contribute to tissue damage and inflammation.
• Over time, these processes can lead to bronchiectasis (damage to the airways) and other structural changes in the lungs.

A clinical staging system has been developed:
* stage I: acute
* stage II: remission
* stage III: recurrent exacerbation
* stage IV: steroid-dependent asthma
* stage V: pulmonary fibrosis