• Bronchiectasis is Found in Patients of All Ages, Genders, and Ethnic Groups
    • However, Older Adults are More Commonly Affected than Younger Age Groups


  • Females are More Commonly Affected than Males in North America

Association with Chronic Obstructive Pulmonary Disease (COPD) (see Chronic Obstructive Pulmonary Disease)

  • Patients with Moderate-Severe COPD Have an Increased Risk of Bronchiectasis (Chest, 2011) [MEDLINE]
  • These Patients Have Severe Airflow Obstruction, Isolation of a Pathogenic Organism from Sputum, and at Least One Hospital Admission for an Exacerbation in the Prior Year
  • These Patients Also Have an Increased Mortality Rate (Hazard Ratio: 2.54) (Am J Respir Crit Care Med, 2013) [MEDLINE]


General Comments

Relative Prevalence of Specific Etiologies

  • Post-Infectious Bronchiectasis Cases are Uncommon in the United States (Except in Native Americans in Alaska), But are Common in Underdeveloped Countries
  • Approximately 25-30% of Bronchiectasis Cases Can Be Traced to a Prior Pulmonary Infection


  • Over 50% of All Bronchiectasis Cases are Idiopathic


Hypogammaglobulinemia (see Hypogammaglobulinemia)

  • Agammaglobulinemia (see Agammaglobulinemia)
    • Autosomal Recessive Agammaglobulinemia: severe hypogammaglobulinemia, antibody deficiency, and increased susceptibility to infection
    • X-Linked Agammaglobulinemia (Bruton Agammaglobulinemia): severe hypogammaglobulinemia, antibody deficiency, and increased susceptibility to infection
      • Most cases do not present prior to 6 mo of age
  • Ataxia-Telangiectasia (see xxx)
  • B-Cell Lymphoma (see Lymphoma): due to increased catabolism of immunoglobulins
  • Biallelic Deficiency of Mismatch Repair Protein PMS2
  • Common Variable Immunodeficiency (CVID) (see Common Variable Immunodeficiency): most cases do not present until the third or fourth decade of life
  • Drug-Related Hypogammaglobulinemia: these cases probably occur in specific predisposed individuals
    • Captopril (see Captopril): may cause IgA deficiency
    • Carbamazepine (Tegretol) (see Carbamazepine): may cause IgA deficiency or reversible hypogammaglobulinemia
    • Chlorpromazine (Thorazine) (see Chlorpromazine): may cause IgA deficiency
    • Hydroxychloroquine (Plaquenil) (see Hydroxychloroquine): may cause IgA deficiency
    • Lamotrigine (Lamictal) (see Lamotrigine): may cause reversible hypogammaglobulinemia
    • Penicillamine (see Penicillamine): may cause IgA deficiency
    • Phenytoin (Dilantin) (see Phenytoin): may cause IgA deficiency or reversible hypogammaglobulinemia
    • Ramipril (Altace) (see Ramipril): may cause hypogammaglobulinemia
    • Sulfasalazine (see Sulfasalazine): may cause IgA deficiency
    • Valproic Acid (Depakote, Depakene) (see Valproic Acid): may cause IgA deficiency
  • Good Syndrome (Immunodeficiency with Thymoma) (see Thymoma)
    • Physiology: B-cell immunodeficiency syndrome
    • Clinical
  • Hyper-IgM Syndrome
    • CD40 Ligand (CD40L or CD154) Deficiency: this X-linked disorder is the etiology of most cases of Hyper-IgM syndrome
    • CD40 Deficiency
    • Activation-Induced Cytidine Deaminase (AID) Deficiency
    • Uracil-Nucleoside-Glycosylase (UNG) Deficiency
  • Immunodeficiency–Centromeric Instability–Facial Anomalies (ICF) Syndrome: normal B-cell counts with agammaglobulinemia
  • Jacobsen Syndrome (Hemizygous Deletion of Part of the Long Arm of Chromosome 11)
  • Immunosuppression
    • Autologous Hematopoietic Stem Cell (HSCT) (Bone Marrow Transplant, BMT) (see Hematopoietic Stem Cell Transplant)
    • Azathioprine (Imuran) (see Azathioprine)
    • Belimumab (Benlysta) (See Belimumab): anti-B cell monoclonal antibody
    • Chemotherapy
    • Corticosteroids (see Corticosteroids)
      • Patients taking ≥12.5 mg prednisone for at least 1 year are at increased risk of hypogammaglobulinemia
      • Patients with hypogammaglobulinemia due to corticosteroid usually retain specific antibody responses: therefore, they are not usually candidates for immunoglobulin replacement therapy
    • Gold (see Gold)
    • Mycophenolate Mofetil (Cellcept) (see Mycophenolate Mofetil): may cause hypogammaglobulinemia
    • Rituximab (Rituxan) (see Rituximab)
    • Tyrosine Kinase Inhibitors
  • Isolated IgA Deficiency (see Isolated IgA Deficiency): few reported cases of bronchiectasis (although these were probably due to undetected IgG deficiencies): most common primary immunodeficiency syndrome (occurs in 1:600 persons)
  • Lymphoproliferative Malignancy
    • Chronic Lymphocytic Leukemia (CLL) (see Chronic Lymphocytic Leukemia): commonly associated with hypogammaglobulinemia and infection
    • Multiple Myeloma (see Multiple Myeloma): antibody deficiency with normal total IgG levels (due to contribution of the paraprotein to the total IgG level and due to tumor cells altering normal regulatory T cells, impairing B-cell maturation)
  • Myelodysplastic Syndrome (see Myelodysplastic Syndrome)
  • Myotonic Dystrophy: increased catabolism of immunoglobulins
  • Nephrotic Syndrome (see Nephrotic Syndrome)
  • Prematurity in Infants: premature infants delivered before the third trimester usually lack adequate maternal immunoglobulin and may also more rapid metabolize the IgG that they have received
  • Protein-Losing Enteropathy: intestinal lymphangiectasia, etc
    • Diagnosis
      • IgG levels are typically affected more than IgM or IgA levels (however, the levels of IgG, IgM, and IgA may all be decreased in severe protein-losing enteropathy)
      • Hypoalbuminemia (see Hypoalbuminemia)
    • Clinical
      • Edema: usually
  • Selective IgG Subclass Deficiency (see Selective IgG Subclass Deficiency): decrease in one or more of the four classes of IgG with normal total IgG is most common type associated with bronchiectasis
  • Severe Burns (see Burns): increased catabolism of immunoglobulins
  • Severe Combined Immunodeficiency (SCID) (see Severe Combined Immunodeficiency)
    • Epidemiology: xxx
  • Specific Antibody Deficiency (SAD)/Specific Polysaccharide Antibody Deficiency (SPAD) (see Specific Antibody Deficiency): poor serological response to polysaccharide antigens (with normal levels of immunoglobulins and IgG subclasses) and normal responses to protein antigens
  • Steinert’s Disease
  • Transcobalamine Deficiency
  • Trisomy 18
  • Wiskott-Aldrich Syndrome



  • Adenovirus-Type 7 (see Adenovirus)
  • Allergic Bronchopulmonary Aspergillosis (ABPA) (see Allergic Bronchopulmonary Aspergillosis)
    • Allergic Bronchopulmonary Aspergillosis Typically Produces Upper Lobe Bronchiectasis (Mainly Apical and Posterior Segments)
  • Influenza Virus (see Influenza Virus)
    • Studies Have Shown Transient Nasal Epithelial Ciliary Loss and Dynein Arm Abnormalities in Children During Viral Upper Respiratory Infection (Influenza, Parainfluenza, etc)
  • Measles Virus (see Measles Virus)
  • Mycobacterium Avium Complex (MAC) (see Mycobacterium Avium Complex)
  • Mycobacterium Tuberculosis (see Tuberculosis)
    • Epidemiology
      • Bronchiectasis May Occur Following Primary Tuberculosis or Reactivation Tuberculosis
    • Diagnosis
      • Tuberculosis Typically Produces Upper Lobe Bronchiectasis (mainly in the Apical and Posterior Segments)
  • Necrotizing Pneumonia and Pulmonary Gangrene (see Necrotizing Pneumonia and Pulmonary Gangrene)
  • Pertussis (see Pertussis)
  • Recurrent Aspiration Pneumonia (see Aspiration Pneumonia)
    • Physiology
      • Bronchiectasis in Association with Recurrent Aspiration Pneumonia Probably Results from Combined Injury from Infection and Gastric Acid

Inhalation Injury

  • Ammonia Inhalation (see Ammonia)
  • Sulfur Mustard Gas Inhalation (see Sulfur Mustard Gas)
  • Smoke Inhalation (see Smoke Inhalation)
  • Recurrent Aspiration Pneumonia (see Aspiration Pneumonia)
    • Physiology
      • Bronchiectasis in Association with Recurrent Aspiration Pneumonia Probably Results from Combined Injury from Infection and Gastric Acid



Bronchiectasis Involves the Destruction of Muscular and Elastic Components of Medium-Sized Bronchial Walls by Mediators Released by Neutrophils (Elastase) and Monocytes (Cytokines), Resulting in >2 mm Dilatation of Medium-Sized Bronchi

Specific Role of Infection in the Pathogenesis of Bronchiectasis

Reversibility of Bronchiectasis

Location of Bronchiectasis

Pathologic Classification (Reid)

General Comments



Arterial Blood Gas (ABG) (see Arterial Blood Gas)


Sputum Gram Stain and Culture (see Sputum Culture)

Classic 3-Layered Sputum

Sputum Culture

Pulmonary Function Tests (PFT’s) (see Pulmonary Function Tests)

General Comments


Bronchoscopy (see Bronchoscopy)

General Comments


Chest X-Ray (CXR) (see Chest X-Ray)

General Comments


Chest Computed Tomography (Chest CT) (see Chest Computed Tomography)

General Comments


High-Resolution Chest Computed Tomography (HRCT) (see High-Resolution Chest CT)

General Comments




General Comments

Serum Alpha-1 Antitrypsin (A1AT) (see Serum Alpha-1 Antitrypsin)

General Comments

Immunoglobulin Levels (see xxxx)

General Comments

Sweat Chloride Test (see Sweat Chloride Test)

General Comments

Electron Microscopic Exam of Sperm or Respiratory Epithelium (Via Nasal Biopsy)

General Comments

Clinical Manifestations

Cardiovascular Manifestations

Cardiovascular Events (Arrhythmias, Ischemia, Congestive Heart Failure, etc)

Otolaryngologic Manifestations

Recurrent/Chronic Rhinosinusitis

Pulmonary Manifestations

Chronic Hypoxemic, Hypercapnic Respiratory Failure (see Respiratory Failure)

Cough with/without Sputum Production (see Cough): most common symptom

Dyspnea (see Dyspnea)

Empyema (see Pleural Effusion-Parapneumonic)

Hemoptysis (see Hemoptysis)

Lung Abcess (see Lung Abscess)

Pneumothorax (see Pneumothorax)

Pulmonary Hypertension/Cor Pulmonale (see Pulmonary Hypertension)

Rales/Rhonchi (see Pulmonary Physical Exam)

Recurrent Pneumonia (see Community-Acquired Pneumonia)

Wheezing (see Wheezing)

Rheumatologic Manifestations

Clubbing (see Clubbing)

Other Manifestations

Amyloidosis (see Amyloidosis)

Brain Abscess (see Brain Abscess)

Fever (see Fever)

Generalized Weakness

Weight Loss (see Weight Loss)



Prompt Removal of Foreign Bodies in Airway


Treatment of Hemoptysis

Intravenous Immunoglobulin (IVIG) (see Intravenous Immunoglobulin)

Postural Drainage

Chest Physical Therapy (PT) (see Chest Physical Therapy)






Clinical Efficacy


Clinical Utility

Fluoroquinolones (see Fluoroquinolones)

Gentamicin (Nebulized) (see Gentamicin)

Tobramycin (Tobi) (see Tobramycin)

Macrolides (see Macrolides)

Penicillins (see Penicillins)

Tetracyclines (see Tetracyclines)

Sulfamethoxazole-Trimethoprim (Bactrim, Septra) (see Sulfamethoxazole-Trimethoprim)

Other Treatments


Inhaled Indomethacin (see Indomethacin)


Oxygen Therapy (see Oxygen)


Prognosis of Bronchiectasis was Previously Poor in the Pre-Antibiotic Era