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Pulmonary Disease in HIV-Infected Patients 

Pulmonary Disease in HIV-Infected Patients
Pulmonary Disease in HIV-Infected Patients

Emily Shuman

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date: 20 May 2022

  1. A. Introduction. Despite widespread use of antiretroviral therapy, pulmonary disease remains a significant cause of morbidity and mortality among patients with HIV infection. One way to approach respiratory complaints in HIV-infected patients is to:

    1. a. Consider the organisms that can cause disease based on the patient’s CD4 count (see Chapter 55).

    2. b. Narrow the list of possible diagnoses by considering the appearance of the chest radiograph (Table 56.1). Remember: these patterns are not mutually exclusive, and each pattern can be caused by many disorders. When it comes to HIV disease, there are few absolute truths—use Table 56.1 as a starting point and modify it based on your clinical experience.

      Table 56.1 Radiographic Patterns in HIV-Associated Pulmonary Disease

      Radiographic Pattern

      Common Causes


      Pneumocystis jirovecii pneumonia (PCP)

      Diffuse interstitial infiltrates


      Disseminated fungal infection


      Kaposi’s sarcoma*

      Congestive heart failure (CHF)

      Viral and atypical pneumonia

      Focal consolidation

      Bacterial pneumonia

      Kaposi sarcoma


      Pleural effusion


      Bacterial pneumonia

      Kaposi’s sarcomaTuberculosis


      Disseminated fungal infection

      * Usually patchy infiltrates.

    3. c. Further narrow the list based on the clinical picture, laboratory data, and results of diagnostic testing.

  2. B. Differential Diagnosis of Pulmonary Infiltrates in HIV

    1. a. Bacterial. Despite an immunocompromised state, bacterial pathogens remain the most likely cause of pneumonia in HIV-infected patients. Pneumonia due to Streptococcus pneumoniae occurs frequently. Remember that Haemophilus influenzae, gram-negative bacilli (including Pseudomonas, particularly in late-stage HIV), Legionella species, and Nocardia can also present as pulmonary disease.

    2. b. Mycobacterial. Tuberculosis and nontuberculous mycobacteria such as Mycobacterium kansasii are not uncommon. Mycobacterium avium complex frequently colonizes sputum but is rarely a pathogen unless CD4 counts fall below 50 cells/µL.

    3. c. Fungal. Cryptococcosis, histoplasmosis, and aspergillosis may each present with pulmonary manifestations in HIV-infected patients.

    4. d. Viral. The respiratory viruses, including influenza, adenovirus, and respiratory syncytial virus, must be remembered. Compared to culture techniques, a nasal swab for polymerase chain reaction (PCR) testing can provide rapid evidence of infection.

    5. e. Pneumocystis jirovecii. See the next section, C.

    6. f. Noninfectious. Both lymphoma and Kaposi’s sarcoma can cause or present with pulmonary disease.

  3. C. Approach to the HIV-Infected Patient with Possible PCP. Whenever a patient with HIV disease presents with respiratory complaints, the diagnosis of Pneumocystis jirovecii pneumonia (PCP) should always be considered because P. jirovecii is an extremely common pathogen.

    1. a. The following questions are important to ask when considering PCP as a possible diagnosis:

      1. i. What is the CD4 count? The CD4 count is indicative of risk for PCP: patients with CD4 counts >200 cells/µL are at much lower risk for PCP than those with counts below 200 cells/µL.

      2. ii. Is the patient receiving PCP prophylaxis? Patients taking trimethoprim-sulfamethoxazole (TMP-SMX) or dapsone are less likely to develop PCP pneumonia.

      3. iii. What is the clinical scenario? Patients with PCP usually present with a subacute onset of shortness of breath (especially on exertion) that is associated with fever, fatigue, weight loss, and a dry cough. Community-acquired pneumonia, on the other hand, usually presents with the acute onset of a productive cough, fever, and evidence of consolidation on lung examination.

      4. iv. Does the physical examination reveal evidence of a different disorder (e.g., tuberculosis, lymphoma, or Kaposi’s sarcoma)?

      5. v. Does the chest radiograph reveal diffuse interstitial infiltrates? Diffuse interstitial infiltrates are the classic radiographic finding in PCP pneumonia; patients may, however, present with minimal changes or atypical findings (e.g., pleural effusions, pneumothorax).

        Hot Key

        The radiographic appearance of the lung fields often looks much worse than predicted by auscultation in patients with PCP; however, a normal chest radiograph does not exclude PCP.

      6. vi. What is the patient’s alveolar-to-arterial (A-a) gradient? The blood gas report allows definition of the degree of hypoxemia as well as evaluation for the necessity of steroid therapy in patients with PCP. (Patients with an A-a gradient >35 usually benefit when treated with corticosteroids.)

        Hot Key

        Oxygen saturation monitoring can be very useful in patients with suspected PCP. Patients who exhibit dramatic desaturation on ambulation may have PCP.

      7. vii. Is the sputum purulent? Finding P. jirovecii organisms is extremely difficult in purulent sputum. On the other hand, culturing sputum for routine pathogens and acid-fast bacillus (AFB) organisms may be diagnostic.

      8. viii. Is the serum lactate dehydrogenase (LDH) elevated? Elevation of serum LDH levels is a common finding in patients with PCP pneumonia. Conversely, a rise in LDH is uncommon in bacterial pneumonia.

    2. b. There are many ways to evaluate patients for the possibility of PCP. The algorithm in Figure 56.1 is our suggested approach. However, it may be modified based on the sensitivity and specificity of the various tests available at your institution.

      Figure 56.1 Algorithm for the assessment of patients with suspected Pneumocystis jirovecii pneumonia (PCP). A-a gradient = alveolar-to-arterial gradient; CXR = chest radiograph.

      Figure 56.1 Algorithm for the assessment of patients with suspected Pneumocystis jirovecii pneumonia (PCP). A-a gradient = alveolar-to-arterial gradient; CXR = chest radiograph.

    3. c. Treatment. First-line therapy for PCP in nonallergic patients is intravenous TMP-SMX, 5 mg/kg every 8 hours. If the A-a gradient is ≥35, corticosteroids (e.g., prednisone) should be added to this treatment regimen. The usual dose is 40 mg twice daily for 5 days followed by 40 mg once daily for 5 days, then a taper to zero over the ensuing 11 days. Treatment of PCP should be continued for 21 days or longer, depending on response. Patients may be switched to oral therapy after they defervesce and are no longer hypoxic on ambulation at room air. Stable, reliable patients who are not initially hypoxic may receive their entire course of therapy orally. TMP-SMX DS (160 mg/80 mg), two tablets orally three times per day, is recommended. Options for TMP-SMX–intolerant patients include intravenous pentamidine, dapsone plus trimethoprim, or clindamycin plus primaquine.

Suggested Further Readings

Maximous S, Huang L, Morris A. Evaluation and diagnosis of HIV-associated lung disease. Semin Respir Crit Care Med 2016;37:199–213.Find this resource:

Montales MT, Chaudhury A, Beebe A, Patil S, Patil N. HIV-associated TB syndemic: a growing clinical challenge worldwide. Front Pub Health 2015;3.Find this resource:

Wang RJ, Miller RF, Huang L. Approach to fungal infections in human immunodeficiency virus–infected individuals: pneumocystis and beyond. Clin Chest Med 2017;38:465–77.Find this resource: