Children with Lung Infection



Causal agent










Nodular or cavitary









Septic embolism











Local infiltrates

Bronchiolitis obliterans with organizing pneumonia

Diffuse alveolar bleeding


Pharmacological toxicity

Graft-versus-host disease

Post-transplantation lymphoproliferative disease

Radiotherapy toxicity

Pulmonary alveolar proteinosis

Diffuse infiltrates


Pharmacological toxicity engraftment syndrome

Early infiltrates

Pulmonary edema

Pulmonary embolism



Aspiration, acute respiratory distress syndrome


Late infiltrates





The spectrum of microorganisms is very wide, so it is very important to identify the causal agent. For this, we must take the following parameters into account:

  1. 1.

    The type of immunosuppression that the patient has.


  2. 2.

    The medical history, physical examination, epidemic status, clinical presentation, and speed at which the respiratory disorder has developed: acute, subacute, or chronic.


  3. 3.

    The timing of the appearance of the respiratory disorder relative to that of the base illness, transplantation, or immunosuppressive drug administration.


  4. 4.

    The preliminary results of general and specific examinations to establish the etiology.


  5. 5.

    The type of radiological infiltrate (diffuse, focal, nodular, cavitated) and the images obtained from computerized tomography (CT scanning), ultrasound scanning, or nuclear magnetic resonance imaging.


  6. 6.

    The drugs and treatments the patient has received, considering that some of them might favor immunosuppression and/or lung damage. The use of immunosuppressive treatments needs to be noted in patients with transplants, such as cyclosporin, steroids, mycophenolate, monoclonal antibodies, or antithymocyte globulins.


  7. 7.

    Chemotherapy drugs such as bleomycin, cyclophosphamide, and methotrexate can cause lung damage, while radiotherapy can cause myelosuppression and lung fibrosis.


Because of their base condition and chemotherapy/radiotherapy, oncological patients have periods of neutropenia and secondary cell immunodeficiency, with a higher risk of developing viral pneumonia due to respiratory syncytial virus (RSV), adenovirus, enterovirus, or varicella zoster; or mycotic pneumonia due to Aspergillus, P. jirovecii, Mucor, Rhizopus, or occasionally Candida. The possibility of pneumonia associated with M. tuberculosis—or, less often, Toxoplasma or Cryptococcus neoformans—must also be taken into account.

In patients who have undergone bone marrow or solid organ transplantation, lung complications will depend on the period of immunosuppression associated with the transplantation.

In general terms, lung infections occurring early after solid organ transplantation are linked to the surgery and invasive procedures performed in hospitalized patients. After the first month and up to 6 months afterward, the level of immunosuppression that is achieved favors infection by organisms that are dormant in the donor or the recipient, opportunistic infections, and infections acquired in the community. After 6 months the predominant infections are those contracted from both viral and bacterial communities (Fig. 25.1). It is important to bear in mind that the risks are higher in lung transplantation when acquired agents have tropisms for the respiratory tract.


Fig. 25.1

Timing of infections in solid organ transplant recipients

During the first 15 days after hemopoietic precursor transplantation, neutropenia and severe damage of the mucosa, due to chemotherapy, favor bacterial infections that can focus on the lung. At the following stage, after bone marrow grafting, CMV is one of the most common problems that can affect the lung, together with opportunistic filamentous fungal infections. At the third stage, 3 months after the transplantation, the cell response and humoral response remain weak, and infections due to encapsulated bacteria, filamentous bacteria, and opportunistic bacteria are frequent (Fig. 25.2).


Fig. 25.2

Timing of infections in hematopoietic precursor transplant recipients

Patients with common variable immune deficiency and agammaglobulinemia present recurrent bacterial pneumonia, normally produced by encapsulated germs; they are rarely present in pneumonia caused by P. jirovecii. Children with T cell immunodeficiency, serious combined immunodeficiencies, etc., have a higher risk of contracting the same type of opportunistic diseases as patients with acquired immunodeficiency syndrome (AIDS), as well as recurrent and persistent infections caused by Candida albicans in the mucosa or the skin. Patients with chronic granulomatous disease suffer lung infections caused by Aspergillus or Staphylococcus aureus—agents that require effective phagocytosis for their destruction. Children with primary immunodeficiency always present severe lung complications: bronchiectasis, empyema, lung abscesses, etc.

In patients with AIDS, there is a long list of associated lung infections, including those caused by P. jirovecii, CMV, Epstein–Barr virus, and mycobacteria, both typical and atypical. These are detailed in the corresponding chapter.

The most frequent etiologies for severe pneumonia according to the type of immunosuppression are listed in Table 25.2.

Table 25.2

Immunosuppression and infectious etiology

Type of immunosuppression

Mechanisms compromised

Favored organisms

Common causes


Engulfment of bacteria and fungi by mononuclear cells (monocytes and macrophages) and polymorphonuclear cells (neutrophils)

Antigen presentation

Staphylococcus aureus, bacilli, Gram-negative aerobes (Pseudomonas aeruginosa, Klebsiella pneumoniae, Escherichia coli), Candida spp., Aspergillus spp.

Neutropenia (leukemia, bone marrow suppression due to chemotherapy)

Chronic granulomatous diseases


Hyper-IgE (Job syndrome)

Humoral immunity

B lymphocytes



Complement activation

Extracellular encapsulated bacteria: Streptococcus pneumoniae, Haemophilus influenzae, Staphylococcus aureus

Primary: agammaglobulinemia, IgA deficiency, IgM deficiency

Secondary: myeloma, Waldenström macroglobulinemia, lymphocyte leukemia


Mediation of opsonization

Attraction of inflammatory cells

Elimination of microorganisms through damage to their membranes

C3-C5: encapsulated bacteria

C5–C9: Neisseria gonorrhoeae, Neisseria meningitidis

C3–C5: encapsulated bacteria

C5–C9: Neisseria gonorrhoeae, Neisseria meningitidis

Cellular immunity

T lymphocytes

Killing of pathogen-infected cells by cytotoxic T (CD8) cells

Macrophage activation by Th1 (CD4) cells

B lymphocytes activation by Th2 (CD4) cells to produce antibodies

Mycobacterium tuberculosis, Mycobacterium avium-c, Nocardia asteroides, Legionella spp., Cryptococcus neoformans, Histoplasma capsulatum, Coccidioides immitis, varicella zoster, herpes simplex, Cytomegalovirus, Epstein–Barr virus, Pneumocystis jirovecii, Toxoplasma gondii


Secondary: malnutrition, lymphoma, leukemia, old age, drugs, AIDS



Blood filtration

Production of bacteria-specific antibodies

Removal of bacteria covered in antibodies

Encapsulated bacteria

Thrombotic thrombocytopenic purpura, Hodgkin lymphoma

AIDS acquired immunodeficiency syndrome, IgA immunoglobulin A, IgE immunoglobulin E, IgM immunoglobulin M, Th1 type 1 helper T cell, Th2 type 2 helper T cell

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Nov 7, 2020 | Posted by in Uncategorized | Comments Off on Children with Lung Infection
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