LIP has an incidence of 16–50 % in children with HIV, commonly at the age of 2–3 years. Currently, it is believed that LIP in children with HIV infection is caused by the immunological responses. Most studies indicate that the proliferating lymphocytes in HIV infected patients are CD8 or cytotoxic/inhibited T lymphocytes. These cells cause immunological impairments via different ways, including T cells activation caused by immunological identification of antigens, production of lymphokines by CD4 lymphocytes such as interleukin-2 and proliferation of effector cells responsible for tissue lesions caused by lymphokines that is mainly CD8 cells in HIV/AIDS. Currently, the following three factors are believed to be related to the pathogenesis of HIV/AIDS. (1) HIV infection causes proliferation of lymphocytes in the body. The lung lesions can be relieved by using the Zidovudine therapy. HIV antigens and antibodies can be found in the bronchoalveolar lavage fluid of LIP patients. (2) HIV and EB virus synergetic infection: Most children with LIP have concurrent EBV infection. Otherwise, EB virus genome can be found that causes lymphatic tissue hyperplasia in lungs of HIV positive children. EB virus infection is transmitted via contacts, with LIP patients as its susceptible population. (3) The immunogenetics basis: It has been demonstrated that more HLA-DR6 can be found in HIV positive patients, with occurrence of CD8 lymphocytosis syndrome and LIP. Generally, the factors of immunological nonspecific stimulation, HIV specific stimulation or EB virus infection and HIV infection contribute to the onset of LIP in HIV positive patients.

Gross lung specimen demonstrates diffuse thickening of the pulmonary interstitium. Microscopy demonstrates mass liked mixed cells infiltration in the septa of pulmonary lobes, alveolar wall, bronchus, bronchioles and perivascular tissues, which is mainly mature lymphocytes and occasionally generative center with no nucleus cleavage. Lymphatic follicle with generative center is common. There are hyperplasia of type II alveolar epithelium, and increased macrophages in the alveolar cavity.

The onset is chronic, with symptoms of cough, dyspnea and hypoxia. Lung auscultation may be negative or may find weakened respiration sound, wheezing and end-inspiratory dry rales. Most of the children patients have bronchospasm, with no cough before demonstration of lesions by chest X-ray. The patients with long term illness course have clubbing fingers/toes and parotid/lymphaden enlargement. The pulmonary functions impaired children have serious hypoxia which causes oxygen dependency. Due to the decrease of lymphocytes and CD4 T cell count, the critical cases with lift threatening conditions are rare, but the patients are more susceptible to opportunistic infections.

Clinical manifestations in pediatric AIDS patients include cough, dyspnea and hypoxia, which have a slowly progressive course. The occurrence of lymphocytosis and hyperglobulinemia with no other isolated pathogens in combination with chest diagnostic imaging findings can define the clinical diagnosis. Based on the findings of bronchoalveolar lavage fluid examination and lung biopsy, the definitive diagnosis can be made.

AIDS children are susceptible to bacterial pneumonia, which is related to their immune deficiency. B cell dysfunction leads to decreased production of antigen specific antibody, T cell functional impairment and neutrocytopenia, which, in combination with intravenous drug use and other factors, result in their susceptibility to various bacteria. Currently, the reported pathogenic bacteria include streptococcus pneumonia, hemophilus influenza, pseudomonas, staphylococcus aureus and legionella.

By microscopic observation, pneumonia caused by streptococcus pneumonia has lesions in different sizes with small spots and flakes of focal inflammation. The lesions are more serious in the inferior lobes and dorsal segment of both lungs. The lesions are in dark red and slightly protrude in the section that is smooth with no particle. In the young children, fusion of multiple small lesions is common, and sometimes even involves the whole lung lobe. Under a microscope, at the center and peripheral areas of the lesions, there are inflammatory bronchi and the lesions are filled with neutrophilic granulocyte as well as lytic and shed epithelial cells. The surrounding alveoli are initially filled with exudates containing abundant proteins, followed by occurrence of neutrophilic granulocyte, erythrocytes as well as shed and enlarged alveolar epithelial cells. The cellulose is rarely found. In the advanced stage of pneumonia, the exudates are commonly transformed into purulent fluid.

By the naked eyes observation, staphylococcus aureus pneumonia has coverage of the pleural surface by a thick layer of fibrinous purulent secretions, protruding grayish yellow or yellowish parenchymal changes under the pleura, extensive hemorrhagic necrosis and multiple small abscesses in the lungs. Once the subpleural small abscesses rupture, pyothorax or pneumopyothorax occurs, sometimes with involved bronchi to form bronchopleural fistula. Microscopic observation demonstrates alveoli filled with bloody edema, occasionally macrophages and small quantity neutrophils. There are also large quantities of Staphylococcus aureus and necrotic tissue debris in the abscess, bronchial lumen filled with pyocyte, seriously damaged mucosa, collapsed parenchymal changes on the cross section to form most abscesses.

The involvement of lungs in HIV positive patients has non-specific symptoms and signs. The clinical manifestations include cough, fever and shortness of breath. The symptoms are obvious, being more acute and serious than those in adult patients. Fever and shortness of breath are especially common in HIV/AIDS children. Its further progression may cause bacteremia and sepsis. By physical examinations, there are tachypnea, tachycardia, pulmonary dry and moist rales and pulmonary parenchymal changes.

Chest X-ray demonstrates pneumococcus pneumonia as high density blurry shadows in the lungs fields, commonly with concurrent pleural effusion or pyothorax. Sometimes nodular lesions and clubbed lesions can also be found at the base of lungs. CT scanning demonstrates thickened bronchial wall and bronchiectasis.

Chest X-ray and CT scanning demonstrate legionella pneumonia as involvement of singular or multiple lung lobes, with a rapid progression. Cavities and empyema are common. Interstitial infiltration may also occur.

Chest X-ray and CT scanning demonstrate bronchogenic staphylococcus aureus pneumonia as multiple small patches of high density shadows in the middle zone of both lungs, with blurry boundary and accompanying transparent areas, which are lesions of focal obstructive emphysema. Dynamic observation of the intrapulmonary lesions demonstrates that the lesions can progress from patches of parenchymal changes into extensive large flakes or segments of lesions within several hours or 1 day. Round or oval shaped low density air sacs occur within 1–2 days after the onset. The rapid progression demonstrated by the diagnostic imaging is characteristic. Sometimes, pulmonary cavities containing gas–liquid level can be found. Pleural effusion, empyema, and pyopneumothorax are also common. By chest X-ray, the secondary blood-borne staphylococcus aureus pneumonia is demonstrated to have patches or spherical high density shadows in middle and lower fields of both lungs.

Pulmonary infection in AIDS children should be firstly differentiated from PCP, which is the most common pulmonary opportunistic infection in AIDS children. Therefore the sputum specimen should be conventionally stained. In combination with the clinical manifestations and imaging findings, differential diagnosis can be made. However, complications of various bacterial infections occur in AIDS children with PCP, which should be paid focused attention. Meanwhile, it should also be differentiated from pulmonary tuberculosis. The clinical manifestations, results of PPD test and the findings of pathogenic examinations should be integrated for the differential diagnosis.

Pneumocystis carinii belongs to the fungus, with lungs as its most common target of invasion. In immunocompetent people, it can be clear out of the body by concurrent actions of cellular immunity and activated macrophages. In AIDS patients, due to their decreased CD4 T cell count and compromised immunity, its clearance ability against Pneumocystis carinii is also decreasing, which enables them to multiply in a large quantity in the alveoli to obstruct the capillaries. Thereafter, large quantity of foamy substances exudates from the alveolar cavity, together with inflammatory cells infiltration and pulmonary interstitial fibrous tissue proliferation, causes a serious of clinical manifestations and X-ray demonstrations.

By the naked eyes observation, the lung tissue has parenchymal changes. In some serious cases, the lungs are swelling and enlarged, with increased weight. The lungs are solid like the liver, in brown, with increased resistance during dissections. The float and sink test demonstrates positive findings. Microscopy demonstrates interstitial pneumonia and alveolar pneumonia, which are characterized by filling of pink foamy or honeycomb liked material in the dilated terminal bronchioles and in the alveolar cavities. The pink foamy or honeycomb liked material contains piles of worms and their disintegrated components; shed alveolar epithelial cells, lymphocytes, plasmocytes, eosinophils, histocytes or alveolar macrophages. There are also congestion and thickening of the pulmonary interstitium with accompanying infiltration of macrophages, lymphocytes and plasma cells. In the serious cases, the lung tissue has parenchymal changes, which are caused by large quantity proliferation of pneumocystis carinii in the alveoli. The infiltration is predominated by plasma cells in infants, and lymphocytes in children, with findings of macrophages and eosinophils.