key: cord-0035436-3gsq724l
authors: Li, Hongjun
title: HIV/AIDS Related Respiratory Diseases
date: 2013-09-30
journal: Radiology of HIV/AIDS
DOI: 10.1007/978-94-007-7823-8_17
sha: 0fd81cf41487d9b2a5991f5a7fe661dc2d72fa64
doc_id: 35436
cord_uid: 3gsq724l

Lungs are the most commonly involved organ by HIV/AIDS related diseases, and pulmonary infections are the main reasons for the increasing death rate from AIDS. Pathogens of HIV related pulmonary infections include parasites, fungi, mycobacteria, viruses, bacteria and toxoplasma gondii. According to international reports, pathogens have different geographical distribution, which is also closely related to the socioeconomic status of the region to produce varied AIDS related diseases spectra. For instance, in the United States, pneumocystis carnii pneumonia (PCP), tuberculosis and recurrent bacterial pneumonia (at least twice within 1 year) occur frequently in HIV infected patients. An international report published 10 years ago indicated that PCP is the most common and serious pulmonary opportunistic infections in HIV infected patients. Now its incidence has dropped with the application of antiretroviral treatment and preventive measures. PCP will continue to occur initially in patients who are aware of their HIV infection. In addition, HIV related viral and parasitic infections have been reported both domestically and internationally. In this section, the clinical manifestations and imaging findings of HIV related pulmonary infections are analyzed and discussed, which provide effective diagnosis basis, so as to reduce the incidence of HIV-related pulmonary infections.

Lungs are the most commonly involved organ by HIV/AIDS related diseases, and pulmonary infections are the main reasons for the increasing death rate from AIDS. Pathogens of HIV related pulmonary infections include parasites, fungi, mycobacteria, viruses, bacteria and toxoplasma gondii. According to international reports, pathogens have different geographical distribution, which is also closely related to the socioeconomic status of the region to produce varied AIDS related diseases spectra. For instance, in the United States, pneumocystis carnii pneumonia (PCP), tuberculosis and recurrent bacterial pneumonia (at least twice within 1 year) occur frequently in HIV infected patients. An international report published 10 years ago indicated that PCP is the most common and serious pulmonary opportunistic infections in HIV infected patients. Now its incidence has dropped with the application of antiretroviral treatment and preventive measures. PCP will continue to occur initially in patients who are aware of their HIV infection. In addition, HIV related viral and parasitic infections have been reported both domestically and internationally. In this section, the clinical manifestations and imaging fi ndings of HIV related pulmonary infections are analyzed and discussed, which provide effective diagnosis basis, so as to reduce the incidence of HIV-related pulmonary infections.

Pneumocystis has been believed to be a kind of protozoon. Recently, based on its ultrastructure and ribosomal RNA phylogenetic analysis, pneumocystis is now believed to be a kind of fungus, with high affi nity to the lung tissues. Due to the compromised immunity, 95 % AIDS patients sustain different types of pulmonary infections, of which PCP is the most common life-threatening opportunistic infection with an incidence rate of about 60-85 %. About 90-95 % patients suffering from AIDS complicated by PCP are adolescents and adults with their CD4 T cell counts being less than 200/ μl. Clinical manifestations of typical PCP are fever, cough (dry cough without phlegm), dyspnea, chest distress and shortness of breath. Dyspnea is shown as progressive difficulty in breathing, which initially occurs after physical activities and develops into diffi culty breathing even in resting state. PCP is commonly accompanied by weight loss, fatigue, anemia, general upset and lymphadenectasis. All these symptoms are non-specifi c, but patients often report subjective feelings of severe symptoms while physical signs are mild. By auscultation, the lungs are normal or with slightly dry, moist rales. These are the clinical fi ndings characteristic to AIDS complicated by PCP. In most patients with PCP, the serum LDH level increases but it is non-specifi c. In cases of AIDS complicated by PCP, the blood PO2 reduces, commonly being lower than 70 mmHg in patients in the middle and advanced stages. The diagnostic imaging for PCP includes chest X-ray and CT scanning. Due to the low resolution of chest X-ray, its demonstrations are negative for PCP patients in the early stage or only include thickened pulmonary markings and decreased pulmonary transparency. However, CT scanning demonstrates tiny lesions or more detailed changes in lungs. Especially with the application of HRCT, the detection rate of PCP lesions has been greatly improved. It has been internationally reported that nearly 10 % of PCP patients show negative fi ndings by the chest X-ray but with abnormal fi ndings by HRCT. Due to the rapid progression of PCP as well as its complex pathological changes, CT scanning demonstrations are diverse with specifi city. According to different pulmonary CT scanning demonstrations in different stages of the illness, PCP is divided into early stage (exudative and infi ltrative stage), middle stage (fusion and parenchymal stage) and advanced stage (absorption or fi brosis stage). The early typical manifestations include intrapulmonary multiple miliary nodules, mainly distributed in both middle and lower lung fi elds. It may be accompanied by enlarged hilar shadow, which should be differentiated from acute miliary tuberculosis.

The middle stage is a period of infi ltration. As the disease progresses, miliary and patchy shadows fuse and expand into a dense infi ltrative shadow with even density, showing a diffuse ground glass liked change. The typical manifestations include bilaterally symmetric foci with the hilus as the center. The foci infi ltrates from the hilus to bilateral pulmonary interstitium, progressing from the both middle lungs to both lower lungs. HRCT can more clearly demonstrate the foci, showing a map liked or gravel road liked appearance, with clearly demonstration of gas containing bronchus penetrating the foci. The pulmonary apex is involved later. The exterior stripe of the lung fi eld has increased transparency, showing typical willow leaf sign or moon bow sign which is the manifestation of compensatory pulmonary emphysema.

During the late compensatory repair period, the intrapulmonary lesions are mainly parenchymal changes and fi brosis, with large fl aky high density shadows as well as cords liked and reticular changes. Pneumothorax, mediastinal emphysema, pneumatocele, pleural effusion and other complications may occur, with an incidence of pneumatocele in about 10-20 % patients. The autopsy grossly demonstrates swelling of the lung tissue, and the alveoli are fi lled with large quantity foamy liquid. The pathological changes mainly manifested as interstitial pneumonia, with early manifestations of increased permeability of the capillary wall basement membrane in the alveolar walls, which leads to fl uid exudation. The Pneumocystis carinii proliferate in large quantity and adhere to cause degeneration of the type I alveolar epithelial cells and shedding of the basement membrane. Vascular congestion, edema as well as infi ltration of lymphocytes, plasma cells and mononuclear cells can be found in the pulmonary interstitium.

Due to the extensive existence of aspergillus in natural world, sputum smear positive often fails to defi ne its invasive infection. In the cases with aspergillus infection, hyphae can be found in the sputum. Fungal infections often occur in patients with CD4 T cell count below 100/μl, of which the most common pulmonary infection is aspergillus infection, followed by penicillium marneffei infection. Pulmonary infections caused by Candida albicans and histoplasma are rarely found. The incidence of cryptococcal pulmonary infection is still in a disagreement, which is increasing recently. There are also some common endemic fungal infections, such as the most commonly found fungal infections of AIDS complicated by penicillium infections in Guangxi Zhuang Autonomous Region and Hong Kong, China. Aspergillus has an extensive existence in the natural world. AIDS complicated by aspergillus infection is related to the application of corticosteroid hormone or broad-spectrum antibiotics, which occurs commonly in the advanced/critical stage of AIDS. The cases of pulmonary fungal infections, with fi ndings of hyphae (aspergillus or candida) or yeast in cytoplasm (Histoplasma capsulatum) in tissue sections and simultaneous fi ndings of histiocytic reactions including the infi ltration of neutrophilic granulocyte and the necrosis of histocytes, can be diagnosed as having invasive fungal infection.

Candida albicans is yeast liked fungus, which is widespread in the natural world. It can parasitize in the mocous of skin, oral cavity, intestinal tract and vagina of the human being. Candida albicans cannot cause disease in immunocompetent people but is pathogenic in immunocompromised population. After its invasion into the tissues, it turns into mycelia and multiplies in large quantity with great toxicity. It also has the ability to fi ght against phagocytosis. Clinically, its infection is characterized by a chronic onset and clinical symptoms of low and moderate grade fever but rarely high fever, cough, shortness of breath, cyanosis, irritation or dysphoria. The pulmonary signs include weakened breathing sounds by auscultation and obvious moist rales of lungs. The serious cases may have symptoms of systemic poisoning. The illness is prolonged and repeated during its whole progression. By diagnostic imaging demonstrations, it can be divided into the following types: (1) Bronchitis type, with chest X-ray demonstrations of increased pulmonary markings in lower fi elds of both lungs; (2) Pneumonia type, commonly with accompanying extrapulmonary lesions. The lesions are mainly located in the middle and lower lung fi elds and lesions in the lower lung fi eld are more common. The apex is generally not involved. The lesions are recurring one after another. A small number of patients may sustain complications of exudative pleurisy. (3) Disseminated type, with miliary shadows, diffuse nodular shadows or multiple small abscesses. The lesions often involve the middle and lower lungs. Chest X-ray demonstrates thickened pulmonary markings and accompanying spots, small fl akes and large fl akes of parenchyma shadows, in manifestations of bronchial pneumonia. In some serious cases, the foci may fuse together and enlarge to involve the entire lobe. CT scanning demonstrates pulmonary nodules and few have ground glass liked changes of the lungs. Pathological changes include acute infl ammatory lesions in the lungs, alveolar exudation and infi ltration of monocytes, lymphocytes and neutrophils. Acute disseminated lesions often cause multiple small abscesses, central caseous necrosis, spores and hyphae in and around the lesions.

Histoplasma capsulatum belongs to moniliales family, deuteromycetes class and fungal kingdom, whose growth requires organic nitrogen. It is often isolated from the soil with abundant contents of birds or bats faeces and spreads along with chickens, birds, dogs, cats, and mice. When the conidia and mycelial fragments of histoplasmosis are inhaled, most can be expelled by the defense mechanism of the human body. Granulomas may form, but in immunocompromised patients, it may cause disseminated histoplasmosis. When the CD4 T cell count in AIDS patients is less than 150/μl, histoplasma capsulatum infection of lungs may occur. Histoplasma capsulatum pneumonia has a higher incidence in South America, Africa and India. In the slight cases, the clinical manifestations are similar to symptoms of the cold, with low-grade fever, cough, and general upset. In the serious cases, there are symptoms of infl uenza, including chills, high fever, cough, chest pain, dyspnea, fatigue and poor appetite. In the cases of acute cavity, thin-walled cavity may form within a month. Complications may be pericarditis, arthritis, skin nodules, rash fi brous mediastinitis and mediastinal granuloma. Diagnostic imaging demonstrations are non-specifi c, with scattering pulmonary acinus exudation, multiple nodules in a diameter of about 3 mm with accompanying thickened septa, and formation of granulomas with accompanying calcifi cation. It should be differentiated from bacterial pneumonia, tuberculosis and other pulmonary fungal infections by laboratory tests to defi ne the diagnosis. The specifi city of the glycogen antigen detection of histoplasma capsulatum is up to 98 %.

Mucor spreads through the respiratory tract. It commonly invades the blood vessels, especially arteries. It reproduces locally or causes thrombosis and embolism. Clinical manifestations are high fever, cough, sputum, shortness of breath, chest distress, chest pain and hemoptysis (pulmonary artery involvement). The diagnostic imaging demonstrates fl akes infl ammatory foci, with manifestations of pulmonary cavity and pulmonary infarction. The pathological changes are hemorrhagic infarction of local tissue, pneumonia and exudation of neutrophils. Hemorrhagic infarction of local tissue may be related to hyphae induced minor arteries lesions.

It is estimated that one third of the world population was/is infected with tubercle bacillus and 9 % of them are AIDS patients. The WHO reported that there are 88,000 newly infected patients of TB each year and 8.4 % of them are caused by AIDS. It is estimated that each year in 1,000 HIV infected patients, 35-162 sustain active TB, and there is a great risk of active TB progressed from the latent tuberculosis infection. HIV infected patients with tuberculosis are commonly young and middle aged adults, with more male patients than female patients. Tuberculosis can occur at any stage of AIDS and at any level of CD4 T cell counts. It has been internationally reported that HIV infection complicated by TB has no specifi c imaging demonstrations. It has an acute onset, with an incidence of acute onset 2.5 times as high as that in non-HIV infected patients. The lesions are morphologically diverse, which are different from non-HIV infected patients with TB. HIV infection complicated by TB has commonly an acute onset, while TB in non-HIV infected patients is commonly secondary to other lesions, with cavities, fi brosis, pleural thickening and calcifi cation. A study conducted in China has demonstrated that for AIDS complicated by TB, the acute cases mainly have military and exudative lesions, with an incidence of 33 and 49 % respectively; while the incidence of chronic cases including cavity, fi brosis and calcifi cation is declining, being 11, 11 and 2 respectively. A later occurrence of tuberculosis in HIV infected patients indicates a more seriously immunocompromised immunity, with less typical clinical manifestations and imaging demonstrations. When the CD4 T cell count level is above 350-400/μl, the systemic symptoms are fever, chills, night sweating, fatigue, poor appetite and weight loss. Respiratory symptoms are cough, expectoration, hemoptysis, chest pain and dyspnea. It manifests as primary tuberculosis, with its foci distributing in the middle and lower lungs, involving multiple lobes and segments. When the CD4 T cell count decrease, the impact of TB increase including the occurrence of extrapulmonary tuberculosis and disseminated disease. When the CD4 T cell count drops below 200/μl, pulmonary tuberculosis manifests as acute onset (such as miliary tuberculosis) or extrapulmonary tuberculosis (such as ileocecal tuberculosis) and peripheral lymph nodes tuberculosis. Its difference from the clinical manifestations of non-HIV infected patients is as the following: (1) More common pulmonary infi ltration with multiple involvements and rare cavities; (2) Higher incidence of dissemination (87-96 %) commonly along with blood fl ow and higher incidence of extrapulmonary tuberculosis (60-70 %); (3) More common lymph node tuberculosis, such as hilar, mediastinal and extrapleural lymphadenectasis; (4) Lower positive rate of tuberculin test (PPD); (5) More patients with no expectoration, with sputum smear for acid-fast bacilli staining is negative; (6) Higher incidence of resistant strains, high recurrence rate, and higher mortality (Table 17 .1 ).

Foci in the cases with AIDS complicated by pulmonary tuberculosis are change quickly. After anti-TB treatment, the lesions are absorbed quickly. Those receiving no anti-TB therapy, the foci tend to fuse together to form a mass or diffusely distribute.

Bacterial septicemia often occurs in AIDS patients. Many opportunistic pathogens can cause respiratory infections, including bacterial bronchitis, pneumonia and pleuritis. The incidence rate of bacterial pneumonia (BP) is 3-5 %. BP has a larger range of impact on HIV infected patients than on non-HIV infected groups. Repeated episode of BP is considered to be the fi rst manifestations of latent HIV infection. Therefore, for those individuals who have recurrent pneumonia without other risk factors, they should be alert to HIV infection. The common pathogenic bacteria include Streptococcus pneumoniae, Staphylococcus aureus, Rhodococcus equi, Haemophilus and pseudomonas aeruginosa. As non-HIV infected patients, the most common pathogens of pneumonia are Streptococcus pneumoniae and Haemophilus infl uenzae. Legionella and Klebsiella are also common. Many factors, such as the reduced T lymphocytes in HIV infected patients, manufacturing disorders of neutrophils, mononuclear cells and cytokines, and dysfunctional B lymphocytes, provide chances for opportunistic bacterial infections. In addition, the application of broad-spectrum antibiotics also increases the chance of opportunistic infections. BP can occur in any stage of HIV and at any level of CD4 T cell count. When the CD4 T cell count decreases, the incidence of BP also increases. The clinical manifestations of HIV infected patients are the same as non-HIV infected patients, with acute onset (3-5 days) , high fever (39-40 °C) , chills, chest pain, dyspnea, cough, purulent sputum (bloody or rusty). Being different from non-HIV infection, pulmonary infection in HIV-infected patients is often recurrent.

The imaging demonstrations of HIV/AIDS related bacterial pneumonia are similar to those in non-HIV infected patients. Most cases of streptococcal pneumonia and haemophilus pneumonia have unilateral, confi ned and partially fused foci with accompanying pleural effusion. The imaging demonstrations include thickened and deranged pulmonary markings, alveolar fi lling of infl ammatory exudates with the progression of the illness, large fl aks infl ammatory infi ltration shadows or parenchymal shadows, bronchial gas fi lling phase in the parenchymal shadows. The lesions distribute along the pulmonary segments or lobes, rarely with accompanying pleural effusion. During the absorption period, the density of the parenchymal shadows gradually reduces and the scope narrows down. There may be cavities in some individual cases. But in most cases it is completely absent after 

Poor effi cacy and more side effects

Favorable effi cacy and less side effects 3-4 weeks. Lesions absorption are slow in elderly patients and recurrent patients, which is diffi cult to be completely absorbed and often develop into organic pneumonia. Rhodococcus equi was initially discovered in 1923 and nominated as corynebacterium equi. After structure analysis of the cell wall, it was found to be different from Corynebacterium, and therefore it is classifi ed into Rhodococcus. Rhodococcus equi is generally considered as the pathogens of horses, pigs and cattle. Human rhodococcus equi infection is rare. But in recent years, due to an increase in patients with immunodefi ciency syndrome, reports of rhodococcus equi induced human respiratory infection and sepsis are increasing. Rhodococcus equi is an intracellular facultative parasitic bacterium. Its optimum temperature for growth is 30 °C, and suitable temperature for its growth is 10-40 °C. The acid-fast staining for rhodococcus equi shows uncertain results. Due to its various morphology, it is commonly mistaken as diphtheroids bacilli, Bacillus or Micrococcus. On sheep blood agar plate, the bacterium can have synergistic hemolysis with staphylococcus aureus, mononuclear Listeria and Corynebacterium pseudotuberculosis. Toxicity mechanisms of Rhodococcus equi has been recently discovered the existence of toxic plasmid, which provides a new idea for the full understanding of its pathogenesis. Clinical symptoms are usually cough, orange red sputum, high fever and other symptoms. E Marchiori et al. in 2005 studied fi ve cases of AIDS complicated by Rhodococcus equi pulmonary infection. All the patients had a case history of cough and fever history for 1-2 months with accompanying shortness of breath and chest pain. Li et al. in 2009 [ 106 ] studied a group of 13 cases. All patients had fever, with a body temperature being 38-40 °C, cough, orange red sputum. The typical clinical manifestations of the disease are fever, dyspnea and chest pain. Other symptoms such as weight loss, diarrhea and joint pain are not representative. Based on the course of the disease, the diagnostic imaging demonstrations of Rhodococcus equi pulmonary infection can be divided into early stage, showing round liked fl aky blurry shadows surrounding unilateral hilum that has blurry boundary; middle stage (parenchymal change), showing central sphere liked high density shadow surrounding unilateral hilum, in parenchymal changes and with clear boundary; advanced stage (necrosis) showing secondary cavity of the pulmonary mass, possibly with hydropneumothorax and pleurisy. The imaging demonstrations are characteristic, but lack of specifi city. And it should be differentiated from pulmonary tumors. The pathological changes include the most commonly chronic suppurative bronchopneumonia and extensive pulmonary abscesses. The histopathology demonstrates massive bleeding in alveolar space, large quantity erythrocytes, intact cellular wall and large quantity epithelial cells. The predominant pathological changes may also be fi broblasts, with parenchymal changes of lung tissue and thickened alveolar septa. Accumulating piles of strip liked purple Rhodococcus equi can be found by PAS staining.

Common pathogenic viruses of the opportunistic pulmonary infections in HIV infected patients are cytomegalovirus (CMV) and infl uenza virus. CMV is the most common pathogen of HIV/AIDS related pulmonary infection. By autopsy, 49-82 % patients with HIV/AIDS have CMV infection, only second to Pneumocystis carinii pneumonia. Moskowitz et al. [ 32 ] reported that among the direct causes of death in AIDS patients, 19 % is due to pulmonary cytomegalovirus infection. Because of the lack of typical clinical manifestations and sensitive examinations for its early diagnosis, the defi nitive diagnosis rate of cytomegalovirus pneumonia is only 13-24 % before autopsy. The clinical manifestations of CMV infection are non-specifi c. The systemic symptoms are fever, soreness of joints and muscles. Respiratory symptoms are paroxysmal dry cough, progressive shortness of breath, diffi culty in breathing during activities. Pulmonary CMV infection may develop secondary fungal infection or be complicated by bacterial, fungal, and Pneumocystis carinii infections. The cytomegalovirus can widely spread in the organs and tissues of the infected patients, and the infections can directly lead to the damage of infected host cells. In addition, the virus can also cause pathogenic effects via immune pathological mechanism. Some scholars classifi ed CMV pneumonia into diffuse, miliary necrosis and cytomegalic. Diffuse and cytomegalic CMV pneumonia are often accompanied by diffuse alveolar damage (DAD), which is more common in the diffuse type of CMV pneumonia but less common in cytomegalic type of CMV pneumonia. The pathological basis of diffuse small nodules in lungs is hemorrhagic necrosis. Sometimes CMV infection is concurrent with other infections in the lungs, and even co-infects one cell. Pulmonary parenchymal changes indicate bacterial and fungal infections, such as fi ndings of inclusion bodies in the cells, commonly known as Eagle's Eye sign. The imaging demonstrations of cytomegalovirus pneumonia are diverse. Some studies summarize that the lungs commonly have manifestations of diffuse interstitial infi ltration or alveolar infi ltration, with ground glass liked changes, pulmonary parenchymal changes, grid liked changes, thickend bronchial wall, bronchiectasis, pulmonary nodules or masses. The principal changes include the early lesions of ground glass liked changes and advanced lesions of pulmonary masses.

Lymphoid interstitial pneumonia is the abnormal hyperplasia of the pulmonary lymphoid tissue. Its occurrence is related to autoimmune diseases, and is believed to be a direct response of the lungs to HIV. The clinical manifestations are recurrent infections, poor appetite, hepatomegaly and splenomegaly, and arrested development. The diagnostic imaging demonstrates no characteristic changes by CT scanning, with thickened bronchial wall, diffuse central lobular nodules or bronchiectasis, grid liked and cords liked shadows in uneven thickness. The pathological changes include accumulating lymphocytes and plasma cells that are mixed to infi ltrate the pulmonary interstitium and expand to surrounding areas of the bronchi.

Toxoplasma pneumonia is caused by the infection of the intracellular parasite, Toxoplasma gondii. Ludlam et al. in 1963 fi rstly proposed the concept of pulmonary toxoplasmosis, which was believed to cause atypical pneumonia [ 107 ] . The clinical manifestations are cough and expectoration. In the serious cases, dyspnea and cyanosis can occur. In the chronic cases, there are long term low grade fever, cough, weight loss and enlarged lymph nodes. The diagnostic imaging demonstrates bronchopneumonia, interstitial pneumonia and pleurisy. (1) Bronchial pneumonia is also known as lobular pneumonia, with scattered patchy and blurry density shadows. (2) Interstitial pneumonia has typical manifestations of reticular and nodular shadows. (3) Pleurisy is rare, showing pleural effusion, limited diaphragmatic activity. The imaging demonstrations are non-specifi c, which can be defi ned in combination with the etiologic examinations. The pathological changes are congestion and edema of the surrounding connective tissue of the alveolar wall and bronchial walls, widened pulmonary interstitium, small quantity serous fi brin exudation from alveoli and pulmonary interstitium, and infi ltration of macrophages and lymphocytes. Toxoplasma cysts and tachyzoites may be found in pulmonary interstitium and macrophages as well as alveolar epithelium.

Kaposi's sarcoma, a vascular tumor, was discovered in 1872, and is also known as multiple hemorrhagic sarcomas, multiple vascular sarcomas, or multiple pigmented sarcomas. Kaposi's sarcoma is believed to be the defi ning tumor of AIDS. Outbreak of KS occurred in male homosexuals in Europe and the United States. Data show that in about 30 % Caucasian homosexuals, Kaposi's sarcoma is a major complication of in HIV/AIDS patients. It has been confi rmed that, though Kaposi's sarcoma has strong invasion, the disease itself has little impact on the mortality of AIDS. The cause of death in majority of the patients is still opportunistic infections. The clinical manifestations include face and neck lesions in dark red to purple red plaques. The plaques do not fade away when pressed, with surrounding brown ecchymosis. It commonly involves multiple organs including lungs, spleen, oral cavity, lymph nodes, gastrointestinal tract and liver. The lungs are the major target of invasion. The diagnostic imaging demonstrates hilar lymphadenectasis and its surrounding nodular infi ltration, bilateral interstitial changes, and pleural effusion that are its typical X-ray demonstration. Early pathological changes are similar to those of common angioma; with gathering of capillaries into groups containing histocytes engulfed hemosiderin and orderly arranged vascular endothelial cells. It further progression see active proliferation of endothelial cells and fi broblasts, increased nuclear mitosis with anaplasia, and scattered lymphocytes and histocytes between blood vessels. In the advanced stage, occlusion and necrosis of the vascular lumen can be found. Irregular lumen and fi ssures of the new capillaries can be commonly found in the tumor, fi lled with blood and common hemorrhage. In China, KS is relatively rare. Its defi nitive diagnosis can be made by pathological examination.

Other HIV/AIDS related malignancies include Burkitt's lymphoma, non-Hodgkin's lymphoma, Hodgkin's lymphoma and lung cancer. In summary, HIV/AIDS related pulmonary infections are important diseases in the disease spectrum of HIV/AIDS imaging. The diagnostic imaging is irreplaceable examinations for pulmonary infections. Early prevention and correct diagnosis are the keys to improve the quality of life and prolong the lives of patients. The complexity and multiplicity of HIV/AIDS related pulmonary diseases present challenges for the clinicians. Firstly, HIV/AIDS related diseases should be optimally classifi ed. Each type should has a disease spectrum, which can be used for exclusion in combination with immunological indices to make the diagnosis and differential diagnosis. The diagnosis of HIV/ AIDS related pulmonary infections should be made in combination with case history and laboratory tests for targeting individualized diagnosis to serve clinical practice.

Carnii Pneumonia (PCP) 

The pathogen is the trophozoites and cysts produced by Pneumocystis carinii, principally living in the lungs. Pneumocystis carinii was used to being categorized as as protozoon, but recently, it is believed to be belonged to fungus according to its ultrastructure and Pneumocystis ribosomal RNA phylogenetic analysis. The main infection route of PCP is airborne transmission and reactivation of in vivo latent Pneumocystis carinii. Infl ammatory and immune responses of the host include phagocytosis of Pneumocystis carinii by the alveolar macrophages, infi ltration of lymphocytes in peribronchial and vascular area, proliferation of type II alveolar cells, local and systemic increase of antibody.

By naked eyes observation, there are extensive and diffuse invasion of lungs, which is soft like waterlogged sponge and in milky white with black spots. The fi lled foamy substance in the alveoli and bronchioles is a mixture of necrotic fungus and immunoglobulin. The alveolar septum has infi ltration of plasma cells and lymphocytes, resulting in thickened alveolar septa up to 5-20 times as the normal thickness that occupy 3/4 of the entire lung volume. The cysts are fi rstly located in the macrophage cytoplasm of the alveolar septa. Subsequently, the alveolar cells containing cysts sheds off into the alveolar space. After the rupture of the cystic wall, sporozoite is discharged to turn into free trophozoites, which gains its access into the alveolar space. The alveolar exudates include plasma cells, lymphocytes and histocytes ( Fig. 17 .1a-c ).

The clinical symptoms include dry cough, shortness of breath and an indoor hypoxia. About 95 % AIDS patients have multi-pathogens induced pulmonary infections. The most signifi cant laboratory abnormality in most PCP patients is hypoxemia. Based on correlation between PCP and arterial oxygen partial difference, hypoxemia is divided into three degrees. The slight cases at indoor conditions have their PaO 2 being above 70 mmHg, or alveolar-arterial oxygen pressure difference being less than 35 mmHg, or both. The moderate and severe cases have their PaO 2 being usually less than 70 mmHg, or alveolar-arterial oxygen pressure difference being above 35 mmHg, or both. The most common manifestations of AIDS complicated by PCP are progressive subacute onset of dyspnea, fever, dry cough and chest distress, the symptoms aggravating in a few days or weeks. Pulmonary examination is usually negative in slight cases. As the disease aggravates, the cases show shortness of breath, cyanosis, tachycardia, and diffuse dry rales. Pneumocystis carinii infection accounts for 60-85 % of AIDS patients, which is one of the major causes of death in AIDS patients.

The diagnostic imaging examinations include chest X-ray, CT scanning and nuclear medicine examination. (1) Chest X-ray is the conventional examination for screening. Early lesions tend to be missed for the diagnosis due to the limited resolution or atypical lung lesions. (2) CT scanning with high resolution is superior to chest X-ray. (3) Nuclear medicine examination demonstrates increased uptake of the isotope-labeled monoclonal antibodies in the lung tissues of the PCP patients.

(1) By tracheal suction or lung tissue biopsy, the detection rate of Pneumocystis carinii is up to 90 %. By tissue section staining, abundant protozoa can be found in intra-alveolar foamy eosinophil substance mass (By methenamine silver nitrate staining, the dark brown round or oval shaped cysts can be found in a diameter of 6-8 μm out of the cells). (2) By ELISA, Pneumocystis IgG antibody can be detected and by latex particle agglutination test, the protozoa antigen can be detected. (3) Molecular biology techniques, such as PCR can be applied for early diagnosis.

The following examinations are non-specifi c, but can be used to assess the severity of PCP and its progression. (1) By arterial blood gas analysis, the patients may show reduced blood oxygen saturation and respiratory alkalosis. (2) By serum enzyme spectrum analysis, the patients may show increased LDH. (3) It can be detected to have increased alveolar-arterial oxygen partial pressure difference.

In the early stage (exudation period), alveolar fl uids exudate, with diffuse granular shadows in the bilateral lung fi elds extend from the hilum to the surrounding. In the middle stage (infi ltration and fusion period), the intrapulmonary lesions fuse, with ground glass liked or cloudy shadows that are bilaterally symmetric like butterfl y wings. In the middle and advanced stages (parenchymal changes period), the lung tissues show parenchymal changes, with high density shadows and accompanying air bronchogram. The lung periphery shows stripes of transparent shadows. In the advanced stage (pulmonary fi brosis period), the pulmonary interstitium is thickened in dense cords liked appearance, with interval irregular patchy shadows. The pulmonary ventilation improves and the lung periphery shows dense parenchymal shadows with emphysema, pneumomediastinum and pneumothorax.

In the early stage (exudation period), the lesions radiatus develop from the hilum to lung fi eld. In the early stage, the diffuse exudative lesions distribute as pulmonary acinus, with changes similar to pulmonary interstitial changes. It was believed to be interstitial pneumonia. However, acute PCP is actually exudation of alveoli and spaces containing 

A male patient aged 31 years was confi rmatively diagnosed as having AIDS by the CDC. He complained of dyspnea, cyanosis and wheezing for 3 weeks, with obviously decreased oxygen saturation. His CD4 T cell count was 45/μl. 

A female patient aged 37 years was confi rmatively diagnosed as having AIDS by the CDC. She complained of dyspnea, cyanosis and wheezing for 8 weeks, with obviously decreased oxygen saturation. Her CD4 T cell count was 45/ μl. 

Patients with acquired immunodefi ciency.

The early symptoms include fever, dry cough and shortness of breath. The advanced symptoms are serious dyspnea, cyanosis, progressive hypoxemia and respiratory failure. By pulmonary examinations, scattered dry and moist rales can be heard.

Trophozoites of Pneumocystis cysts can be found by liquid Giemsa staining.

Slight and moderate interstitial infl ammation responses mainly involve lymphocytes and alveolar macrophages. The detection of cysts containing sporozoites is the basis to defi ne the diagnosis.

Chest X-ray Chest X-ray demonstrations of PCP can be classifi ed into four types. (1) Early pulmonary interstitial infi ltration and diffuse miliary alveolar exudation; (2) In the middle stage, there are alveolar exudates, with fusion and parenchymal changes; (3) In the middle-advanced stage, diffuse parenchymal changes; (4) Pulmonary interstitial fi brosis and lung cavity or lung bulla, as well as pneumothorax and emphysema.

For the cases with negative or atypical fi ndings by chest X-ray, CT scanning with high resolution should be performed. CT scanning demonstrates early lesions of multiple symmetric diffuse miliary nodal shadows, which have clear boundaries. In the middle stage, there are thin cloudy shadows or ground glass liked density shadows. In the middleadvanced stage, the lung tissues show parenchymal shadows, with trachea-bronchial sign. In the outer strip of the lung, a transparent area in shape of willow leaf can be demonstrated. In the advanced stage, fi brous cords liked shadows are demonstrated some lung tissues with compensatory emphysema and even pulmonary pseudocysts.

The intake of the isotope-labeled monoclonal antibody by lung tissues of PCP patients increases.

HIV/AIDS related PCP should be differentiated from bacterial pneumonia, pulmonary tuberculosis, viral pneumonia, fungal pneumonia, ARDS, and lymphocytic interstitial pneumonia (LIP).

Bacterial pneumonia has more focal lesions but less diffuse lesions.

Pulmonary mycobacterium tuberculosis infection has manifestations of military pulmonary tuberculosis by chest X-ray, which is diffi cult to be differentiated from early PCP. HIV/ AIDS related PCP shows miliary nodules, which further fuse into cloudy or ground glass liked shadows or parenchymal changes. The lesions are commonly symmetrical, with the hilus as the center. The clinical manifestations include fever, dry cough or accompanying diffi culty breathing, and even cyanosis. But in the cases of pulmonary Mycobacterium tuberculosis infections, most show miliary nodules, which further fuse into large nodules or mass. After about 2 weeks treatment in the early stage, the military nodules in both lungs can be absent, with common clinical symptom of high fever. Correlation studies of miliary tuberculosis and peripheral blood CD4 T cell count have demonstrated that the general incidence of miliary tuberculosis is low, only 6-9 %, but it is the main manifestation of HIV/AIDS related pulmonary miliary tuberculosis. Generally, when CD4 T cell count is below 200/μl, the incidence of cavity lesions is 29 %, noncavity lesions 58 %, complicated by pleural effusion 11 % and lymphadenectasis 20 %. When CD4 T cell count is between 200 and 390/μl, the incidence of cavity lesions and non-cavity lesions each accounts for 44 %, complicated pleural effusion 11 % and lymphadenectasis 14 %. When CD4 T cell count above 400/μl, the manifestation is commonly pneumonia type, in fl aky shadows or parenchymal shadows in just one pulmonary segment. The incidence of cavity lesions is 63 %, non-cavity lesions 33 %, complicated by pleural effusion 3 % and no lymphadenectasis.

Chest X-ray demonstrates cytomegalovirus pneumonia negative in 1/3 patients. The foci are commonly bilateral, with reticular particles in 33 % patients, alveolar foci in 22 % patients, nodular foci in 11 % patients, complicated by cavity in 11 % patients, cysts in 6 % patients, pleural effusion in 33 % patients and lymphadenectasis in 11 % patients.

The incidence of diffuse foci in the cases of cryptococcus neoformans pneumonia is 76 %, interstitial foci or mixed foci 76 %, alveolar foci 19 %, nodular foci 5 %, lymphadenectasis 11 % and pleural effusion 5 %.

HIV/AIDS related PCP is more likely to occur in children with AIDS, which presents diffi culty for its differentiation form lymphoid interstitial pneumonia. However, lymphoid interstitial pneumonia commonly has a chronic onset, with commonly manifestations of cough and dry rales. Systemic lymphadenectasis and enlargement of salivary glands can also be found. By lung tissues biopsy, EBV-DNA1 can be detected, which provides basis for their differentiation.

Pneumocystis, a unicellular organism, is the pathogen of Pneumocystis carinii pneumonia. Pneumocystis carinii pneumonia is one of common opportunistic infections in AIDS patients, which is also the leading cause of death in AIDS patients. In the initial episode of PCP, most patients have a CD4 T cell count of less than 100/μl. Diagnostic imaging demonstrates bilaterally symmetrical ground glass liked shadows, which can be diffusely distributed and tend to mainly involve the periphery of the hilus or the middle and lower lung fi elds. HRCT scanning is commonly applied to assess early PCP that is demonstrated negative by chest X-ray. HRCT scanning demonstrates bilaterally symmetric patchy or fused ground glass liked shadows. The pathological basis of ground glass liked shadows and parenchymal areas refl ect that the acinus is fi lled by the foamy exudates, which are composed of surface active substances, cellulose and cell debris. All of the ground glass liked shadows, overlapping septa and the intralobular linear shadows are in gravel road liked manifestation. The septa and intralobular linear shadows demonstrate pulmonary interstitial edema or cellular infi ltration.

In the middle-advanced stage of PCP, there are manifestations of small pulmonary nodules, pulmonary parenchymal changes, thickened interlobular septa, intralobular linear shadows, mass like lesions, pleural effusion, and lymphadenectasis. The cysts tend to mainly involve the upper lobes, which can be unilateral or bilateral pulmonary cysts, pneumothorax, mild or severe interstitial fi brosis and traction bronchiectasis. HRCT scanning demonstrations of PCP are non-specifi c. Its diagnosis should be in combination with HIVPH13 and etiological examinations.

Bacterial Infections

Mycobacterium tuberculosis is still an important pathogen for pulmonary infection in HIV positive patients. Since the mid-1980s, the main cause of the increasing incidence of tuberculosis is the prevalence of HIV infection. The incidence of tuberculosis in AIDS patients is 200-500 times higher than the general population. HIV infection is the most dangerous factor for progression of latent tuberculosis into active tuberculosis. Tubercle bacillus belongs to Mycobacterium family of Mycobacterium genus, which is divided into types of human, bovine and murine. The main cause of human tuberculosis is human Mycobacterium tuberculosis, which is known as acid-fast bacilli. Tubercle bacillus wall is the complex containing high molecular weight fatty acids, lipids, proteins and polysaccharides, which are related to its pathogenicity and immune responses. Lipid can cause the infi ltration of human monocytes, epithelial cells and lymphocytes to form tuberculous nodules. Its protein contents can cause allergic reactions, and infi ltration of neutrophils and mononuclear cells. Polysaccharides participate in certain immune responses (such as agglutination). These pathogenic factors lay the foundation for the occurrence of tuberculosis in AIDS patients.

Human immunity, allergic responses as well as the number and pathogenicity of tubercle bacilli are closely related to the quality, range, spreading rate and the progression of tuberculosis. Its pathological changes are characterized by exudation, infi ltration, proliferation and hyperplasia, degenerative necrosis (caseous necrosis) and cavity formation.

The manifestations include congestion, edema and infi ltration of leukocytes. The exudative lesions occur in early stage of tuberculosis infl ammation or when the lesions deteriorate. It can also be found in the serosa tuberculosis. There is neutrophilic granulocytes in the exudative lesions, which are gradually substituted by monocytes (phagocytes). The engulfed tubercle bacilli can be found in the large mononuclear cells. The exudative lesions are absorbed and dissipated through the phagocytosis of the mononuclear-phagocyte system, even with no scar.

When large mononuclear cells engulf and digest tubercle bacilli, the phospholipid of the bacteria render the large mononuclear cells to enlarge and be fl at, similar to epithelial cells, which is known as epithelioid cells. These epithelioid cells gather into groups, with central Langhans giant cells that pass the messages of the bacteria antigens to lymphocytes. Surrounding the Langhans giant cells, there are often many lymphocytes to form typical tuberculous nodules, which are characteristic lesions of tuberculosis. This is why it is called Tuberculosis. In the tuberculous nodules, tubercule bacilli are usually undetectable. Proliferation based lesions often occur in the cases with less bacteria invasion and when human cells mediated immunity is predominant.

Degeneration often occurs on the basis of the exudative or proliferative lesions. Tubercle bacilli overcome macrophages and then continually proliferate in large quantity. After the cells become cloudy and swelling, the foci show fatty degeneration, dissolved into fragments, until the occurrence of necrosis. After the death of infl ammatory cells, proteolytic enzymes are released to dissolve the tissues that results in necrosis, which is coagulative necrosis. By naked eyes observation, they are yellowish gray, with loose and brittle quality like caseous. Therefore it is known as caseous necrosis. Microscopic examination demonstrates an area of solid and Eosin staining red necrotic tissues with no tuberculosis.

Tubercle bacilli in the foci of caseous necrosis proliferate in large quantity to cause liquefaction, which is related to infi ltration of neutrophile granulocytes and large monocytes. Part of liquefi ed caseous necrotic substances can be absorbed and part can be discharged by the bronchus to form cavities. Otherwise, it may cause intrapulmonary spreading along with bronchi. The small caseous necrosis or proliferative lesions can be shrunk and absorbed after treatment, with only residues of slight fi brous scars. Due to the compromised immunity in AIDS patients, the lesions rarely show fi ber tissues proliferation, but form cords liked scar. Calcifi cation rarely occurs.

If the necrotic lesions erode the blood vessels, tubercle bacilli can cause systemic miliary tuberculosis along with blood fl ow, including brain, bones and kidneys. Large quantity sputum containing tubercle bacilli gains its access into the gastrointestinal tract. It can also cause intestinal tuberculosis and peritoneal tuberculosis. Pulmonary tuberculosis can cause tuberculosis pleurisy via direct spreading to the pleura ( Fig. 17 .19a-c ). 

Clinically, it is a chronic progression, with rare acute onset. The clinical symptoms are commonly systemic, with fever and fatigue. The respiratory symptoms include cough and hemoptysis. Pulmonary TB can be divided into primary and secondary, with the initial episode commonly being primary (type I). The residual bacteria after primary infection can cause secondary infection (type II-IV) when the immunity is compromised via spreading along blood fl ow or direct spreading.

It is common in HIV positive children. Most cases are asymptomatic, sometimes with symptoms of low grade fever, mild cough, sweating, rapid heartbeat, and poor appetite.

HIV/AIDS related miliary tuberculosis is one of the major manifestations of pulmonary tuberculosis, which is more common. The onset of acute miliary tuberculosis is rapid, with symptoms of chills and high fever with a body temperature up to 40 °C, mostly remittent fever or continuous fever. There may be decreased leukocytes count and accelerated sedimentation rate. The progression of subacute and chronic hematogenous disseminated pulmonary tuberculosis is relatively slow.

Infi ltrative pulmonary tuberculosis in AIDS patients commonly occurs in both middle and lower lung fi elds, with fl aky and fl occulent foci or parenchymal changes in lobes or segments. Caseous lesions are rare. The early stage of infi ltrative pulmonary tuberculosis is commonly asymptomatic, with later occurrence of fever, cough, night sweating, chest pain, weight loss, expectoration and hemoptysis.

This type of pulmonary TB rarely occurs in AIDS patients.

In non-AIDS patients, chest X-ray demonstrates three major changes, namely cavity, fi brosis, and bronchial dissemination. In the AIDS patients, the pulmonary manifestations include single or multiple nodular shadows with clear boundaries.

Tuberculous pleuritis is an exudative infl ammation caused by the direct invasion of tubercle bacillus from the primary lesion near the pleura into the pleura, or hematogenous dissemination via the lymphatic vessels to the pleura. The routes for occurrence of tuberculous pleurisy include: (1) The bacteria in the hilar lymph tuberculosis counterfl ow to the pleura along lymph vessels. (2) TB lesions adjacent to pleura rupture to cause direct access of the tubercle bacilli or products of tuberculosis infection into the pleural cavity. (3) Acute or subacute hematogenous disseminated tuberculosis causes pleuritis. (4) Due to the increased allergic responses, the pleura highly respond to tuberculosis toxins to cause exudation. (5) Thoracic tuberculosis and rib tuberculosis rupture into the pleural cavity. Clinically, pleuritis can be divided into three types, dry pleuritis, exudative pleuritis and tuberculous empyema (rare). The common clinical manifestations are fever, cough with accompanying chest pain of the affected side and shortness of breath.

(1) Sputum smear examination is simple to manipulate, with high accuracy rate. The fi ndings of the tubercle bacilli can defi ne the diagnosis. It still is the golden criteria for the diagnosis of pulmonary tuberculosis. (2) Sputum tubercle bacilli culture has high reliability. Tubercle bacilli drug sensitivity test can be performed but requires 6-8 weeks to obtain the results. Therefore, its application is limited.

(1) Tuberculin purifi ed protein derivative (PPD) test is commonly used. Its positive result is one of the evidence confi rming a past history of TB infection.

(2) BACTEC test can be performed to detect the metabolites of mycobacterium tuberculosis. Generally, mycobacterium can be detected in 2 weeks. The quantity of mycobacteria can affect the period required for test results. (3) PCR has poor specifi city but high sensitivity of up to 98-100 %.

Both can be applied to observe the enlarged lymph nodes in the chest and mediastinum. In addition, they can be applied to obtain specimens for biopsy, which facilitates the diagnosis and differential diagnosis.

Diagnostic imaging examinations include chest X-ray and CT scanning. Chest X-ray can demonstrate the location, quality and range of the lesions. It can also help to assess the therapeutic effi cacy. CT scanning can demonstrate small or hidden lesions, with a high resolution.

Primary pulmonary tuberculosis, also known as primary syndrome, is rare in adult AIDS patients. Chest X-ray demonstrates intrapulmonary patchy or large fl aky parenchymal changes, hilar and mediastinal lymphadenectasis in connection to irregular cords liked shadows (located between intrapulmonary lesion and the hilum). Lymph node tuberculosis is demonstrated to have mediastinal lymphadenectasis that sometimes fuse into mass. In AIDS patients, simple mediastinal lymph node tuberculosis is more common than primary syndrome.

Tuberculosis (1) The acute cases are demonstrated to have diffused miliary nodules in both lungs with even distribution, even size and even density. (2) The subacute and chronic cases are demonstrated to have nodules in both lungs, with uneven distribution, uneven size and uneven density. Sometimes calcifi cation occurs in the nodules, with fi brous cords and thickened pleura.

Infi ltrative pulmonary tuberculosis are demonstrated to have patchy parenchymal changes in the middle and lower lung fi elds as well as parenchymal changes, cavities and fi brous cords liked foci in the segments and lobes. It can also occur in the upper lung fi elds, commonly with accompanying mediastinal and hilar lymph node tuberculosis.

It commonly occurs in the advanced stage of AIDS,, with manifestations of pulmonary interstitial fi brosis and formation of cavities. This type of pulmonary tuberculosis is less common.

It rarely occurs, mostly in the early stage of AIDS. It is rare in the middle and advanced stages of AIDS. Dry pleuritis has manifestations of blunt costophrenic angle and limited diaphragm mobility. Exudative pleuritis is manifested as small quantity pleural effusion and thickened pleura, commonly with encapsulated effusion of the lateral pleura. Calcifi cation is rare.

A male patient aged 28 years was confi rmatively diagnosed as having AIDS by the CDC. He complained of dull chest pain, dyspnea, fever, night sweating, fatigue and anorexia. His CD4 T cell count was 65/μl. 

A female patient aged 36 years was confi rmatively diagnosed as having AIDS by the CDC. She complained of dull chest pain, dyspnea, fever, night sweating and fatigue. Her CD4 T cell count was 85/μl. A male patient aged 41 years was confi rmatively diagnosed as having AIDS by the CDC. He was infected HIV via blood transfusion, with complaints of cervical lymph node tuberculosis, ascites and abdominal infection, fungal stomatitis, biliary stones with infection and severe anemia. His CD4 T cell count was 33/μl. A female patient aged 39 years was confi rmatively diagnosed as having AIDS by the CDC. She complained of fever and night sweating. Her CD4 T cell count was 73/μl. A female patient aged 35 years was confi rmatively diagnosed as having AIDS by the CDC. She was hospitalized due to complaints of chest distress, cough and expectoration for 2 months, with after noon low grade fever and weight loss. On admission, she was confi rmed HIV positive and a CD4 T cell count of 120/μl. A female patient aged 37 years was confi rmatively diagnosed as having AIDS by the CDC. She complained of fever and chest pain for 2 months, with acid-fast bacilli positive in the pleural fl uid culture. Her CD4 T cell count was 71/μl. A female patient aged 40 years was confi rmatively diagnosed as having AIDS by the CDC. She complained of fever and chest pain for 2 months, with acid-fast bacilli positive in the pleural fl uid culture. Her CD4 T cell count was 891/μl.

A female patient aged 34 years was confi rmatively diagnosed as having AIDS by the CDC. She complained of fever and chest pain for 2 months, with acid-fast bacilli positive in the pleural fl uid culture. Her CD4 T cell count was 51/μl. 

Cough expectoration, chest pain, dyspnea, fever, night sweating, fatigue, anorexia, lymphadenectasis and rapid progression of the conditions.

PPD skin test with a resulted diameter of more than 5 mm should be considered as tuberculosis infection. But its positive rate remains low.

The culture of sputum and bronchoalveolar lavage fl uid can detect the pathogens.

Nucleic acid analysis or DNA probe technique, PCR and chromatography can be applied to detect tubercle bacilli.

The commonly used diagnostic imaging examinations include chest X-ray and CT scanning. The main demonstrations include (1) intrapulmonary and extrapulmonary lymphadenectasis; (2) miliary tuberculosis manifestations;

(3) infi ltrative (pneumonia type) pulmonary tuberculosis; (4) Pulmonary interstitial fi brosis, cavity, pulmonary emphysema, nodules, emphysema, and bronchiectasis with accompanying infections. In the cases with their CD4 T cell count being above 400/μl, the imaging demonstrations are similar to those of non-HIV/AIDS patients with pulmonary tuberculosis. In the cases with their CD4 T cell count being above 400/μl, the manifestations are intrapulmonary large fl aky parenchymal changes, surrounding satellite lesions as well as mediastinal and hilar lymphadenectasis. Sometimes the manifestations may be only mediastinal lymphadenectasis and their fusion into mass. In the cases with CD4 T cell count being above 200/μl, there may be accompanying extrapulmonary tuberculosis, such as tuberculous peritonitis, bone tuberculosis, brain tuberculosis and splenic tuberculosis. In the cases with their CD4 T cell count being lower than 100/μl, the manifestations are mostly miliary tuberculosis.

HIV/AIDS related tuberculosis should be principally differentiated from pneumocystis carinii pneumonia, fungal infections, other pneumonia and lung cancer. 

HIV/AIDS related tuberculosis should be differentiated from PCP. PCP is mainly manifested as multiple lesions with hilum as the center to extending symmetrically to outside of the lungs. In the advanced stage, PCP has main lesions of pulmonary interstitial fi brosis, with less accompanying mediastinal and hilar lymphadenectasis. The laboratory tests can facilitate to defi ne the diagnose.

HIV/AIDS related tuberculosis should be differentiated from fungal infections. Fungal infections are relatively less common than tuberculosis. The imaging fi ndings of HIV/AIDS related pulmonary fungal infections are diverse, with manifestations of miliary, fl aky fl occulent liked, parenchymal, mass, and interstitial changes. In general, the diffuse lesions are mainly interstitial changes, while confi rmed lesions, compared to TB lesions, are more likely to have thick walled cavities. Satellite lesions of fungal infections are less than those of tuberculosis, with less accompanying mediastinal and hilar lymphadenectasis. Sometimes laboratory tests are necessary to defi ne the diagnosis.

HIV/AIDS related tuberculosis should be differentiated from non-tuberculosis mycobacteria pneumonia. Their imaging fi ndings are similar to each other, which presents challenges for their differential diagnosis. Molecular biology examinations play an important role in the differentiation.

HIV/AIDS related tuberculosis should be differentiated from other pneumonia. Non-bacterial pneumonia (mycoplasma, viral and allergic) often shows patchy shadows, which are similar to the manifestations of early infi ltrative pulmonary tuberculosis. When bacterial pneumonia shows lobar lesions, it may be confused with tuberculous caseous pneumonia, which should also be differentiated for the diagnosis. Symptoms of mycoplasma pneumonia are mild, with imaging fi ndings being always inconsistency with the clinical symptoms, which usually subside within 2-3 weeks. In the cases of allergic pneumonia, eosinophils in the blood increase, with intrapulmonary mobile shadows, which are the basis for their differentiation. Bacterial pneumonia can have acute onset, with chills, high fever, rust colored sputum, and streptococcus pneumoniae positive. Recovery is rapid after antibiotic treatment and all these symptoms can subside within 1 month.

HIV/AIDS related tuberculosis should be differentiated from pulmonary abscesses. In the cases of infi ltrative pulmonary tuberculosis with cavities, it should be differentiated from pulmonary abscess. Especially, tuberculosis with cavities in the apical segment of inferior lobe should be differentiated from acute pulmonary abscess. Chronic fi brous cavity tuberculosis should be differentiated from chronic pulmonary abscess. The key points for the differentiation are tubercle bacilli positive by sputum culture in the cases of TB, while tubercle bacilli negative by sputum culture in the cases of abscesses. Pulmonary abscess has an acute onset, with increased leukocytes and neutrophils as well as favorable therapeutic effi cacy of antibiotics. But sometimes tuberculosis with cavity may develop into bacterial infection, with undetectable tubercle bacillus by sputum culture.

HIV/AIDS related tuberculosis should be differentiated from lung cancer. The central type of lung cancer has nodular shadow in the hilum or hilar and mediastinal lymph node metastasis, which should be differentiated from lymphatic tuberculosis. The peripheral type of lung cancer has small fl aky infi ltration and nodules in the periphery of the lungs, which should be differentiated from tuberculoma or tuberculosis infi ltrative lesions. Lung cancers occur commonly in people aged above 40 years. The central type mainly is squamous carcinoma and the cases often have a history of long term smoking, with symptoms of no fever but diffi culty breathing or chest distress as well as gradually increasing chest pain. There are also symptoms of irritated cough with blood phlegm and progressive weight loss. The cases with supraclavicular metastasis have palpable harden lymph nodes. The intrapulmonary nodules can lobulated with fi ne spikes, no satellite lesions, generally no calcifi cation and possible vacuole sign. The peripheral type of lung cancer shows pleura invagination sign. Tuberculin test often shows negative in the cases of lung, positive or weakly positive in the cases with TB, and negative or weak positive in AIDS patients.

HIV infection is known to be the main factor for the development of latent tuberculosis into active tuberculosis. immunosuppression are similar to those in the cases with primary tuberculosis, with characteristic abnormal manifestations of hilar and/or mediastinal lymphadenectasis and parenchymal changes of the air chambers. CT scanning demonstrates enlarged nodules with low density. Enhanced scanning demonstrates marginal enhancement of the lymph nodes. The incidence of military tuberculosis in AIDS patients is increasing due to reduced thymic T lymphocytes in AIDS patients and the defects of delayed allergic responses, which result in the formation of granulomas and impaired functions to kill bacilli and confi ne the lesions.

Nontuberculous mycobacteria (NTM) refer to the mycobacteria except for mycobacterium tuberculosis complex (human, cattle, African and vole) and mycobacterium leprae. The most commonly known nomination is nontuberculous mycobacteria (NTM). More than 100 kinds of NTM have been found so far. According to Berger Manual of Systematic Bacteriology, NTM is divided into two categories, rapid growth type and slow growth type.

NTM are widely spread in nature, such as soil, dust, fl owing water and raw milk. Under a microscope, NTM is morphologically similar to tubercle bacilli, with red stained fi ndings by acid-fast staining. According to the growth of NTM in solid medium, the Runyon classifi cation divides NTM into the following four groups, light chromogenic bacteria; dark chromogenic bacteria that can cause cervical lymphnoditis in children, intrapulmonary or extrapulmonary infections and abrasive abscess; non-chromogenic bacteria including mycobacterium avium complex, intracellular mycobacteria that can cause pulmonary infections, lymphnoditis, arthritis and meningitis; rapid growth bacteria including mycobacterium fortuitum, mycobacterium, mycobacterium abscessus that can cause pulmonary diseases and skin infections.

Immunocompromised populations, such as HIV infected patients, patients with neoplasms, patients with long-term use adrenocortical hormone or immunosuppressive agents, are more susceptible to disseminated NTM infection. Immunocompetent people may have mycobacterium kansasii and mycobacterium avium infections. It was reported in the United States that the occurrence of mycobacterium avium complex infection in HIV positive patients is up to more than 95 %. The pathological changes of NTM infections are similar to those of tuberculosis. NTM lymphnoditis is pathologically characterized by granulomatous infl ammation.

Tuberculous nodules formed by epithelioid cells and Langhans giant cells are rare, with no accompanying central caseous necrosis. Due to the weak pathogenicity of NTM, the pathological changes are slight, but there is difference in the pathological changes of NTM infections in terms of location, type and host. Cavities are common in the cases with pulmonary NTM infection, commonly being multiple or multilocular thin wall cavities. The pleuron is rarely involved, with non-specifi c pathological changes of infl ammation but with large quantity pathogens of NTM.

Patients often have a history of chronic obstructive pulmonary disease, tuberculosis, silicosis, pulmonary abscess, bronchiectasis, cystic fi brosis, diabetes, ulcer as well as use of hormone or immunosuppressive agents. Its occurrence is more common in males than in females. The symptoms include cough, expectoration, hemoptysis, chest pain, diffi culty breathing, low grade fever, weight loss and fatigue. The symptoms are nonspecifi c and the conditions progress slowly.

For patients with suspected diagnosis of pulmonary NTM infection, sputum smear for acid-fast staining, sputum culture and bronchial lavage specimen culture can be performed. The positive fi ndings should be identifi ed with two to three times repeated culture. The same fi nding of NTM can defi ne the diagnosis.

Pathological biopsy can be performed for the diagnosis of NTM lymphnoditis.

Using 16S-23 SrDNA gene spacer sequence (IGS) of NTM for PCR-restriction fragment length polymorphism analysis (PCR-RFLP), NTM species can be identifi ed, which is more accurate, faster and simpler than the conventional morphological and biochemical examinations.

Mycobacterium tuberculosis and NTM have common antigen. PPD skin test produces cross-reaction, but there are still differences between mycobacterium tuberculosis and NTM. PPD-T of the mycobacterium tuberculosis and PPD-NTM of NTM are simultaneously obtained for Mantoux skin tests. The induration diameter of PPD-T in NTM patients is generally within 15 mm. For the cases with the induration diameter of PPD-NTM skin test being 5 mm larger or over 25 % larger than that of PPD-T skin test, NTM infection can be confi rmed.

Both are the most commonly used imaging examinations.

A female patient aged 26 years was confi rmatively diagnosed as having AIDS by the CDC. She complained of cough and chest distress for half a month, fever for 10 days, 1 day after cesarean section and fi nding of HIV positive for 1 day. Her CD4 T cell count was 54/μl, with Treponema pallidum antibody negative and PPD test negative.

Imaging demonstrations include various lesions such as infi ltration, cavity, nodules, fi brous caseation and extensive fi ber contraction in unilateral or bilateral lungs. The incidence of cavity is up to 80 %, being singular or multiple. Cavities caused by intracellular Mycobacterium are mostly found in the pleura, with thin wall and less surrounding exudates. 

The incidence of non-tuberculous mycobacterial infections in AIDS patients is high. MAC infection is usually caused by the initial exposure rather than the reactivation of latent pathogens. In patients with complications of MAC related lung diseases, most of the imaging fi ndings are normal. The most common manifestation is mediastinal or hilar lymphadenectasis. And the pulmonary symptoms are similar to those of tuberculosis. In the cases with multiple patchy parenchymal changes, cavities can be found, as well as nodules with blurry boundaries, pleural effusion and rarely found miliary nodules. Sputum or bronchoalveolar lavage fl uid culture positive, clinical symptoms, imaging fi ndings, and response to treatment can defi ne the diagnosis.

Staphylococcus aureus is a Gram positive coccus and is coagulase positive staphylococcus. The pathogenic substances of staphylococcus aureus mainly are toxins and enzymes, such as hemolytic toxins, leukocidin and enterotoxin, which play a role in hemolysis, necrosis, killing leukocytes and vascular spasm. The staphylococcus aureus coagulase is the main reason for suppurative infection.

Pneumonia caused by inhaled staphylococcus aureus through the respiratory tract often shows lesions in the large lobes or extensive fusion of bronchopneumonia lesions. Bronchial and alveolar rupture allows gas to enter the pulmonary interstitium, which is communicated with the bronchi. In the cases of bronchiolar blockage by necrotic tissues or pus, the one-way valve effect is formed to cause tension pulmonary emphysema. In the cases with superfi cial pulmonary emphysema with excessively high tension, it ruptures to form pneumothorax or pyopneumothorax, as well as bronchooleural fi stula ( Fig. 17.45a, b ) . 

The symptoms include chills, persistent high fever, cough, expectoration, chest pain and other symptoms. There is no sign in the early period. Symptoms are scattered moist rales in both lungs, being in consistency to severe toxic symptoms and respiratory symptoms. Yellow purulent sputum is the typical characteristics of staphylococcus aureus pneumonia. In the cases with larger lesions or fusion of lesions, signs of parenchymal changes, pneumothorax or pyopneumothorax can be found.

In the sputum or pleural fl uid smears examinations, the bacteria with a concentration being no less than 107 cfa/ml is the pathogen, the bacteria with a concentration being 105-107 cfa/ml is the suspected pathogen, and the bacteria with a concentration being less than 105 cfa/ml is the contaminated bacteria.

There are increased WBC count and neutrophils, leftward migration of the nucleus and possibly no increase of WBC count in AIDS patients.

Immunofl uorescence, enzyme-linked immunosorbent assay and counter immunoelectrophoresis can be performed to detect serum antigen or antibody of the pathogenic bacteria, which can defi ne the diagnosis. Polymerase chain reaction has certain signifi cance in pathogen detection.

The protected bronchoscopic specimen (PBS) and bronchoalveolar lavage (BAL) can be applied to collect the specimen, which has reduced chances of specimens contamination by oral bacteria.

Biphasic TV monitors guided pulmonary puncture and suction for pulmonary tissues examinations can be performed to detect the real pathogenic bacteria.

Both are the most commonly used imaging examinations.

The diagnostic imaging demonstrates staphylococcus aureus pneumonia as lesions in the inner zone of both middle lower lungs. There are singular or multiple parenchymal changes in patchy or lobar distribution that may fuse into large fl akes. It may be complicated by cavity and pulmonary emphysema, with surrounding compensatory emphysema.

A male patient aged 37 years was confi rmatively diagnosed as having AIDS by the CDC. He complained of high fever with a body temperature of about 39 °C and chest pain for 2 months. His CD4 T cell count was 31/μl. 

Chills, fever, cough, expectoration, chest pain and other symptoms commonly; hemoptysis and dyspnea rarely

The patients may be found with fever appearance, rarely shortness of breath and cyanosis. In the serious cases, the body temperature can be as high as 39-40 °C and blood pressure decreases, with signs of shock. By chest examinations, decreased ipsilateral respiratory motion; increased or decreased fremitus, dull sound in percussion; bronchial breathing sounds or moist rales by auscultation; rarely pleural friction and weakened breathing sounds.

Increased WBC count and neutrophils, possible the nucleus left shift; no increase or even decrease of WBC count in AIDS patients; Staphylococcus aureus positive by blood culture.

Sputum or pleural fl uid smears examinations for pathogenic bacteria culture is positive, and antibiotic sensitivity test is positive.

By chest X-ray and CT scanning, the most common demonstrations are lesions of bronchial pneumonia. The fi ndings of pulmonary emphysema and cavities can facilitate the diagnose.

The lesions should be differentiated from infi ltrative parenchymal bronchioloalveolar carcinoma. The smaller lesions should be differentiated from pulmonary infarction. The large lesions should be differentiated from obstructive pneumonia. It is diffi cult to identify the types of common bacterial pneumonia simply by chest X-ray and CT scanning. In combination to the laboratory tests, the diagnosis can be defi ned.

The incidence of pyogenic bacterial infection is increasing in AIDS patients, which is caused by their weakened cellular and humoral immunity. The manifestations of these most common bacterial infections are similar to those of non-HIV infected patients by chest X-ray. Bacterial pneumonia and purulent bronchitis are the most common causes of pulmonary infections in AIDS patients. Particularly, they are frequently found in patients with a history of intravenous drug abuse and smokers. They are histologically characterized by infl ammations of the bronchi and bronchioles as well as infl ammatory exudates and mucus in the airway lumens. CT scans facilitates the diagnosis of bronchiolitis and early bronchial pneumonia. The demonstrations are characterized by (1) small centrilobular nodular shadows, which is the cross sectional demonstration of bronchioles fi lled with infl ammatory substances and its surrounding infl ammations; 

Rhodococcus equi infection is one of the zoonotic diseases, which commonly occurs in the grazing areas. Patients with T lymphocyte immunodefi ciency caused by AIDS and other factors are especially susceptible to the infection. Rhodococcus equi was fi rstly discovered in 1923 and was nominated as corynebacterium equi. After structure analysis of the cell wall, it was found that the bacterium is quite different from Corynebacterium, and therefore classifi ed as Rhodococcus. Rhodococcus equi infection in human is rare. But in recent years, due to an increase of patients with immunodefi ciency syndrome, reports on rhodococcus equi caused human respiratory infections and sepsis are increasing. In the past, the toxicity mechanism of Rhodococcus equi was mostly speculated. Until recently, the damage process of toxic plasmid to human tissue is discovered, which presents a new way for the study of the pathogenesis of Rhodococcus equi infections.

Rhodococcus equi is one of the facultative parasites in the cells and its optimum growth temperature is 30 °C, with a suitable growth temperature of 10-40 °C. Acid-fast staining of Rhodococcus equi shows uncertain results. Due to its morphological diversity, it is often mistaken as diphtheroid bacillus, bacillus or micrococcus. In sheep blood agar, rhodococcus equi can have synergistic hemolysis with staphylococcus aureus, Listeria monocytogenes and corynebacterium pseudotuberculosis, which is a characteristic manifestation of Rhodococcus equi. The most common pathological changes in Rhodococcus equi infection are chronic purulent bronchitis and extensive lung abscess. Imaging often demonstrates subacute pneumonia, commonly with cavities.

The clinical manifestations are poor appetite, drowsiness, fever and shortness of breath. Studies by E Marchiori et al. [ 30 ] in 2005 revealed that all the 5 cases of AIDS complicated by rhodococcus equi pulmonary infection have cough and fever lasting for 1-2 months, with accompanying shortness of breath and chest pain. All the 13 cases, studied by Li et al. in 2011 [ 106 ] , have fever with a body temperature up to 38-40 °C and cough. In addition, there are also expectoration with orange red sputum in 10 cases, hemoptysis in 4 cases, dyspnea in 11 cases, moist rales of lungs in 13 cases, emaciation in 6 cases, poor appetite in 6 cases, diarrhea in 2 cases, joint pain in 1 case, oral candidiasis infections in 13 cases, oral herpes in 4 cases, chest pain in 4 cases, no obvious symptoms in 1 case and hepatitis B in 3 cases. Typical clinical manifestations of this disease are fever, cough, dyspnea and chest pain, while others such as emaciation, diarrhea and joint pain are not representative symptoms.

Identifi cation of the Bacteria Various specimens were inoculated on blood plates at a temperature of 35 °C for 18-24 culture, with bacteria growth of 18 strains. They are biologically characterized by a diameter of about 0.5 mm, non-transparent and slight yellowish colonies. After 48-72 h, the colonies expand to 1-2 mm, which can be emulsifi ed in mucous fl uid liked state. Most of the colonies produce orange and orange red pigments, which can be cultured in ordinary agar.

Histopathological fi ndings are typical for Rhodococcus equi infection. H&E staining demonstrates mainly bleeding in the alveolar space, large quantity epithelial cells, possibly predominant fi broblasts, parenchymal changes of lung tissue and thickened alveolar septa. PAS staining demonstrates scattered or clustered rhodococcus equi in pink or purplish red.

Both are the most commonly used imaging examinations.

Biphasic TV monitor guided lung puncture can be performed to suck lung tissues for biopsy, based on which the real pathogenic bacteria can be detected.

The typical demonstrations include central hilar sphere liked shadow with increased density in unilateral lung, accounted for 70 %. There are also manifestations of exudative infi ltration and large fl aky or spherical mass shadows in the right or left hilar area. The lesions are in patchy or fl aky appearance, radiating from the hilum to the lung fi eld with blurry boundaries.

A male patient aged 30 years was confi rmatively diagnosed as having AIDS by the CDC. He complained of recurrent fever, cough and chest pain for 13 days; and was found HIV positive for 8 days. He was also a carrier of hepatitis C virus, with symptoms of fever with no known causes, cough, chest distress and weak limbs. By examinations, he was found to have complexion of chronic conditions; many moist and dry rales by cardiopulmonary auscultation. He had a past history of HIV positive for 8 years, with drug abuse and extramarital affairs. The history of present illness includes fever, paroxysmal cough with a little whitish yellow thick sputum since May 8, 2008 . He also had subjective paroxysmal dull pain in the left chest, and hemoptysis once which was bright red with blood clot in a volume of about 80 ml. His CD4 T cell count was 10/μl. By sputum culture, Rhodococcus equi was found positive. After receiving antibiotic treatment, his conditions improved and he was discharged from the hospital. 

Catalase test of the strain is positive, which is confi rmed as Rhodococcus equi by API CORYNE system.

Examinations H&E staining demonstrates mainly bleeding in the alveolar space, large quantity epithelial cells or mainly fi broblasts, parenchymal changes of lung tissue and thickened alveolar septa. PAS staining and Masson staining demonstrate scattered or clustered distribution of rod rhodococcus equi in pink or purplish red.

AIDS complicated by pulmonary rhodococcus equi infection shows subacute infl ammation. Firstly, there are exudates in the surrounding area of unilateral hilum as well as sphere shaped mass shadows which is centrally dense and peripherally blurry, with its apex pointing to the hilum. The lesions can be complicated by cavities and fl uid level, with thick wall of the cavities. As the disease progresses, the abscess cavities have increased tension, with gradually thinner abscesss cavity walls and uneven wall thickness, even showing pleural effusion. These are its characteristic imaging fi ndings.

It often needs to be differentiated from Pneumocystis carinii pneumonia, tuberculosis, staphylococcus aureus pneumonia, central type lung cancer and other diseases. Imaging fi ndings of Pneumocystis carinii pneumonia usually are ground glass liked changes in the lung fi eld, with parenchymal changes and centrilobular nodules. Tuberculosis often shows miliary tuberculosis, with lymphadenectasis, large tubercles and parenchymal changes. These characteristic pathological and imaging fi ndings of staphylococcus aureus pneumonia are similar to those of bronchial pneumonia (lobular pneumonia). The lesions are nodules with blurry boundaries in a diameter of 4-10 mm. The disease progresses rapidly, while pulmonary rhodococcus equi infection has a chronic progression. HRCT scanning demonstrates staphylococcus aureus pneumonia as centrilobular nodules and branch linear shadows (tree buds sign), which can be found in 40 % patients, with 15-30 % will develop into commonly singular pulmonary abscess. Chest CT scanning demonstrates round liked abscess cavity with thick wall and liquid level in it. The inner wall of the abscess cavity is often irregular, with various changes within short period. The central type of lung cancer is commonly demonstrated as round liked shadow of unilateral hilum with rough boundary. Lobulation or bronchial stenosis sometimes occurs. However, AIDS complicated by Rhodococcus equi pneumonia is demonstrated as sphere liked mass in the hilum; mostly sphere liked increased density shadow with hilum as the center. The shadow is centrally dense and peripherally blurry, with no bronchial stenosis.

Rhodococcus equi was fi rstly discovered in 1923 and was nominated as corynebacterium equi. After structure analysis of the cell wall, it was found that the bacterium is quite different from Corynebacterium, and therefore classifi ed as Rhodococcus. Rhodococcus equi is generally believed to be the pathogen for horses, pigs and cattle. [ 106 ] showed a CT4 T cell count of lower than 49/μl. All the results are in consistency. In conclusion, AIDS complicated by pulmonary Rhodococcus equi infection is mainly subacute infl ammation. There are exudation around the unilateral hilum as well as centrally dense and peripherally blurry sphere shaped mass shadows, with secondary cavities and parenchyma changes and even pleural effusion. All of these are characteristic imaging demonstrations.

Most cases of HIV positive complicated by respiratory or pulmonary diseases are caused by Aspergillus fumigatus. Aspergillus fumigatus belongs to filamentous fungi, which is a common opportunistic fungus and has a wide distribution in the nature. As conditional pathogenic bacteria, it can parasitize in the human skin and upper respiratory tract. Human has certain resistance to Aspergillus so it commonly fails to cause diseases. In immunocompromised AIDS patients, the pathogenic bacteria can pass through the defects in the skin and mucous membrane into the blood flow to infect the tissues and organs.

Aspergillus commonly violates bronchus and lung, with involvements of rhinal sinuses, external auditory canal, eye and skin. Otherwise, it disseminates to organs of the body along with blood fl ow. The early lesions are diffuse infi ltrative and exudative changes. And advanced lesions are necrosis, pyogenesis or granuloma. Large quantity hyphae can be found in the lesions. The hyphae penetrate the blood vessels to cause vasculitis, perivascular infl ammation and thrombosis. And thrombosis can cause ischemia and necrosis of the tissue. According to the pathological changes and imaging fi ndings, it can be divided into three major types: vascular invasion type, bronchopneumonia type and allergic bronchopulmonary aspergillosis type. (1) The vascular invasion type is the result caused by toxins released in the process of aspergillus spreading extensively from the primary focus to the lungs. Vascular infi ltration of the pulmonary parenchyma and coagulative necrosis are believed to be the cause of vascular occlusion and pulmonary infarction. (2) Bronchopneumonia type is acute bronchitis caused by inhalation of Aspergillus spores. In the cases of hyphae invasion into the lung tissues, extensive infi ltrative pneumonia or focal granuloma are resulted in. It can also cause necrosis, pyogenesis and multiple small abscesses. Spherical pulmonary aspergillosis is often secondary to bronchiectasis, tuberculosis, carcinous cavity and other lung diseases. Mycelia multiply and gather in the cavities of the lungs to form a spherical mass with fi brin and mucosal cells, which are called aspergillar glomera, which do not invade the lung tissue. (3) Allergic bronchopulmonary aspergillosis type is the proliferation and germination of inhaled Aspergillus spore in the airway, often showing obvious related mucosal lesions and eventually resulting in bronchiectasis ( Fig. 17.64a-c ) .

The cases with acute onset have symptoms of high fever or irregular fever, cough, shortness of breath and green purulent sputum. The cases with a chronic onset have symptoms of repeated cough and hemoptysis, which are similar to those of tuberculosis. The pulmonary signs are not obvious, with occasional fi ndings of moist rales.

Most cases are asymptomatic and sometimes there are fever, cough, shortness of breath, and mucous purulent sputum.

The main symptoms are persistent fever, cough and chest pain. In the serious cases, there is dyspnea.

By microscopic examination of sputum, Aspergillus hyphae can be found. The culture for aspergillus fumigatus is positive.

Serum IgE is commonly above 2,500 μg/L. Skin test for aspergillus antigen is positive. Serum anti-Aspergillus antigen IgG antibody precipitin is positive.

Puncture of lungs and pleura for biopsy facilitates the diagnosis of pulmonary fungal infections.

Both are the most commonly used imaging examinations.

HIV/AIDS related aspergillus bronchopneumonia is commonly demonstrated to have increased pulmonary markings, diffuse patchy blurry shadows and mass shadows in both lungs. Spherical pulmonary aspergillosis is commonly demonstrated to have sphere liked aspergillar glomera suspending in the cavities to form a crescent shaped transparent area, in characteristic meniscus sign, rolling ball sign and fi ngertip sign. Meniscus sign is nominated due to a meniscus liked space between the aspergillar glomera growing in the cavity and the cavity wall. Rolling ball sign means that the aspergillar glomera moves along with the changes of posture. Fingertip sign indicates that the substance formed by aspergillar glomera in dilated bronchi is in a fi nger shape, sometimes in V shape sign and Y shape sign. Invasive lesions refer to lesions invading or destroying lung structures, such as pneumonia, parenchymal changes and necrosis. A female patient aged 28 years was confi rmatively diagnosed as having AIDS by the CDC. She complained of cough and chest distress, with increased eosinophilic granulocytes. Her CD4 T cell count was 45/μl. A male patient aged 36 years was confi rmatively diagnosed as having AIDS by the CDC. He complained of high fever or irregular fever, cough and shortness of breath. His CD4 T cell count was 96/μl. 

A male patient aged 38 years was confi rmatively diagnosed as having AIDS by the CDC. He complained of high fever or irregular fever, cough and shortness of breath. His CD4 T cell count was 76/μl. 

A male patient aged 35 years was confi rmatively diagnosed as having AIDS by the CDC. He was hospitalized due to complaints of fever for 1 week, chest distress and shortness of breath for 1 day. On admission, he was confi rmed as HIV positive, with a CD4 T cell count of 9/μl. By physical examinations, he was in poor physical conditions, respiratory rate 27/min, lips cyanotic, coarse breathing sounds of both lungs with small quantity dry rales. His conditions progressed rapidly and death occurred due to respiratory failure after 3 days. 

Lung and pleura puncture for biopsy can detect the growth of Aspergillus hyphae.

Sputum culture can detect Aspergillus hyphae, with fi ndings of Aspergillus fumigatus positive.

In the cases with allergic bronchopulmonary aspergillosis, the serum IgE is above 2,500 μg/L. Skin test of aspergillus antigen is positive. The serum anti-Aspergillus antigen IgG antibody precipitin is positive.

Characteristic CT scanning demonstrations of HIV/AIDS related parasitic aspergillar glomera include pulmonary cavities or cavity lesions with spherical contents, smooth boundaries of the spherical contents with even density, lunate shaped or ring shaped transparent shadows between cavity or cavity walls and the contents, migration of the contents with the body postures. According to the pathological and imaging demonstrations, it can be divided into three major types:

In the early stage, CT scanning demonstrates soft tissue density nodules or light ground glass liked halo sign around the mass, which is the evidence for the diagnosis of the invasion 

type pulmonary aspergillosis. Air cresent sign refers to round pulmonary infi ltration with accompanying central necrosis and surrounding lunate or ring shaped cavity. Other noncharacteristic CT scanning demonstrations include multiple lobular parenchyma lesion shadows or lobular fusion shadows, parenchyma lesion shadows in the lobes, segments and subsegments, nodular or mass shadows and thin/thick wall cavities or low density areas in the mass shadows.

It is demonstrated to have parenchymal lesions around the airway or/and central small nodules in the lower lobes. The parenchymal lesions prove the occurrence of mycotic bronchopneumonia.

The most common imaging fi nding is the thickened bronchial wall. Central bronchiectasis is its characteristic demonstration. In the cases of dilated bronchi containing sputum bolt or mucus, it shows fi ngertip shaped or toothpaste shaped shadow, which should be considered as its characteristic demonstration.

HIV/AIDS related pulmonary aspergillosis should be differentiated from congenital bronchial atresia. Most cases of the congenital bronchial atresia are atresia at the proximal pulmonary segment of the bronchi, often with a clearly defi ned mass. In the typical cases, there are bronchial branches and more branches in fi ngertip shape, pointing to the pulmonary hilum. Confi ned pulmonary air retention in the pulmonary lobe and segment of the atresic bronchi is the important evidence for the diagnosis of congenital bronchial atresia.

HIV/AIDS related pulmonary aspergillosis should be differentiated from allergic bronchial-pulmonary aspergillosis.

In the cases of allergic bronchial-pulmonary aspergillosis have no clearly defi ned mass, with demonstrations of V shaped, Y shaped, grapes shaped or fi ngertip shaped shadows with clearly defi ned boundaries, which are characteristic in those patients with bronchial asthma or a case history of exposure to dusts containing fungi. There is also increased proportion of eosinophilic granulocytes in the peripheral blood. Detection of aspergillus in phlegm can defi ne the diagnosis.

HIV/AIDS related pulmonary aspergillosis should be differentiated from central lung cancer. Central lung cancer also can cause mucus impaction of the distal bronchi, with manifestations of bronchial arctia and/or truncation, and the surrounding soft tissue mass shadows.

HIV/AIDS related pulmonary aspergillosis should be differentiated from pulmonary cavities and abscesses induced by dissolved tuberculoma, secondary pulmonary TB, chronic lung abscess and peripheral lung cancer as well as cystic bronchiectasis. Except aspergilloma, spheric morphology caused by other causes is commonly irregular. The cavity contents cannot migrate with body postures, which is the key point for the differential diagnosis.

HIV/AIDS related pulmonary aspergillosis can be caused by many pathogenic bacteria and aspergillus fumigatus is the most common one. The infection is often caused by inhaled aspergillus fumigatus in the environment. Vascular invasion type of pulmonary aspergillosis usually has multiple lesions and nodular changes. Generally in pathology, the center of nodule presents typical pale color; commonly with fi brous ring surrounding the nodules resulted from hemorrhage and/or lung parenchymal changes. Histologically, they are characterized by coagulative necrosis of the lung tissues, infi ltration of large quantity hyphae in the necrotic tissue, pulmonary vascular infi ltration, but usually without responses of vasculitis and thrombosis. The enzymes released by neutrophile granulocytes can cause the separation of necrotic tissue from its adjacent lung tissues to form necrotic mass in the cavities. Airway invasion type of pulmonary aspergillosis, also called aspergillus bronchopneumonia, accounts for 15-30 % of invasive aspergillosis. The most common imaging fi ndings are unilateral/bilateral fl aky parenchymal changes, centrilobular small nodules and branches liked linear shadows (tree buds sign). Histologically, it is characterized by necrosis and infi ltration of neutrophil granulocytes. The lesions surround the bronchiole and the bronchiole. The invasion of the pulmonary artery can cause bleeding of the adjacent pulmonary parenchyma. Allergic bronchopulmonary aspergillosis rarely has lesions, with no unknown pathogenesis, which is generally believed to be related to type I and type II allergic reactions. It usually shows obvious asthma related mucosal lesions. Hyphae generated by aspergillus fumigatus can induce the production of mucus and additional mucosal lesions, eventually leading to bronchiectasis. Dilatate bronchial lumen is fi lled with mucus or with absence of epithelium, which is replaced by a granulomatous infl ammatory infi ltration. The most common imaging manifestations are migratory fl occulent, branched Y shaped and V shaped (fi ngertip sign) shadows in the pulmonary parenchyma, which are related to the infi ltration of eosinophils.

Pathologically, bronchial cystic dilatation in the pulmonary segment and sub-segment occurs, with large quantity eosinophils in the bronchial mucus and scattered broken aspergillus hyphae. In combination with the case history, the diagnosis can be defi ned.

Compromised immunity is an important cause of cryptococcosis, especially in patients with AIDS or abnormal lymphoproliferative diseases. Cryptococcus neoformans, a single phase mould, exists widely in the natural world. The cryptococcus has a diameter of less than 10 μm, which can be inhaled into the human body via respiratory tract. Under the impact of a high concentration carbon dioxide, it forms a clearly defi ned protective layer composed of polysaccharide capsule to antagonize the defense mechanisms of the host. Thus, lung infection occurs after its inhalation in immunocompetent people, which is commonly asymptomatic. of cryptococcus, Inhalation of cryptococcus by AIDS patients can lead to hilar lymphadenopathy, as well as singular or multiple subpleural small nodules, being similar to those in the cases of Mycobacterium tuberculosis infection.

In the early stage of cryptococcal infection, only a mild infl ammatory reaction or diffuse infi ltrative exudative changes occur. But in the advanced stage, necrosis, suppuration or granuloma is formed. Large quantity hyphae can be found in the focus. In the cases with hyphae penetrating the blood vessels, vasculitis, perivascular infl ammation and thrombosis occur. And thrombosis leads to ischemia and necrosis of the tissue (Fig. 17.77 ).

Pulmonary cryptococcus infection in AIDS patients often is extensively disseminating, with symptoms of fever, cough, diffi culty breathing, expectoration, chest pain caused by pleuritis, and even acute respiratory distress syndrome (ARDS). 

HIV/AIDS related pulmonary cryptococcus infection has no characteristic imaging demonstrations. Chest X-ray and CT scanning show multiple morphology of the lesions. In the slight cases, there are thickened pulmonary markings in both lower lungs or isolated nodular shadows, and occasionally cavities. In the cases of acute interstitial infl ammation, there are diffuse infi ltrative or miliary foci, with infi ltration, nodules or exudation in any lobe which is more common in bilateral middle and lower lungs, in unilateral lung or confi ned to one lobe. The foci may be isolated huge spherical or multiple nodular, without obvious surrounding infl ammatory responses, similar to those of tubercles or tumors. Otherwise, they are diffuse miliary shadows or fl aky infi ltrative shadows. A male patient aged 60 years was confi rmatively diagnosed as having AIDS by the CDC. He was hospitalized on 2009-2-19 due to headache and vomiting for more than 10 days. In the CSF, Cryptococcus was found. By blood and sputum culture, cryptoccocus was detected. The diagnosis was cryptococcal meningitis, cryptococcal pneumonia and cryptococcal sepsis. After receiving amphotericin B antifungal treatment and dehydration, headache and vomitting were relieved. But chest CT scanning reexamination demonstrated increased pulmonary lesions, which was considered as tuberculosis. On 2009-4-1, he was given HERV anti-tuberculosis treatment. Twenty days ago he sustained weakened lower limbs, which gradually aggravated and completely paralyzed in the recent 1 week, His CD4 T cell count was 34/μl. 

HIV/AIDS related pulmonary cryptococcus infections should be differentiated from tuberculosis, primary or metastatic lung cancer. Tuberculosis mostly is secondary tuberculosis, which is caused by repeated infections of tubercule bacillus. Lesions show fl aky or fl occulent shadows in the two upper lungs, with blurry boundaries. The wrapped necrotic foci by fi bers develop into nodules. It can also show miliary shadows, mostly with mediastinal lymphadenectasis. It should also be differentiated from primary or metastatic lung cancer.

Cryptococcus is a relatively common pathogen of pulmonary fungal infection, and mostly develops in AIDS patients. Usually, it is a disseminated disease, with common involvement of the central nervous system and the lungs. In immunocompetent patients, the nodular granuloma caused by the pathogen is similar to those of other pulmonary fungal infections. In patients with serious immunosuppression, wide tissue infi ltration of the pathogens may occur in the lungs. 

liked shadows, parenchymal changes of air cavity and miliary nodules. The pathogenic fungi can be found mainly in the pulmonary interstitium. Imaging fi ndings include singular or multiple nodules or masses, parenchymal changes of lung lobes and lung segments with clear or unclear boundaries in size of 1-10 cm. There may be also miliary lesions, lymphadenectasis and cavity shadows.

Candida is an opportunistic pathogen, which widely exists in nature. Candida albicans parasitize in the oral cavity, laryngopharynx, upper respiratory tracts, vaginal and intestinal mucosa of human being. Pulmonary and bronchial moniliasis is commonly caused by candida albicans which has the strongest pathogenicity. After its invasion into the tissues, candida transforms into hyphae and multiplies in a large quantity, with strong toxicity and ability to fi ght against phagocytosis. AIDS patients may have disseminated pathological changes. Only when the immunity is compromised, the pathogen invades into the bronchus or lungs to cause diseases. Therefore, pulmonary candida infection is commonly secondary.

Candidosis can cause acute infl ammation in bronchus and lungs, mainly exudation of neutrophils, which can be divided into two types: bronchitis type and pneumonia type. The pathological changes in the early stage are acute suppurative infl ammation, accompanied with the formation of abscesses. By the naked eyes observation, they are large fl aky parenchymal changes, with central grayish white coagulative necrosis. Under a microscope, the lesions are large fl aky caseous necrosis, accompanied with the formation of abscesses, and surrounding infi ltration of hyphae and phagocytes. In the advanced, there are caseous necrosis, formation of cavities, fi brosis and granuloma.

Symptoms in AIDS patients are mild, with frequent cough, with a small amount of white mucous phlegm or thick phlegm, no fever or low grade fever; scattered spots of white membranes in the mucosa of oral cavity, throat and bronchus. Dry rales can be heard occasionally in both lungs.

In AIDS patients, the manifestations are mostly acute pneumonia or sepsis, with chills, fever, cough, expectoration of white mucous jelly liked phlegm or thick phlegm often with blood or necrotic tissue. The thick sputum, candidal hyphae and shedding cell debris can be condensed into small colloid clumps, with yeast smell. Other symptoms include even haemoptysis and diffi culty breathing. Dry and moist rales can be heard in lungs.

Symptoms may be diffi culty breathing, rhinocnesmus, runny nose and sneezing. Wheezing rales can be heard in both lungs. 

Chest X-ray Chest X-ray demonstrates nodular shadows and fl aky parenchyma changes in unilateral or bilateral lungs. Sometimes there is miliary infection.

CT scanning demonstrates most lesions in the middle and lower lung fi elds, with rare involvement of the apex. There are thickened lung markings or diffuse small fl aky/patchy shadows, some of which can fuse into large fl aky dense shadows, with blurry boundaries. Nodules, due to bleeding around it, may be surrounded by ground glass liked shadows, which is necrotic bronchopneumonia, usually accompanied with a large quantity neutrophils.

Cough expectoration with white mucous phlegm or thick phlegm, hemoptysis and shortness of breath.

Examinations of the oral cavity and the throat demonstrate spots liked white membrane covering the surface, and dry and moist rales in the lungs.

Successive cultures of phlegm, lung tissue, pleural fl uid or cerebrospinal fl uid repeatedly demonstrate the same strain of candida, or direct microscopic fi ndings of large quantity pseudohyphae or hyphae and groups of spores can defi ne the diagnosis.

It is demonstrated to have thickened and deranged lung markings in double lung, diffuse small fl aky/patchy shadows, fusion of some small shadows into large fl aky dense shadows, with blurry boundaries, enlarged hilum and blurry structures. The conditions progress rapidly, with repeated lesions occurrence.

HIV/AIDS related pulmonary candida infection should be differentiated from bacterial pneumonia. Bacterial pneumonia often has symptoms such as high fever, cough, expectoration, chest pain and shortness of breath. CT scanning demonstrates fl occulent infi ltrative shadows or parenchyma changes and cavities. The pathogen can be detected in the sputum or chest liquid.

HIV/AIDS related pulmonary candida infection should be differentiated from virus pneumonia. Viral pneumonia fi rstly causes upper respiratory tract infection, which spread downward to cause pulmonary infl ammation. The demonstrations

A male patient aged 40 years was confi rmatively diagnosed as having AIDS by the CDC. He complained of high fever, cough, expectoration, chest pain and shortness of breath, with pulmonary parenchymal changes sign and moist rales. His CD4 T cell count was 18/μl. include ground glass liked changes in the lung fi elds or mass shadows. The defi nitive diagnosis should be based on throat swabs, virus isolation from the sputum and serum specifi c antibodies test.

HIV/AIDS related pulmonary candida infection should be differentiated from pulmonary tuberculosis. In the early stage, the symptoms and signs include irritative dry cough, expectoration, hemoptysis and cavities in lungs. (Detailed manifestations of tuberculosis see the section about tuberculosis in this chapter) Its diagnosis mainly should be based on chest X-ray and fi ndings of tubercule bacillus in sputum or other specimens, or tuberculosis specifi c pathological changes.

HIV/AIDS related pulmonary candida albicans is a widespread dimorphism bacteria. The oval shaped budding yeasts and hyphae both can be found in the tissues. Candidiasis is a common disease in AIDS patients. Chest X-ray demonstrates unilateral or bilateral patchy parenchymal changes of the air cavity and nodules with unclear boundaries. Miliary lesions are common. HRCT demonstrates multiple nodular shadows in both lungs, often accompanied with parenchymal changes. Its defi nitive diagnosis should be based on the fi ndings of candida albicans in the tissues.

Penicillium marneffei (PM) is a newly found penicillium in 1956, which is a special strain with a distribution in South East Asia and Southern China. Rhizomys is its natural host. In 1973, Disalvo et al. [ 12 ] reported the fi rst case of natural human PM infection. In 1984, the fi rst case of human PM infection in China was reported in Guangxi Zhuang Autonomous Zone. PM is an opportunistic pathogen and immunocompromised people are susceptible to its infection. Its spreading is along with soil contaminated by Rhizomys feces to invade human body via the respiratory tract, the digestive tract and skin defects. PM infection is believed to be one of the most common opportunistic infections in AIDS patients in Southeast Asia, which has an increasing incidence.

PM is the only dimorphic fungus in hyphomycetes penicillium, which is a special strain of penicillium. At different culture temperatures, it shows conversion of biphasic forms: fungal phase at 25 °C and yeast phase at 37 °C. The fungal phase is the hyphae of many cells, with certain biological morphology, such as penicillus, conidiophore, chain liked conidiospore and chains between spores. The yeast phase shows unicellular or bicellular form. In the growth process of PM, large quantity bright rosy or dark rosy pigments are produced, which is characteristically PM. The pigment of yeast phase is secondary metabolites of cells with strong hydrophobicity, which can promote the adhesion of conidiums in fungal phase and cells in yeast phase to the alveolar macrophages and other cells surface in the human body. The pigment monoclonal antibody (MAb) can interrupt the pathological process of adhesion. In addition, this pigment can determine the expression of cluster-encoding genes Mbr through diffusion and penetration of drugs to the cell membrane, thus preventing the penetration of hydrophilic antifungal drugs, such as fl uconazole. That is to say, it improves the natural antifungal resistance level of PM. The soluble components of the pigment in fungal phase can trigger the generation of anti-conidium antibody (only IgG) in animals to prevent its spreading in the body. The phenomenon proves that, in terms of tissue invasion, fungal phase is less powerful than yeast phase. Conidium in fungal phase is the carrier of pathogen while the cells in yeast phase are the real pathogenic factors.

When PM spreads to the target organ along with the blood fl ow, it is engulfed by mononuclear phagocytes. In the cases of replication itself and further spreading, reactive proliferation of phagocytes is caused. Mononuclear phagocyte system has strong defense ability. In the cytoplasm of proliferated mononuclear phagocytes, various amounts of PM can be found. PM mainly invades into the body via the respiratory tract, digestive tract and skin defects. In immunocompetent people, local abscesses form in the invasion site, which is characterized by the thick mucus fl uid, with mainly necrosis and liquefaction. Vascular reactions and exudation of neutrophil leukocytes and body fl uids is less than abscesses induced by common purulent bacteria. The clinical manifestation is confi ned suppurative infl ammation. When the immunity is compromised, due to the insuffi ciency of immunologic factors, it is diffi cult for the immune cells to restrict and digest the engulfed pathogens, which leads to confi ned suppurative reaction. Therefore, it often presents with diffuse lesions. The pulmonary lesions are principally interstitial exudative infl ammation.

The typical penicillium marneffei disease has acute or subacute onset, along with fever, chills and shivers, cough and expectoration, hemoptysis, shortness of breath, abdominal pain, diarrhea, bloody stool, fatigue, central necrotic papula mainly in the head and face and scattering in the trunk and extremities as well as hepatosplenomegaly.

Bone marrow smear and PAS staining can be performed to detect the pathogen. Blood, bone marrow, pleuroperitoneal fl uid, phlegm and skin defect tissue are collected for the culture at double temperatures with Sabouraud'Broth medium. At the temperature of 25 °C, the colony is in dark red with villous surface, with surrounding red wine liked pigments to gradually spreading into the medium.

Biopsy of lymph nodes and skin defects with PAS staining and Wright & Gimsa staining can be performed.

WBC count, hemochrome, platelets, AST and CD4 T cell count.

CT scanning and routine chest X-ray are the diagnostic imaging examinations of choice, which can facilitate to understand the size, morphology, location, quantity and density of the lesions.

It demonstrates multiple small nodular shadows in the lungs, multiple honeycomb liked cavities in both lungs and mediastinal lymphadenectasis. Abdominal scanning demonstrates different degrees of hepatic, splenic and retroperitoneal lymphadenectasis, which can fuse into a huge mass.

Routine Chest X-ray It demonstrates thickened, deranged and blurry pulmonary markings, small cavities, military nodular shadows, mass liked shadows, spots and patchy shadows, ground glass liked changes, pleuritis and pleural effusion. A female patient aged 35 years was confi rmatively diagnosed as having AIDS by the CDC. Her husband had a history of drug abuse and she complained of abdominal pain and fever for more than 2 months, with accompanying face rash and diarrhea. Her CD4 T cell count was 5/μl. By examinations, she sustained skin palpula, abdominal tenderness, central concave skin rashes on the face, neck, and upper limbs. There was a palpable mass in the upper left abdomen, hard and tenderness, in a size of 12 × 12 cm. More than 2 months before her admission, she had persistent dull abdominal pain that is commonly in the upper left abdomen, with accompanying fever and face skin rashes that is gradually increasing and spreads to the neck and upper limbs. She also had hepatosplenomegaly, abdominal aortic lymphadenectasis and ascites. A female patient aged 51 years was confi rmatively diagnosed as having AIDS by the CDC. She had an unhealthy sexual life, with complaints of fever and cough for more than 1 month. Her CD4 T cell count was 7/μl. A male patient aged 35 years was confi rmatively diagnosed as having AIDS by the CDC. He had been found to be HIV positive for 5 years, with complaints of irregular fever, cough, fatigue and dizziness for 10 days to be hospitalized. By examinations, his CD4 T cell count was 40/μl, HIV positive, Subcultivation of strains demonstrated typical biphasic penicillium. By fungus culture, typical penicillus was found. By bone marrow smear, the round corpuscles mainly located in the macrophages. A male patient aged 32 years was confi rmatively diagnosed as having AIDS by the CDC. He had a history of extramarital affair, with complaints of fever, cough, chest distress, shortness of breath, fatigue, poor appetite, poor sleep, weight loss and shortness of breath after activities for more than 3 months. His CD4 T cell count was 23/μl. 

Chest X-ray and CT Scanning Both demonstrate multiple nodules in different sizes and cavity shadows. The cavities cluster into honeycomb liked changes with uneven thickness of the walls, clear boundaries and surrounding infl ammatory exudates. Some of the nodules infuse into mass dense shadows. Lesions in both lungs have a symmetrical or asymmetric distribution, with no characteristic leions. Mediastinal lymph nodes are obviously enlarged.

Sputum smear for direct microscopy demonstrates candida.

PMs are found by fi brobronchoscopy lavage smear and biopsy.

(1) Candida skin test shows positive. (2) Fluorescent antibody test for PMs is performed in procedures of direct smear, fungal colony culture and histopathological examination of the tissue sections.

Metabolites test of PM and PCR can be performed to determine the gene sequences of PM for the early diagnosis.

HIV/AIDS related penicillium marneffei pneumonia should be differentiated from bronchiectasis and blood borne staphylococcus aureus pulmonary abscess.

Although the cases of bronchiectasis are demonstrated to have clustering round shadows on the cross sections, the wall is thinner and even, accompanying to the spots liked vascular shadows. Some lesions have typical railway liked bronchial dilation signs.

It is demonstrated to have multiple small cavity lesions in both lungs in line with the evenly distributing blood borne lesions. The lesions are rarely clustering. The wall of the cavities is thick and even with surrounding marginal exudates and blurry boundaries.

With the steady increasing of HIV infections, reports on the complication of PM disease have also been increasing recently. The disease can be localized but mostly disseminated, with the involvement of lungs, liver, skin, lymph nodes and other tissues and organs. Therefore, it is known as penicilliosis marneffei or disseminated penicillium marneffei infection in literature reports.

Due to the insuffi cient knowledge about the disease, diagnosis is delayed or missed. In Thailand, penicilliosis marneffei has been the indicator disease of AIDS. About 20 % AIDS patients are infected by PM and 70 % have necrotic papula, which is characteristically disseminated penicillium marneffei infection. CT scanning demonstrates HIV/AIDS complicated by disseminated penicillium marneffei infection as fl aky parenchyma shadows in the lungs, clustering of cavities and nodular shadows, mediastinal lymphadenectasis and pleural infl ammation responses, which can facilitate its clinical diagnosis.

Mucormycosis is a rare kind of conditional fungal disease, with its pathogen, mucor, distributing widely in the natural world. It generally fails to cause diseases, but can cause systematic infections in immunocompromised people. Mucor often invades into the human body via the nose to cause paranasal sinuses and orbital infections, which can further invade into the brain to cause meningitis and frontal abscesses. Pulmonary mucormycosis is only second to the nasal-cerebral infection. It can spread via the respiratory tract to cause pulmonary infections. In addition, there are also skin and gastrointestinal mucormycosis as well as disseminated mucormycosis.

The pathological changes of HIV/AIDS related pulmonary mucormycosis are mainly hemorrhagic necrotic infl ammation. The defense mechanism of immunocompetent people is to kill the fungal spores with the phagocytosis of macrophages and oxidation killing mechanism. In immunocompromised or immunodefi cient patients, the macrophages are often too weak to restrain the engulfed spores from germinating. Therefore, the disease occurs. Vascular vessels are susceptible to the invasion of mucor, especially the arteries. Mucor can locally multiply to cause the formation of blood clots and embolization, and disseminate to other organs along with the blood fl ow. The main lesions are hemorrhage and necrosis of local tissues and exudation of neutrophils. The lesions of hemorrhage and necrosis are possibly related to the arteriole lesions caused by hyphae.

The clinical manifestation of HIV/AIDS related pulmonary mucormycosis is a nonspecifi c pneumonia. The most common symptoms reported in literatures are persistent high fever, cough, hemoptysis, chest pain and diffi culty breathing. It has a rapid progression, with a high mortality rate of 65-96 %. Lung lesions are hemorrhagic infarction or pneumonia, which can cause high fever, cough, expectoration, shortness of breath, chest distress, chest pain, hemoptysis (pulmonary artery involved) and other symptoms. Moist rales can be heard in both lungs and pleural rubs can be heard in the cases of pleura involvement.

1. Assisted by bronchofi broscopy, lung biopsy can be performed. 2. Histological examinations include bronchial lavage fl uid examination, exploratory thoracotomy and puncture of lung tissues for biopsy. 3. Chest X-ray and CT scanning are conventional effective examinations.

The lesions are frequently found in the dorsal and medial segments of both lungs. Early exudation shows miliary shadows, cavity shadows with no wall or with thin wall and small bronchiectasis shadows. Their further progression may cause fusion infi ltration, parenchymal changes, nodules, masses, thick-walled cavities and pleural effusion, with accompanying mediastinal lymphadenectasis.

1. The fi ndings of mucor or their hyphae by sputum and bronchofi broscopic biopsy. 2. The diagnostic imaging demonstrates lesions commonly in the dorsal and medial segments of both lungs. There are diffuse scattering miliary shadows, cavity shadows with no wall or with thin walls and small bronchiectasis shadows. They further progress into fusion infi ltration, parenchymal changes, nodules, masses, thick-walled cavities and pleural effusion. 3. Often with accompanying mediastinal lymphadenectasis.

Chest X-ray of pulmonary mucormycosis demonstrates progressive infi ltrated parenchymal changes, or masses, nodules, cavities and pleural effusion. It needs to be differentiated from miliary tuberculosis. HIV/AIDS related miliary tuberculosis are commonly demonstrated as chronic blood borne disseminated tuberculosis, with lesions distributing symmetrically in both lungs. Its long term progression causes fusion into masses. Otherwise, it can be cured by anti-TB therapies. The early lesions are no-wall cavities or thin wall cavities and small bronchioectasis shadows, based on which the differential diagnosis can be made.

Almost all cases of HIV/AIDS related pulmonary mucormycosis are found in immunocompromised patients. Chest X-ray demonstrates parenchyma changes and isolated or multiple nodules or masses. The parenchyma changes are patchy or fuse, with unilateral or bilateral distribution. About 20 % patients have pleural effusion and less than 10 % patients have hilar or mediastinal lymphadenosis. CT scanning demonstrates singular or multiple nodules or masses, commonly with clustering or honeycomb liked cavities. 

Cytomegalovirus pneumonia has extensive pathological changes in the lungs. Pathologically, it shows interstitial pneumonia, with the lesions randomly blood borne distributing in the lungs. The distribution can be diffuse, panlobular or focal. The target cells of pathological changes include alveolar cells and macrophages. Diffused pulmonary interstitial edema and fi brosis as well as alveolar swelling, focal necrosis, bleeding and hyperplasia occur after CMV infections to cause hypoxemia. Gross observation of fresh specimens demonstrates pulmonary surface edema and fl aky blooding spots. Fixed specimens demonstrate brown hard lung tissues. Under a microscope, pulmonary interstitial congestion as well as infi ltration of lymphocytes and mononuclear cells can be found, with the involved epithelial cells enlarged. In the pulmonary interstitium and alveoli, there are intranuclear inclusions, cytoplasmic inclusions and fl uid containing abundant proteins. The classical intranuclear inclusions can be found in the cells, purplish red or purplish blue, round or oval, with surrounding halos in eagle eyes sign. Atypical cytomegalic inclusions in cells are slender, long and round liked with abundant cytoplasm and accentric nucleolus, which are blurry, unclear and atypical ( Fig. 17 .97a-e ). Immunohistochemitry demonstrates HIV P24 antigen positive.

The systemic symptoms of CMV infection include fever, joint and muscle soreness and pain, abdominal distension and orthostatic hypotension. The respiratory symptoms include paroxysmal dry cough, diffi culty breathing, cyanosis and three depressions sign. According to the imaging fi ndings of CMVP, CMV pneumonia can be classifi ed as diffuse, miliary and mass types, among which the diffuse type is the most common.

Cytomegalovirus can be separated from respiratory secretions culture and urine culture by using human embryonic fi broblasts. By urine sediment smear, giant cell with inclusions can be found. By using immunofl uorescence, indirect hemagglutination inhibition and complement fi xing test, the antibody titer can be found increased. Indirect immunofl uorescence test and immunoenzymic staining test can be applied to detect the anti-CMV-IgG and IgM antibody. In addition, enzyme-linked immuno sorbent assay (ELISA) can also be performed to detect the anti-CMV-IgG and IgM antibody. CMV-IgM antibody positive indicates a recent infection, which has diagnostic value. A single serum CMV-IgG antibody positive indicates a previous infection. And during the acute and recovery phases, double serum CMV-IgG antibody titer being no less than four times increase has diagnostic value, indicating a recent infection.

PCR can be applied to quantitatively determine the viral load in the whole blood, blood plasma, leukocytes, urine, bronchoalveolar lavage fl uid (BALF), cerebrospinal fl uid and the tissue specimens, which is believed to be the best way for the diagnosis of invasive CMV infection.

Chest X-ray is the most commonly used examination. Chest CT scanning is superior to chest X-ray in terms of resolution and detection rate of the lesions.

Pulmonary demonstrations by CMVP include diffuse interstitial infi ltration and alveolar infi ltration to form reticular shadows, nodules and parenchymal changes. A baby boy aged 6 months was confi rmatively diagnosed as having AIDS by the CDC. He was infected via vertical transmission from mother to child, with recurrent cough after being born and the most recent cough for 4 days as well as wheezing cough in throat for 1 day before he was hospitalized. He had a past history of premature birth, with primary apnea and bronchial pneumonia and was hospitalized for treatment. Later, he was admitted for three times due to cough, which was diagnosed as interstitial pneumonia. By examinations, WBC 16.3 × 10 9 /L, LYM lymphocyte count 11.7 × 10 9 /L, CMV-Ab weak positive, blood sedimentation 11 mm/h, and tuberculosis antibody negative. After treated by broad-spectrum antibiotic therapy, the therapeutic effi cacy is unfavorable. 

Cytomegalovirus (CMV) infection is an important cause of pneumonia in patients with compromised immunity. Imaging fi ndings include nodular shadows with blurry boundaries and bilateral fl aky parenchymal changes of the lungs. The nodules tend to be bilaterally symmetric or asymmetric, with centrilobular distribution. Histopathological manifestations are nodular alveolar hemorrhage, necrosis and infl ammatory lesions, and diffused alveolar lesions. The nodules tend to have a centrilobular distribution, indicating occurrence of bronchiolitis. In AIDS patients, if the diameter of nodules is under 10 cm, it is most likely to be viral infection. The size of the nodules can facilitate the differential diagnosis of pulmonary infections.

Herpes simplex viral pneumonia (HSVP) often occurs in the upper respiratory tract, and rarely in the lower respiratory tract. Human herpes simplex virus can be divided into two types, namely herpes simplex virus type I (HSV-I) and herpes simplex virus type II (HSV-II). Herpes simplex viral pneumonia mostly occurs in patients with immunodefi ciency.

Herpes simplex viral pneumonia can be caused by HSV-I and HSV-II, both of which have a nucleocapsid with 20 surfaces. The thickness of the nucleocapsid is about 100 nm, which is composed of 162 capsomeres. The nucleocapsid contains the core of the virus DNA. The virion gains the phospholipid rich viral envelope when it passes through the nuclear envelope. The nucleocapsid gemmates after it passes through the nuclear membrane and is released to the cell surface. The nucleocapsid can also be released outside the cells or gains its access into the neighbour cells for further reproduction. Herpes simplex virus replicates itself in the cell nucleus to produce histopathologic changes of herpes virus replication, with visible Cowdry A type intranuclear inclusions. The pathogenesis process of herpes simplex virus infection in the body can be divided into fi ve stages: initial skin mucosa infection, acute ganglia infection, latent infections, re-activation, and recurrent infections in susceptible hosts. Patients infected by herpes simplex virus can produce IgM, IgG and IgA antibodies to fi ght directly against virus protein, which may play a role in changing the severity of the infection. Interferon also participates in the control of herpes simplex infection by inhibiting the virus or regulating the defense mechanism. Genetic factors may be also related to the herpes virus infection. Cellular immunity can confi ne the infection. Herpes virus cannot reproduce in the alveolar macrophages of human body, which is also the reason why herpes virus is less than cytomegalovirus in lungs. Currently, it is believed that herpes simplex virus is an important pathogen of respiratory infections, especially in immunocompromised patients. Localized herpes simplex viral pneumonia occurs due to the direct spreading of virus in the upper and lower respiratory tract. Diffuse herpes simplex viral pneumonia is caused by the virus spread from the reproductive organs lesions or oral lesions (most possibly blood borne). Viremia caused by HSV-I or HSV-II has been reported, and both are related to diffused infections. But in patients without herpes simplex viral infection in skin mucosa, herpes simplex viral pneumonia can also occur.

Herpes simplex viral pneumonia is caused by the direct spreading of the virus from the upper and lower respiratory tract. Diffuse herpes simplex viral pneumonia is cause by the spreading of the virus from the reproductive organs lesions or oral lesions (most possibly blood borne). Viremia cause by either HSV-I and HSV-II have been reported, both of which are related to diffuse infections. In such cases, the lung tissues may have infl ammatory infi ltration, lung parenchyma necrosis, bleeding, cellular swelling and round, diffuse interstitial pneumonia. And in most cases, there are accompanying cellular changes of herpes virus infection such as the intranuclear eosinophilic inclusions, necrotic herpes simplex viral trachitis. Herpes simplex viral bronchitis has demonstrations of mucosa erythema, edema, exudation and ulcer, with coverage of the surface by fi brous purulent membranous secretions.

The common initial clinical symptoms of herpes simplex viral pneumonia are shortness of breath, cough, and fever with a body temperature being higher than 38.5 °C, decreased WBC count, hypoxemia, respiratory dysfunctioning and azotemia. HSV pneumonia may be accompanied by mucocutaneous lesions by HSV, which show earlier than those of pneumonia. There may be concurrent fungus, cytomegalovirus or bacteria infection. Herpes simplex viral tracheobronchitis may show tracheal or bronchial spasm or stenosis.

Etiological Examinations HSV can be detected in tracheobronchial secretions, bronchoalveolar lavage fl uid and lung tissues. Early sampling should be performed under the guidance of a bronchofi broscope.

Tissue culture is the most sensitive and specifi c method for the diagnosis, which can also be used for the classifi cation of the virus.

Papanicolaou (Pap) or Tzank test is a fast and cheap method for cellular diagnosis.

ELISA can be used to detect herpes simplex virus, with a sensitivity of up to 95 % and a high specifi city.

Chest X-ray demonstrations are less valuable for the differential diagnosis. Pulmonary CT scanning can be applied for the differential diagnosis.

Herpes simplex viral pneumonia includes three types, namely local, multiple or diffuse interstitial infi ltration. In the early stage, typical hilar or diffuse interstitial shadows with increased density can be found, with thickened bronchial wall. As the disease progresses, cloudy or patchy alveolar tamponade and fusion can be found. Chest X-ray may demonstrate negative for herpes simplex viral trachitis and bronchitis. 

Herpes simplex viral pneumonia should be differentiated from bacterial pneumonia, CMV pneumonia, and infl uenza pneumonia.

HIV/AIDS related herpes simplex viral pneumonia is mostly demonstrated by multiple signs, including small nodules, ground glass liked shadows and patchy parenchymal changes. The nodules are in centrilobular distribution, mostly with accompanying branches liked shadows (tree buds sign). Chest X-ray demonstrates diffuse lung parenchymal changes. Imaging fi nding are parenchymal change areas with bilaterally blurry boundaries. Generally, the nodules have a diameter of 2-10 mm. CT scanning with high resolution demonstrates nodules with surrouding ground glass liked density lesions.

Lymphoid/Lymphocytic interstitial pneumonia (LIP) is more common in children with AIDS. The CDC in the United States has defi ned LIP in children under the age of 13 years as the diagnostic indicator of AIDS. The predictive diagnostic criteria include chest X-ray demonstration reticular nodular changes in pulmonary interstitium of both lungs for no less than 2 months, undetectable pathogens and no responses to the antibiotic therapy.

Currently, HIV/AIDS related lymphocytic interstitial pneumonia is considered to be related to HIV and Epstein-Barr virus, human T cell leukemia-lymphoma type I virus (HTLV-I) and HIV-I. The infection of the above viruses causes pulmonary lymphatic hyperplasia and other systemic diseases.

About 22-75 % children with HIV infection sustain LIP, and 3 % in adults. Most cases of non-HIV infected patients with lymphoid interstitial pneumonia are women, at average age of 56 years old, more commonly in the age group of 40-50 years old and above 70 years old. The pathological manifestations are infi ltration of small and mature lymphocytes as well as plasma cells in alveolar septum and the alveolus, extensive interstitial fi brosis and non-caseous granuloma. It is characterized by diffuse infi ltration of lymphocytes, plasmocytes and histocytes in the pulmonary interstitium. The lymph follicle with germinal center is more common. Hyperplasia occurs in type II alveolar epithelium, and the macrophage increases in the alveolar cavity. There are rare or mild intraalveoli organization and macrophage aggregation. Staining of the immune globulin light chain demonstrates poly-clone B cells.

The clinical symptoms are in progressive development, with cough and suffocation, rare hemoptysis and Sjogren syndrome commonly in mouth and eyes. By examinations, the signs have slight difference between adults and children. In children, there are lymphadenectasis, hepatosplenomegaly, enlargement of parotid gland, clubbing fi ngers and wheezing sound. In adults, there are lymphadenectasis, slight fi ne bubbling rales, as well as hepatosplenomegaly and enlargement of parotid gland in 1/3 patients.

1. Peripheral hemogram demonstrates increased lymphocytes and eosinophilic granulocytes. 2. Myelogram demonstrates increased lymphocytes, plasmocytes and eosinophils. 3. Blood biochemical examination demonstrates increased immune globulin, predominantly lgM. 4. Blood gas analysis demonstrates hyoxemia. 5. Pathogenic examinations by bronchofi broscopy, bronchial alveolar lavage and biopsy can defi ne the diagnosis. 6. Pulmonary function examinations demonstrate restrictive ventilatory disorder, lower lung compliance and impaired diffusion function. Impaired diffusion function is a more sensitive indicator in monitoring the progress of the disease. 7. Chest X-ray is the most commonly used imaging examination, while chest CT scanning is commonly applied for the differential diagnosis.

Chest X-ray demonstrates HIV/AIDS related lymphoid interstitial pneumonia as reticular or reticular nodular shadows of lung markings in both lungs. HRCT demonstrates bilateral diffuse ground glass liked density shadows. Perivascular thin-walled pneumatocele is common. Pneumatocele induced by LIP is commonly found in the middle lung fi eld, which probably is due to the valve effects caused by infi ltration of cells around bronchioles. Manifestations of pneumatocele, together with ground glass liked density shadows, highly indicate LIP. Centrilobular and subpleural small nodules and thickened intralobular septa can be occasionally found. Dysfunctional diffusion is a more sensitive indicator in monitoring the progress of the disease.

HIV/AIDS related lymphoid interstitial pneumonia should be differentiated from allergic pneumonia, carcinomatous lymphangitis and pneumocystis carinii cysts.

CT scanning with high resolution demonstrates characteristic lesions of HIV/AIDS related lymphoid interstitial pneumonia, including intralobular linear shadows and honeycomb liked changes, with common involvement of the subpleural area and the basal lung. Its characteristic manifestations are clustering gas containing thin-walled cyst in a diameter of 2-10 mm, with clear cyst wall. Shared wall between cysts is its characteristic demonstration. The surrounding ground glass liked density indicates infl ammation. Intralobular linear shadows indicate interstitial fi brosis.

Pulmonary toxoplasmosis (PT) is caused by the toxoplasma parasitizing in cells. Ludlam et al. fi rstly proposed the concept of pulmonary toxoplasmosis in 1963 [ 107 ] , arguing that toxoplasma can cause atypical pneumonia. Later, there are some pathological reports about pulmonary toxoplasmosis or disseminated toxoplasmosis with lung involvement. In recent years, due to the global prevalence of AIDS, the incidence of pulmonary toxoplasmosis is increasing, with most cases being disseminated toxoplasmosis with lung involvement. PT has been one of the important opportunistic infections in patients with immunosuppression, especially AIDS patients.

HIV/AIDS related pulmonary toxoplasmosis is a zoonotic disease, with cats as its main transmission source, followed by pigs and sheep. People are infected by intake the water or food contaminated by cats' feces or without cooked meat. Immunocompromised AIDS patients are susceptible to this disease, and its occurrence is rare in immunocompetent people. After its invasion into the human body, the sporozoite in the cystozygote and intracystic cystozoite overfl ows to penetrate the intestinal wall mucosa and spread to the whole body tissues along with blood or lymph fl ow. The brain, heart, lymph nodes, and lung are the most vulnerable tissues and organs for the infection. Any abnormality in the process of defense mechanism can cause impaired immune functions to eliminate the toxoplasma, which ultimately causes systemic and pulmonary infections. Pulmonary toxoplasma infection may also be caused by the blood borne spreading of reactivated toxoplasma infection in other body parts, with no exclusion of reactivated pulmonary infection or primary pulmonary infection.

Ludlam et al. generally nominated toxoplasmosis as atypical pneumonia [ 107 ] . Catterall et al. divided toxoplasmosis into three types: necrosis, infl ammatory infi ltration and toxoplasma invasion [ 109 ] . It can also be classifi ed as type A: subclinical or occult infection; type B: interstitial and atypical pneumonia; type C: necrotic pneumonia; type D: lobar pneumonia; and type E: granulomas pneumonia (toxoplasmoma). By naked eyes observation, the involved lungs are solid, with congestion and red brown section. The pleura have bleeding spots, with moderate peribronchial lymphadenectasis. Under a light microscope, there is exudation of serous fl uids in alveolar cavities, occasional formation of transparent membrane or fi brin purulent exudation, infi ltration of small quantity neutrophils, proliferation and shedding of alveolar wall cells, and trophozoite and/or cysts of toxoplasma in epithelial cells and macrophages. The pulmonary interstitium may have infi ltration of lymphocytes and plasmocytes as well as visible fi broblasts and macrophages. The granuloma changes are also found in the lung tissues, with central stripes or localized necrosis and surrounding lymphocytes and small quantity multinucleated giant cells. It is diffi cult to fi nd toxoplasma in granuloma, but it can be found in the normal tissues around or near the granuloma.

Almost all cases of AIDS complicated by pulmonary toxoplasmosis are caused by disseminated toxoplasmosis with pulmonary involvement. It is commonly diffuse pulmonary infl ammation with serious symptoms, including high fever, cough, cyanosis, breathing diffi culty, possible occurrence of skin rashes, lymphadenectasis and meningitis. The chronic cases may have long-term low grade fever, cough, and weight loss.

Direct light microscopy of the specimen smear and enprint such as blood, cerebrospinal fl uid, bone marrow, anterior aqueous humor, phlegm, urine, saliva, and other osmotic solutions, as well as lymph nodes, muscle tissue or other living tissues can be performed for pathogen examinations.

Sabin proposed that the staining test have high sensitivity and specifi city according to the fi ndings that mixture of fresh toxoplasma with normal serum can be stained deep by alkaline methylene blue staining, while its mixture with immune serum can be stained light or blank by the same staining.

Other assays including indirect fl uorescent antibody, indirect blood coagulation, and complement fi xation test can provide valuable reference for the diagnosis.

Toxoplasm is tested in pathological eaminations that can provide valuable reference for the diagnosis.

Chest X-ray is the most commonly used diagnostic imaging examination. And chest CT scanning can be applied for the differential diagnosis.

Imaging fi ndings of HIV/AIDS related pulmonary toxoplasmosis can be divided into four types: bronchial pneumonia, interstitial pneumonia, pleuritis and complication of cardiovascular disease. The type of bronchial pneumonia is also known as lobular pneumonia, with thickened pulmonary markings that distribute along with the bronchi in the middle and lower lung fi elds, scattered patchy shadows with uneven density and blurry boundaries, fusion of some shadows into large fl aky shadow and widened hilar shadow. The type of interstitial pneumonia is demonstrated as reticular and nodular shadows. The interstitial lesions widen the space between the bronchiole and the alveolar wall, with stripes and fl occulent shadows. The type of pleuritis is rare, with signs of pleural effusion. The type of complication of cardiovascular disease is demonstrated as heart failure (acute pulmonary edema), with signs of pericardial effusion.

A male patient aged 39 years was confi rmatively diagnosed as having AIDS by the CDC. He complained of cough and fever. His CD4 T cell count was 29/μl. 

By direct light microscopy, toxoplasma tachyzoites can be found in the specimens such as blood, cerebrospinal fl uid, bone marrow, anterior aqueous humor, phlegm, urine, saliva, and other osmotic solutions, as well as lymph nodes, muscle tissues or other living tissues.

The fl uorescent antibody and complement fi xation test are positive.

The biopsy tissue culture and inoculation test are positive.

In the lesions and their surrounding tissues of interstitial e c d Fig. 17 . 105 (continued) pneumonia, necrotic bronchitis or granuloma, Toxoplasma can be found.

The diagnostic imaging demonstrates any one type of pulmonary toxoplasmosis, including bronchial pneumonia, interstitial pneumonia, pleuritis and cardiovascular disease, can be used as the evidence for the diagnosis of pulmonary toxoplasmosis. The type of bronchial pneumonia is also known as lobular pneumonia, with thickened pulmonary markings with a distribution in both middle and lower lung fi elds along with the bronchi, scattered patchy shadows with uneven density and blurry boundaries, fusion of some patchy shadows into large fl aky shadow and widened hilum. The type of interstitial pneumonia has typical demonstrations of reticular and nodular shadows. The interstitial lesions widen the space between the bronchiole and the alveolar wall, with strip and fl occulent shadows. The type of pleuritis is rare, with signs of pleural effusion. The type of cardiovascular disease may have signs of heart failure (acute pulmonary edema), and signs of pericardial effusion.

HIV/AIDS related pulmonary toxoplasmosis should be clinically differentiated from infectious mononucleosis and mycoplasma pneumonia.

with primary pulmonary lesions. Pulmonary low malignant B cell lymphoma is the most common primary pulmonary lymphoma which is derived from mucosa related lymphoid tissue. The manifestations include slowly decreased alveolar transparency. Pulmonary high malignant B cell lymphoma is extremely rare, which often occurs with singular lesion and primary disease such as immunodefi ciency.

HIV/AIDS related malignant lymphoma is mostly caused by compromised immunity. HIV/AIDS related Hodgkin's lymphoma is relatively rare. There are also reports about HIV/AIDS related T cell lymphoma with pulmonary involvement.

HIV/AIDS related malignant lymphomas are mostly highly malignant large cells lymphoma. Cerebral lymphoma is one of the defi ning diseases of AIDS. It has been reported that the clinical incidence of pulmonary infi ltration by malignant lymphoma is 10-20 %, but 29-50 % by autopsy.

In the early stage, it is commonly asymptomatic. With its progression, symptoms of dry cough, suffocation, and small quantity clear phlegm occur. Mediastinal lymphadenosis includes lymphadenectasis to compress the trachea by, blood vessels and nerves and lead to breathing diffi culty, superior vena caval obstruction syndrome, and hoarse voice. The pulmonary parenchyma lesions include reticular structure in the lungs. The clinical symptoms are cough, expectoration, suffocation and breathing diffi culty.

A male patient aged 43 years was confi rmatively diagnosed as having AIDS by the CDC. He complained of chest distress and cough for more than 1 month. His CD4 T cell count was 56/μl. In patients with HIV/AIDS related Kaposi's sarcoma, its serologic positive rate is 100 %. Kaposi's sarcoma cells can produce IL-6, during which IL-6 plays a role as an autocrine factor to maintain the cell growth, paracrine cytokines, stim-ulate proliferation of other interstitial cells and induct the vascular growth. Therefore, Kaposi's sarcoma is a kind of tumor with abundant blood vessels. Before the application of HARRT, the incidence of Kaposi's sarcoma in male homosexuals is 21 %. After the clinical application of HARRT treatment, the incidence is decreasing. In addition to HHV-8, some studies indicated that most patients with Kaposi's sarcoma have HIA-DR5 alleles, suggesting a possible relationship between Kaposi's sarcoma and the heredity.

There is no obvious difference between HIV/AIDS related Kaposi's sarcoma and classic Kaposi's sarcoma in pathological changes. Early pathological manifestations are chronic infl ammation or granulomatous infl ammation, with formation of new vascular and lymphatic vessels and accompanying edema and bleeding. The fi ndings of large and protruding endothelial cells in granuloma tissue with accompanying erythrocytic exudation and hemosiderin particles have great signifi cance for the early diagnosis. The pathological changes in the advanced stage are signifi cant proliferation of the endothelial cells, and proliferation of fi broblasts around capillaries. In the advanced stage, the lesions are often accompanied by extensive connective tissue hyperplasia, which presents diffi culty for its differentiation from common sarcoma. When it is diffi cult to defi ne the diagnosis by light microscopy, immunohistochemical examinations can be used to defi ne the diagnosis. The pathological changes are characterized by lesions confi ned to the epithelial lamina propria, gathering of spindle cells with mild heteromorphism around many lacuna vasorum with irregular lumen, erythrocytic exudation and hemosiderin sedimentation. The atypical lacuna vasorum can be compressed by proliferative spindle cells to be absent. Vascular endothelial cells and peripheral spindle cells may have mitotic phase in the advanced stage, with increased heteromorphism cells. The infl ammatory cells are mainly plasma cells, with acidophilic corpuscles and PAS staining positive, which can assist the pathological diagnosis.

Pulmonary Kaposi's sarcoma in AIDS patients rarely has symptoms. It is commonly concurrent with pulmonary opportunistic infections, with symptoms of cough, diffi culty breathing and fever. Other symptoms are related with the location of the tumors. The involvement of trachea or bronchi can cause luminal stenosis. The mediastinal tumor can compress and obstruct lymph vessels to cause pulmonary edema or a large quantity pleural fl uids, which result in respiratory diffi culty, and even respiratory failure.

(1) Sampling by bronchoscopy or endoscopy to prepare pathological section. (2) Chest X-ray demonstrates its typical manifestation of pleural effusion.

DR demonstrates enlarged and deranged hilum in both lungs in bird nest liked appearance. There is light density fl aky shadows in the both lower lungs. CT scanning demonstrates multiple rounds liked nodular shadows in the middle and lower lung fi elds of both lungs with clear boundaries. There are also mediastinal and hilar lymphadenectasis, with common involvement of the pleura and bilateral pleural effusion in a small quantity.

A male patient aged 33 years was confi rmatively diagnosed as having AIDS by the CDC. He had been detected as HIV positive for 5 months, with complaints of recurrent cough and nausea for 10 days and was hospitalized on Jan. 7, 2004. The transmission route was unknown because he denied histories of intraveneous drug abuse, paid blood donation, blood transfusion and unhealthy sexual behaviors. Five months ago, he was diagnosed as AIDS in the stage of AIDS in our hospital, and hospitalized to treat PCP, with a CD4 T cell count of 17/μl. His symptoms were quickly relieved after PCP treatment and he continued the antiviral therapy for almost 5 months after being discharged. By physical examinations, he was in poor spiritual condition, a light blue nodule in size of 0.5 × 0.5 cm in the left upper chest wall with medium hardness, palpable lymph nodes in size of 1.0 × 2.0 in the opisthotic area and inguen, no tenderness and being movable. By the digital rectal examination, a palpable prominent nodule with wide base at 4 cm 7 points away from the anus, with fl exible texture and smooth surface. By the auxiliary examinations, WBC 3.9 × 10 9 /L, NEμT 48.3 %, LYM 34.9 %, MON 7.4 %, EOS 9.0 %, RBC 3.27 × 10 12 /L, HGB 126 g/L, PLT 210 × 10 9 /L, routine urine test normal, blood sedimentation 16 mm/h. By hepatitis B examinations, HBsAg, Anti-HBe and Anti-HBe positive. His CD4 T cell count was 91/μl. By abdominal B ultrasound, multiple low echo nodules in the abdominal cavity, the largest in size of 1.2 × 1.0 cm, which are suspected to be enlarged lymph nodes. On Jan. 14, he received inguinal lymph node biopsy, with pathological report of Kaposi's sarcoma. During the treatment and following up, the involvement of lungs, digestive tract, lymph nodes and skin is suspected, with the diagnosis of phase II Kaposi's sarcoma and chemotherapy was recommended. Reexamination by chest X-ray demonstrated normal cardiopulmonary phrenic. Abdominal B ultrasound failed to fi nd enlarged lymph nodes. CT scanning demonstrated shrinkage of lesions in both lungs and mediastinal lymph nodes, with only palpable soybean sized submandibular lymph node. By examinations after chemotherapy, CD4 T cell count 67/μl, viral load 63,000 copies/ml. The patients had multimorphological erythema drug eruptions, which was suspected as drug allergies of chemotherapy, which were absent after symptomatic treatment. The following ups so far show no recurrence of Kaposi's sarcoma, with his CD4 T cell count fl uctuating around 400/μl. He can work as usual. A male patient aged 36 years was confi rmatively diagnosed as having AIDS by the CDC. He had a history of homosexual behaviors, with complaints of fever and cough for 2 months as well as chest distress for more than 20 days. Since, July 2010, fever with a body temperature of about 37.5-37.8 °C occurs, with cough, yellowish bloody sputum, and dark purplish patchy skin rashes.

By examinations, his anti-treponema pallidum antibody positive, multiple dark purplish patchy skin rashes on the face, eyelid, lower jaw, hairline, chest and abdomen with skin surface desquamation, palpable bilateral cervical lymphadenectasis and the largest in size of 10 × 19 mm. By laboratory tests, WBC 5.98 × 10 9 /L, N 78.74 %, RBC 2.22 × 10 12 /L, HGB 71 g/L, PLT 204 × 10 9 /L, CD4 12/μl. 

A male patient aged 27 years was confi rmatively diagnosed as having AIDS by the CDC. He complained of cough for more than 2 months, chest distress for more than 1 month, and bloody sputum for half a month and was hospitalized.

He had a history of homosexual behaviors. By examinations on admission, multiple round purplish blue skin rashes nodules on the limbs. His CD4 T cell count was 9/μl. demonstrations can also be fl aky fl occulent areas with blurry density or parenchymal density areas along with bronchi. 3. Lung puncture for histopathological biopsy demonstrates irregular vascular lumen in the dermis, proliferation of endothelial cell with accompanying heteromorphism. In some cases, there are tumor masses composed of spindle cells and epithelial cells.

Other Sarcoma and Vascular Tumor HIV/AIDS related Kaposi's sarcoma should be differentiated from other sarcoma and vascular tumor. KS invasion of the digestive mucosa can cause bleeding and upper gastrointestinal symptoms. The pathological lesions can be diagnosed by upper gastrointestinal endoscopy or biopsy. In the cases of no fever and exclusion of infections, the typical imaging demonstrations and bronchoscopy fi ndings can defi ne the diagnosis of pulmonary KS.

HIV/AIDS related Kaposi's sarcoma should be differentiated from Pneumocystis carinii pneumonia. The lesions of PCP are mostly symmetric ground glass liked density shadows extending outwards from the hilum in both lungs. In the middle and advanced stages, nodules, fi brosis and cavities occur, rarely with pleural effusion.

Lung cancer commonly refers to the cancer in lung parenchyma, usually does not include those mesodermal tumors originating from other pleura, or other malignancies like carcinoid, malignant lymphoma, or metastatic malignancies for other body parts. Therefore, the following lung cancer we are discussing about refers to the malignancies originating from bronchial, or bronchiolar epithelial cells, accounting for 90-95 % of the lung parenchyma malignancies. The cause of lung cancer is still not completely known. Data have indicated that the risk factors of lung cancer include smoking (including second-hand smoke), asbestos, radon, arsenic, ionizing radiation, halogen alkenes, polycyclic aromatic compounds and nickel.

Long-term smoking can cause proliferation of the bronchial mucosal epithelial cells and proliferation of squamous epithelium to induce squamous epithelium carcinoma or undifferentiated small cell carcinoma. Non-smokers can also develop lung cancer, but adenocarcinoma is more common among them.

Long-term exposure to radioactive substances, like uranium and radium, and its derivatives; carcinogenic hydrocarbons, like arsenic, chromium, nickel, copper, tin, ferri, coal tar, bitumen oil, petroleum, asbestos and mustard gas, all can induce lung cancer, which is commonly squamous carcinoma and undifferentiated small cell carcinoma.

Some chronic pulmonary diseases, such as tuberculosis, silicosis and pneumoconiosis, can concurrent with lung cancer. In the cases with these chronic pulmonary diseases, the incidence of cancer is higher than the general population. In addition,bronchopulmonary chronic infl ammation and pulmonary fi brous scar lesions may cause metaplasia or hyperplasia of squamous epithelium during their healing processes, based on which some cases can develop into cancer.

The internal factors of the human body include family heredity, compromised immunity, metabolism and endocrine dysfunction.

The lung cancers distribute more in the right lung than in the left lung, more in the upper lobe than in the lower lobe. Its locations range from the major bronchus to the bronchioles. The central type of lung cancer has its origination from the major bronchial lobes and locates adjacent to the pulmonary hilum. The peripheral type of lung cancer has its origination from the lower parts of pulmonary segment bronchi and locates in the peripheral areas in the lungs. In the growth process of the lung cancer, it causes the extension and dilation of the bronchial walls, and penetrates the bronchial walls to invade the adjacent lung tissues and form masses. Meanwhile it intrudes into the bronchi to cause luminal stenosis or obstruction. With its further progression and dissemination, it spreads from the lungs and directly extends into the chest walls, mediastinum, heart, major vessels and other adjacent organs and tissues. Lung cancer can also transfer to other parts of the body along with blood and lymph fl ows or disseminates to other pulmonary lobes via the respiratory tract. The growth rate and transferring paths of lung cancer depend on its histological types, differentiation degree and other biological characteristics.

Lung cancer has no special symptoms in the early period, only has the common symptoms with common respiratory diseases, including cough, bloody sputum, low grade fever, chest pain and chest distress. Therefore, it is often misdiagnosed.

(1) Face and neck edema; (2) Hoarse voice is the most common symptom; (3) Shortness of breath.

Lung cancer tends to occur distant metastases in the early stage. In the cases with metastatic lesions to the brain, the patients sustain persistent headache and blurry vision. In the cases with metastatic lesions to the bone, bone destruction may occur to cause fracture.

(1) Restrictive wheezing sound, mostly occurring in the inspiratory phase and recurring after cough; (2) Hoarse voice, caused by lymph nodes transferring to compress and invade the recurrent laryngeal nerve; (3) Superior vena cava syndrome, caused by the compresses or invasion to the superior vena cava by the mass and venous obstruction, with edema in the head, face, neck, and upper limbs, varicose veins and edema in the upper chest, and accompanying dizziness, chest distress, shortness of breath and other symptoms; (4) Horner's syndrome, with enophthalmos of the affected side, blepharoptosis, shrinkage of the pupils, eye fi ssure stenosis, increased skin temperature in the upper chest of the affected side and no sweating due to compression or invasion of the apical cancer to the cervical sympathetic ganglia; (5) Should and arm pain, which is radial burning pain in the shoulder and upper limbs of the affected side due to compression or invasion of apical cancer to the brachial plexus nerve; (6) Phrenic nerve paralysis, with symptoms of shortness of breath and chest distress due to invasion to the phrenic nerve; (7) Dysphagia, caused by compressed esophagus by mediastinal lymphadenectasis; and diffi culty breathing caused by compressed trachea by mediastinal lymphadenectasis; (8) Pericardial effusion, shortness of breath, arrhythmia and heart dysfunctions due to pericardial invasion; (9) Pleural metastasis, with chest pain and cancerous pleural effusion; (10) Lung cancer metastasis, spreading of lung cancer along with blood fl ow to the bone, liver, brain, kidney, adrenal gland and subcutaneous tissues. Intrapulmonary metastasis is also common. Metastasis to different locations shows different symptoms and signs. (11) Extrapulmonary signs, commonly including joint pain or joint hypertrophy, clubbing fi ngers and mental disorders.

The diagnostic imaging is the most commonly used and an important examination for the diagnosis of lung cancer. It can facilitate to fi nd some specifi c manifestations in the lesions, which provide clues for the diagnosis of lung cancer. It is also the main basis for the staging of lung cancer, but fails to defi ne the qualitative diagnosis. Chest X-ray is the main examination for the diagnosis of lung cancer. Anteroposterior and lateral chest X-ray are used for preliminary screening. Chest CT is the diagnostic imaging examination of the choice for the diagnosis of lung cancer. For the central type of lung cancer in the early stage, there are direct signs to defi ne the diagnosis. In the early stage, thin layer scanning with a layer thickness of 1.5-4 mm can be performed to observe the bronchial changes. MR imaging can demonstrate intraluminal nodules, luminal thickness and luminal stenosis of the bronchi from the transverse, coronal, and sagittal perspectives. MR imaging demonstrates favorably cancer in the lesions of obstructive pneumonia, and masses covered by the hilum. PET/CT scanning can be used for the screening of lung cancer metastasis and assessing the therapeutic effi cacy after treatment. DSA is used for infusion chemotherapy of bronchial artery in the cases of primary lung cancer.

Bronchoscopy is an important examination for the diagnosis of lung cancer. The pathological changes of the endothelium and the lumen of bronchi can be directly observed by using bronchoscopy. For the cases with caner or cancerous infi ltration by bronchoscopy, sampling of the tissues under the guidance of bronchoscopy for biopsy can be performed. Otherwise, bronchial secretions can be suctioned under the guidance of bronchoscopy for cytological examinations to defi ne the diagnosis and the histological classifi cation.

In most cases of primary lung cancer, the shed cancer cells can be found in the sputum, which can also facilitate to defi ne its histological classifi cation.

After several examinations and short-term exploratory therapies, the qualitative diagnosis cannot be defi ned and the possibility of lung cancer cannot be excluded. Therefore, exploratory thoracotomy can be performed if the patient's physical conditions permit.

Chest X-ray Early lesions are confi ned within the bronchi, causing valve ventilatory disorder and changes of obstructive emphysema. The manifestations include restrictive pulmonary gas increase and sparse lung markings. In the cases with certain degree of bronchostenosis due to unfavorable discharge of the secretions, obstructive pneumonia occurs, showing patchy blurry shadows. In the cases with complete blockage of the bronchi, obstructive atelectasis occurs, showing decreased pulmonary volume, increased density and migration of the mediastinum to the affected side. Obstructive pulmonary bronchiectasis has demonstrations of intrapulmonary cords liked shadows. Lung A male patient aged 41 years was confi rmatively diagnosed as having AIDS by the CDC. He complained of repeated cough for more than 1 month and reported to have a history of unhealthy sexual behaviors. His CD4 T cell count was 65/ μl. cancer in the middle and advanced stages are mainly manifested as hilar mass and atelectasis. The mass has a high density with clear boundary. However, the cancer cannot be observed due to its common immersion in the large fl aky obstructive pneumonia lesion or large quantity pleural effusion. Atelectasis is commonly manifested as shrinkage of pulmonary segments or shrinkage of unilateral lung, with high density. The shadow of atelectasis widens at the hilum to show prominent mass. In the cases of central type lung cancer in the right upper lobe, a transverse S shape is at the hilum (commonly known as Pancoast cancer). Early diagnosis of central type lung cancer by plain chest X-ray only shows some indirect pulmonary manifestations caused by bronchial obstruction. And these indirect signs are not characteristically lung cancer.

In the cases of local obstructive emphysema, these indirect signs can be caused by foreign substances in the bronchi or early infl ammation. Obstructive pneumonia is diffi cult to be differentiated from common pneumonia. Obstructive atelectasis needs to be differentiated from many other conditions.

(1) Pathological changes in the bronchial lumen including polypoid, nodular or fl at papula masses. Benign tumor has smooth boundary and malignant tumor has unsmooth boundary, commonly with wider base and thickened lumen wall. Even the slight bronchial changes caused by the central type of lung cancer can be demonstrated by thin layer CT scanning, including slightly thickened bronchial wall, intraluminal small nodules and lumen stenosis or obstruction. In the middle and advanced stages, the direct signs of the central type lung cancer include thickened bronchial wall, irregular or unsmooth lining of the bronchial lumen. Bronchial obstruction is suddenly truncation or gradual thinning of the lumen to obstruction. (2) Hilar mass locates adjacent or around the bronchi, with smooth or arch shaped boundary. The indirect signs of the central type lung cancer in the middle and advanced stages include secondary changes to bronchial stenosis. Obstructive pneumonia is manifested as patchy blurry shadows or parenchymal changes of the pulmonary segments/lobes, and decreased lung volume.

MR imaging demonstrates the tumor as long T1 and long T2 signals. In the cases of central type lung cancer with secondary obstructive atelectasis and obstructive pneumonia, enhanced T1 demonstrates the tumor in the lesion of pulmonary atelectasis and obstructive pneumonia. The signal of atelectasis is higher than that of the tumor.

PET/CT scanning can demonstrates increased and thick stained metabolites of metastatic lesions or residual lesions, which has a diagnostic sensitivity of above 90 %, and a reported specifi city of 80-90 %. In addition, it can be applied for the clinical consideration of it hilar, mediastinal lymph node metastasis and extrathoracic distant metastasis, which is an important method to decide clinical stages before lung cancer therapy. But PET has false negative diagnosis in the diagnosis of lung cancer with decreased metabolites, especially the alveolar cell carcinoma. For the diagnosis of pneumonia and pulmonary tuberculosis, it also has false positive results. DSA can demonstrate the blood supply of the tumors. Miliary tuberculosis is more common in young adults, with obvious symptoms of systemic toxicity. Anti-tuberculosis drug therapy can relieve the symptoms, with gradually absorbed lesions. (3) Chest X-ray demonstrates hilar lymph node tuberculosis as mass shadows in the hilum of lung, which may be misdiagnosed as the central type lung cancer. Hilar lymph node tuberculosis is more common in teenagers, commonly with symptoms of tuberculosis infection but rarely hemoptysis. Lung cancer can be concurrent with pulmonary tuberculosis.

(1) Bronchial pneumonia; Obstructive pneumonia induced by early lung cancer can be misdiagnosed as bronchial pneumonia. Bronchial pneumonia has an acute onset with more obvious symptoms of infection. Chest X-ray demonstrates patchy or spots shadows, with blurry boundaries and uneven density. The lesions are not confi ned within one segment or one lobe. (2) Pulmonary abscesses; Central necrosis and liquefaction of the lung cancer results in cancerous cavities. By Chest X-ray, the central type lung cancer can be misdiagnosed as pulmonary abscesses. In the acute period, a pulmonary abscess has obvious symptoms of infection, with large quantity purulent sputum. Chest X-ray demonstrates thin cavity wall, smooth inner wall, liquid level and infl ammatory changes in the surrounding lung tissues or pleura.

Pulmonary benign tumors including hamartomas, fi broma and chondroma have slow growth. Chest X-ray demonstrates round liked mass shadow, with homogeneous density without lobation.

Joint United Nations Programme on HIV/AIDS (uNAIDS)

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Pulmonary cryptococcosis: localized and disseminated infections in 27 patients with AIDS

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CD4+ T cell-mediated fatal hyperinfl ammatory reactions in mice infected with Penicillium marneffei

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Pulmonary toxoplasmosis

A female patient aged 35 years was confi rmatively diagnosed as having AIDS by the CDC. She complained of cough, fever and no sputum. Her CD4 T cell count was 45/ μl. 

Filariform larvae of strongyloides stercoralis invade into skin or mucosa and reach the lungs through lymphatic vessels or venous system and the right heart. They develop into schistosomula in 3-30 days. A few schistosomula develop mature in the lungs or bronchi. Most schistosomula penetrate the pulmonary capillaries into alveoli to cause a series of respiratory symptoms. In the cases of serious infection and in patients with compromised immunity, disseminated lesions occur in lungs and other organs.

HIV/AIDS related pulmonary strongyloidiasis can have manifestations of local small bleeding spots, pimples, migratory linear or strips urticaria on skin, as well as manifestations of allergic bronchitis, lobular pneumonia or asthma. AIDS patient may have severe diffuse infection and systemic infection, with symptoms of fever, severe cough, expectoration, hemoptysis, shortness of breath, breathing diffi culty, and asthma.

1. Laboratory tests 2. The pathological examinations include biopsy tissue culture and inoculation test. 3. Chest X-ray is the most commonly used examination.

There are demonstrations of small spots and fl aky shadows, thickened hilar shadow and thickened pulmonary markings. Mitchell reported in 1992 that interstitial or alveolar infi ltration in both lungs accounts for 62 %, nodular shadows in both lungs 15 %, hilar or mediastinal lymphadenectasis 26 %, pleural fl uids 42 %, septal line 25 %, mediastinal lymphadenectasis and ascites are the important clues for the diagnosis.

1. The clinical manifestations of HIV/AIDS related pulmonary strongyloidiasis are non-specifi c. Its diagnosis depends on the etiological examinations. The fi ndings of Strongyloides sterocralis in the patient's sputum and feces can defi ne the diagnosis.

increases to 20 × 10 9 ⁄L; eosinophils granulocytes 25-30 %, or even as high as 70-80 %; the serum total lgE level increases by 50 %; 90 % cases with blood serum lgG and lgE of fi lariform larvae antigen positive. In the cases with femal strongyloides stercoralis parasitizing in the bronchial epithelium, rhabditiform larva, fi lariform larva, schistosomula, adult strongyloides stercoralis and the eggs can be found in fresh phlegm, which can defi ne the diagnosis. 3. Pathological examinations including biopsy tissue culture and inoculation test are positive. 4. By chest X-ray, the lungs have small spots and fl akes of shadows, thickened hilar shadow and thickened pulmonary markings.

HIV/AIDS related pulmonary strongyloidiasis should be differentiated from HIV/AIDS related pulmonary toxoplasmosis, infectious mononucleosis and mycoplasma pneumonia.

Pulmonary infi ltration of HIV/AIDS related malignant lymphoma commonly has three types: Primary pulmonary lymphoma, which is rare and accounts for 0. 3. The diagnostic imaging examinations are the most commonly used examinations for the diagnosis.

The imaging demonstrations of HIV/AIDS related malignant lymphomas include: 1. Mediastinal lymphadenectasis is the most commonly found pulmonary manifestations of malignant lymphoma. The lesions are mainly located in anterior and middle mediastinum, in asymmetric wave liked or lobulated mass. It occurs unilaterally or bilaterally, isolated or fusion. 2. The incidence of pulmonary parenchymal lesions is 20-30 %. Chest X-ray demonstrates mediastinal lymph nodes extending directly into the lungs, which is susceptible to confusion with pneumonia. They are demonstrated as round shadows in the lung fi elds or distribute in the whole lung fi elds. Chest X-ray demonstrates the lymphatic spread of lesions as military nodules in different sizes or isolated intrapulmonary nodules or cavities, commonly accompanying with mediastinal hilar lymphadenectasis. In the cases with its occurrence secondary to endobronchial membrance, obstructive pneumonia or atelectasis can be caused. Some patients may have diffuse pulmonary interstitial changes. Pulmonary infi ltration by non-Hodgkin's lymphoma can also be divided into four types: (1) Nodular type; (2) Pneumoniaalveolar type; (3) bronchial-vascular-lymphatic type, which can be further divided into the central bronchialvascular type, and diffuse lymphatic type; (4) diffuse lymphatic type can have lesions of reticular or reticular nodular infi ltration and its progression into patchy changes. 3. Miliary-blood borne spreading type is rare. 4. The pleural lesions is mainly pleural effusion, with bloody or serous pleural fl uid.

A male patient aged 41 years was confi rmatively diagnosed as having AIDS by the CDC. He complained of chest distress and chest pain for more than 2 months. His CD4 T cell count was 36/μl. 

(1) Tuberculoma is diffi cult to be differentiated from the peripheral type of lung cancer. Tuberculoma is more common in young adults, with a long term course of illness. The lesions are commonly found in the apical posterior segment of the upper lobe or dorsal segment of the lower lobe. Chest X-ray demonstrates the lesions with uneven density and satellite lesions. (2) Miliary tuberculosis is diffi cult to be differentiated from diffuse bronchioloalveolar carcinoma.