Differential Diagnosis in Internal Medicine From Symptom to Diagnosis_2 ppt

Siegenthaler, Differential Diagnosis in Internal Medicine, © 2007 Thieme All rights reserved. Usage subject to terms and conditions of license. 518 18 Pulmonary Opacities K. E. Bloch and E. W. Russi 18 18 Siegenthaler, Differential Diagnosis in Internal Medicine, © 2007 Thieme All rights reserved. Usage subject to terms and conditions of license. 519 18.1 Infectious Pulmonary Infiltrates (Pneumonias) 521 Bacterial Pneumonia 523 Classification 523 Clinical Presentation of Bacterial Pneumonias 524 Pneumonias Due to Gram-Positive Microorganisms 524 Pneumonias Due to Gram-Negative Bacteria and Microorganisms not Identifiable under Light Microscopy 526 Pneumonia Due to Multiple Gram-Positive and Gram-Negative Organisms (“Mixed Flora”) 528 Pulmonary Tuberculosis 530 Primary Tuberculosis 531 Postprimary Pulmonary Tuberculosis 531 Exsudative Pulmonary Tuberculosis 531 Tuberculous Cavity 531 Miliary Tuberculosis 533 Fibroproliferative Tuberculosis 534 Tuberculoma 534 Disease Due to Mycobacteria Other Than Tuberculosis (MOTT) 535 Viral Pneumonia 536 Influenza Pneumonia 536 Adenovirus Pneumonia 536 Severe Acute Respiratory Syndrome (SARS) 536 Hantavirus Pneumonia 536 Pneumonia Due to Nonpneumotropic Viruses 536 Fungal Pneumonia 537 Fungus Infection in Immunocompromised Patients 537 Pneumonia Due to Yeasts and Molds 537 Pneumocystis carinii Pneumonia 537 Endemic Fungal Infection 539 Allergic Bronchopulmonary Aspergillosis and Mycetoma 539 Pulmonary Parasitosis 540 18.2 Noninfectious Pulmonary Infiltrates 540 Physical or Chemical Pneumonitis 540 Radiation Pneumonitis 541 Lipoid Pneumonia 541 Infiltrates Due to Chronic Congestive Heart Failure 541 Pulmonary Infarction − Infarction Pneumonia 543 Pneumonia Associated with Bronchiectasis 545 Pneumonia Due to Bacterial Superinfection 545 Chronic Pneumonia 545 Other Noninfectious Pulmonary Infiltrates 545 18.3 Eosinophilic Pulmonary Infiltrates 546 Transient Eosinophilic Pulmonary Infiltrates (Löffler) 546 Pulmonary Eosinophilia with Parasitosis and Tropical Pulmonary Eosinophilia 546 Allergic Bronchopulmonary Aspergillosis (ABPA) 546 Drug-Induced Pulmonary Eosinophilia 547 Acute Eosinophilic Pneumonia 547 Chronic Eosinophilic Pneumonia 547 Eosinophilic Infiltrates with Asthma 547 Allergic Granulomatosis and Angiitis (Churg−Strauss Syndrome) 547 Hypereosinophilic Syndrome 547 Diagnostic Criteria: 547 18.4 Diffuse Parenchymal Lung Disease (DPLD)/Pulmonary Fibrosis 548 Idiopathic Interstitial Pneumonia 549 Idiopathic Pulmonary Fibrosis (IPF) 550 Nonspecific Interstitial Pneumonia (NSIP) 551 Cryptogenic Organizing Pneumonia (Idiopathic Bronchiolitis Obliterans Organizing Pneumonia [BOOP]) 551 Pulmonary Opacities 520 Acute Interstitial Pneumonia (AIP, Hamman−Rich Syndrome) 553 Respiratory Bronchiolitis-Associated Interstitial Lung Disease (RB-ILD) 554 Desquamative Interstitial Pneumonia (DIP) 554 Lymphoid Interstitial Pneumonia (LIP) 554 Interstitial Pneumonia in Association with Collagen Vascular Disease 554 Toxic and Drug-Induced Interstitial Pneumonia 556 Extrinsic Allergic Alveolitis (Hypersensitivity Pneumonitis) 556 Pneumoconiosis 557 Silicosis 557 Silicatosis and Other Pneumoconioses 559 Diffuse Granulomatous Pulmonary Diseases 561 Other Diffuse Parenchymal Lung Diseases and Orphan Lung Diseases 561 Alveolar Cell Carcinoma, Bronchoalveolar Cell Carcinoma, and Pulmonary Adenomatosis 561 Lymphangiosis Carcinomatosa 561 Kaposi Sarcoma 561 Pulmonary Hemosiderosis 561 Goodpasture Syndrome 561 Antiphospholipid Syndrome 564 Pulmonary Alveolar Proteinosis (PAP) 564 Microlithiasis Alveolaris 564 Langerhans Cell Histiocytosis 564 Lymphangioleiomyomatosis (LAM) 564 Formation of Cysts and Honeycombing 565 18.5 Pulmonary Nodules 566 Solitary Pulmonary Nodules 567 Malignant Neoplasms 567 Benign Tumors 569 Inflammatory Pulmonary Nodules 569 Tuberculoma 569 Echinococcosis 569 Pulmonary Nodules of Various Etiology 570 Multiple Pulmonary Nodules 570 Metastasis 570 Wegener Granulomatosis 570 Arteriovenous Aneurysms 572 18.6 Cavernous and Cystic Lung Diseases 573 Tuberculous Cavitary Lesion 573 Pulmonary Abscess 573 Pulmonary Abscess Due to Aspiration 573 Pulmonary Abscess Formation as a Complication of Bacterial Pneumonia 574 Metastatic Lung Abscess 574 Lung Cysts 574 Cavernous and Cystic Lesions of Various Etiologies 574 18.7 Atelectasis 57 4 18.8 Middle Lobe Syndrome 576 18.9 Opacities in the Cardiophrenic Angle 578 Cysts and Hernias 578 Lung Sequestration 578 18 Pulmonary Opacities Siegenthaler, Differential Diagnosis in Internal Medicine, © 2007 Thieme All rights reserved. Usage subject to terms and conditions of license. 521 Radiologic Morphology of Pulmonary Opacities By definition, the diagnosis of pulmonary opacities re- quires a radiographic examination. Although the pres- ence of opacities may be suspected on clinical grounds, chest percussion and auscultation are often normal or equivocal. Opacities of the lung parenchyma may be re- lated to extravascular fluid accumulation (exudate, tran- sudate) and to infiltration of inflammatory, fibrotic, or neoplastic cells. The following discussion refers to con- ventional chest radiography. A larger amount of anatomi- cal information, and a significantly higher spatial resolu- tion, can be obtained by a computed tomography (CT) scan of the chest including spiral acquisition in thin slices and visualization in high-resolution techniques, with and without application of a contrast agent. However, a CT scan is generally not performed as the initial radiologic examination due to its higher costs and radiation expo- sure. For the description of CT images a specialized no- menclature, different from that used to describe conven- tional chest radiography, is applied. Pulmonary opacities are characterized by their size, dis- tribution, and pattern. Size. Based on their size and extension, localized opaci- ties (such as those found in lobar pneumonia or tuber- culoma) are differentiated from diffuse opacities (such as those found in fibrosing alveolitis, or pneumoconiosis). Pattern of Infiltrates. Inflammatory or neoplastic infil- trates are typically associated with opacities that pre- serve the lung structure. Infiltrates may occur with an aci- nar or interstitial pattern: ț Acinar Infiltrates. Diseases that affect the pulmonary acini (e. g., pneumoconioses) have the following characteristics: − homogeneous density − tendency for confluence − air bronchograms − absence of lung volume loss. ț Interstitial Infiltrates. Diseases that predominantly af- fect the pulmonary interstitium (e. g., fibrosing alve- olitis) have the following characteristics: − ground-glass opacity − inhomogeneous density − linear and reticular densities (Kerley A, B, and C lines) − noduli − “honeycombing” − loss of lung volume. Consolidation. This term refers to a dense opacity that conceals the structure of the affected lung parenchyma. Consolidation is seen in pneumonia, lung cancer, or metastasis. Mass Lesions. A typical characteristic of a pulmonary mass is its tendency to encroach upon adjacent lung parenchyma and other structures. This is not only seen in neoplasia but also in inflammatory diseases (pulmonary abscess). Nodules. A nodule is defined as a rounded, clearly de- lineated opacity of less than 3 cm in diameter. Solitary or multiple pulmonary nodules may be related to cancer, in- fection, or organic and inorganic dust exposure (such as found in silicosis). Opacities with Central Hypodensity. These opacities occur due to necrotic destruction such as found in an ab- scess (bacterial abscess, cavity due to infection with My- cobacterium tuberculosis), pulmonary infarct, neoplasia, or vasculitis (Wegener granulomatosis). Mixed Patterns of Pulmonary Opacities. The simul- taneous occurrence of various types of opacities is com- mon. Additional Diagnostic Criteria. Certain lung diseases are associated with a distinct distribution and pattern of radiologic opacities. The high-resolution CT scan may be diagnostic in some of these diseases (e. g., Langerhans cell histiocytosis, lymphangioleiomyomatosis, or asper- gilloma). In contrast, other diseases occur with variable, nonspecific findings that preclude a definitive diagnosis by chest radiography or even by CT scan (e. g., sarcoido- sis, or amiodarone pneumopathy). 18.1 Infectious Pulmonar y Infiltrates (Pneumonias) Infectious pulmonary infiltrates result from an inflam- matory response to the infection caused by microor- ganisms. The clinical manifestation is determined by the type of the infectious agent (bacteria, viruses, fungi, or parasites) and the immunologic response of the host. The following discussion is arranged according to the in- fectious agent (Tab. 18.1). Infectious Pulmonary Infiltrates (Pneumonias) Siegenthaler, Differential Diagnosis in Internal Medicine, © 2007 Thieme All rights reserved. Usage subject to terms and conditions of license. 522 Table 18.1 Classification of inflammatory infiltrates Infectious pneumonia Bacterial pneumonia − due to Gram-positive organisms − Streptococcus pneumoniae (pneumococci type 1−90) − Streptococcus − Staphylococcus − Actinomyces − Nocardia − due to Gram-negative organisms and organism not identifiable by light-microscopy − Haemophilus influenzae − Klebsiella − Branhamella (Moraxella) catarrhalis − Escherichia coli − Proteus − Pseudomonas − Serratia − Mycoplasma pneumoniae − Chlamydia pneumoniae − Chlamydia psittaci (ornithosis) − Brucella (Bang pneumonia) − Legionella pneumophila − Rickettsia (Q-fever) − Bacillus anthracis − due to Gram-positive and Gram-negative anerobic organisms (Bacteroides, Fusobacterium) − due to Mycobacterium tuberculosis complex − M. tuberculosis − M. bovis − M. africanum − due to atypical mycobacteria − M. avium-intracelluare complex − M. kansasii − M. fortuitum, M. abscessus, and M. chelonei Viral pneumonia − Influenza virus − Adenovirus − Coronavirus (SARS) − Hantavirus − pneumonia due to virus not primarily affecting the lungs (measles, Epstein−Barr virus) Fungal pneumonia − fungal infection in the immunocompromised host − candidiasis (moniliasis) − aspergillosis − Pneumocystis carinii − Mucor mycosis (geotrichosis) − cryptococcosis (torulosis) − endemic fungal infections − blastomycosis − histoplasmosis − coccidioidomycosis Pneumonia due to parasites − Toxoplasma gondii Noninfectious pneumonia Physical−chemical pneumonia Pneumonia with eosinophilia (see Eosinophilic Pulmonary Infiltrates p. 546) Inflammatory pulmonary infiltrates in collagen vascular disease (see Diffuse Parenchymal Lung Disease/Pulmonary Fibrosis p. 548) Due to circulatory failure − cardiogenic pulmonary edema − infarction pneumonia 18 Pulmonary Opacities Siegenthaler, Differential Diagnosis in Internal Medicine, © 2007 Thieme All rights reserved. Usage subject to terms and conditions of license. 523 Prognostic Factors in Community-Acquired Pneumonia Infectious Pulmonary Infiltrates (Pneumonias) In a patient with community-acquired pneumonia, the severity of the illness and the need for hospital care have to be assessed. The following factors may aid in this assessment: −age 50 years − co-morbidity such as a neoplasia, congestive heart failure, chronic obstructive lung disease, or renal and hepatic diseases − altered consciousness − tachycardia  125 beats/min. − respiratory rate  30/min. − systolic blood pressure  90 mmHg − body temperature  35 °C or  40 °C. If none of the above-mentioned risk factors is present, the clinical course is generally favorable and treatment of the pneumonia may be performed at home. The following findings represent additional risk factors: − acidosis: arterial pH  7.35 − serum urea ͧ 30 mg/dL (11 mmol/L) − serum sodium  130 mmol/L − serum glucose ͧ 250 mg/dL (14 mmol/L) − hematocrit  30% − leukocyte count  4000 × 10 6 /L or  20 000 10 6 /L − arterial oxygen partial pressure: Po 2  60 mmHg − multilobar pulmonary infiltrates − pleural effusion. Bacterial Pneumonia Bacterial pneumonias are still among the leading causes of death due to infectious diseases despite the wide- spread use of antibiotics. The organisms responsible vary according to where the infection is acquired (at home, in the hospital or another institution, in the in- tensive care unit), host factors such as the age of the patient, co-morbidities, and the individual immune re- sponse. Streptococcus pneumoniae (pneumococcus), Haemophilus influenzae, Gram-negative enteric bacilli, Staphylococcus aureus, and Legionella pneumophila are the most common causes of bacterial pneumonia. To- gether with Mycoplasma pneumoniae, Chlamydia pneu- moniae, and the respiratory viruses, they account for the majority of community-acquired pneumonias. In con- trast, hospital-acquired pneumonias are more com- monly caused by Gram-negative organisms. Classification According to Where the Infection Was Acquired and the Host Defense. One of the major determinants of the type of microorganism and course of the pneumonia is whether it has been acquired in the community (“com- munity-acquired pneumonia”) or in a special setting such as in a hospital (“hospital-acquired pneumonia”), nursing home, prison, or in other institutions where many people live closely together. Another major determinant of the susceptibility to certain infections, and of particular clinical presenta- tions, is the ability of a patient to create an effective im- mune response. In nonimmunocompromised patients, bacterial pneumonias generally occur with an acute course (with high fever, cough, and production of putrid sputum), whereas bacterial pneumonias may initially have a less dramatic course in the immunocompromised host. Nevertheless, neither the clinical presentation, laboratory tests, nor the radiographic appearance allows a reliable diagnosis of the infectious agent of pneumonia. Thus, the term atypical pneumonia is inappropriate and, at best, of historical interest. Originally, atypical pneu- monias were thought to be caused by microorganisms other than Streptococcus pneumoniae. The first recog- nized “atypical agents” were Mycoplasma pneumoniae; subsequently Chlamydia pneumoniae and Legionella pneumophila were identified. Since pneumonia caused by Streptococcus pneumoniae and other bacteria may have a clinical and radiologic presentation similar to in- fections by the “atypical agents,” the distinction between typical and atypical pneumonia is clinically useless. According to the Infectious Agent. Another classification of pneumonia is based on the microorganism. However, the identification of the agents responsible is often not feasible or successful. Even in patients hospitalized for treatment of pneumonia, the microorganism is iden- tified in less than half of cases. Other Classifications. These are based on the mode of transmission of the infection and the radiologic appear- ance. These classifications may help to identify the potential spectrum of microorganisms responsible: for example, community-acquired aspiration pneumonia is generally caused by a mixed flora of anaerobic and aero- bic bacteria. In contrast, in hospital-acquired aspiration pneumonia, Gram-negative bacteria are often involved. Hematogeneous pneumonias are often caused by Staphylococcus spp. Special conditions predispose the patient to certain infections. Examples are HIV infection (Pneumocystis carinii, Mycobacterium tuberculosis, and mycobacteria other than tuberculosis), chemotherapy- induced agranulocytosis (bacterial pneumonias, inva- sive fungal infections), prolonged corticosteroid therapy (Pneumocystis carinii), and immunoglobulin def iciency (infections by capsulated microorganisms). Siegenthaler, Differential Diagnosis in Internal Medicine, © 2007 Thieme All rights reserved. Usage subject to terms and conditions of license. 524 a b Fig. 18.1 Pneumococcal pneumonia. Homogeneous confluent infiltrate of the right upper lobe (lobar pneumonia) in a 32- year-old man. a Posterio-anterior view. b Lateral view. 18 Pulmonary Opacities Although often used, the radiologic classification based on the extension and pattern of infiltrates is clini- cally of minor relevance. The following patterns may be identified: localized or diffuse forms, unilateral or bi- lateral, and lobar or segmental pneumonic infiltrates. If the opacities are confluent and show an air broncho- gram the pattern is called acinar. If the infiltrates are ill- defined of linear, reticular, or nodular shape, and if there is no air bronchogram, the pattern is called interstitial. A solitary abscess is a typical complication of aspiration pneumonia. Multiple pulmonary abscesses suggest a hematogenic spread, such as occurs in staphylococcal infection. Pulmonary infarction may occur as a con- sequence of an invasive Aspergillus infection or may occur in Pseudomonas aeruginosa pneumonia. Clinical Presentation of Bacterial Pneumonias Pneumonias Due to Gram-Positive Microorganisms As already observed by Hans Gram in 1884, the majority of bacterial pneumonias are caused by Gram-positive bacteria, namely Streptococcus pneumoniae, staphylo- cocci, and streptococci. Peptococci and peptostreptococci, Actinomyces israelii, Nocardia asteroides, Bacillus an- thracis, and Mycobacterium tuberculosis are also positive for staining. Pneumococcus Pneumonia. Currently, 20−60 % of com- munity-acquired bacterial pneumonias are caused by Streptococcus pneumoniae, and 5% of patients with this infection still die as a consequence. Patients with a com- promised immune defense system, immunoglobulin deficiency, hemoglobinopathies, or following splen- ectomy are at particular risk. The clinical presentation of Pneumococcal pneumonia classically starts with sudden onset, high fever, chills, and pleuritic chest pain. Untreated, the fever remains at Siegenthaler, Differential Diagnosis in Internal Medicine, © 2007 Thieme All rights reserved. Usage subject to terms and conditions of license. 525 Fig. 18.2 Staphylococcus pneumonia with focal and confluent infiltrates in the middle and lower lobes in a patient with Hodgkin lymphoma (lobu- lar pneumonia or bronchopneumonia) in a 33- year-old man. Infectious Pulmonary Infiltrates (Pneumonias) temperatures up to 39−40 °C. The pulse rate is also ele- vated. The following findings can occur: ➤ Chest percussion: dullness, increased fremitus. ➤ Auscultation: bronchial breath sounds, end-inspira- tory rales, often perioral herpes infection, leukocyto- sis up to 30 000/μL (30 × 10 9 /L) with pronounced left shift, toxic granulations, and lymphopenia. ➤ Radiologic: in the chest radiograph the infiltrates are dense, homogeneous, and clearly delineated with air bronchograms. They may extend to entire lobes (lobar pneumonia) (Fig. 18.1) or consist in one, or more rarely, in multiple ill-defined infiltrates. ➤ Sputum: microscopic examination of the frothy sputum reveals Gram-positive diplococci. Abundant amounts of Gram-positive diplococci identified in putrid sputum are diagnostic for Streptococcus pneu- moniae. Since pneumococci are normal saprophytes of the oropharyngeal mucosa (carrier rate 5−70%), only moderate or minor amounts of Gram-positive diplococci do not allow a definitive identification of Streptococcus pneumoniae. ➤ Blood cultures: in hospitalized patients blood cultures are positive in one-fourth to one-third of cases. The resorption of infiltrates takes place within four to eight weeks. Delayed resorption of infiltrates may indi- cate another diagnosis (tuberculosis, neoplasia) or a complication, and may occur in patients in a reduced general condition, such as from alcohol abuse, diabetes, or chronic obstructive airway disease. Complications of Pneumococcal pneumonia include atelectasis, pleural empyema, parapneumonic effusion, delaye d resorption, pulmonary abscess formation (in approximately 2% of cases), and pericarditis. Minor ef- fusions are common (60%), major effusions are rare (5%). Metastatic spread of the infection leading to septic arthritis, endocarditis, meningitis, or peritonitis is mainly seen in immunocompromised patients or after splenectomy. Streptococcal and Staphylococcal Pneumonia. While streptococcal pneumonias are relatively rare in adults, staphylococcal infection accounts for 3−5% of bacterial pneumoniasinoutpatients,andfor 6−24 %inhospitalized patients. Streptococcal and staphylococcal pneumonias mayoccurasacomplicationofinfluenzaviralinfection.In addition, streptococcal pneumonia may result from a spread of an upper airway infection to the lungs. Strepto- coccal and staphylococcal pneumonias generally have an acute course with severe febrile illness. The chest radio- graph shows multiple patchy infiltrates spreading over one or several lobes (bronchopneumonia; Fig. 18.2). Ab- scess formation is a common complication that typically occurs in staphylococcal pneumonia. The diagnosis is confirmed by blood cultures, which are positive in approximately 20% of staphylococcal pneumonias. Pulmonary Actinomycosis and Nocardiosis. Pulmonary actinomycosis has a prolonged course with fever, phlegm, pleural pain, and leukocytosis. It is commonly associated with manifestation of the infection at other sites, in particular in the oral cavity and the jaw. The Siegenthaler, Differential Diagnosis in Internal Medicine, © 2007 Thieme All rights reserved. Usage subject to terms and conditions of license. 526 Fig. 18.3 Combined Pneumocystis carinii and Nocardia asteroides pneu- monia in a in a 50-year-old male patient receiving chemotherapy. 18 Pulmonary Opacities typical radiologic manifestation includes pleural-based infiltrates that may extend beyond the visceral pleura to the chest wall or to adjacent lobes. The microscopical identification of Actinomyces in the sputum or bronchial washings suggests the diagnosis (yellow sulfur granula corresponding to Actinomyces israeli colonies). The definitive cultural diagnosis may require several weeks. Pulmonary infection by the mandatory aerobic and weakly acid-fast staining Nocardia spp. (Nocardia asteroides, Nocardia brasiliensis) predominantly occurs in the immunocompromised host or in patients with preexisting chronic lung diseases, e. g., pulmonary alve- olar proteinosis (Fig. 18.3). Pneumonias Due to Gram-Negative Bacteria and Microorganisms not Identifiable under Light Microscopy ThisincludespneumoniasduetoHaemophilusinfluenzae, Gram-negative Enterobacteriaceae (Klebsiella pneu- moniae, Escherichia coli, Proteus, Enterobacter, and Serra- tia), Pseudomonas aeruginosa, and Branhamella (Morax- ella) catarrhalis. Legionnaires disease, Q-fever, and Bang disease are also caused by Gram-negative bacteria (i. e., Legionella pneumophila, Rickettsia, and Brucella, respec- tively). Mycoplasma pneumoniae and Chlamydia pneu- moniae are both common causes of community-acquired pneumonias.Thesemicroorganismscannot bevisualized by light microscopy due to their small size. It has been estimated that 9−20% of community-acquired pneu- monias and more than 40 % of hospital-acquired pneu- monias are due to Gram-negative bacteria. Haemophilus influenzae Pneumonia. Haemophilus influ- enzae in its capsulated or uncapsulated form is thought to cause 3−10% of community-acquired pneumonias. It commonly occurs in patients with chronic lung disease, such as chronic obstructive pulmonary disease (COPD) or bronchiectasis, who are also susceptible to Klebsiella infection. Pneumonias Due to Gram-Negative Enterobacteria. Kleb- siella spp. along with Haemophilus influenzae are the most common Gram-negative microorganisms causing community-acquired pneumonia. Alcoholics, diabetics, and patients with chronic airway disease are most sus- ceptible. The clinical presentation is similar to that of other bacterial pneumonias such as caused by Strepto- coccus pneumoniae. The diagnosis is made by identifica- tion of Klebsiella pneumoniae (Gram-negative, capsu- lated diplobacillus) in the sputum or blood culture (50− 70% of blood cultures are positive). Siegenthaler, Differential Diagnosis in Internal Medicine, © 2007 Thieme All rights reserved. Usage subject to terms and conditions of license. 527 Infectious Pulmonary Infiltrates (Pneumonias) Pseudomonas aeruginosa Pneumonia. This predomi- nantly occurs in severely ill, hospitalized patients, and in patients with bronchiectasis. More than 40% of hospi- tal-acquired pneumonias are due to Pseudomonas and other Gram-negative bacteria. These nosocomial pneu- monias may be related to long-term antibiotic therapy, immunosuppression, cytotoxic chemotherapy, or me- chanical ventilation. Bacteriemic Pseudomonas aerugi- nosa pneumonia is associated with a high mortality rate (i. e., 60−70 %) despite appropriate antibiotic treatment. Mycoplasma Pneumonia. Mycoplasma pneumoniae are estimated to be the causative agent in 3−35% of commu- nity-acquired pneumonias. The microorganisms are spread to close contacts by aerosol formation during coughing. Mycoplasma pneumonias are therefore com- monly observed in preschools and schools, and among military personnel. The incubation period is approxi- mately three weeks. Following the infection, lifelong immunity develops. Mycoplasma pneumoniae infections may pass without apparent symptoms, but more severe infec- tions, with fever, bronchitis, and pneumonia, may also occur. The disease usually starts with headaches, malaise, and fever. The cough is usually nonproductive. Less than 10% of patients present clinically with a typi- cal pneumonia. Pulmonary auscultation may be normal. Associated symptoms may include pharyngitis, rhi- nosinusitis, and otitis (sometimes with protracted hemorrhagic, bullous myringitis). The chest radiograph in Mycoplasma pneumonia shows nonspecific alterations, usually consisting in bronchopneumonic infiltrates. Mycoplasma infections may be associated with extrapulmonary manifestations such as hemolysis (cold agglutinins), a rash, and arthritis. This small microorganism cannot be seen under light microscopy. A cultural identification may take several weeks and is therefore clinically not useful. Instead, a serologic examination (complement fixation) may sug- gest a Mycoplasma infection by an increase in IgM and, subsequently, in IgG antibodies. A four-fold increase in antibody titers over the course of the disease or an in- dividual titer of  1:32 are suggestive of the diagnosis. An increase in antibodies may be expecte d within seven to nine days after infection with a maximal response after three to four weeks. Chlamydia Pneumonia. Chlamydia are mandatory intra- cellular microorganisms. Worldwide, their main mani- festation consists of genitourinary and ophthalmic in- fections (Chlamydia trachomatis). Pulmonary infections are due to Chlamydia pneumoniae and, less frequently, Chlamydia psittaci. The clinical presentation of Chlamydia pneumoniae is nonspecific. Symptoms may start acutely with pharyn- gitis and a hoarse voice. Pulmonary infiltrates may occur as ground-glass opacities and be unilatral or bi- lateral. A serologic diagnosis is not feasible, since immuniza- tion without previous clinical manifestation is common. Legionella Pneumonia (Legionnaires disease). Legionella are ubiquitous organisms that are commonly found in water from sprinklers, air conditioners, and humidifica- tion systems. The infection occurs by inhalation of aero- sol of water containing Legionella. It is not always as- sociated with clinical disease; 1.5−20% of healthy sub- jects have circulating antibodies. Legionella pneumonia may be acquired in the com- munity and in the hospital and its prevalence varies largely, i. e., 1−22.5%. Men are more commonly affected than women and there is a seasonal predilection in the period from June through November. Symptoms at the beginning of the disease include fatigue, malaise, joint pain, and headache. One to two days after infection, the disease manifests fever, nonpro- ductive cough, pleuritic chest pain, nausea, vomiting, di- arrhea, abdominal pain, and abnormal neurologic signs. A laboratory examination may reveal a moderate leukocytosis, proteinuria hematuria, and hypophos- phatemia. Radiologically, diffuse, patchy, and homogeneous confluent infiltrates are found (Fig. 18.4). Pleural ef fu- sion is present in 50% of patients, but abscess formation is rare. The diagnosis of Legionella infection is based on culture, serologic, and immunologic testing. In clinical practice, identification of Legionella antigen in the urine is most useful, as it provides a rapid diagnosis within hours, whereas the cell culture diagnosis takes several days. Rickettsia Pneumonia. This is caused by Coxiella burnetii, a Gram-negative coccus, which presents clinically as Q-Fever. Although Q-fever was first described in Queensland the letter Q stands for query, alluding to the unknown etiology of the disease at that time. As Coxiella is found in animal milk and secretions, farmers, animal dealers, and veterinarians are exposed to the infection. It can present as a flulike disease with fever, cough, my- algia, and headaches. During physical examination splenomegaly, enlarged and tender cervical lymph nodes, and bradycardia may be found. Rickettsia pneu- monia cannot be distinguished clinically, radiologically, or histologically from pneumonia due to Mycoplasma pneumoniae. The chest radiograph may show segmental consolidation of lower lobes, patchy infiltrates, and ground-glass opacities. The differential diagnosis includes infectious mono- nucleosis. Additional information on Q-fever is provided in Chapter 4. Brucella Pneumonia. Pulmonary infiltrates in Bang dis- ease are rare and have no typical appearance. Infiltrates may appear in the perihilar area. Diagnosis is made serologically. Clinical presentation is described in Chap- ter 4. Branhamella catarrhalis Pneumonia. Branhamella or Moraxella catarrhalis, a Gram-negative diplococcus, may cause bronchopneumonia in patients with COPD or with immunosuppression. Siegenthaler, Differential Diagnosis in Internal Medicine, © 2007 Thieme All rights reserved. Usage subject to terms and conditions of license. [...]... made in spontaneous sputum or 537 Siegenthaler, Differential Diagnosis in Internal Medicine, © 2007 Thieme All rights reserved Usage subject to terms and conditions of license 18 Pulmonary Opacities Fig 18.14 Invasive aspergillosis of the lung in a patient with ill-defined pneumonic infiltrates in both lower lobes a Right lower lobe b Left lower lobe a b 538 Siegenthaler, Differential Diagnosis in Internal. .. Diagnosis in Internal Medicine, © 2007 Thieme All rights reserved Usage subject to terms and conditions of license 18 Pulmonary Opacities Fig 18.18 Interstitial pulmonary infiltrates in a patient with congestive heart failure a b Fig 18.19 Right-sided interlobar effusion (vanishing tumor) in a 46-year-old man Before (a) and after (b) treatment 542 Siegenthaler, Differential Diagnosis in Internal Medicine, ... pathogenesis is similar Initially, the alveolar epithelium and the capillary endothelium are damaged directly by toxic substances such as oxygen radicals, cytotoxic drugs (bleomycin), or indirectly by immunologic mechanisms that results in release of mediators from inflammatory cells Subsequent to the injury to epithelial and endothelial cells, inflammatory cells migrate into the interstitium and the... typical symptoms, including minor hemoptysis, suggest the diagnosis of pulmonary emboli with infarction A typical, wedge-shaped infiltrate extending from the hilum to the chest wall is not always seen and the infiltrates may be difficult to differentiate from a bronchopneumonia of another origin However, spiral-angio-CT demonstrates the intravascular emboli and confirms the diagnosis Major pulmonary infarction... result from hematogeneous spread from an intra-abdominal abscess Elderly persons and patients with impaired upper airway reflexes (due to neurologic disease or after upper airway surgery [such as tonsillectomy]), alcoholics, and 528 Siegenthaler, Differential Diagnosis in Internal Medicine, © 2007 Thieme All rights reserved Usage subject to terms and conditions of license Infectious Pulmonary Infiltrates... The differential diagnosis of aspiration pneumonia related to infection with anaerobic organisms includes massive aspiration of acidic gastric content, which may cause an acute respiratory distress syndrome (ARDS) by chemical irritation The radiologic findings include varying diffuse, patchy, or confluent infiltrates and consolidation (Fig 18.6) 529 Siegenthaler, Differential Diagnosis in Internal Medicine, ... uncomplicated pulmonary infarction without secondary infection, and bronchopneumonia In pericarditis and myocardial infarction, the character of chest pain is not pleural, i e., it is not influenced by respiration and dyspnea is not the main symptom In pulmonary edema, the sputum may be frothy but frank hemoptysis does not occur 544 Siegenthaler, Differential Diagnosis in Internal Medicine, © 2007 Thieme... inorganic dust exposure are discussed below 545 Siegenthaler, Differential Diagnosis in Internal Medicine, © 2007 Thieme All rights reserved Usage subject to terms and conditions of license 18 Pulmonary Opacities 18.3 Eosinophilic Pulmonary Infiltrates Definition and Classification These infiltrates are due to a heterogeneous group of diseases that have in common a pulmonary infiltration with eosinophilic... Churg−Strauss syndrome have to be considered Drug-Induced Pulmonary Eosinophilia Eosinophilic pulmonary infiltrates have been described with the use of various drugs, most commonly with nonsteroidal anti-inflammatory drugs (NSAIDs), certain antibiotics, L-tryptophan, and recombinant granulocyte− macrophage colony stimulating factor (GM-CSF) Acute Eosinophilic Pneumonia Clinical Features Symptoms include fever,... reaction) are common, in particular in persons with repetitive or chronic exposure wool, or by contaminated meat The most common form is cutaneous infection Gastrointestinal manifestations include abdominal pain, diarrhea, and life-threatening gastrointestinal hemorrhage Recently, anthrax has gained renewed interest since it has been used in biological warfare and bioterrorism Inhalation of even small . Russi 18 18 Siegenthaler, Differential Diagnosis in Internal Medicine, © 20 07 Thieme All rights reserved. Usage subject to terms and conditions of license. 519 18.1 Infectious Pulmonary Infiltrates (Pneumonias) 521 Bacterial. chest pain. Untreated, the fever remains at Siegenthaler, Differential Diagnosis in Internal Medicine, © 20 07 Thieme All rights reserved. Usage subject to terms and conditions of license. 525 Fig the infection at other sites, in particular in the oral cavity and the jaw. The Siegenthaler, Differential Diagnosis in Internal Medicine, © 20 07 Thieme All rights reserved. Usage subject to