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İstanbul Aydın Üniversitesi Tıp Fakültesi

Dr. Ahu Senem Demiröz

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pulmonary infections pneumonia pathogens medical research

Summary

This document provides an overview of various pulmonary infections, detailing the causes, symptoms, and characteristics of bacterial infections such as pneumonia caused by Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis and Staphylococcus aureus. It also discusses viral infections, and opportunistic infections.

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Pulmonary infections Dr. Ahu Senem Demiröz • mutations in MYD88: severe necrotizing pneumococcal infections • congenital defects in IgA production: increased risk for pneumonias caused by encapsulated organisms such as pneumococcus and H.influenzae • defects in TH1 cell–mediated immunity:increase...

Pulmonary infections Dr. Ahu Senem Demiröz • mutations in MYD88: severe necrotizing pneumococcal infections • congenital defects in IgA production: increased risk for pneumonias caused by encapsulated organisms such as pneumococcus and H.influenzae • defects in TH1 cell–mediated immunity:increased infections with intracellular microbes such as atypical mycobacteria. • cigarette smoke compromises mucociliary clearance and pulmonary macrophage activity, • alcohol impairs neutrophile function as well as cough and epiglottic reflexes(thereby increasing the risk for aspiration). Streptococcus pneumoniae • increased frequency in two clinical settings: • (1) chronic diseases such as CHF, COPD, or diabetes; • (2) congenital or acquired defectsin immunoglobulin production • decreased or absent splenic function • numerous neutrophils in sputum containing the typical gram-positive, lancet-shaped diplococci supports the diagnosis • S. pneumoniae is a part of the endogenous flora in 20 % of adults • Isolation of pneumococci from blood cultures is more specific but less sensitive • Pneumococcal vaccines containing capsular polysaccharides from the common serotypes are used in individuals at high risk for pneumococcal sepsis Haemophilus influenzae • Encapsulated forms can cause a particularly lifethreatening form of pneumonia in children, often after a respiratory viral infection. • Encapsulated H. İnfluenzae type b was formerly an important cause of epiglottitis and suppurative meningitis in children • vaccination in infancy has significantly reduced the risk. • Adults at risk for developing infections include those with chronic pulmonary diseases such as chronic bronchitis, cystic fibrosis, and bronchiectasis. • H. influenzae is the most common bacterial cause of acute exacerbations of COPD Moraxella catarrhalis • second most common bacterial cause of acute exacerbation of COPD in adults • Along with S. pneumoniae and H. influenzae, M. catarrhalis is one of the three most frequent causes of otitis media (infection of the middle ear) in children Staphylococcus aureus • an important cause of secondary bacterial pneumonia in children and healthy adults after viral respiratory illnesses • Staphylococcal pneumonia is associated with a high incidence of complications: lung abscess and empyema. • in association with right-sided staphylococcal endocarditis is a serious complication of intravenous drug abuse. • an important cause of nosocomial pneumonia Klebsiella pneumoniae • most frequent cause of gram-negative bacterial pneumonia. • debilitated and malnourished individuals, particularly chronic alcoholics • Thick and gelatinous sputum is characteristic Pseudomonas aeruginosa • association with infections in cystic fibrosis, • most commonly is seen in nosocomial settings • neutropenic, usually secondary to chemotherapy; • in victims of extensive burns; • in patients requiring mechanical ventilation • propensity to invade blood vessels at the site of infection • organisms invading the walls of necrotic blood vessels (Pseudomonas vasculitis), leading to secondary coagulative necrosis of the pulmonary parenchyma • Pseudomonas bacteremia is a fulminant disease, with death often occurring within a matter of days Legionella pneumophila • Pontiac fever is a related self-limited upper-respiratory tract infection caused by L. pneumophila, without pneumonic symptoms • artificial aquatic environments, such as watercooling towers and within the tubing system of domestic water supplies • transmission : inhalation of aerosolized organisms or aspiration of contaminated drinking water • Predisposing condition : • cardiac, renal, immunologic, or hematologic disease. • Organ transplant recipients • fatality rate of 30% to 50% in immunosuppressed individuals Bacterial pneumonia • Two patterns of anatomic distribution: • lobular bronchopneumonia • lobar pneumonia • In lobar pneumonia, four stages of the inflammatory response 1. congestion, 2. Red hepatization 3. gray hepatization 4. resolution, • Complications of pneumonia • abscess formation; • Empyema • bacteremic dissemination to the heart valves, pericardium, brain, kidneys, spleen, or joints, causing metastatic abscesses, endocarditis, meningitis, or suppurative arthritis CommunityAcquired Viral Pneumonias • propensity to infect and damage resspiratory epithelium • interstitial inflammation, some outpouring of fluid into alveolar spaces may also occur, so that on chest films the changes may mimic those of bacterial pneumonia. • damage leading to necrosis of the respiratory epithelium inhibits mucociliary clearance and predisposes to secondary bacterial infections • infants,older adults, malnourished patients, alcoholics, and immunosuppressed individuals. Influenza Infections • Singlestranded RNA virüs • The viral surface has a lipid bilayer containing the viral hemagglutinin and neuraminidase, which determine the subtype (e.g., H1N1, H3N2) • The type A viruses infect humans, pigs, horses, and birds and are the major cause of pandemic and epidemic influenza infections. • Epidemics of influenza occur through mutations of the hemagglutinin and neuraminidase antigens that allow the virus to escape most host antibodies (antigenic drift). • Pandemics, which last longer and are more widespread than epidemics, may occur when both the hemagglutinin and neuraminidase are replaced through recombination of RNA segments with those of animal viruses, making all animals susceptible to the new influenza virus (antigenic shift). Hospital-Acquired Pneumonias • severe underlying disease, • immunosuppressed, • on prolonged antibiotic regimens. • on mechanical ventilation are a particularly high-risk group • Gram-negative rods (members of Enterobacteriaceae and Pseudomonas spp.) and S. aureus are the most common • S. Pneumoniae is not a common pathogen in the hospital setting. Aspiration Pneumonia • Debilitated or unconscious patients • pneumonia is partly chemical, due to the extremely irritating effects of the gastric acid, and partly bacterial. • often necrotizing, pursues a fulminant clinical course • frequent cause of death in individuals predisposed to aspiration. • In those who survive, abscess formation is a common complication Lung Abscess • localized area of suppurative necrosis within the pulmonary parenchyma, • resulting in the formation of one or more large cavities • Aspiration of infective material: oral surgery, anesthesia, coma, or alcoholic intoxication, andin debilitated patients with depressed cough reflexes. • Aspiration of gastric contents, • As a complication of necrotizing bacterial pneumonias: S. aureus, Streptococcus pyogenes,K. pneumoniae, Pseudomonas spp., and, rarely, type3 pneumococci. Mycotic infections and bronchiectasis also may lead to lung abscesses • Bronchial obstruction, bronchogenic carcinoma obstructing a bronchus or bronchiole. Impaired drainage, distal atelectasis, and aspiration of blood and tumor fragments • Septic embolism, from infective endocarditis of the right side of the heart. • Hematogenous spread of bacteria • Anaerobic bacteria are present in almost all lung abscesses • abscesses resulting from aspiration of infective material are more common on the right side (with its more vertical airways) • Complications: • abscesses rupture into the pleural cavity and produce bronchopleural fistulas, • pneumothorax or empyema. • embolization of septic material: meningitis or brain abscess. • Secondary amyloidosis may develop in chronic cases Histoplasmosis, Coccidioidomycosis, and Blastomycosis • isolated pulmonary involvement, as commonly seen in infected immunocompetent individuals, • disseminated disease in immunocompromised individuals. • Clinic: • (1) acute (primary) pulmonary infection, • (2) chronic (granulomatous) pulmonary disease, • (3) disseminated miliary disease. • In the vulnerable host, chronic cavitary pulmonary disease develops • predilection for the upperlobe, resembling the secondary form of tuberculosis. • perihilar mass lesions that resemble bronchogenic carcinoma radiologically. • cough, hemoptysis, and even dyspnea and chest pain. • In infants or immunocompromised adults, particularly those with HIV infection, disseminated disease (analogousto miliary tuberculosis) may develop. • there are no well-formed granulomas. • focal collections of phagocytes containing yeast forms are seen within the liver, spleen, lymph nodes, lymphoid tissue of the gastro intestinal tract, and bone marrow • Disseminated disease produces a febrile illness marked by hepatosplenomegaly, anemia, leukopenia, and thrombocytopenia. • Cutaneous infections with disseminated Blastomyces organisms frequently induce striking epithelial hyperplasia, which may be mistaken for squamous cell carcinoma. Pneumonia in the Immunocompromised Host • The more common pulmonary pathogens include • (1) bacteria (P.aeruginosa, Mycobacterium spp., L. pneumophila, and Listeria monocytogenes); • (2) viruses (cytomegalovirus and herpesvirus); • (3) fungi (P. jiroveci, Candida spp., Aspergillus spp.,and Cryptococcus neoformans Cytomegalovirus Infection • Cells infected by the virus exhibit gigantism of both the cytoplasmand the nucleus. • The nucleus typically contains a large inclusion surrounded by a clear halo (“owl’s eye”), • the classic form of symptomatic disease thatboccurs in neonates—cytomegalic inclusion disease • Transmission of CMV can occur by several mechanisms, depending on the age group: • A fetus can be infected transplacentally from a newly acquired or reactivated infection in the mother (congenital CMV infection). • The virus can be transmitted to the infant through cervical or vaginal secretions at birth, or later through the breast milk of a mother with an active infection (perinatal CMV infection). • Preschool children, especially in day care centers, can acquire it through saliva. Toddlers so infected readily transmit the virus to their parents. • In patients older than 15 years of age, the venereal route is the dominant mode of transmission, but spread also may occur through contact with respiratory secretions and by the fecal-oral route. • Iatrogenic transmission can occur at any age through organ transplantation or blood transfusion Pneumocystis • P. jiroveci (previously P. carinii), an opportunistic infectious agent formerly considered to be a protozoan, is now classified as a fungus. • all individuals are exposed to Pneumocystis during the first few years of life, but in most the infection remains latent. • Reactivation with development of clinical disease occurs almost exclusively in immunocompromised individuals. • susceptibleto infection with P. jiroveci • AIDS • severely malnourished infants • İmmunosuppressed individuals • confined to the lung, where it produces an interstitial pneumonitis • characteristic intraalveolar foamy, pink-staining exudate with hematoxylin-eosin (H&E) stain (“cotton candy” exudate) • radiographic evidence of bilateral perihilar and basilar infiltrates is typical. Candidiasis • Systemic candidiasis (with associated pneumonia) is a disease restricted to immunocompromised patients • C. albicans demonstrates yeastlike forms (blastoconidia), pseudohyphae, and true hyphae • special “fungal” stains (Gomori methenamine-silver, periodic acid–Schiff) • Candidiasis can involve the mucous membranes, skin, and deep organs (invasive candidiasis). • Superficial infection on mucosal surfaces of the oral cavity. This is the most common presentation. • Vaginitis • Esophagitis • Skin infection: onychomycosis, paronychia, folliculitis, intertrigo, balanitis, Diaper rash • Chronic mucocutaneous candidiasis • Invasive candidiasis • 1) renal abscess, • (2) myocardial abscess and endocarditis, • (3) brain involvement (most commonly meningitis, but parenchymal microabscesses occur), • (4) endophthalmitis (virtually any eye structure can be involved), • (5) hepatic abscesses, • (6) Candida pneumonia, Cryptococcosis • an opportunistic infection in immunocompromised hosts, particularly patients with AIDS or hematolymphoid malignancies. • 5- to 10-μm yeast, has a thick, gelatinous capsule and reproduces by budding • pseudohyphal or true hyphal forms are not seen. • India ink or periodic acid–Schiff staining effectively highlights the fungus • usually manifests as pulmonary, central nervous system, or disseminated disease • inhalation of aerosolized contaminated soil or bird droppings The Opportunistic Molds • Mucormycosis is caused by the class of fungi known as Zygomycetes. • Rhizopus and Mucor are the two fungi of medical importancewithin the Zygomycetes class. • Their hyphae are nonseptate and branch at right angles • rhinocerebral and pulmonary mucormycosis, • propensity to colonize the nasal cavity or sinuses • direct extension into the brain, orbit, and other head and neck structures. • Patients with diabetic ketoacidosis are most likely to develop a fulminant invasive form of rhinocerebral mucormycosis. • Pulmonary disease can be localized (e.g., cavitary lesions) or may manifest radiologically with diffuse “miliary”involvement • invasive aspergillosis: • the hyphae of Aspergillus organisms are septate and branch at more acute angles • necrotizing pneumonia • Systemic dissemination, especially to the brain, is a complication that is often fatal. • Allergic bronchopulmonary aspergillosis: type I hypersensitivity against the fungus • Aspergilloma (“fungus ball”) formation occurs by fungal colonization of preexisting pulmonary cavities • predilection for invading blood vessel walls, causing hemorrahage, vascular necrosis and infarction

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