الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Hospital – acquired pneumonia (HAP) or nosocomial pneumonia (NP) is defined as pneumonia that occurs 48 hours or more after hospital admission while, ventilator associated pneumonia (VAP) refers to pneumonia that arises more than 48-72 hours after endotracheal intubation. HAP accounts up to 25% of all ICU infections and for more then 50% of antibiotic prescribed. However the incidence of VAP varied between 9-27% of all intubated patients in different studies.
Time of onset of pneumonia is an important epidemiologic variable and risk factor for specific pathogens and outcomes in patients with HAP and VAP. Early – onset HAP and VAP, defined as occurring within the first 4 days of hospitalization, usually carry a better prognosis, and are more likely to be caused by antibiotic sensitive bacteria. Late-onset HAP and VAP (5 days or more) are more likely to be caused by multidrug resistant (MDR) pathogens, and are associated with increased patient mortality and morbidity.
HAP may be caused by a wide spectrum of bacterial pathogens; may be polymicrobial, and are rarely due to viral or fungal pathogens in immunocompetent hosts. Common pathogens include aerobic Gram-negative bacilli, such as Pseudomonas aeruginosa, Echerichia coli (E-coli), Klebsiella pneumoniae, and Acinetobacter species. Infections due to Gram-positive cocci such as Staphylococcus aureus, particularly methicillin resistant Staphylococcus aureus (MRSA), have been rapidly emerging in the USA. Pneumonia due to Staphylococcus aureus is more common in persons taking drugs by injection, in patients with diabetes mellitus, head trauma, thermal injury, wound infection, and those hospitalized in ICU or who have received prior antibiotic therapy.
Significant growth of oropharyngeal commensals (viridians group Streptococci, coagulase negative Staphylococci, Neisseria species, and Corynebacterium species) from distal bronchial specimens is difficult to interpret, but these organisms can produce infection in immunocompromised hosts and some immunocompetent patients. Rates of polymicrobial infection vary widely, but appear to be increasing and are especially high in patients with ARDS.
The frequency of specific MDR pathogens causing HAP may vary by hospital, patient population, exposure to antibiotics, type of ICU patient, and may change over time, emphasizing the need for timely, local surveillance data.
Rates of HAP due to MDR pathogens have increased dramatically in hospitalized patients, especially in intensive care and transplant patients.
For HAP to occur, the delicate balance between host defenses and microbial propensity for colonization and invasion must shift in favor of the ability of the pathogens to persist and invade the lower respiratory tract. Sources of infection for HAP include healthcare devices or the environment (air, water, and equipment) and can occur with transfer of microorganisms between staff and patients. A number of host-treatment-related colonization factors, such as the severity of the patient’s underlying disease, prior surgery, exposure to antibiotics, other medications, and exposure to invasive respiratory devices and equipment, are important in the pathogenesis of HAP and VAP.
HAP requires the entry of microbial pathogens into the lower respiratory tract, followed by colonization, which can then overwhelm the host’s mechanical (ciliated epithelium and mucus), humoral (antibodies and complement), and cellular (polymorphonuclear leucocytes, macrophages, and lymphocytes and their respective cytokines) defenses to establish infection.
Aspiration of oropharyngeal pathogens or leakage of bacteria around the endotracheal tube cuff is the primary route of bacterial entry into the trachea. The stomach and sinuses have been suggested as potential reservoirs for certain bacteria colonizing the oropharynx and trachea but their importance remain controversial. Some investigators postulate that colonization of the endotracheal tube with bacteria may result in embolization into the alveoli during suctioning or bronchoscopy. Inhalation of pathogens from contaminated aerosols, and direct inoculation are less common. Hematogenous spread from infected intravascular catheters or bacterial translocation from the gastrointestinal tract lumen is quite rare.
The conventional clinical diagnosis HAP was based on a body temperature of 38.3 degrees C or greater, a leukocyte count less than 4000 cells/mm3 or greater than 12 000 C/mm3, purulent secretions, and the presence of new and persistent pulmonary infiltrates, however, these manifestation are not specific and qualitative sputum cultures can identify pathogenic and nonpathogenic organisms. The principal promise of bronchoscopy for the diagnosis consists of the ability to retrieve uncontaminated lower respiratory secretions and quantitative cultures should allow a valid differentiation of colonization from infection. The protected specimen brush (PSB) and the bronchoalveolar lavage (BAL) represent the two principal bronchosopic techniques.
Quantitative endotracheal aspirates (QEA) compares reasonably well with more invasive techniques for diagnosing VAP. The results of quantitative cultures from EA are reproducible. Quantitative culture of EA is a good diagnostic test when a non-invasive test has been chosen for the diagnosis of VAP.
The diagnosis of HAP is difficult, and most studies of non intubated patients have involved clinical diagnosis, with sputum culture, but bronchoscopy has been used less often.
The aim of this study was to assess risk factor , common bacterial pathogens and prognosis hospital acquired pneumonia, the utility of different methods to collect the respiratory secretions which may be noninvasive (induced sputum) , less invasive (endotracheal aspirate) or invasive (bronchoalveolar lavage) for diagnosis of HAP, and to determine multidrug resistant pathogen.
This study was conducted on 100 patients selected from those who were admitted to the main university hospital, mainly who were admitted to the intensive care units and who fulfilled the inclusion criteria: (hospital admission for at least 48 hours and developed clinical manifestation of HAP (Presence of a persistent new and /or progressive infiltrates with at least two of the following; fever or hypothermia, Leucocytosis or leucopenia, or purulent aspirates).
All patients were subjected to demographic evaluation (age, sex, onset of HAP, duration of mechanical ventilation, duration of hospital stay, prior surgeries, prior antibiotics, paralytic agent, intravenous sedation, H2 blockers or antacids and history of associated diseases, burn, nasogastric intubation etc….).
Clinical examination , laboratory investigations (including vital signs and parameters necessary to calculate Acute Physiology and Chronic Health Evaluation (APACHE) II score, C-reactive protein (at admission , day 3, 5, and 7 of hospital admission), plain x-ray chest, arterial blood gases, electrocardiogram (ECG) and bacteriological examination including examination of induced sputum , EA and BAL specimens (including Gram and Ziehl Neelsen stains, quantitative cultures for aerobes ,anaerobes and for fungi, blood culture, identification of pathogens by specific techniques, cultures for Legionella antibodies for Legionella pneumophilia in acute and convalescence states, and susceptibility test for antibiotics) . The growth of a potential pathogens in count >106, 105 and 104cfu/mL for induced sputum, EA and BAL fluid respectively was taken as the diagnostic threshold of HAP.
Lastly evaluation of treatment outcome was carried on clinical laboratory and radiological bases.