10-11, 12, 13, 14-10 Pneumonia Super Outline (Palmieri, Elswafi ...

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10-11, 12, 13, 14-10 Pneumonia Super Outline (Palmieri, Elswafi ...

  1. 1. 10-11, 12, 13, 14-10 Pneumonia Super Outline (Palmieri, Elswafi, Martin, Williams) - Outline<br />Total lecture hours: 2 Palmieri/Elswafi, 3 Williams, 4 Martin (lots of redundancy) – 9 lecture hours in total<br />Anatomy<br /><ul><li>Alveoli: concentrically arranged, free edge reinforced by thick bundles of connective tissue (entrance rings)
  2. 2. Alveolar septal tissues include
  3. 3. epithelial type I cells
  4. 4. epithelial type II cells
  5. 5. capillary endothelial cells
  6. 6. Note the thin alveolar septal tissue barrier over much of the surface.
  7. 7. The barrier for O2 diffusion across the thin portions of the septa into erythrocytes (EC) consists of
  8. 8. epithelium
  9. 9. common basement membrane
  10. 10. endothelium
  11. 11. Normal Flora (Respiratory)
  12. 12. The lower respiratory system is generally devoid of resident bacteria
  13. 13. Transient populations are effectively cleared by the host defenses
  14. 14. Successful pathogens are those that can persist despite the host defense systems</li></ul>Bacterial<br /><ul><li>Immune Defense (Immunology)
  15. 15. Ciliated respiratory epithelium
  16. 16. Cough reflex
  17. 17. Alveolar macrophages
  18. 18. Other immune cells (lymphocytes, neutrophils
  19. 19. Alveolar lining fluid which contains surfactant, various immunoglobins, complement components, phospholipids, enzymes, albumin, transferrin.
  20. 20. Lymphoid tissue
  21. 21. Pathogen Defense (Virulence)
  22. 22. Ways pathogens avoid phagocytosis
  23. 23. Capsule production!
  24. 24. Cytotoxicity
  25. 25. Hiding (growing) in pulmonary or phagocytic cells
  26. 26. Mimicry
  27. 27. Ways pathogens survive phagocytosis
  28. 28. Inhibition of lysosome/phagosome fusion
  29. 29. Phagosome lysis or escape
  30. 30. Growth in the phagolysosome
  31. 31. Pathogens
  32. 32. A HUGE variety of organisms have been implicated in LRT infections. The following is a list of the most common/important agents
  33. 33. Bacterial: Most Common Agents
  34. 34. More common:
  35. 35. Streptococus pneumoniae
  36. 36. Haemophilus influenzae
  37. 37. Klebsiella pneumoniae
  38. 38. Staphylococcus aureus
  39. 39. Gram-negative diplococci
  40. 40. Atypical Pneumonia:
  41. 41. Mycoplasma pneumoniae
  42. 42. Chlamydia pneumoniae
  43. 43. Legionella pneumophila
  44. 44. Some others:
  45. 45. Group A and B streptococci
  46. 46. Mycobacterium tuberculosis
  47. 47. Pseudomonas aeruginosa
  48. 48. Bacillus anthracis and others
  49. 49. Escherichia coli
  50. 50. anaerobes (important in aspiration pneumonia)
  51. 51. Pathophysiology, Diagnosis, Treatment
  52. 52. Pneumonia
  53. 53. A clinical syndrome
  54. 54. Streptococcus pneumonia (50%)
  55. 55. Haemophilus influenzae (10%)
  56. 56. Type B, childhood vaccine
  57. 57. requires X and V factors
  58. 58. Pneumonia develops when host defenses are overwhelmed by an infectious pathogen. This may occur because of :
  59. 59. inadequate immune response (often the result of underlying comorbid illness such as congestive heart failure, diabetes, renal failure, chronic obstructive lung disease, or malnutrition)
  60. 60. anatomic abnormalities (endobronchial obstruction, bronchiectasis)
  61. 61. immune dysfunction associated with acute illness (sepsis, extrapulmonary infection)
  62. 62. therapy-induced dysfunction of the immune system (corticosteroids, endotracheal intubation)
  63. 63. Seeding
  64. 64. Inhalation
  65. 65. Aerosolized droplets accounts for the transmission of respiratory viruses, such as influenza, which is highly contagious and often occurs in epidemics. Similar means of spread produce pneumonias
  66. 66. Mycobacterium tuberculosis is spread from person to person by aerosolized droplets.
  67. 67. Legionella pneumophila is the species most likely to be spread by inhalation of aerosolized organisms that originate in contaminated freshwater
  68. 68. Aspiration
  69. 69. Nasopharyngeal organisms occurs in nearly all persons during sleep and is probably responsible for most bacterial pneumonias
  70. 70. The pulmonary consequences from the abnormal entry of fluid, particulate exogenous substances, or endogenous secretions into the lower airways.
  71. 71. There are usually two requirements to produce aspiration pneumonia:
  72. 72. Compromise in the usual defenses that protect the lower airways including glottic closure, cough reflex, and other clearing mechanisms
  73. 73. An inoculum deleterious to the lower airways by a direct toxic effect, a large enough bacterial inoculum, or obstruction of the airway
  74. 74. The term aspiration pneumonia usually reserved for pneumonitis resulting from the altered clearance defenses and usually refers to an infection caused by less common and often less virulent bacteria, primarily anaerobes and enterobacteriace, which are constituents of the normal flora in a susceptible host.
  75. 75. Primary Mechanism
  76. 76. Microaspiration of colonized oropharyngeal secretions
  77. 77. Oral Colonization: Haemophilus influenzae and Streptococcus pneumoniae
  78. 78. Anaerobic Bacteria
  79. 79. Elderly Patients: Enterobacteriaceae, Pseudomonas aeruginosa, and Staphylococcus aureus.
  80. 80. Recumbent Position
  81. 81. MC Site: Posterior segment of upper lobes and apical segments of lower lobes
  82. 82. Upright or Semirecumbent Position
  83. 83. MC Site: Basal segments of the lower lobes
  84. 84. Risks
  85. 85. Altered Consciousness
  86. 86. Alcoholism
  87. 87. Seizures
  88. 88. Cerebrovascular Accident
  89. 89. Head Trauma
  90. 90. General Anesthesia
  91. 91. Drug Overdose
  92. 92. Dysphagia
  93. 93. Esophageal Disorders: Strictrures, neoplasm, diverticula, TE fistula, incompetent cardiac sphincter
  94. 94. Neurologic Disorders
  95. 95. Multiple Sclerosis, Parkinson’s Disease, Myasthenia gravis, Pseudobulbar palsy
  96. 96. Stroke patients
  97. 97. Not protected by feeding tubes
  98. 98. Mechanical disruption of the usual defense barriers
  99. 99. Nasogastric tube, endotracheal intubation, tracheostomy, upper gastrointestinal endoscopy, bronchoscopy
  100. 100. Other
  101. 101. Protracted vomiting, gastric outlet obstruction, large-volume nasogastric tube feedings, pharyngeal anesthesia, general debility, recumbent position
  102. 102. Types
  103. 103. Chemical Pneumonitis
  104. 104. The aspiration of substances that are toxic to the lower airways, independent of bacterial infection (gastric acid).
  105. 105. This form of aspiration pneumonia commonly follows a fulminate course that may result in acute respiratory distress syndrome (ARDS)
  106. 106. Hypoxemia results from pulmonary edema, reduced surfactant activity, reflex airway closure, atelectasis, alveolar hemorrhage, infiltration of polymorphoneculear leukocytes and fibrin and hyaline membrane formation.
  107. 107. Lung function demonstrates decreased compliance, abnormal ventilation-perfusion, and reduced diffusing capacity.
  108. 108. The lung becomes grossly edematous and hemorrhagic with alveolar consolidation.
  109. 109. Diagnosis — The diagnosis of acid pneumonitis is usually presumptive based upon the clinical features and course. After aspiration, chest x-ray changes are noted in as little as two hours.
  110. 110. Aspiration of gastric contents requires a pH of <2.5 to produce chemical pneumonitis.
  111. 111. Abrupt onset of symptoms with prominent dyspnea
  112. 112. Fever, which is usually low-grade
  113. 113. Cyanosis and diffuse crackles on lung auscultation
  114. 114. Severe hypoxemia and infiltrates on chest radiograph involving dependent pulmonary segments
  115. 115. Treatment — Patients with an observed aspiration should have immediate tracheal suction to clear fluids and particulate matter that may cause obstruction.
  116. 116. The major therapeutic approach is to support pulmonary function.
  117. 117. Demonstrated benefit from positive-pressure ventilation support
  118. 118. The use of corticosteroids in the treatment of chemical pneumonitis is controversial with mixed results reported.
  119. 119. The acid-injured lung is highly susceptible to bacterial challenge with 13 to 26 percent of patients developing pulmonary superinfections within 7 days .
  120. 120. Antimicrobial agents are commonly given and must cover gram negative m/o as well as anaerobes.
  121. 121. Outcomes vary
  122. 122. Bacterial Infection
  123. 123. The most common forms of aspiration pneumonia are caused by bacteria that normally reside in the oral-pharyngeal area or stomach.
  124. 124. Anaerobic bacteria are the dominant organisms in the upper airways and most common cause of infection.
  125. 125. Major M/O include: Peptostreptococcus, Fusobacterium nucleatum, Prevotella, and Bacteroides spp.
  126. 126. Gram-negative bacilli, E. coli, Klebsella, Proteus spp., P. aurgenosa, Serratia spp., etc were the most common isolates (49 percent) followed by anaerobes (16 percent) and S. aureus (12 percent) due to difficulty in culturing and identifying anaerobic m/o.
  127. 127. patients with gram-negative bacilli isolated often also have anaerobes involved
  128. 128. Highly variable depending upon the bacteria involved and the status of the host.
  129. 129. Compared to most cases of community-acquired pneumonia, the tempo of the disease in this type of aspiration pneumonia is often relatively slow.
  130. 130. Most patients present with the common manifestations of pneumonia including cough, fever, purulent, sputum and dyspnea, but the process evolves over a period of several days or weeks instead of hours
  131. 131. Some patients have a relatively abrupt and more toxic course with chills and rigors onset suggestive of a pyrogenic pneumonia due to common bacterial pathogens, including Streptococcus pneumoniae, H. Influenza, S. aures, etc.
  132. 132. Clindamycin is more effective for treatment than penicillin agents today due to development of resistance in the anaerobic m/o most commonly involved with micro-aspiration
  133. 133. Beta-lactam beta lactamase combination anti-pseudomonal penicillins (piperacillin-tazobactam or ticarcillin-clavulanate)
  134. 134. Or
  135. 135. antipsuedomonal cephalosporin agents such as cefepime or ceftadizime indicated for treatment of suspected gram negative
  136. 136. Or
  137. 137. Antipseudomonal carbapenem, (inipenem or meropenem).
  138. 138. Aminoglycocide agents alternative for gram negative agents including pseudomonas in combination with fluoroquinolones
  139. 139. Fluoroquinolones, levofloxacin and gatifloxacin indicated but clinically moxifloxacin and trovafloxacin, have best anaerobic activity in addition to good gram negative coverage and are more appropriate.
  140. 140. If MRSA suspected, linezolid or vancomycin employed
  141. 141. Mechanical obstruction
  142. 142. Aspiration pneumonia may involve fluid or particulate matter, which are not inherently toxic to the lung, but can cause airway obstruction or reflux airway closure.
  143. 143. Intratracheal instillation of fluids in limited quantities results in transient, self-limited hypoxemia. On occasion, this may trigger pulmonary edema, more severe hypoxemia, and reduced lung compliance .
  144. 144. This reaction is reversible by vagotomy or administration of atropine or isoproterenol.
  145. 145. This type of aspiration pneumonia is difficult to recognize clinically, but the appropriate treatment would be removal of the offending agents and positive-pressure breathing with 100 percent oxygen combined with isoproterenol.
  146. 146. Particulate matter
  147. 147. Money and toys
  148. 148. Teeth
  149. 149. Large food particles-such as peanuts which are often not visible on x-ray
  150. 150. Medical devices
  151. 151. Fluids  
  152. 152. Saline , water, juices, etc
  153. 153. Barium
  154. 154. Gastric contents with a pH exceeding 2.5
  155. 155. Bacterial superinfection is a frequent complication when the obstruction or partial obstruction persists for more than one week, with anaerobic m/o being most common
  156. 156. Hematogenous
  157. 157. Causes pneumonia, accounts for occasional cases of staphylococcal pneumonia in patients with tricuspid valve endocarditis or septic thrombophlebitis. This mechanism is also responsible for various gram-negative bacillary pneumonias in patients with bacteremi
  158. 158. Associated with spread of infectious agent via circulatory system to lung secondary to development of septacemia from distant infected site.
  159. 159. May have any organism that becomes bacteremic, from Candida septicemia, Klebsiella, E. coli, P. aurgenosa, etc.
  160. 160. Commonly associated with right heart disease and emboli of infected vegetations associated with endocarditis and valular heart disease
  161. 161. Most common organism is S. aures, associated with I.V. drug abusers which produces classic cannon ball defects on CXR
  162. 162. Spread from pulmonic and tricuspid value vegetations with any organism producing pathology, from S. viridians to Candida
  163. 163. Environmental
  164. 164. This category includes Hypersensitivity Lung Disease.
  165. 165. These conditions produce 15 to 20% of all COPD.
  166. 166. Related to development of interstitial lung disease as well as COPD, CA and pnuemonitis in patients.
  167. 167. X-ray distribution and resp. changes provide some clues to but not definitive etiology.
  168. 168. Mineral dust more related to restrictive changes on PFT while organic dust and chemical agents more associated with obstructive patterns seen with asthma and COPD.
  169. 169. Small, round, millenary opacities on CXR related more commonly with silicosis or coal workers pneumoconiosis
  170. 170. Linear opacities more associated with asbestosis
  171. 171. The size of particles and composition of gaseous agent also determine the presentation on X-ray and distribution of pathological agent:
  172. 172. Particles >10-15 um generally do not penetrate beyond upper respiratory tract.
  173. 173. Particles < 10um penetrate below larynx in larger airways
  174. 174. Particles 2.5 um-10um (associated with crustal elements like silica, iron and aluminum) tend to deposit high in the tracheo-bronchial tree
  175. 175. Particles < 2.5 um tend to penetrate to lower airways, bronchioles and alveoli
  176. 176. Particles < 1 um (ultrafine particles) have diffuse distribution in all areas of lung
  177. 177. The size of particles and composition of gaseous agent also determine the presentation on X-ray and distribution of pathological agent:
  178. 178. Water soluble gases like ammonia or sulfa oxide tend to cause upper airway bronchoconstrictive processes
  179. 179. Less soluble agents like phosgene or nitrogen dioxide penetrate to bronchioles and alveoli and are associated with more severe respiratory perfusion/ventilation damage and ARDS
  180. 180. Inorganic Dusts & Respiratory Response
  181. 181. Asbestos (asbestosis)
  182. 182. Pulmonary Fibrosis (PF), Lung CA, mesothelioma
  183. 183. Asbestos is generic term for several mineral silicates
  184. 184. Widely distributed world wide, was widely utilized up to 1980 for insulation so extensive exposure
  185. 185. Produces acute pneumonitis, pleural and pulmonary fibrosis, diffuse interstitial fibrosis as well as highly associated with Cancer of the lung and respiratory tract.
  186. 186. Produces restrictive pattern with decrease with decrease in both lung volume and diffusion
  187. 187. CXR associated with pleural plaques in linear pattern, most commonly in lower lung fields.
  188. 188. Occasionally have pleural effusion in acute episodes, frequently bloody.
  189. 189. On C.T., classic is cardiac margin occluding “ground glass” perihilar changes.
  190. 190. Pneumonitis and interstitial pneumonia can be seen in few weeks or delayed for months and years.
  191. 191. Lung CA delayed >15 years classically after prolonged exposure to agent.
  192. 192. Risk of lung CA greatly multiplied by concurrent or history of smoking!
  193. 193. Mesothelioma both pleural and peritonial , although less common than lung CA, occurs in association with asbestos and may be seen with short term exposure as much as 4 decades before
  194. 194. Risk of mesothelioma not related to smoking!
  195. 195. Silica (silicosis)
  196. 196. PF, CA, silcotuberculosis, COPD, PMF
  197. 197. Pulmonary fibrosis generally occurs after years of exposure to silica although an acute syndrome is associated with large volume exposure.
  198. 198. May be rapidly progressive with fibrosis and interstitial pneumonitis in spite of removal from exposure.
  199. 199. Characterized by diffuse milinary infiltration and consolidation (“crazy paving”)
  200. 200. Simple silicosis from long term (15-20 year) exposure presents as rounded opacities in upper lobes accompanied by hilar node calcification
  201. 201. Silica is cytotoxic to alveolar macrophages and patients are at greater risk of lung infections from organism like M. tuberculosis, atypical mycobacterium and fungi.
  202. 202. Also associated with exacerbation of autoimmune connective tissue disorders such as RA, SLE and scleroderma
  203. 203. Coal Dust
  204. 204. PMF, COPD (Coal workers pneumoconiosis)
  205. 205. Seen in up to 50% of coal miners after 20 years of work in mines.
  206. 206. Less common in miners of bituminous coal found in the west than miners of anthracite coal found in Europe and Eastern US
  207. 207. CXR resembles silicosis, small, round opacities more common in upper lobes.
  208. 208. Complicated CWP presents with large nodules (> 1cm up to involvement of entire lobe) seen primarily in upper lobe. More severe restrictive and obstructive lung disease associated.
  209. 209. Highly associated with development of COPD.
  210. 210. Effects are synergistic and additive to effects of cigarette smoking
  211. 211. Beryllium
  212. 212. Lung CA, Acute pneumonitis, chronic granulomatous disease
  213. 213. Beryllium is a light weight utilized in control of nuclear reactions due to ability to quench neutrons and in production of electronics, ceramics, etc.
  214. 214. Exposure can produce an acute pneumonitis but more associated with a chronic granulomatous inflammatory disease similar to sarcoidosis
  215. 215. Disease is secondary to cell mediated immune response.
  216. 216. Test for beryllium disease is beryllium lymphocyte proliferation (BeLPT)
  217. 217. Presents on CXR similar to sarcoidosis with nodules along septal lines but has less hilar adenopathy.
  218. 218. PFT yield both restrictive and obstructive changes along with decreased diffusion capacity.
  219. 219. Chronic beryllium disease is one of best examples of genetic-environmental interaction.
  220. 220. Susceptibility to CBD is highly associated with HLA-DP alleles that possess a glutamic acid in position 69 of the beta chain
  221. 221. Other metals
  222. 222. Pneumonitis, CA, asthma (Aluminum, Chromium, Cobalt, Nickel, titanium, Tungsten)
  223. 223. Organic dusts & Respiratory response
  224. 224. Hypersensitivity Pneumonitis (again)
  225. 225. An inflammatory disorder of the lung involving the alveolar walls and terminal airways.
  226. 226. Induced by inhalation of a variety of organic agents that induce an immunologic reaction within the pulmonary parenchyma.
  227. 227. Immune complex-induced inflammatory reactions initiate acute lung injury then T cell-mediated hypersensitivity reactions perpetuate it and induce chronic inflammatory, granulomatous, and fibrotic responses in the interstitium of the lungs.
  228. 228. Numerous inciting agents, with more than 300 identified, include but are not limited to, agricultural dusts, bioaerosols, fungi, bacterium, virus, and certain chemicals.
  229. 229. Klebsiella oxytoca, Mycobacterium avium complex (MAC), actinomycetes spores, aspergillus, micropolyspora faeni, Cladosporium cladosporioides, diphenylmethane diisocyanate (MDI), toluene diisocyanate, metalworking fluid aerosols, feather duvets, etc.
  230. 230. EPIDEMIOLOGY — The prevalence and incidence are thought to be low but widely unknown.
  231. 231. Most knowledge has been derived from studies of chemical workers, farmers and bird fanciers.
  232. 232. The prevalence and incidence of HP varies considerably depending upon intensity of exposure to inciting antigens, season, geographical conditions, local practices and customs, proximity to certain industries, and host risk factors.
  233. 233. Many persons with mild or subclinical HP escape detection or are misdiagnosed as suffering from viral illnesses or asthma, either of which may have nonspecific clinical findings which mimic HP.
  234. 234. Only a small proportion of exposed individuals develop clinically significant HP, and genetic factors have been postulated to play a major role in determining an individual's risk of disease.
  235. 235. A wide range of occupations and avocations that result in contact with airborne organic antigens increase the risk of developing HP.
  236. 236. Farmer's lung is one of the most common forms of HP, affecting 0.4 to 7 percent of the farming population
  237. 237. Chemical workers lung, related in part to exposure with isocyanates in US in relatively rare.
  238. 238. Bird fanciers lung has variable occurrence as well with estimates range from 20 to 20,000 affected individuals per 100,000 persons at risk.
  239. 239. Bagassosis sugar cane workers response to fungal antigens.
  240. 240. High rates noted with sporadic outbreaks of HP among other populations :
  241. 241. 52 percent of exposed office workers with humidifier lung
  242. 242. 37 percent of lifeguards exposed to a public swimming pool
  243. 243. 27 percent of workers at an injection molding plant manufacturing polyurethane foam parts for automobiles
  244. 244. 15 percent of office workers exposed to a contaminated forced air system
  245. 245. Cigarette smoking is associated with a decreased risk of HP. These observations may reflect diminished antibody responses to inhaled antigens among smokers.
  246. 246. Once the disease is established, however, smoking does not appear to attenuate its severity, and may predispose to a more chronic and severe course .
  247. 247. Clinical picture is interstitial pneumonitis
  248. 248. Can be acute, sub-acute or chronic in presentation
  249. 249. Acute presents as cough, fever, chills, malaise and dyspnea as quickly as 6 to 8 hours post exposure.
  250. 250. Sub acute presents over weeks with cough, dyspnea, progressing to cyanosis and hypoxia.
  251. 251. Acute and sub-acute signs, symptoms and manifestation disappear in days, weeks or month if exposure is removed.
  252. 252. Chronic only seen with continued exposure to antigen and may be indistinguishable from pulmonary fibrosis from a variety of causes with clubbing, chronic cyanosis, pulmonary hypertension and respiratory failure.
  253. 253. Diagnosis
  254. 254. See elevation in acute reactants, ESR, C-reactive protein, rheumatoid factor, neutrophilia
  255. 255. It is on note that eosinophilia if not a feature of HP.
  256. 256. Serum precipitins against suspected agents (thermophilic actinomycetes, apsergillus, cladosporium spp, mycobacterium avium complex, isocyanates, etc) are suggestive but not diagnostic due to wide exposure among population.
  257. 257. CXR is non-specific with diffuse infiltrates or discrete nodular infiltrates both seen.
  258. 258. Differentiate from other interstitial lung disorders made often by history, drugs exposed to, history of collagen vascular disease like RA or Crohn’s, etc.
  259. 259. Prevention
  260. 260. Diminishing exposure to provocative antigens. This may be accomplished by minimizing contact with potential inciting agents, reducing microbial contamination, or using protective equipment.
  261. 261. Indoor microbial contamination is usually related to problems with moisture control.
  262. 262. Stagnant water is prone to microbial overgrowth. humidity should be maintained below 60 percent, water damage cleaned aggressively, carpeting should be avoided if possible and kept dry if not and water in heating, ventilating, and air conditioning systems should not be re-circulated and cleaned regularly.
  263. 263. Treatment
  264. 264. Antigen avoidance 
  265. 265. Glucocorticoids — accelerate initial recovery from farmer's lung and bird fancier's lung, however, the long-term outcome appears unchanged by glucocorticoid treatment
  266. 266. The majority of persons with HP experience near total recovery of lung function, which in some cases may take several years after the inciting exposure ceases
  267. 267. Cotton Dust
  268. 268. byssinosis-(asthma like syndrome), COPD
  269. 269. Grain Dust
  270. 270. Asthma, COPD, HP
  271. 271. Other Ag. Dusts
  272. 272. Asthma, COPD, HP
  273. 273. Toxic Chemicals have been demonstrated to produce COPD, hypersensitivity pneumonitis, pneumoconiosis, pulmonary edema, ARDS, and CA
  274. 274. Infiltrates with Eosinophilia
  275. 275. First described by Loeffler as migratory pulmonary infiltrates and peripheral eosinoophilia of unknown cause.
  276. 276. Idiopathic causes:
  277. 277. Loeffler’s syndrome
  278. 278. Acute eosinophilic pneumonia
  279. 279. Chronic eosinophilic pneumonia
  280. 280. Allergic granulomatosis of Churg and Strauss
  281. 281. Hypereosinophilic syndrome
  282. 282. Known etiologies:
  283. 283. Allergic bronchopulmonary mycoses (aspergillus, penicillium, candida, helminthosporium spp)
  284. 284. Parasitic infestations
  285. 285. Drug reactions
  286. 286. Eosinophilia-myalgia syndrome
  287. 287. Most common form of eosinophilic pneumonia.
  288. 288. Associated with bronchial asthma.
  289. 289. Most common agent is A. fumigatus
  290. 290. Asthma due to IgE mediated hypersensitivity, while bronchiectasis associated form immune complex reaction in airways.
  291. 291. Parasite
  292. 292. Most often with filarial infections but also seen with Ascaris, Ancyclostoma, Toxocara, Strongyloides, Wuchereria bancrofti
  293. 293. Rare in US unless international travel but seen recently with Iraq and Afghanistan veterans.
  294. 294. Drug-Induced
  295. 295. Most common cause of eosinophilic pulmonary infiltrates in US.
  296. 296. Most commonly associated with nitrofurantion with onset 2 to 10 days after exposure to drug.
  297. 297. Also seen with thiazides, penicillin, sulfonamides, chlorpropamide, tricyclic antidepressants, gold salts, isoiazide, indomethacin, etc.
  298. 298. Recently reported with anti-TNF-alfa therapy
  299. 299. Contiguous Spread
  300. 300. Reactivation
  301. 301. Risks
  302. 302. Smoking
  303. 303. Smoking alters mucociliary transport, humoral and cellular defenses, and epithelial cells, and increases adhesion of Strep. pneumoniae and H. influenzae to the oropharyngeal epithelium. Accordingly, a large proportion of patients hospitalized with pneumonias are current smokers
  304. 304. Age: >65 y.o.
  305. 305. COPD
  306. 306. Immunosuppression
  307. 307. Respiratory therapy
  308. 308. Comorbidity
  309. 309. Neoplasm
  310. 310. Neurological disease
  311. 311. Alcoholism
  312. 312. Alcohol adversely affects many aspects of the respiratory tract defense mechanisms.
  313. 313. facilitates bacterial colonization of the
  314. 314. oropharynx by Gram-negative bacilli
  315. 315. impairs cough reflexes
  316. 316. alters swallowing and mucociliary transport
  317. 317. impairs the function of lymphocytes, neutrophils,
  318. 318. monocytes, and alveolar macrophages.
  319. 319. Each of these alterations contributes to the reduced bacterial clearance from the airways found in these patients.
  320. 320. Close contact with infected persons
  321. 321. Institutionalization
  322. 322. Oropharyngeal colonization
  323. 323. Strep. Pneumonia > Staph. Aureus > Gram-negative bacilli > Haemophilus influenzae
  324. 324. Miscellaneous
  325. 325. Soldiers
  326. 326. Painters
  327. 327. South African gold miners
  328. 328. Recent hospitalization (especially S. pneumonia)
  329. 329. Defined as pneumonia that occurs more than 48 hours after hospital admission, excluding any infection incubating at the time of admission.
  330. 330. It has been suggested that this definition is no longer adequate because cases can occur within 48 hours of hospitalization, particularly as a consequence of emergency intubation, or cardiopulmonary resuscitation
  331. 331. Ventilator-associated pneumonia (VAP) can be regarded as a particular subgroup of HAP for which the incidence, etiology, investigation and outcome are somewhat different.
  332. 332. It should be remembered that patients recently discharged from hospital who develop pneumonia may have an illness with features more in keeping with hospital-acquired rather than community-acquired infection.
  333. 333. Pathogens with high rate of resistance
  334. 334. Aerobic gram negative bacilli (Enterobacter spp, Escherichia coli, Klebsiella spp, Proteus spp, Serratia marcescens, and Hemophilus influenzae)
  335. 335. Gram-positive organisms such as Streptococcus pneumoniae and Staphylococcus aureus
  336. 336. Signs & Symptoms
  337. 337. Respiratory
  338. 338. Cough
  339. 339. Fever
  340. 340. Chest Pain
  341. 341. Tachypnea
  342. 342. Sputum
  343. 343. Non-respiratory
  344. 344. Confusion
  345. 345. Headache
  346. 346. Myalgia
  347. 347. Abdominal pain
  348. 348. Nausea
  349. 349. Vomiting
  350. 350. Diarrhea
  351. 351. The classic signs of:
  352. 352. consolidation
  353. 353. dullness to percussion
  354. 354. crackles
  355. 355. increased tactile fremitus
  356. 356. bronchial breathing
  357. 357. Found in only one third of adults admitted to hospital with radiographically confirmed CAP
  358. 358. 5–10% of adults who have CAP in the community
  359. 359. Radiologic Findings
  360. 360. Lobar
  361. 361. Relatively homogeneous regions of increased lung opacity and air bronchograms
  362. 362. The entire lobe need not be involved, and in fact, with early therapy, consolidation does not usually affect the entire lobe
  363. 363. Pathologically, the infecting organism reaches the distal air spaces, resulting in edema filling the alveoli
  364. 364. The infected edema fluid spreads centripetally throughout the lobe via communicating channels to adjacent segments
  365. 365. Air bronchograms are common
  366. 366. Lobular
  367. 367. Characterized on x-ray by relatively homogeneous regions of increased lung opacity and air bronchograms
  368. 368. The entire lobe need not be involved, and in fact, with early therapy, consolidation does not usually affect the entire lobe
  369. 369. Pathologically, the infecting organism reaches the distal air spaces, resulting in edema filling the alveoli
  370. 370. The infected edema fluid spreads centripetally throughout the lobe via communicating channels to adjacent segments.
  371. 371. Air bronchograms are common
  372. 372. Bronchopneumonia
  373. 373. Results from inflammation involving the terminal and respiratory bronchioles rather than the distal air spaces. Since the process focuses in the airways, the distribution is more segmental and patchy, affecting some lobules and sparing others
  374. 374. Interstitial
  375. 375. Looks awful
  376. 376. Ground glass attenuation
  377. 377. Bilateral, patchy & diffuse
  378. 378. W /WO airspace consolidation
  379. 379. Geographic distribution with spared areas
  380. 380. Mixed
  381. 381. Mixed interstitial and alveolar opacities (ground-glass pattern) are findings compatible with PCP in a HIV positive patient
  382. 382. Klebsiella pneumoniae
  383. 383. Enterobacteriaceae
  384. 384. Extensive capsular polysaccharide
  385. 385. Staphylococcus aureus
  386. 386. Community acquired
  387. 387. Community-acquired pneumonia (CAP) affects approximately 4.5 million adults in the United States annually.
  388. 388. About one third of these adults require hospitalization.
  389. 389. The mortality rate among hospitalized patients with CAP varies each year and can reach 35 percent.
  390. 390. Streptococcus pneumoniae causes up to 70 percent of CAP cases
  391. 391. Atypical pathogens are responsible for 30 to 40 percent of cases and may be copathogens in other cases
  392. 392. Possible contradiction (Williams): S. aureus most likely pneumonia cause in 2006-2007 Flu Season
  393. 393. Things to keep in mind:
  394. 394. Flu first
  395. 395. Then 2nd pneumonia – S. aureus
  396. 396. “Don’t miss this”
  397. 397. (I think this is a semantics problem, not a contradiction. Be aware.)
  398. 398. Determining the pathogen is difficult
  399. 399. 50% of cases: pathogen is not identified
  400. 400. Suggests atypical agent
  401. 401. In a study of patients with a mean age of 41 years, for example, Mycoplasma pneumoniae accounted for 22.8% of community-acquired pneumonias, Chlamydia pneumoniae for 10.7%, and influenza A for 2.7%
  402. 402. See “Atypical Pneumonia” below
  403. 403. Most common cause of Community-Acquired Pneumonia
  404. 404. Before antibiotics, S. pneumoniae was synonymous with pneumonia.
  405. 405. Today S. pneumoniae accounts for about ½ the community acquired cases where agents are identified.
  406. 406. The elderly and the very young are most at risk.
  407. 407. Few virulence factors known besides polysaccharide capsule
  408. 408. α-hemolytic, non-typeable (non-groupable)
  409. 409. Rust-colored sputum
  410. 410. Often sequel to influenza
  411. 411. Gram-negative diplococci
  412. 412. Neisseria
  413. 413. Moraxella catarrhalis
  414. 414. Atypical Pneumonia
  415. 415. Atypical organisms such as Mycoplasma pneumoniae, Chlamydia pneumoniae, and Legionella pneumophila are implicated in up to 40 percent of cases of community-acquired pneumonia
  416. 416. Mycoplasma pneumoniae
  417. 417. Smallest free-living organism, no cell wall
  418. 418. Most common cause of atypical pneumonia
  419. 419. Mycoplasma pneumoniae causes a wide range of respiratory infections, including
  420. 420. Pneumonia
  421. 421. Tracheobronchitis
  422. 422. upper respiratory tract infection
  423. 423. Only 3 to 10 percent of persons infected with M. pneumoniae develop pneumonia.
  424. 424. Because M. pneumoniae infection becomes more common with increasing age, it is particularly important to consider this agent in elderly patients.
  425. 425. M. pneumoniae infection occurs throughout the year but can cause periodic outbreaks within small communities.
  426. 426. Transmission is by person-to-person contact, and infection spreads slowly, most often within closed populations (e.g., households, schools, businesses).
  427. 427. M. pneumoniae infection may be associated with several extrapulmonary manifestations.
  428. 428. Skin manifestations include
  429. 429. erythema multiforme
  430. 430. erythema nodosum
  431. 431. maculopapular and vesicular eruptions
  432. 432. urticaria.
  433. 433. Neurologic derangements include
  434. 434. aseptic meningitis
  435. 435. cerebral ataxia
  436. 436. Encephalitis
  437. 437. Guillain-Barré syndrome
  438. 438. transverse myelitis.
  439. 439. S/S
  440. 440. Onset is insidious, over several days to a week.
  441. 441. Constitutional symptoms, which usually are present, include headache exacerbated by a cough, malaise, myalgias, and sore throat.
  442. 442. The cough is usually dry, paroxysmal, and worse at night.
  443. 443. The clinical course of pneumonia caused by M. pneumoniae is usually mild and self-limited.
  444. 444. The mortality rate is approximately 1.4 percent.
  445. 445. However, pulmonary complications can be significant and include effusion, empyema, pneumothorax, and respiratory
  446. 446. The production of cold agglutinins can result in hemolytic anemia, especially when M. pneumoniae titers are high. Finally, complications such as myocarditis, pancreatitis, pericarditis, and polyarthritis can occur.
  447. 447. Diagnosis
  448. 448. The WBC count is generally not helpful in mycoplasmal pneumonia because results may be normal or elevated
  449. 449. M pneumoniae is difficult to culture and requires 7-21 days to grow; culturing is successful in only 40-90% of cases and does not provide information to guide patient management
  450. 450. Hemolytic anemia has been described but is rare.
  451. 451. Sputum Gram stains and cultures are usually not helpful because M pneumoniae lacks a cell wall and cannot be stained. 
  452. 452. Elevated erythrocyte sedimentation rates may be present but are nonspecific.
  453. 453. Serum cold agglutinins may be positive but are nonspecific
  454. 454. PCR can accurately identify the pathogen
  455. 455. Not practical or readily available
  456. 456. Eosinophil cationic protein (ECP) measures damage to the respiratory epithelium
  457. 457. May be used more in the future for Dx
  458. 458. High-resolution CT scans of the chest are more sensitive than chest radiography in elucidating lung disease.
  459. 459. Radiographic findings vary, but abnormalities are usually more striking than the findings upon physical examination. 
  460. 460. Bronchopneumonia often involves a single lower lobe. Lobar consolidation is rare.
  461. 461. Platelike atelectasis is noted as thin, flat areas of collapsed lung and is often seen on a lateral image of the chest.
  462. 462. Reticulonodular or interstitial infiltrates, primarily in the lower lobes, may resemble other diseases with granulomatous pathology, such as tuberculosis, mycoses, and sarcoidosis. 
  463. 463. Hilar adenopathy is sometimes mistaken for malignancy.
  464. 464. Pleural effusions develop in less than 20% of patients; when present, they can be seen on lateral decubitus films.
  465. 465. Treatment
  466. 466. Chlamydia pneumoniae
  467. 467. Obligate intracellular pathogen
  468. 468. Unusual life cycle (EB and RB forms)
  469. 469. Chlamydia pneumoniae is an obligate intracellular organism capable of persistent latent infection.
  470. 470. Humans are the only known reservoir.
  471. 471. Transmission results from contact with respiratory secretions, with an incubation period of several weeks.
  472. 472. By the age of 20 years, one half of persons in the United States have detectable levels of antibody to C. pneumoniae. The antibody is present in 75 percent of elderly persons.C. pneumoniae infection is more likely to occur in older patients with comorbid diseases than in those who are otherwise healthy.
  473. 473. Patients with C. pneumoniae infection often present with sore throat, headache, and a cough that can persist for months if treatment is not initiated early.Sputum is usually scant or nonexistent, and a low-grade fever is usually present.
  474. 474. Chest radiographs tend to show less extensive infiltrates than are seen with other causes of pneumonia, although significant infiltrates have been reported.
  475. 475. Most cases of C. pneumoniae infection are mild,
  476. 476. Severe disease can occur, necessitating admission to an intensive care unit. The mortality rate has been estimated to be 9 percent, and death usually is associated with secondary infection and underlying comorbid disease
  477. 477. Legionella pneumophila
  478. 478. Legionnaire’s disease
  479. 479. water source reservoir
  480. 480. require iron and cysteine for growth
  481. 481. problematic in aged, smokers, drinkers, immunocompromised
  482. 482. Legionella species are intracellular organisms. Legionella pneumophila is the most pathogenic species, and several serotypes have been identified.
  483. 483. Serotype 1 has been associated with most reported human cases of pneumonia caused by L. pneumonphila.
  484. 484. Infection occurs from exposure to legionella organisms in the environment.
  485. 485. Person-to-person spread has not been reported.
  486. 486. Legionellae are found most commonly in freshwater and man-made water systems.
  487. 487. Risk factors for the development of legionellosis include
  488. 488. overnight stays outside the home.
  489. 489. recent home plumbing work
  490. 490. renal or liver failure
  491. 491. Diabetes
  492. 492. Malignancy
  493. 493. Other conditions that compromise the immune system
  494. 494. The pathogens also can be found in moist soil, especially near streams and ponds.
  495. 495. Man-made systems for heating and cooling water can be prime environments for the proliferation of legionellae, because of conditions such as temperatures between 32°C (89.6°F) and 45°C (113°F), stagnation of water, and the presence of scale sediment and amebas.
  496. 496. Condensers, cooling towers, respiratory therapy equipment, showers, water faucets, and whirlpools have been associated with outbreaks of legion.
  497. 497. Others
  498. 498. Group A and B streptococci
  499. 499. Mycobacteria
  500. 500. M. tuberculosis
  501. 501. M. avium-intracellulare
  502. 502. found in birds
  503. 503. TB-like disease in immunocompromised
  504. 504. MAC is especially common in soil in the South-Eastern United States
  505. 505. Up to 40% of US patients with advanced AIDS have had MAC
  506. 506. Most common bacterial opportunistic infection (OI) in adults infected with HIV in the developed world.
  507. 507. Most found in US – Rare in Africa.
  508. 508. Annual frequency in AIDS – 10-20%.
  509. 509. Occurs late in HIV infection.
  510. 510. Mean CD4+ Count ~ 10-30/μL. (TB occurs early.)
  511. 511. Inhaled or ingested from environment.
  512. 512. Spreads via lymphatics then hematogenously.
  513. 513. Taken up in reticuloendothelial organs.
  514. 514. Primary
  515. 515. None-tubercular pulmonary disease, more common than T.B. in US, endemic to most of N. America
  516. 516. Age > 50
  517. 517. Nonsmoking Women > Males
  518. 518. No underlying disease identified absolutely
  519. 519. Radiography reveal nodular bronchiectatic changes with midzone involvement
  520. 520. Secondary
  521. 521. White Middle-Aged/Elderly Men
  522. 522. 30-70
  523. 523. M>F
  524. 524. Smokers &/or Alcoholics
  525. 525. Resembles TB
  526. 526. Prior Bronchiectasis
  527. 527. Healed TB
  528. 528. Pneumoconisosis
  529. 529. Cystic Fibrosis
  530. 530. Prior Malignancy
  531. 531. S/S
  532. 532. Disseminated MAC
  533. 533. Fever
  534. 534. Night Sweats
  535. 535. Diarrhea
  536. 536. Weight Loss and wasting syndrome in HIV patients
  537. 537. Malaise
  538. 538. Anemia
  539. 539. Elevated LFTs
  540. 540. Alkaline Phosphatase
  541. 541. Gastrointestinal MAC
  542. 542. Chronic Diarrhea & Abdominal Pain
  543. 543. Malabsorption
  544. 544. Cholestatic Jaundice
  545. 545. Diagnosis
  546. 546. Repeated cultures of MAC from sputum or bronchial wash
  547. 547. Positive blood cultures in severely compromised
  548. 548. Imaging studies consistent with pulmonary disease
  549. 549. Treatment:
  550. 550. Clairthromycin daily (or Azithromycin) and ethambutol for 18 to 24 months
  551. 551. Some recommend adding rifampin or floroquinolone in those with secondary or more advanced disease
  552. 552. Hypersensitivity-Pneumonitis due to NTM
  553. 553. “Hot Tub Lung”
  554. 554. Treated with avoidance and glucocorticosteroids
  555. 555. Resistant MAC Treatment
  556. 556. 4 Drug Therapy
  557. 557. Rifabutin or rifampin +
  558. 558. Clarithromycin or azithromycin +
  559. 559. Ethambutol +
  560. 560. Streptomycin (f0r 2 months)
  561. 561. Treat for 18-24 Months
  562. 562. Treat for 12 Months after sputum is negative for MAC
  563. 563. M. kansasii
  564. 564. Second most common cause of NTM in US
  565. 565. Generally > 60 years of age
  566. 566. Generally predisposing lung disease
  567. 567. Closely resembles acute TB in S/S
  568. 568. Treated with INH, rifampin and ethambutol.
  569. 569. If resistant to rifampin, then clarithromycin or azithromycin may be subsituted.
  570. 570. Pseudomonas aeruginosa
  571. 571. mucoid capsule; particularly difficult in cystic fibrosis patients
  572. 572. Bacillus anthracis
  573. 573. Francisella tularemia
  574. 574. Enterics and Anaerobes
  575. 575. Important in Aspiration Pneumonia
  576. 576. Aspiration of particulate material can produce acute airway obstruction and death by asphyxiation; aspiration of smaller particles may produce atelectasis of a pulmonary segment or even an entire lung with dyspnea, wheezing, and cyanosis
  577. 577. Primary Mechanism
  578. 578. Microaspiration of colonized oropharyngeal secretions
  579. 579. Risks
  580. 580. Altered Consciousness
  581. 581. Dysphagia
  582. 582. Neurologic Disorders
  583. 583. Mechanical disruption of the usual defense barriers
  584. 584. Other
  585. 585. Because the concentration of aerobic bacteria in upper respiratory tract secretions is high, and that of anaerobic bacteria is about 10 times greater, aspiration of even small quantities of oropharyngeal secretions introduces an enormous bacterial challenge to the lungs
  586. 586. Prevotella (formerly oral strains of Bacteroides) e.g., P. melaninogenica
  587. 587. Fusobacterium nucleatum
  588. 588. microaerophilic streptococci
  589. 589. Peptostreptococcus
  590. 590. Multiple organisms are recovered from most patients with aspiration (polymicrobial infections)
  591. 591. Very high mortality with massive aspiration + Mendelson 70%
  592. 592. 20% for aspiration + empyema
  593. 593. Uncomplicated 5% mortality
  594. 594. Prevention
  595. 595. Bacterial pneumonia can be prevented in various ways,
  596. 596. reducing risk factors
  597. 597. Smoking
  598. 598. Alcoholism
  599. 599. Vaccination
  600. 600. Influenza vaccine
  601. 601. subjects over 65 years of age
  602. 602. cases of chronic diseases
  603. 603. medical and nursing home employees
  604. 604. Pneumococcal vaccine
  605. 605. subjects older than 65
  606. 606. younger patients who have:
  607. 607. cardiovascular or pulmonary diseases
  608. 608. diabetes mellitus
  609. 609. alcoholism
  610. 610. liver cirrhosis
  611. 611. cerebrospinal fluid leaks
  612. 612. immunodepression (including human immunodeficiency virus infection, chronic renal failure, organ transplant recipients, hematologic and lymphatic malignancies, asplenia, and sickle cell disease
  613. 613. Complications
  614. 614. Abscess
  615. 615. Cavities develop when necrotic lung tissue is discharged into communicating airways, resulting in either necrotizing pneumonia (multiple small cavities, each <2 cm in diameter, in one or more bronchopulmonary segments or lobes) or lung abscess (one or more cavities >2 cm in diameter)
  616. 616. Empyema
  617. 617. Most empyemas evolve from parapneumonic effusions. Inadequate treatment of the underlying infection results in bacterial invasion of the pleural space with accumulation of large volumes of pleural fluid
  618. 618. There is progressive thickening of the pleura and adjacent soft tissues with the development of a pleural peel, an inelastic fibrous membrane which encases the lung and restricts function
  619. 619. Bronchiectasis
  620. 620. Chronic bronchial dilatation with parenchymal infection and inflammatory reaction
  621. 621. loss of parenchyma between the crowded airways, and the large caliber of the lumen near the pleural surface, compared to airways in the lower lung
  622. 622. Treatment
  623. 623. Antibiotic treatment is empiric and includes coverage for both typical and atypical organisms. Doxycycline, a fluoroquinolone with enhanced activity against Streptococcus neumonia, or a macrolide is appropriate for outpatient treatment of immunocompetent adult patients</li></ul>Viral<br /><ul><li>Note: Martin likes coronavirus (SARS) and influenza for pneumonia
  624. 624. “Considers them to be important” – hint hint
  625. 625. Viral respiratory tract infections are the most common cause of symptomatic human disease among children and adults.
  626. 626. They account for more time lost from school and work than any other infection.
  627. 627. Approximately 1-3 respiratory tract illnesses occur in adults, compared with 2-7 respiratory tract illnesses in children, each year. These infections may cause a wide variety of diseases, from the common cold to severe pneumonia, and may result in significant morbidity and mortality.
  628. 628. The incidence of viral pneumonia has increased during the past decade.
  629. 629. The increase primarily is because of improved diagnostic techniques and the growing population of patients who are immunocompromised.
  630. 630. In the past, the diagnosis of viral pneumonia was made essentially on clinical grounds.
  631. 631. Over the past 10 years, new biotechnology has greatly facilitated the diagnosis of viral pneumonias.
  632. 632. Clinicians are able to obtain a virologic diagnosis with a high degree of sensitivity and specificity, often within a few hours of the diagnostic procedure.
  633. 633. Furthermore, improved approaches to prevention and treatment of viral pneumonias have also become available
  634. 634. The 4 most frequent etiologies of viral pneumonia in adults are
  635. 635. influenza virus
  636. 636. enveloped, single-stranded, RNA viruses of the family Orthomyxoviridae and are the most common viral cause of pneumonia.
  637. 637. They are classified as types A, B, and C and are distinguished by the antigenic differences in the internal proteins.
  638. 638. Influenza virus is capable of undergoing minor or major changes in antigenicity, which allows the virus to evade the preexisting immunity in the population.
  639. 639. Influenza epidemics occur during the winter months and are associated with significant morbidity and mortality.
  640. 640. Patients at increased risk for severe disease, which can lead to death, include:
  641. 641. Patients with chronic obstructive pulmonary disease (COPD)
  642. 642. congestive heart failure
  643. 643. hemoglobinopathies
  644. 644. immunosuppression.
  645. 645. Influenza virus is transmitted from person to person primarily by droplet and aerosol exposure to the virus. The incubation period is 1-5 days after exposure.Two influenza types have emerged of particular importance
  646. 646. H5N1 avian influenza strain
  647. 647. H1N1 swine influenza strain
  648. 648. Respiratory syncytial virus (RSV)
  649. 649. Second most common viral cause of pneumonia.
  650. 650. It is a medium-sized virus of the Paramyxoviridae family but consists of only 1 serotype. Structurally, RSV has 10 unique viral polypeptides, 4 of which are associated with virus envelope, and 2 of these (F and G) are important for infectivity and pathogenicity. Classic RSV infection causes syncytia formation in cell culture, giving the virus its name.
  651. 651. RSV is the most frequent cause of lower respiratory tract infection among infants and children and is highly contagious, spreading via droplet and fomite exposure.
  652. 652. Most children are infected before age 5 years, but the immunity is incomplete, and reinfection may occur later in life; the likelihood of more severe disease and pneumonia increases with advancing age.
  653. 653. RSV is a well-established cause of pneumonia in the elderly population and in adults who are immunocompromised.
  654. 654. Infection may occur seasonally during the winter months or as outbreaks in hospitals and nursing homes
  655. 655. Adenovirus
  656. 656. Enveloped DNA viruses that cause upper and lower respiratory tract infections.
  657. 657. Pneumonia is less common in adults outside of military recruit camps and similar facilities, but fulminant disease has been described in the immunocompromised population and can occur in apparently healthy hosts.
  658. 658. Although 51 serotypes exist, classified into 7 subgroups or species (A-G), pulmonary disease is predominantly caused by serotypes 1, 2, 3, 4, 5, 7, 14, and 21.
  659. 659. Adenoviruses are spread through droplet and fomite transmission; close living arrangements (eg, college campuses, military camps) are likely places for outbreaks.
  660. 660. newly identified, more virulent strain, serotype 14 (subgroup B), has been reported to cause severe respiratory illness and pneumonia.
  661. 661. In 2005, surveillance of civilian and military populations initially reported emergence of this strain, with outbreaks occurring subsequently at military training centers throughout the United States; in 2007, adenovirus serotype 14 caused a large, sustained outbreak of febrile respiratory illness among military trainees in Texas, in a residential care facility in Washington State more recently, and in a community-wide setting in Oregon.6,7,8,9
  662. 662. In the Oregon community outbreak, the median age was 52 years, and 76% required hospitalization, 47% required critical care, 24% required vasopressors, and 18% died; the majority of these patients were otherwise immunocompetent adults
  663. 663. Parainfluenza virus (PIV)
  664. 664. from the family Paramyxoviridae and is characterized by nucleocapsids, which develop in the cytoplasm of infected cells, with hemagglutinin present in the virion envelope.
  665. 665. These can be separated into 4 subtypes based on antigenic characteristics. This virus is spread via droplet and fomite exposure.
  666. 666. Parainfluenza is a common virus that infects most persons during childhood. PIV type 3 is endemic year round, and types 1 and 2 peak during the fall season.
  667. 667. Immunity is short term, and recurrent upper or lower respiratory tract infections occur throughout life.
  668. 668. The infections vary from a mild illness to life-threatening croup, bronchiolitis, or pneumonia. Infection in hosts who are immunocompromised can result in life-threatening pneumonia with lung injury and respiratory failure
  669. 669. Human metapneumovirus
  670. 670. relatively newly discovered respiratory pathogen, initially described in the Netherlands in 2001.
  671. 671. It is also in the Paramyxoviridae family (like RSV and PIV) and is a pleomorphic-shaped virus surrounded by surface protein projections.
  672. 672. This virus is a ubiquitous organism, and most surveys indicate that by age 5 years, almost all children have been exposed to it.
  673. 673. However, reinfection occurs throughout life, including in adults. This virus is spread via droplet and fomite exposure.
  674. 674. As with other viruses, the severity of infection increases with older age and with comorbid (cardiopulmonary disease) or immunosuppressive conditions.
  675. 675. The most common diagnoses associated with adult hospitalizations with hMPV infection are
  676. 676. COPD exacerbations
  677. 677. Bronchitis and pneumonia.
  678. 678. In immunocompromised hosts (eg, hematologic malignancies), severe pneumonitis requiring intensive care or resulting in death has been reported
  679. 679. Coronavirus
  680. 680. Coronaviruses are from the family Coronaviridae and are single-stranded RNA viruses, the surface of which is covered by crownlike projections, giving the virus its name.
  681. 681. This virus is spread via droplet and fomite exposure. Long known to cause upper respiratory infections, coronaviruses were not felt to significantly cause pneumonia until relatively recently; strains 229E and OC43 have been shown to cause pneumonia in adults.3
  682. 682. However, it was the severe acute respiratory syndrome (SARS) pandemic in 2003 that brought the ability of this virus to cause life-threatening pneumonia to worldwide attention.
  683. 683. The SARS coronavirus (SARS-CoV) quickly spread from China to the rest of the world, affecting more than 8000 patients in 29 countries and resulting in 774 deaths.
  684. 684. The mode of transmission was thought to be primarily via droplet and/or fomite. After intensive infection control measures by the World Health Organization, the global transmission was halted in June 2003.14
  685. 685. Viral isolation and genomic sequencing have revealed that this virus originated in the masked palm civet cat (Paguma larvata), raccoon dog (Nyctereutes procyonoides), and possibly the Chinese ferret-badger (Melogale moschata), with subsequent interspecies jumping, during which a partial loss of genome probably led to more efficient human-to-human transmission
  686. 686. Cytomegalovirus
  687. 687. Immune competent
  688. 688. “Mononucleosis”
  689. 689. High Fevers (6 weeks), Chills, Profound Fatigue, Malaise, Myalgias, Headache, Arthralgias
  690. 690. Rarely exudative pharyngitis and cervical lymphadenopathy
  691. 691. Neonate
  692. 692. Pneumonitis
  693. 693. Perinatal infection occurs with contact maternal cervicovaginal sections during delivery or from breast milk ingestion after delivery.
  694. 694. infection may become apparent as early as 3 weeks and as late as 3-6 months
  695. 695. Sepsis-like syndrome commonly and associated with HSM abnormal blood counts with lymphopenia, neutropenia, and thrombocytopenia, abnormal tranaminases and pneumonitis
  696. 696. Immunocompromised
  697. 697. Fever, Leukopenia, Hepatitis, Pneumonitis, gastritis, colitis, retinitis
  698. 698. Transplanted organ is often the targeted organ.
  699. 699. Marrow transplant is associated with CMV pneumonia in 15-20% with a case fatality of >80%
  700. 700. CMV
  701. 701. Also Varicella, Herpes Simplex associated with immunocompromised and viral pneumonia
  702. 702. Influenza virus types A and B are responsible for more than one of community-acquired viral pneumonia cases, particularly during influenza outbreaks.
  703. 703. RSV ranks second among the common causes of viral pneumonia in adults, followed by adenovirus and PIV</li></ul>Fungal<br /><ul><li>Endemic Infections
  704. 704. Infection by organism, widely present but not normally a component of the host normal flora
  705. 705. Generally, but not always, infection occurs only with compromise in immune function
  706. 706. Examples would include Coccidioidomycosis, Histoplasmosis, Blastomycosis, Cryptococcus
  707. 707. Mucormycosis-Mucor, Rhizopus, rhizomucor
  708. 708. Especially associated with uncontrolled DM patients
  709. 709. Produces severe sinusitis as well as progressive lung tissue destruction with pneumonia
  710. 710. Patient often critical rapidly
  711. 711. Treated with Amp. B.
  712. 712. Pneumocystis jirovecii
  713. 713. Formally pneumocystis carinii
  714. 714. Treated with TMP-SMX or clindamycin + pirmiquin or pentamidine
  715. 715. Manifest with cough, hypoxia, chest pain, high and undulating fever with frequently night sweats
  716. 716. Opportunistic Infections
  717. 717. When infections are developed secondary to organism that are normally components of the hosts flora secondary to compromise in normal immune response
  718. 718. Examples: Candidia, Aspergillus
  719. 719. Mycosis
  720. 720. Yeast-normally present in rounded cellular form
  721. 721. Candidia-cryptococcus
  722. 722. Molds-normally present in environment in filamentous form as hyphae
  723. 723. Aspergillus, rhizapus
  724. 724. Dimorphic fungi are organism exist as yeast in tissue and molds with hyphae in environment
  725. 725. Immunocompromised patient
  726. 726. Cryptococcus is found world wide. The other major fungi are geographically restricted and are dimorphic, existing as a mold form in the environment and as a yeast form in tissue.
  727. 727. Widely disseminated, almost all adults have antibody to Cryptococcal neoformans antigens.
  728. 728. C. neoformans is associated with bird droppings and is found world-wide.
  729. 729. C. gattii is also associated with eucalyptus trees and can be pathogenic.
  730. 730. Cryptococcus exists only as a yeast form both in the environment and in the infected person. There is no mycelial (mold) form.
  731. 731. Treatment
  732. 732. Treatment:
  733. 733. Induction: Amphotericin B, Flucytosine
  734. 734. Consolidation: Fluconazole or Voriconazole
  735. 735. Fluconazole is continued indefinitely in HIV patients unless CD4+ count due to HAART rises to > 100 for > 6 months.
  736. 736. Primary Prophylaxis: Not Recommended
  737. 737. Incidence of Cryptococcal Disease has fallen due to HAART and daily fluconazole gave no survival advantage.
  738. 738. Treatment: Crytpococcal meningoencephalitis is uniformly fatal if untreated
  739. 739. Medical therapy (2002 IDSA guidelines)
  740. 740. Amphotericin B (0.7 mg/kg daily) & flucytosine (100 mg/kg per day in four divided doses) for two weeks of induction therapyif clinical response during inductiond/c ampho/flucytosine; start high-dose fluconazole (400mg/d if normal hepatic/renal fxn) for consolidation x 8 weeks; followed by fluconazole 200mg/d for long term chronic suppression
  741. 741. Monitoring of treatment
  742. 742. Amphoserum creatinine and electrolytes.
  743. 743. Infusion related reactions (fever/chills)pretreatment w acetaminophen, diphenhydramine, or corticosteroids
  744. 744. Flucytosineserum levels 2 hours after an oral dose; concern bone marrow toxicity; caution w impaired renal fxn
  745. 745. FluconazoleLFTs
  746. 746. H. capsulatum
  747. 747. Most prevalent endemic mycosis in N. America
  748. 748. General Range: Ohio & Mississippi Valleys
  749. 749. Infection is by inhalation of wind blown earth in which the fungus lives.
  750. 750. Dimorphic fungus; Mycelial form in soil and yeast form at body temperature
  751. 751. Yeast within macrophage
  752. 752. Temperate zones worldwide; specific endemic areas include the mississippi, ohio, and St lawreence River valleys, the caribbean, southern mexico, central america
  753. 753. Fungus is found in high concentrations in soil contaminated with bird or bat excreta (associated with jobs/hobbies such as construction, spelunking, bird handling)
  754. 754. Occurs in 5-27% of patients with AIDS living in endemic areas
  755. 755. Opportunistic pathogen, causing disseminated disease in patients with AIDS or with other forms of impaired cellular immunity
  756. 756. CD4 count <100 cells/microL
  757. 757. AIDS defining illness in 50% of affected patients
  758. 758. Self-Limited Pulmonary Disease in Immune competent*
  759. 759. Granuloma formtion and calcifications
  760. 760. Mimicking “healed” or “latent” tuberculosis
  761. 761. *In the immune competent, this form of pulmonary Histoplasmosis needs no treatment.
  762. 762. Clinical Presentation
  763. 763. Isolated Pulmonary Involvement <5% of patients
  764. 764. Pulmonary Involvement in dissemenated disease 70%: cough and dyspnea
  765. 765. Disseminated histoplasmosis: febrile, wasting illness. HSM, adenopathy, skin and mucosal lesions, diarrhea, meningitis, cytopenias, and a sepsis-like syndrome
  766. 766. Immunocompromised: Active, Acute Infection with initial flu like symptoms progressive to more severe and persistent symptoms of cough, SOB, chest pain, fever, night sweatsin compromised.
  767. 767. Yields: Chronic Fibrocavitary Pulmonary Disease
  768. 768. Mimicking “active” tuberculosis
  769. 769. Untreated yields: Disseminated Disease
  770. 770. Febrile, wasting illness, anemia, thrombocytopenia, lympadenopathy, hepatosplenomegaly, and abnormal liver function tests (LFTs)
  771. 771. Diagnosis
  772. 772. Self-Limited Pulmonary Disease
  773. 773. Looks like TB but it isn’t and patient has been exposed in an Endemic Area
  774. 774. Chronic Fibrocavitary Pulmonary Disease
  775. 775. Sputum Culture positive for H. capsulatum and CXR compatible
  776. 776. Disseminated
  777. 777. Blood Culture positive for H. capsulatum
  778. 778. Histoplasma Antigen in Blood or Urine
  779. 779. Diagnosis: visualization of the organism within cells on a Wright’s stained smear of peripheral blood or a buffy coat
  780. 780. Dx of organism in tissue or BAL
  781. 781. Treatment
  782. 782. Treatment for all of the deep fungal diseases is with sequential amphotericin B & itraconazole or either voriconazole or fluconazole.
  783. 783. Treatment: Amphotericin B x 7-14 days Induction itraconazole
  784. 784. Secondary Prophylaxis: 50-80% will relapse if lifelong therapy is not maintained; amphotericin relapse rats of 3-19%, itraconazole prevents relapse in up to 95% of cases, fluconazole relapse rate of 12-18%
  785. 785. Primary Prophylaxis: Itraconazole 200mg/day, effective in patients with CD4 count <100 cells/microL living in endemic areas
  786. 786. C. inmitis
  787. 787. General Range: Lower Sonoran Desert
  788. 788. Infection is by inhalation of wind blown earth.
  789. 789. Endemic to sothwestern US, northern mexico and parts of central and south-america
  790. 790. Occurs in ~27% of HIV patients living in endemic areas
  791. 791. Presentation
  792. 792. Primary Pulmonary Infection
  793. 793. Valley Fever: “Flu-Like” Symptoms to Severe Pneumonia (40%)
  794. 794. Begins 10-14 days after exposure with fever, cough, chest pain, malaise, erythema nodosum
  795. 795. Course: Spontaneous improvement and recovery in several weeks
  796. 796. No treatment in immune competent host
  797. 797. No Symptoms in 60%
  798. 798. Chronic Fibrocavitary Disease produced.
  799. 799. Disseminated Disease can occur in compromised patients
  800. 800. Immediate or by Reactivation if immunosuppression occurs
  801. 801. Wide spectrem of presentation in HIV
  802. 802. Non-immunocompromised: Focal pneumonia, skin involvement, and meningitis
  803. 803. Extrathoracic manifestations, disseminated diseaes, and unusaul sites of involvement
  804. 804. Pulmonary Disease (85%): fever, cough, and dyspnea
  805. 805. Xray: diffuse infiltrates are the MC radiographic findings (60%)
  806. 806. Focal alveolar infiltrates 65%; nodules 25%; hilar adenopathy 20%; cavities 15%; pleural effusions 5%
  807. 807. Diagnosis
  808. 808. Primary pulmonary disease or prior infection
  809. 809. Looks like TB but it isn’t and patient was exposed in the endemic area and is skin test positive with Coccidioides antigen. (May have low level of antibody.)
  810. 810. Disseminated disease –
  811. 811. Complement fixation (CF) quantitative antibody determination shows an increasing antibody titer.
  812. 812. Paradox – antibody is not protective
  813. 813. Diagnosis:
  814. 814. Definitive diagnosis visualization of the fungus from a clinical specimen or recovery in culture
  815. 815. Sputum culture yield 16%; BAL often required
  816. 816. Papanicolaou or Gomori methenamine silver stains
  817. 817. Cultures of BAL require 5 days to grow
  818. 818. 80% positive tube precipitin or complement fixation serology
  819. 819. Treatment
  820. 820. Diffuse pulmonary involvement have high mortality 70% w median survival of 1 month
  821. 821. Amphotericin B
  822. 822. Fluconazole and itraconazolecoccidioidal meningitis
  823. 823. Secondary prophylaxis: lifelong mainentance therapy is requierd.
  824. 824. Fluconazole is the preferred agent
  825. 825. Primary Prophylaxis: prior infection does not predict the development of active coccidiodomycosis in the hiv INFECTED POPULATION.
  826. 826. No DEFINITIVE RECOMMENDATIONS EXISTS
  827. 827. Immunocompromised
  828. 828. Amphotericin B if widely disseminated and acutely ill
  829. 829. Replaced largely by Voriconazole as treatment of choice
  830. 830. Also responds to azole drugs, fluconazole and itraconazole
  831. 831. PEARLS
  832. 832. Histoplasma & Coccidioides mimic Mycobacterium tuberculosis clinically & radiologically but not epidemiologically.
  833. 833. Histoplasma & Coccidoioides mimic each other & Mycobacterium avium complex (MAC) epidemiologically.
  834. 834. Histoplasma, Coccidioides, & MAC are found in earth, are geographically restricted, & are not transmissible person to person.
  835. 835. Acute lung disease caused by H. capsulatum or C. inmitis does NOT need treatment in the Immune Competent.
  836. 836. Overall, world wide, fungal lung disease is much less common than M. tuberculosis of the lung
  837. 837. P. braziliensis
  838. 838. B. dermatiditis
  839. 839. Endemic area as for Histoplasmosis (Ohio & Mississippi Valleys) plus areas of Ontario & Manitoba.
  840. 840. The lung is the portal of entry.
  841. 841. All who are infected need treatment.
  842. 842. Dimorphic fungus
  843. 843. Endemic to the midwestern and south central US
  844. 844. Inhalation of the organism into the lung
  845. 845. Majority of immune competent patients will have dissemination to skin, mucosa, bone, or genitourinary tract, weeks to years after infection.
  846. 846. Minority of immune competent patients with lung Blastomycosis will have self limited disease.
  847. 847. Those with self-limited lung disease cannot be distinguished from those whose disease will disseminate.
  848. 848. Symptoms of disseminated disease are fever, weight loss, lassitude.
  849. 849. CXR lesions found in 2/3s of patients with dissemination.
  850. 850. Uncommon, but serious complication of advanced HIV disease
  851. 851. CD4 count <200 cells/microL
  852. 852. Course in HIV may be fulminant with a 40% early mortality in HIV infected patients
  853. 853. Clinical Presentation: pulmonary disease (80%); 42% disseminated disease to multiple visceral organs including skin, liver, lymph nodes, and meninges as well as the lungs
  854. 854. Fever, weight loss, and cough, pleuritic chest pain and significant dyspnea
  855. 855. XRAY: 40% focal lobar infiltrates, 40% miliary or diffuse interstitial infiltrates
  856. 856. Diagnosis:
  857. 857. cytologic or histologic stain or culture of variety of clinical specimens including sputum, BAL , tissue biopsy, and CSF
  858. 858. Culture requires 2-4 weeks
  859. 859. Serologic tests are frequently negative and unreliable
  860. 860. Treatment:
  861. 861. Amphotericin B
  862. 862. Itraconazole for focal, non-life threatening infections
  863. 863. ***CHRONIC maintenance therapy is indicated. Itraconazole has become the preferred agent
  864. 864. Aspergillus pneumonia
  865. 865. A. fumigatus common opportunistic agent producing infection in compromised host
  866. 866. Creates cavitations with pneumonia and pulmonary infection and resembles T.B. on X-Ray
  867. 867. Common cause of sinusitis
  868. 868. Exacerbations common with drawl of steroids
  869. 869. Treatment is Voriconazole or Amphotericin B and Itraconazole
  870. 870. Candidia
  871. 871. More than 150 species of Candidia identified, only a few know to cause human infections
  872. 872. C. albicans, C. krusei, C. glabrata, C. tropicalis, etc.
  873. 873. Relatively rare to see pneumonia compared to other organ involvement
  874. 874. Spreads by hematogenous spread, in fact is 4th most common isolate from blood cultures and #1 noscomal infection.
  875. 875. Treatment is fluconazole, voriconazole and Amp. B . Responds to echinocandins as well. </li></ul>Nonsocomial (redundant, but specific info)<br /><ul><li>Definitions
  876. 876. Hospital Acquired (HAP) Ventilatory Associated (HAP) 85% of HAP
  877. 877. VAP developed by 20% of intubated patients
  878. 878. HAP: occurs 48 hours or more post admission, but was not incubating at the time of admission
  879. 879. VAP: occurs more than 72 hours after admission, following intubation
  880. 880. HCAP: any patient hospitalized for 2+ days within 90 days of the infection onset
  881. 881. Nursing home or long-term care resident
  882. 882. Received recent antibiotics
  883. 883. Chemo
  884. 884. Wound care within the past 30 days
  885. 885. Attended a hospital or hemodialysis clinic
  886. 886. Risks
  887. 887. Mechanical ventilation and intubation increases the risk 6-21x
  888. 888. Age >70 years
  889. 889. Chronic lung disease
  890. 890. Depressed consciousness
  891. 891. Aspiration
  892. 892. Chest surgery
  893. 893. The presence of an intracranial pressure monitor or nasogastric tube
  894. 894. H-2 blocker or antacid therapy
  895. 895. Transport from the ICU for diagnostic or therapeutic procedures
  896. 896. Previous antibiotic exposure, particularly to third generation cephalosporins
  897. 897. Reintubation
  898. 898. Hospitalization during the fall or winter season
  899. 899. Mechanical ventilation for acute respiratory distress syndrome (ARDS)
  900. 900. Frequent ventilator circuit changes
  901. 901. Nursing Home
  902. 902. Organisms
  903. 903. Hospital Acquired Pneumonia (HAP)
  904. 904. Early onset
  905. 905. S. pneumonia, Hib, MSSA
  906. 906. Late onset
  907. 907. P. aeruginosa, MRSA, resistant GNB
  908. 908. Gram negative bacteria (other) > P. aeruginosa > S. aureus > Candida
  909. 909. Purulent Bronchitis
  910. 910. Purulent sputum
  911. 911. Normal CXR
  912. 912. Typical in patients on ventilators
  913. 913. P. aeruginosa: High mortality (50%)
  914. 914. Monotherapy is not adequate
  915. 915. High failure rates
  916. 916. Relapse
  917. 917. Resistance
  918. 918. Empirical therapy
  919. 919. 2 active drugs
  920. 920. Beta lactam + aminoglycoside
  921. 921. Beta lactam + fluuroquinolone
  922. 922. VAP
  923. 923. Resistance: P. aeruginosa, MRSA, A. baumannii, S. maltophilia
  924. 924. Late onset
  925. 925. High mortality (39%)
  926. 926. 65% died with high-risk pathogen
  927. 927. Found in resistance list
  928. 928. Acinetobacter spp
  929. 929. Resistant to many antibiotics
  930. 930. Most active agents
  931. 931. Carbapenems
  932. 932. 1st line
  933. 933. A. baumannii
  934. 934. Extended spectrum Beta lactamases
  935. 935. Plasmids
  936. 936. Resistant to ceftazidime, cephalosporins, penicillins
  937. 937. K. pneumonia
  938. 938. Emerged in U.S. in the 1980s
  939. 939. Colistin
  940. 940. Sulbactam
  941. 941. 4-15% of VAP
  942. 942. Found in ICU patients almost predominantly
  943. 943. Risks
  944. 944. Prior antibiotics
  945. 945. Prolonged ICU stay
  946. 946. Mechanical ventilation
  947. 947. HCAP:</li></ul>MRSAPseudomonas aeruginosaAcinetobacter spp.MDR EnterobacteriaceaeHospitalization > 48 hrsXXXXHospitalization for 2 days in prior 90 daysXXXXNursing home or extended-care facility residenceXXXXAntibiotic therapy in preceding 90 daysXXChronic DialysisXHome Infusion TherapyXHome Wound CareXFamily Member w MDR infectionX<br /><ul><li>HAP/VAP/HCAP suspected onset > 5 days or risk factors for MDR pathogens Yes Broad spectrum therapy
  948. 948. No Limited spectrum therapy
  949. 949. No Risk
  950. 950. HCAP: No Risk Factors for MDR Pathogen
  951. 951. Streptococcus pneumoniae
  952. 952. Haemophilus influenzae
  953. 953. Methicillin-sensitive Staphylococcus aureus
  954. 954. Antibiotic-sensitive enteric gram-negative bacilli
  955. 955. Escherichia coli
  956. 956. Klebsiella pneumoniae
  957. 957. Proteus species
  958. 958. Serratia marcescens
  959. 959. Risk
  960. 960. Streptococcus pneumoniae
  961. 961. Haemophilus influenzae
  962. 962. Methicillin-sensitive Staphylococcus aureus
  963. 963. Antibiotic-sensitive enteric gram-negative bacilli
  964. 964. Escherichia coli
  965. 965. Klebsiella pneumoniae
  966. 966. Proteus species
  967. 967. Serratia marcescens
  968. 968. MDR Pathogens
  969. 969. Pseudomonas aeruginosa
  970. 970. Klebsiella pneumoniae (ESBL)
  971. 971. Acinetobacter species
  972. 972. MRSA
  973. 973. Legionella pneumophila
  974. 974. Drugs
  975. 975. Antipseudomonal cephalsporin (cefepime, ceftazidime)
  976. 976. or
  977. 977. Antipseudomonal carbepenem (imipenem or meropenem)
  978. 978. or
  979. 979. B-Lactam/B-lactamase inhibitor (piperacillin-tazobactam)
  980. 980. PLUS
  981. 981. Antipseudomonal fluoroquinolone (ciprofloxacin or levofloxacin)
  982. 982. or
  983. 983. Aminoglycoside (amikacin, gentamicin, or tobramycin)
  984. 984. PLUS
  985. 985. Linezolid or vancomycin
  986. 986. Nursing home pneumonia
  987. 987. Etiology and Management is between community- and hospital-acquired pneumonia in etiology and management
  988. 988. S. pneumoniae and gram-negative bacilli
  989. 989. H. influenzae and Moraxella catarrhalis are next most common.
  990. 990. Epidemiology
  991. 991. Leading cause of death among all nosocomial infections.
  992. 992. Second most common cause of nosocomial infections in the USA.
  993. 993. Associated morbidity of nosocomial pneumonia is so high that is estimated that 5 days are added to the hospital length of stay (los).
  994. 994. Health care cost are astronomical
  995. 995. Treatment
  996. 996. Antibiotics are classified by mechanism of action
  997. 997. Cell wall Inhibition or Peptoglycan destruction
  998. 998. Penicillins
  999. 999. Cephalosporins
  1000. 1000. Glycopeptides
  1001. 1001. Monobactams
  1002. 1002. Carbapenems
  1003. 1003. Daptomycin
  1004. 1004. Membrane Permeability Disruption
  1005. 1005. Polymycins
  1006. 1006. Detergents
  1007. 1007. Antimetabolites/Folic Acid
  1008. 1008. Sulfas
  1009. 1009. Clotrimazole
  1010. 1010. Inhibition of DNA:
  1011. 1011. Replication
  1012. 1012. Fluroquinolones
  1013. 1013. Repair
  1014. 1014. Metronidazole
  1015. 1015. Imidazoles
  1016. 1016. Transcription
  1017. 1017. Rifampin
  1018. 1018. Rifamycin
  1019. 1019. Inhibition of Protein Synthesis:
  1020. 1020. Anti 30S
  1021. 1021. Tetracycline
  1022. 1022. Glycylcyclines
  1023. 1023. Aminoglycosides
  1024. 1024. Oxazolidones
  1025. 1025. Anti 50S
  1026. 1026. Chloroamphenicol
  1027. 1027. Macrolides
  1028. 1028. Lincomycins
  1029. 1029. Ketolides
  1030. 1030. New Drugs
  1031. 1031. Linezolid
  1032. 1032. Oxazolidinones
  1033. 1033. Inhibits synthesis at 70S
  1034. 1034. Gram positive
  1035. 1035. Novel mode of action lacks cross resistance problems
  1036. 1036. MRSA is still resistant
  1037. 1037. E. faecium too
  1038. 1038. Ertapenem
  1039. 1039. Carbapenem
  1040. 1040. Gram positive and negative
  1041. 1041. Limited use with Enterococcus, P. aerugonisa
  1042. 1042. Resistance in some ESBLs
  1043. 1043. Daptomycin
  1044. 1044. Cyclic lipopeptide
  1045. 1045. Concentration dependent
  1046. 1046. Gram positive
  1047. 1047. No cross resistance
  1048. 1048. Resistance with MRSA, S. aureus, E. faecalis
  1049. 1049. POOR EFFICACY IN PULMONARY INFECTIONS
  1050. 1050. Tigecycline
  1051. 1051. Glycylcyclines
  1052. 1052. Bacteriostatic
  1053. 1053. Inhibits translation at 30S
  1054. 1054. Gram positive and negative
  1055. 1055. Not very useful with Pseudomonas
  1056. 1056. Biliary/fecal excretion
  1057. 1057. P450 NOT AFFECTED
  1058. 1058. Few drug interactions
  1059. 1059. Standard dose
  1060. 1060. Initial dose of 100 mg IVfollowed by 50 mg IV q12h
  1061. 1061. Indicated in patients ≥18 years of age
  1062. 1062. Renal impairment
  1063. 1063. No dosage adjustment necessary
  1064. 1064. Not dialyzable
  1065. 1065. Hepatic impairment
  1066. 1066. No dosage adjustment necessary in patients with mild to moderate impairment
  1067. 1067. In patients with severe hepatic impairment (Child Pugh C), the initial dose is 100 mg IV followed by 25 mg IV q12h
  1068. 1068. Flouroquinolones
  1069. 1069. Gemifloxocin- Factive
  1070. 1070. Levofloxacin- Levaquin
  1071. 1071. Gatifloxocin- Tequin
  1072. 1072. Moxifloxacin- Avelox
  1073. 1073. Mechanism of action is dual by inhibiting DNA Gyrase and Topoisomerase lV

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