Pneumonia CLASS

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					Pneumonia – The Captain Of
the men of Death

Bangar Raju Dept of Microbiology KMC-IC

Acute and Subacute Pneumonia
Basic Concepts and Clinical Examples

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Common Definitions
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URTI (Upper Respiratory Tract Infection) Contaminated LRTI (Lower Larynx Respiratory Tract Sterile Infection) Pneumonia (Infection involving the Alveolar spaces or interstitial spaces)
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Common Definitions
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Bronchitis Bronchiolitis /Croup Community Acquired Pneumonia (CAP) Nursing Home Pneumonia Nosocomial Pneumonia Ventilator Associated Pneumonia (VAP)
These diagnoses attempt to imply a specific mechanism of acquisition and likely organisms (often erroneously)

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Other Definitions
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Cavities Abscesses (not all cavities are abscesses) Empyema (in contrast to sympathetic effusions or transudates)

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Very Important to Remember

Not all Pulmonary Inflammatory Processes with Fever, Cough, Dyspnea and sputum production are Infections

Also Think about:
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Toxins Malignancy Collagen Vascular Diseases (RA,SLE) Pulmonary Emboli
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Definitions used for Pneumonia
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Acute vs. Chronic (time) Typical vs. Atypical (clinical characteristics) Alveolar vs. Interstitial (X-ray pattern) Community Acquired vs. Nosocomial (location of illness onset)
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Acute
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vs
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Chronic
Insideous Onsetvague recollection by patient with nonspecific symptoms Presents for care late in illness (weeks or even months) Slowly evolves with or without therapy

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Rapid onset – exact time often recognized by patient (sudden fever, rigors, chest pain, SOB) Presents for medical care shortly after onset Rapid deterioration with or without therapy

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Acute can evolve into chronic, because nothing is that simple!
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Acute
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vs.
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Chronic
Mycobacterium Aspergillus Nocardia Actinomycosis Histoplasmosis Gram negatives Anaerobic (aspiration)

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S. pneumoniae SARS Coronavirus Staphylococcus Klebsiella pneumoniae Influenza A Legionella Histoplasmosis Anaerobic (aspiration)

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Typical
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vs.
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Atypical
Slow onset Patient appears relatively well Non-productive or dry cough No left shift in WBC Sputum + WBC no bugs Interstitial or patchy infiltrate

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Sudden onset Toxic patient appearance Productive cough High fever (>39 C) Elevated WBC with left shift Sputum + WBC & bugs Defined consolidation

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Typical
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vs
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Atypical
Mycoplasma Chlamydia Legionella Viruses

S. pneumoniae Hemophilus influenza Staph aureus Klebsiella pneumoniae
Respond to βlactames

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Respond to macrolides and quinolones
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Community Acquired Pneumonia
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Pneumonia is the 6th leading cause of death & leading infectious cause in US Incidence of 267/100,000 in an Ohio study with fatality rate of ~9 % Translates to : 485,000 hospitalizations (?1 million in other estimates) in US with 45,000 deaths ($ 9 billion) and 3 million outpatients treated

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Classification
ACUTE PNEUMONIAS Community acquired  Person to person transmission
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S. pneumoniae, Mycoplasma pneumoniae, Haemophilus influenzae, S. aureus, S. pyogenes, K. pneumoniae, N. meningitidis, B. catarrhalis, influenza virus Legionella pneumophila, Francisella tularensis, Coxiella burnetii, C. psittaci, Yersinia pestis (plague), Bacillus anthracis (anthrax), Pseudomonas pseudomallei (melioidosis), Pasteurella multocida (pasteurellosis)

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Animal or environmental exposure
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Pneumonia in the infant & young child
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Chlamydia trachomatis, Respiratory Syncytial virus & other respiratory viruses, S. aureus, Group B Streptococcus, Cytomegalovirus, S. pneumoniae, H. influenza type b

Nosocomial pneumonia  Enterobacteriaceae, Pseudomonas aeruginosa, Acinetobacter calcoaceticus, Staphylococcus aureus

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MOST LIKELY ORGANISMS
Neonatal (0-1 mo): Escherichia coli, Group B Streptococcus Infants (1-6 mo): Chlamydia trachomatis , Respiratory Syncytial Virus Children (6 mo-5 yr): Respiratory Syncytial Virus, Parainfluenza Viruses Children (5-15 yr): Mycoplasma pneumoniae , Influenza Virus Type A Young Adults (16-30) :Mycoplasma pneumoniae, Streptococcus pneumoniae Older Adults: Streptococcus pneumoniae, Haemophilus influenzae

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Types of pneumonia:
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Typical Pneumonia Syndrome Atypical Pneumonia Syndrome Chronic Pneumonias Pneumonias of the Newborn Period and Infancy Pneumonia in the AspirationProne Patient Pulmonary Infection in the Immunocompromised Host
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Acquisition of Infection
1.

2.

3.

4.

Colonization of upper airway followed by aspiration of a pathogen (S.pneumo) Infection of upper airway and inhalation/aspiration of infecting organism (RSV, mycoplasma) Direct lower airway inhalation of infecting organism (Influenza, M.Tb,SARS CoV) Hematogenous spread to lung (varicella)
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Transmission
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Person to Person Influenza, M. tuberulosis, SARS CoV, S. pneumoniae, Varicella, chlamydia, group A strep Environment Aspergillosis (air, water) Legionella (water) Histoplasmosis (bird droppings & bat caves) Psittacosis (pet birds) Anthrax (soil)

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Virulence Properties of Pathogens

Adhesion molecules that bind to cell receptors  HA of influenza binds sialic acid  G protein of RSV binds to glycoaminoglycans

Mechanisms to evade innate host defenses  NS1/2 proteins of RSV block α-interferon

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Virulence Properties of Pathogens
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Ability to avoid adaptive immune mechanisms IgA protease of pneumococcus gene recombination by influenza Production of toxins capillary leak Hantavirus via β-3 integrins EF & LF toxins of B. anthracis Pseudomonas type III protein, Exotoxin A Evolution of antibiotic resistance β-lactamases by bacteria amantadine resistance by influenza
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Pathogenesis of Pneumonia:
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A microorganism enters the alveoli and proceeds to grow in the rich environment provided by the lung. The organism contains a capsule or is intracellular and can avoid phagocytosis for a period of time. As a result of tissue injury an inflammatory response occurs. Tissue injury can occur due to exotoxins produced by a bacteria, cell lysis caused by a virus, or death of alveolar macrophages and dumping of their lysosomal contents in the alveoli due to growth of an organism in the phagocyte.
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Vascular permeability increases and PMNs arrive at the area attempting to contain and eliminate the organisms. Along with PMNs come many of the serum components. Meanwhile other alveolar macrophages are being recruited to the area of inflammation. This accumulation of micro organism, immune cells, and serum components causes the alveoli to fill up and can result in spread to other alveoli in close proximity
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This inflammatory response is what is described as an opacity or consolidation when viewing a X-ray film. Not only are serum components coming into the alveoli but certain products made by the microorganism are able to leave the lung and exert systemic effects. Examples include endotoxin from gram negative bacteria eventually resulting in fever and septic shock, and cell wall components of gram positive bacteria that can eventually lead to fever production and septic shock.
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The deleterious effects on the host fall into two categories:
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Systemic effects such as fever, shock, (particularly associated with gram negative bacteria) and wasting (chronic tuberculosis). Interference with the ability of the lungs to carry out air exchange.

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Due to thickening of the membrane that separates erythrocytes from inspired air in the alveoli.

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Complications of PneumoniaTwo types of complications: 1. Complications that occur during the acute phase of the infection.  Pleural effusion: Sterile effusion into the pleural space surrounding the lungs.  Empyema: A pleural effusion that is grossly purulent (contains bacteria and white blood cells).  Fluid and electrolyte: Dehydration and hypernatremia (high concentration of sodium in the blood).  Hematologic: Anemia seen in chronic pneumonia, disseminated intravascular coagulation (usually gram negative pneumonia), and thrombocytopenia (Influenza binding to platelets).

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Hepatic: Bacterial pneumonias can commonly be associated with mild elevations of liver enzymes without evidence of liver invasion. Sometimes jaundice can occur and can indicate a poor prognosis.  Renal: In cases of severe pulmonary infections protein catabolism markedly increases.  This results in an azotemia (nitrogenous products in the blood).  This condition is transient and renal damage does not occur (No large increase in creatinine).
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2. Chronic complications
Abnormalities in pulmonary function: Usually manifested as a decrease in arterial PO2.  Chronic pneumonia  Bronchiectasis: Is a disorder characterized by irreversible destruction and dilatation of airways.
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Mechanisms invaders use to avoid the normal defense mechanisms
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Avoid phagocytosis Capsule production Toxin production Being too large to phagocytize- parasites and fungi Replication inside the cells Mimicry Inhibition of lysosome fusion with phagosome Escape from the phagosome Resistance to killing and digestion in the phagolysosome Growth in the phagocytic cell

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Typical Pneumonia Syndrome
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The signs and symptoms are also seen in other syndromes (some infections of the immunocompromised host, and in the aspirationprone patient, pneumonias of the newborn and infant). This is because the other syndromes also include bacteria that elicit respiratory symptoms, sudden onset, and purulent sputum. The immune status of the patient tend to increase the chances of acquiring a different set of bacterial pathogens

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Etiology and epidemiology
Community Acquired

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Common
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Uncommon
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S. pneumoniae - most common cause of community-acquired bacterial pneumonia H. influenzae K. pneumoniae S. aureus S. pyogenes P. aeruginosa N. meningitidis

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Rare  Y. pestis
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B. pseudomallei Acinetobacter calcoaceticus
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Klebsiella pneumonia

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   

acquired by bronchogenic spread of the pathogen. also manifest itself as a suprainfection in patients previously infected by an upper or lower respiratory viral infection. There is no age-specific predisposition, however the incidence of infection increases with advancing age. Most patients are adults above the fifth decade and who have some underlying chronic obstructive pulmonary disease (COPD), cardiovascular or other chronic disease. Streptococcus pneumoniae is a bacterial pathogen that affects children and adults worldwide. It is a leading cause of illness in young children and causes illness and death among the elderly and persons who have certain underlying medical conditions.

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Klebsiella pneumonia:

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The organism colonizes the upper respiratory tract and can cause the following types of illnesses:  Disseminated invasive infections, including bacteremia and meningitis;  Pneumonia and other lower respiratory tract infections;  Upper respiratory tract infections, including otitis media and sinusitis.
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In adults, 60%-87% of pneumococcal bacteremia is associated with pneumonia. Severe pneumococcal infections result from dissemination of bacteria to the bloodstream and the central nervous system. At least 500,000 cases of pneumococcal pneumonia are estimated to occur annually in the United States. S. pneumoniae accounts for approximately 25%-35% of cases of community-acquired bacterial pneumonia in persons who require hospitalization. Concomitant bacteremia occurs in approximately 10%-25% of adult patients who have pneumococcal pneumonia

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H. influenzae and K. pneumoniae are more commonly seen in patients with COPD, alcoholics, and the elderly. S. aureus infections are most common in IV drug users, the elderly, in people with a recent influenza virus infection, and in individuals with cystic fibrosis. P. aeruginosa is also often seen as a cause of pneumonia in patients with cystic fibrosis and on respirators are more likely to develop pneumonia due to P. aeruginosa.

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S. pyogenes pneumonia is less common today due to the use of antibiotics to treat upper respiratory tract infections. N. meningitidis is occasionally seen in epidemics in military recruits. Y. pestis infections are due to environmental exposure to an infected rat population. B. pseudomallei infections are due to exposure with contaminated soil in Southeast Asia.
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Clinical, Radiological, and Laboratory Features
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Systemic complaints include malaise, and high fever however pulmonary symptoms predominate. Pulmonary symptoms include any combination of symptoms listed below:
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Dyspnea Chest discomfort Pleuritic pain Cough productive of purulent or blood-tinged sputum Tachypnea Tachycardia
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In advanced cases :
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Cyanosis Confusion Early on in disease a fine crepitant rales over the involved portion of the lung (s). Progression to lobar consolidation results in:
Dullness to percussion  Vocal fremitus  Bronchial breathing
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Chest sounds include:
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Certain radiological patterns when present may be of diagnostic value:
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Klebsiella pneumoniae infection: ("bulging fissure" sign) Upper lobar consolidation with a bowing fissure. Staphylococcus aureus infection: Multiple bilateral nodular infiltrates with central cavitation. In children one can see ill-defined, thin walled cavities ("pneumatoceles"), bronchopleural fistulas, and empyema. Pseudomonas aeruginosa infection: microabscesses which may coalesce into large abscesses. Lung necrosis: often seen with Gram-negative rod infections (Klebsiella, Proteus, E. coli).

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Klebsiella and chronic bronchitis:

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Atypical Pneumonia Syndrome:
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These infections can involve Mycoplasma, Chlamydia, Rickettsia, other bacteria, viruses, or fungi. Determining the causative agent requires knowing what the common causes of atypical pneumonia are, as well as knowing the epidemiology, clinical picture, radiologic findings, and laboratory findings. This will provide the presumptive diagnosis.

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Etiology and Epidemiology

Bacteria
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Mycoplasma pneumoniae most common Legionella sp. (Legionnaire's disease) Francisella tularensis (tularemia) Bacillus anthracis (anthrax) Chlamydia psittaci (psittacosis) Chlamydia trachomatis* Chlamydia pneumoniae Coxiella burnetii (Q fever)

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Viruses
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Influenza Parainfluenza Respiratory syncytial virus Adenovirus

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Fungi
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Histoplasma capsulatum (histoplasmosis) Coccidioides immitis

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The most common pathogen of this group is Mycoplasma pneumoniae. It ranks second only to S. pneumoniae among all pneumonias due to infectious diseases. The other relatively common cases of atypical pneumonia are Chlamydia pneumoniae, the Influenza viruses and Legionella spp
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M. pneumoniae is now known to be the cause of pneumonia in 20% to 25% of all age groups and to persist in certain persons for weeks to months, resulting in prolonged reduced pulmonary clearance and airway hyperresponsiveness. C. pneumoniae causes approximately 10% of community-acquired pneumonia. The other agents are uncommon in adults or are due to exposure of the host to an unusual source

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Clinical, Radiologic, and Laboratory Features
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Symptoms of atypical pneumonia include fever, nonproductive cough, and prominent constitutional signs (severe headache, malaise, myalgias) onset is usually more insidious. Signs of pulmonary consolidation are rarely present. The radiographic findings usually appear as interstitial patchy bronchopneumonic infiltrates. There is a lot of overlap in the manifestations of atypical pneumonia.
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Diagnosis
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Direct isolation of the organism is not usually performed due to the hazardous nature of some organisms (F. tularensis) and due to the specialized culture techniques needed to allow growth of the organism. Microscopic examination of the sputum is not performed unless a Legionella sp. infection is suspected. This organism is stained with direct fluorescent antibody staining. An indirect Fluorescent Antibody test to detect antibodies to Mycoplasma pneumoniae is very useful.
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Acute infiltration

segmental pnuemonia

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

BILATERAL

ASPERGILLOSIS

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Serologies for the various causes of atypical pneumonia include:
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Mycoplasma pneumoniae= complement fixation test, IgM by latex agglutination or ELISA, cold agglutinins Legionella pneumophila= rapid microagglutination test, test for Legionella antigen in the urine. Chlamydia spp.= microimmunofluorescence, ELISA Coxiella burnetii= complement fixation test. Skin testing for histoplasmosis and coccidioidomycosis is performed only if a previous skin test was negative.

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A four fold or greater rise in titer between the acute and convalescent sera is confirmatory of an acute infection. A combination of the clinical, epidemiologic, radiographic, and laboratory features can specify a certain etiology so that empiric treatment can begin.

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Chronic Pneumonias:
These pneumonias develop gradually over a period of weeks to months and are caused by numerous microorganisms.  Noninfectious as well as infectious processes can result in chronic pneumonia Bacteria:
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Mycobacteria  M. tuberculosis
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M. kansasii seen often in immunocompromised M. avium-intracellulare patients and AIDS patients

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Mixed anaerobic oral flora Actinomyces israelii Nocardia asteroides Burkholderia pseudomallei
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Fungi
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Blastomyces dermatitidis most common Coccidioides immitis Histoplasma capsulatum Cryptococcus neoformans Sporothrix shenkii Paracoccidioides brasiliensis Entamoeba histolytica = usually get dysentery first

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Protozoa
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Helminths
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Paragonimus westermani Echinococcus granulosus
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Early diagnosis of chronic pneumonias requires useful epidemiologic characteristics relate to
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endemic areas of infection, the host factors that increase the susceptibility to infection.

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Dark-skinned people and pregnant women show an increased tendency to develop disseminated or chronic pulmonary forms of Coccidioides immitis. White-skinned males are more likely to develop chronic cavitary histoplasmosis. Nocardiosis, cryptococcoses and mycobacterial disease are associated with hosts with defects in cell-mediated immunity. Opportunistic fungal infections are also more common in immunocompromised patients (histoplasmosis, blastomycosis, coccidioidomycosis).
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Clinical, Radiologic, and Laboratory Features:
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Often times the patient experiences low grade fever, anorexia, significant weight loss, a productive cough, hemoptysis, chest pain and dyspnea (onset very gradual). A putrid odor of the sputum is a sure indication of an anaerobic infection. Also, certain microorganisms can infect extrapulmonary sites which helps to narrow down the number of possible causative agents. Skin - N.A. blastomycosis, coccidioidomycosis, Nocardiosis, cryptococcoses, S.A. blastomycosis. Mucosa - histoplasmosis, N.A. and S.A. blastomycosis, coccidioidomycosis, tuberculosis.

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ASPERGILLOMA INFILTRATION IN ASPERGILLOSIS:

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Central Nervous System - cryptococcoses, coccidioidomycosis, tuberculosis, nocardiosis. Bone - N.A. blastomycosis, coccidioidomycosis, tuberculosis cryptococcoses (see cells in urine). Other Sites - liver, spleen, adrenal glands, and GI tract are affected occasionally by tuberculosis and histoplasmosis.

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Diagnosis
These are five basic modalities that can aid in diagnosis:  Smears and cultures of sputum.  Smears and cultures from extrapulmonary sites.  Skin testing.  Serologic testing.  Invasive diagnostic methods.  One should begin with an examination of the sputum.

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A Gram stain, acid fast stain, NaOH wet mount, or 10% KOH wet mount can be helpful depending on the clinical and epidemiological circumstances. Gram stain for stainable bacteria like Burkholderia. An acid fast stain for Mycobacteria. Chest radiographs of Mycobacterial pneumonia can reveal granulomatous lesions called ghon complexes. A modified acid fast stain for Nocardia. KOH wet mounts for fungal infections and a NaOH wet mount for Paragonimus westermanii infections.

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Skin testing is of limited value for determining a fungal etiology, however, it is very useful in the diagnosis of tuberculosis. Conversion from a recent negative skin test to a positive test is a strong indication of tuberculosis in adults.

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The Mantoux test requires 48-72 hours before it is read. The zone of induration is read not the zone of erythema.
Whether a reaction to the Mantoux tuberculin skin test is classified as positive depends on the size of the induration and on the person's risk factors for TB.

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Serology can be very useful in assisting in diagnosis. There are serologic tests for Nocardia and for melioidosis. Serology is very useful in diagnosis of fungal and parasitic infections. Complement fixation, hemagglutination, and immunodiffusion tests are available to assist in diagnosis of fungal and parasitic chronic pneumonias.

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Treatment Due to the large diversity of organisms in this group antibiotic treatment should not be instituted until your sure of the cause of the infection.

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Pneumonias of the Newborn Period and Infancy: Etiology and Epidemiology  The causes of pneumonia occurring in pediatric patients vary according to the age of the patient. day 0 to 2 weeks:  Group B Streptococcus; Streptococcus agalactiae  Some Gram-negative enteric bacilli (ex. E. coli)  Staphylococcus aureus  U. urealyticum is a common cause of pneumonia

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Newborn infants born before 34 weeks of gestation.  Congenital infections (Toxoplasma gondii, Rubella, Cytomegalovirus, Herpes simplex virus: TORCH infections) others that cause congenital infections= Treponema pallidum, and Mumps

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2 weeks to 6 months  Chlamydia trachomatis causes afebrile pneumonia  Respiratory syncytial virus  Parainfluenza virus 6 months to 5 years  Respiratory syncytial virus (RSV)  Parainfluenza virus  Adenovirus  Influenza virus  Echoviruses  Coxsackie viruses  S. pneumoniae  H. influenzae type B 5 years and older  Mycoplasma pneumoniae  S. pneumoniae

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Congenital infections:  Pneumonias acquired in utero and are hematogenously transmitted (also termed transplacental transmission). Five organisms are seen most often.  They are remembered by the acronym "TORCH." Toxoplasma gondii, Treponema pallidum, Rubella virus, Cytomegalovirus, and Herpes simplex viruses cause .  These infections are frequently able to infect other areas of the body such as the liver, spleen, brain, kidney, bone, and skin.
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Infections acquired during labor and delivery:
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The organisms are transmitted to the infant by upward spread of bacteria from the maternal genital tract into the amniotic cavity. The fetus aspirates or inhales the infected amniotic fluid prior to birth. Group B Streptococcus (S. agalactiae), E. coli, and Klebsiella pneumoniae are the cause of pneumonia in these infants

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Infections acquired after birth:
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These pneumonias present at various times after birth. The organisms can include RSV, parainfluenza, influenza virus, echoviruses, coxsackie viruses, adenoviruses, Chlamydia trachomatis, Staphylococcus aureus, and Gram-negative enteric bacteria. The virus infections are usually acquired in late fall to early spring.
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Clinical, Radiologic, and Laboratory Features





 

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Many different agents can cause pneumonia in these patients. As a result the clinical, radiologic, and laboratory features are highly variable. In viral and Chlamydial pneumonic infections the patient experiences apnea, tachypnea, lethargy, and respiratory distress. Little to no sputum is produced. X-rays reveal diffuse, interstitial or patchy infiltrates. Rarely one sees consolidation.
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Diagnosis
The etiologic agent most likely to cause infection depends on  the age of the patient,  the mother acquired a TORCH infection during pregnancy,  the mother's vagina was colonized with a particular organism,  the clinical and radiologic features, as well as the presence of infection in other body sites.
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Pneumonia in the Aspiration-Prone Patient




Aspiration is a process in which matter present in the oropharynx is carried through inhalation into the lower tracheobronchial tree. Usually the matter is cleared from the lungs however, if the person is compromised in some fashion or inhales large amounts of matter a pneumonia can result.

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Aspiration Pneumonia:
 



Aspiration of bacteria from the oropharynx. Patients have a cough, fever, purulent sputum, and radiographic evidence of infiltrate. Treatment requires antibiotics.

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Epidemiology and Etiology The following conditions predispose patients to aspiration pneumonia.  Altered Level of Consciousness  Alcoholism  Seizures  Drugs  Anesthesia  Central nervous system disorders  hospital-acquired.

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      

Trauma Dysphagia Esophageal disorders Neurological disorders Mechanical Disruption of Functional Barriers Nasogastric tubes Aspiration pneumonia is an endogenous infection. The infection is usually polymicrobial. The microorganisms can vary depending on whether the infection is community-acquired
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COMMUNITY ACQUIRED Obligate anaerobes  Fusobacterium spp.  Bacteroides spp.  Prevotella spp.  Porphyromonas spp.  Peptostreptococci spp. Aerobes  Streptococcus pneumoniae Rarely  Klebsiella pneumoniae  Staphylococcus aureus
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HOSPITAL ACQUIRED

Obligate anaerobes  Fusobacterium spp.  Bacteroides spp.  Prevotella spp.  Porphyromonas spp.  Peptostreptococci spp. Aerobes  Staphylococcus aureus  Klebsiella pneumoniae  Proteus sp.  Pseudomonas sp.  Serratia sp.  Escherichia coli
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Clinical, Radiographic, and Laboratory Features :






Aspiration pneumonia is much like "typical" pneumonia. However, the possibility of necrotizing pneumonia and lung abscess are more likely in aspiration pneumonia. Often times the sputum has a very foul odor that is pathognomonic for anaerobic lung infections.

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Diagnosis:


  

This syndrome is a lot like "Typical" pneumonia except for recurrent chills, pneumonia in dependent lung segments, and growth of normal flora on routine sputum culture. Some patients (50%) will produce foul smelling sputum. To get a definitive diagnosis translaryngeal aspiration must be performed. This is a dangerous procedure and usually the patients are treated empirically on the basis of predicted bacteriology.
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Epidemiology and Etiology Most pulmonary infections of the immunocompromised patient are bacterial. The following organisms can cause infections: Bacteria (most common to least common)  Klebsiella pneumoniae  Escherichia coli  Pseudomonas aeruginosa  Serratia sp.  Streptococcus pneumoniae  Staphylococcus aureus  Listeria monocytogenes

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Mycobacterium tuberculosis  Mycobacterium avium-intracellular  Mycobacterium kansasii  Nocardia sp.  Legionella sp. Viruses  Cytomegalovirus  Herpes simplex  Varicella-zoster  Measles  Adenovirus Protozoa  Pneumocystis jirovecii  Toxoplasma gondii

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Fungi  Histoplasma capsulatum  Cryptococcus neoformans  Coccidioides immitis Fungi seen only in immunocompromised patients:  Aspergillus sp.  Mucor sp.  Candida albicans
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Diagnosis :
 






A very good history and physical exam will help a lot. Knowledge of the most common organism causing pneumonia in a particular circumstance is also important. Acute onset of symptoms usually indicate a bacterial or Aspergillus infection. Subacute onset of symptoms indicate a viral, Pneumocystis, or Nocardial infection. A chronic onset of symptoms suggest infection due to mycobacteria, Nocardia, or fungi.
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





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Usually sputum is not produced in sufficient amounts to aid in diagnosis. Blood cultures can be useful and should be obtained. Skin tests are often useless because the person is unable to mount a T cell response. If samples prove useless and the patient is rapidly deteriorating even during empiric antimicrobial treatment then translaryngeal aspirates, open lung biopsy, or percutaneous needle biopsy are necessary to determine the exact etiologic agent.
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How to Diagnose Pneumonia
and cure the patient (your goal)
 



Clinical history Physical examination & lab tests Chest X-Ray

? Enough for Therapy


Diagnostic Microbiology

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Diagnostic Tools




History Cough (>90%), sputum (66%), dyspnea (66%), chest pain (50%), fever & chills, myalgias, diarrhea, headache, sore throat, rhinitis Rate of onset, season, location, travel, exposure to ill persons, animals, environment, and immunosuppressive conditions





Physical Exam Temperature, RR, intercostal and accessory muscle use, rales, wheezes, rhonchi, pleural rubs Overall state of health (age), BP, RR, Pulse, O2 saturation (Vital Signs) Provide decision making and prognostic information

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To make a diagnosis :
     



The clinical and epidemiological data are quite useful in narrowing down the number of possible etiological agents. Is the pneumonia acute, subacute, or chronic in onset? Acute usually means 24 to 48 hours between onset of generalized symptoms and development of pneumonia. A subacute pneumonia usually requires 1 to 2 weeks to develop into pneumonia. In a chronic onset the disease process is much slower and may require 4 to 6 weeks to develop into pneumonia. If the pneumonia was acquired in the hospital (a nosocomial infection) a different set of organisms will be suspect than when the pneumonia is community-acquired. The age of the patient will also help to narrow down the number of possible agents since certain organisms are more common at certain ages.

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Diagnosis
The diagnosis of pneumonia is not particularly difficult.
   



The problem often is determining the causative agent. This is often quite difficult because: Of the large number of organisms capable of causing pneumonia, Clinical findings associated with many of these agents are very similar, Less invasive procedures (sputum samples, blood cultures) for definitive diagnosis are commonly contaminated with normal flora or negative for growth of the etiological agent, and The invasive procedures (translaryngeal aspirate, lung biopsy, etc.) used for definitive diagnosis are rarely performed

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Determining the definitive diagnosis
  

A presumptive diagnosis is necessary to start treatment of the patient. However, to ensure successful treatment of the patient the etiologic agent should be determined. Other laboratory tests are useful in determining the definitive diagnosis.

These tests include:
 





Culture of the sputum sample for bacteria, or fungi. Blood samples that are cultured for bacteria, fungi or viruses, the white blood cell count is performed, and the differential is obtained (A sedimentation rate can also be performed). Serology to detect antibodies produced against the pathogen or as a result of infection with the pathogen (cold agglutinins for Mycoplasma pneumoniae, detection of antibodies to the capsule of S. pneumoniae). For gram stains and culture.

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





Antigen tests to detect certain antigens produced by the pathogen (polysaccharide testing for S. pneumoniae and H. influenzae). Skin tests to detect delayed type hypersensitivity reactions to certain pathogens (M. tuberculosis, some of the fungi). In certain cases sputum and blood collection is not able to determine the etiologic agent. Other techniques have been developed to avoid the contamination of the sample with normal flora.

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





These techniques include translaryngeal aspiration, bronchoscopy, needle biopsy of the lung, and open lung biopsy. These techniques are often required when an anaerobic bacterial, a fungal, a gram negative bacillary, or a parasitic infection, is suspected. Obtain pleural fluids or fluids from other affected areas
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Diagnosis of pneumonia requires a new infiltrate on CXR

* But not always !!!!
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Old or New Infiltrate ?

That is the question

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Microbiological Diagnosis
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History not definitive for determining causative agent Physical Examination not definitive of causative agent Epidemiology may be helpful and in some rare cases is critical X-rays usually provide a hint–at best

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Microbiological Tests
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

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Commonly available Sputum gram and acid fast stains Sputum Cultures Blood Cultures (>1) Pleural fluid gram stain and culture Nasal cultures for virus Antigen detection for viruses (RSV, Influenza) Special stains for PCP

Less Commonly available  Urine antigen detection (legionella, pneumococcus)  Serum antigen detection (Aspergillus, Histoplasma, Cryptococcus)  RT-PCR for virus, chlamydia, Mycobacterium  Serology for Psittacosis

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Diagnostic Tools

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Interpretation of Gram Stained Sputum Always use in conjunction with culture

Adequate & Useful  <10 epithelial cells  >25 PMNs  Dominant flora



 

Inadequate & Unhelpful >25 epithelial cells No dominant flora Few PMNs

Remember: DO NOT USE CULTURE ALONE !!!!
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What does this Sputum Gram stain mean?

Culture: Normal flora and 1+ S. pneumoniae
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Answer


 

Gram stain shows respiratory epithelial cells with attached bacteria No neutrophils Conclusion: Inadequate sputum and culture results not valid usually (exception M. Tb, legionella, PCP, virus)

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What does this Sputum gram stain mean?

Culture: normal oral flora
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Answer


Many PMNs and many gram positive diplococci in predominance Rare or no epithelial cells Conclusion: consistent with pneumococcal pneumonia (even without culture confirmation because pneumococcus is fastidious organism)

 

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What does this gram stain mean?

Culture: 3+ Moraxella catarrhalis
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Answer
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

Many PMNs and no epithelial cells Many intacelluar Gram negative diplococci Conclusion: good specimen and consistent with Moraxella or Meningococcal pneumonia

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What does this gram stain mean?

Culture: 2+ Pseudomonas, 1+ Staph aureus,
Normal oral flora

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Answer
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


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Many respiratory epithelial cells Rare PMNs Mixed bacterial flora Conclusion: inadequate sputum indicative of upper tract contamination. Results of culture not reliable as they reflect mouth flora (exceptions are M. Tb, legionella, viruses)

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Sputum Acid Fast Stain




PMNs and Epithelial cells relevant if negative. AFB seen in moderate numbers. Conclusion: Consistent with tuberculosis or atypical mycobacterial infection

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Results of Extensive Laboratory Evaluation


  

Sputum gram stain & culture (25%) Blood cultures (10%) Antigen detection tests (10%) Serology (10%)

Total specific diagnoses: 50-70%

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Specific therapy is generally best
   


 

S. pneumoniae → β-lactam Haemophilus → β-lactamase stable β-lactam Moraxella → β-lactamase stable β-lactam Mycoplasma → Macrolide or quinolone Chlamydia → Macrolide or quinolone Gram negative bacilli → β-lactam Influenza → consider neuraminidase inhibitor

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Empiric Antibiotic choices for CAP
 

Quinolone (levofloxacin, moxifloxacin) Third generation cephalosporin (Ceftriaxone) plus Macrolide (Azithromycin)

Other Issues to consider: drug allergies, antibiotic resistance in community

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Nosocomial Pneumonia

Nosocomial Pneumonia
  



2nd leading cause of nosocomial infection Accounts for 13-18% on infections Leading cause on bacterial nosocomial infection related death Increases LOS by 7-9 days

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Treatment
 



Early : Before Day 5 Absence of risk factors : Abdominal surgery, aspiration, coma, DM, renal failure, head trauma, underlying lung disease, prolonged steroids, ICU, prior antibiotic treatment. Treatment same as community acquired; Levofloxacin or Ceftriaxone

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Practical Dx and Treatment
 Make

your best assessment on clinical grounds + sputum gram stain  Start BROAD  Know your ICU flora  Rapidly adjust based on micro data  Keep duration of Abx appropriate

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Tuberculosis
The three stages of tuberculosis (TB): 1. primary infection within the lung tissue: this is the usual way how tuberculosis starts. 2. latent or dormant stage of tuberculosis: often tuberculosis goes "underground", on the surface not progressing for up to 1 or 2 years, but the TB bacterium is live wherever it incubates and there are silent tissue reactions. 3. active tuberculosis in various organ systems: tuberculosis tends to express itself in 11 different organ systems masquerading as distinct clinical entities despite the same underlying TB pathogen.
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Tuberculosis

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



 



When the bacterium is inhaled, it forms the primary infection within the lung tissue, which may go undetected, if no cough or other symptoms develop. On other occasions TB might be diagnosed at this stage and treated very effectively. It may then lay dormant (latent of dormant stage of TB) and take several months or 1 to 2 years before it gets reactivated. All along the TB bacterium is alive, but surrounded by granulation tissue (one of the histological markers, with live tuberculosis bacteria in the center). The third stage is active tuberculosis in various organ systems (pulmonary TB, meningeal TB, miliary TB, tuberculous peritonitis, lymph gland TB, tuberculous pericarditis, TB of bones and joints, liver TB, gastrointestinal TB, TB of wounds and skin, Genitourinary TB).

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





Tuberculosis symptoms: In primary infection with TB (the first stage of TB) the patient just does not feel well. There likely is a cough for a few weeks, but a smoker might think that it is just a smoker's cough, whereas a non smoker may blame it on a "regular cold or virus". In primary TB infection there is formation of granular tissue around the TB bacteria as a result of an inflammatory reaction.
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      



This is called a "caseous nidus" and this can rupture open and get coughed up. The result is that the patient may see some cottage cheese like material mixed into the phlegm that was coughed up. At this point in time there would be subtle X-ray changes on a chest Xray. In adults there would be nodular scars on the upper lung fields, called "Simon foci", from which the TB continues in the later stages. In children the initial nodular changes are in the middle and lower lobes of the lungs, which in that age group are better perfused. Children also get a prominent hilar lymph gland reaction as well as more commonly pleural effusions, which shows up on X-rays. After the dormant stage there is a sudden occurrence where TB either flares up in the lungs or as tuberculous meningitis as a neurological disease. TB is a great masquerator as it can also present as various system diseases.

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

An induration of 5 or more millimeters is considered a positive reaction for the following people: People with HIV infection Close contacts of people with infectious TB People with chest x-ray findings suggestive of previous TB disease People who inject illicit drugs and whose HIV status is unknown

   

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

   

An induration of 10 or more millimeters is considered a positive reaction for the following people: People born in areas of the world where TB is common (foreign-born persons) People who inject illicit drugs but who are known to be HIV negative Low-income groups with poor access to health care People who live in residential facilities (for example, nursing homes or correctional facilities)

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

People with medical conditions that appear to increase the risk for TB (not including HIV infection), such as diabetes Children younger than 4 years old People in other groups likely to be exposed to TB, as identified by local public health officials
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






An induration of 15 or more millimeters is considered a positive reaction for people with no risk factors for TB. In most cases, people who have a very small reaction or no reaction probably do not have TB infection. Positive tests in children is highly suggestive of infection. False-positive reactions can be caused by infection with nontuberculous mycobacteria or vaccination with BCG.

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Tuberculosis treatment
Signs and symptoms as well as treatment are very much determined by the anatomical location of TB. Treatments used for the various forms of tuberculosis. Primary pulmonary TB or early stage 3 pulmonary disease  When the tests are positive for TB, this condition is treated for 3 months with a combination of rifampin, clarithromycin and ethambutol.  More serious invasive cases are treated with 4 to 6 drug combinations simultateously.  In the past partial lung resections were often done, which is now reserved for the resistant cases in a young patient who is otherwise healthy.

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Case 1





A 73 years old woman comes to Emergency Department complaining of fever, cough and SOB in early January. PMH –, Hypothyroidism PE – acutely ill, Temp -39ºC RR-24 BP-nl, Chest shows rales in the bases and wheezes

What other history Do you want?

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What other history Do you want?
   

Exposure to illness Exposure to children Travel Immunizations

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



  

She got back from a trip to China 1 week ago. She spent time with the grandchildren: ages 2-7yo for the holidays. She a had a pneumovax at age 65 She had her flu shot in the Fall Her only exposure to illness was some man coughing next to her.

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Case 2
     

A 30 year old man with SLE is admitted with Fever and cough in June. He has a severe headache and nausea Cough is productive of scant sputum. No exposure to illness He is a married banker. No children. No travel. He owns a parakeet and a cat

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Case 2
   

He is very ill appearing’ Temp 40.5, RR-36, SBP -88 He has rhonchi and rales in both lungs Room air blood gas-7.36/24/52

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What tests? What drugs?

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Case 3

 




66 year old diabetic post severe CVA is a chronic ventilator patient on 5200. You are called for a temp and the patient is stable so you order “pancultures” Two days later the sputum culture is growing 3+ Stenotrophomonas and 2+ ORSA. The patient is still having low grade fevers. What do you do?

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Take Home Messages
 


 

All patients with pneumonia are not alike. Think about the age, setting, time of year, exposures. Try to get sputum! Don’t just respond to a culture without checking the gram stain. In very ill ICU patients, start broad and narrow based on micro data.
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