Nasopharyngeal organisms occurs in nearly all persons during sleep and is probably responsible for most bacterial pneumonias
The pulmonary consequences from the abnormal entry of fluid, particulate exogenous substances, or endogenous secretions into the lower airways.
There are usually two requirements to produce aspiration pneumonia:
Compromise in the usual defenses that protect the lower airways including glottic closure, cough reflex, and other clearing mechanisms
An inoculum deleterious to the lower airways by a direct toxic effect, a large enough bacterial inoculum, or obstruction of the airway
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.
The most common forms of aspiration pneumonia are caused by bacteria that normally reside in the oral-pharyngeal area or stomach.
Anaerobic bacteria are the dominant organisms in the upper airways and most common cause of infection.
Major M/O include: Peptostreptococcus, Fusobacterium nucleatum, Prevotella, and Bacteroides spp.
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.
patients with gram-negative bacilli isolated often also have anaerobes involved
Highly variable depending upon the bacteria involved and the status of the host.
Compared to most cases of community-acquired pneumonia, the tempo of the disease in this type of aspiration pneumonia is often relatively slow.
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
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.
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
Beta-lactam beta lactamase combination anti-pseudomonal penicillins (piperacillin-tazobactam or ticarcillin-clavulanate)
Antipseudomonal carbapenem, (inipenem or meropenem).
Aminoglycocide agents alternative for gram negative agents including pseudomonas in combination with fluoroquinolones
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.
If MRSA suspected, linezolid or vancomycin employed
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.
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 .
This reaction is reversible by vagotomy or administration of atropine or isoproterenol.
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.
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
Associated with spread of infectious agent via circulatory system to lung secondary to development of septacemia from distant infected site.
May have any organism that becomes bacteremic, from Candida septicemia, Klebsiella, E. coli, P. aurgenosa, etc.
Commonly associated with right heart disease and emboli of infected vegetations associated with endocarditis and valular heart disease
Most common organism is S. aures, associated with I.V. drug abusers which produces classic cannon ball defects on CXR
Spread from pulmonic and tricuspid value vegetations with any organism producing pathology, from S. viridians to Candida
An inflammatory disorder of the lung involving the alveolar walls and terminal airways.
Induced by inhalation of a variety of organic agents that induce an immunologic reaction within the pulmonary parenchyma.
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.
Numerous inciting agents, with more than 300 identified, include but are not limited to, agricultural dusts, bioaerosols, fungi, bacterium, virus, and certain chemicals.
EPIDEMIOLOGY — The prevalence and incidence are thought to be low but widely unknown.
Most knowledge has been derived from studies of chemical workers, farmers and bird fanciers.
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.
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.
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.
A wide range of occupations and avocations that result in contact with airborne organic antigens increase the risk of developing HP.
Farmer's lung is one of the most common forms of HP, affecting 0.4 to 7 percent of the farming population
Chemical workers lung, related in part to exposure with isocyanates in US in relatively rare.
Bird fanciers lung has variable occurrence as well with estimates range from 20 to 20,000 affected individuals per 100,000 persons at risk.
Bagassosis sugar cane workers response to fungal antigens.
High rates noted with sporadic outbreaks of HP among other populations :
52 percent of exposed office workers with humidifier lung
37 percent of lifeguards exposed to a public swimming pool
27 percent of workers at an injection molding plant manufacturing polyurethane foam parts for automobiles
15 percent of office workers exposed to a contaminated forced air system
Cigarette smoking is associated with a decreased risk of HP. These observations may reflect diminished antibody responses to inhaled antigens among smokers.
Once the disease is established, however, smoking does not appear to attenuate its severity, and may predispose to a more chronic and severe course .
Can be acute, sub-acute or chronic in presentation
Acute presents as cough, fever, chills, malaise and dyspnea as quickly as 6 to 8 hours post exposure.
Sub acute presents over weeks with cough, dyspnea, progressing to cyanosis and hypoxia.
Acute and sub-acute signs, symptoms and manifestation disappear in days, weeks or month if exposure is removed.
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.
See elevation in acute reactants, ESR, C-reactive protein, rheumatoid factor, neutrophilia
It is on note that eosinophilia if not a feature of HP.
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.
CXR is non-specific with diffuse infiltrates or discrete nodular infiltrates both seen.
Differentiate from other interstitial lung disorders made often by history, drugs exposed to, history of collagen vascular disease like RA or Crohn’s, etc.
Diminishing exposure to provocative antigens. This may be accomplished by minimizing contact with potential inciting agents, reducing microbial contamination, or using protective equipment.
Indoor microbial contamination is usually related to problems with moisture control.
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.
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
Recent hospitalization (especially S. pneumonia)
Defined as pneumonia that occurs more than 48 hours after hospital admission, excluding any infection incubating at the time of admission.
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
Ventilator-associated pneumonia (VAP) can be regarded as a particular subgroup of HAP for which the incidence, etiology, investigation and outcome are somewhat different.
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.
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
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%
Onset is insidious, over several days to a week.
Constitutional symptoms, which usually are present, include headache exacerbated by a cough, malaise, myalgias, and sore throat.
The cough is usually dry, paroxysmal, and worse at night.
The clinical course of pneumonia caused by M. pneumoniae is usually mild and self-limited.
The mortality rate is approximately 1.4 percent.
However, pulmonary complications can be significant and include effusion, empyema, pneumothorax, and respiratory
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.
Transmission results from contact with respiratory secretions, with an incubation period of several weeks.
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.
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.
Chest radiographs tend to show less extensive infiltrates than are seen with other causes of pneumonia, although significant infiltrates have been reported.
Most cases of C. pneumoniae infection are mild,
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
Other conditions that compromise the immune system
The pathogens also can be found in moist soil, especially near streams and ponds.
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.
Condensers, cooling towers, respiratory therapy equipment, showers, water faucets, and whirlpools have been associated with outbreaks of legion.
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
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
Prevotella (formerly oral strains of Bacteroides) e.g., P. melaninogenica
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)
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
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
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
Viral respiratory tract infections are the most common cause of symptomatic human disease among children and adults.
They account for more time lost from school and work than any other infection.
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.
The incidence of viral pneumonia has increased during the past decade.
The increase primarily is because of improved diagnostic techniques and the growing population of patients who are immunocompromised.
In the past, the diagnosis of viral pneumonia was made essentially on clinical grounds.
Over the past 10 years, new biotechnology has greatly facilitated the diagnosis of viral pneumonias.
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.
Furthermore, improved approaches to prevention and treatment of viral pneumonias have also become available
The 4 most frequent etiologies of viral pneumonia in adults are
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
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.
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.
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.
RSV is a well-established cause of pneumonia in the elderly population and in adults who are immunocompromised.
Infection may occur seasonally during the winter months or as outbreaks in hospitals and nursing homes
Enveloped DNA viruses that cause upper and lower respiratory tract infections.
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.
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.
Adenoviruses are spread through droplet and fomite transmission; close living arrangements (eg, college campuses, military camps) are likely places for outbreaks.
newly identified, more virulent strain, serotype 14 (subgroup B), has been reported to cause severe respiratory illness and pneumonia.
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
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
from the family Paramyxoviridae and is characterized by nucleocapsids, which develop in the cytoplasm of infected cells, with hemagglutinin present in the virion envelope.
These can be separated into 4 subtypes based on antigenic characteristics. This virus is spread via droplet and fomite exposure.
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.
Immunity is short term, and recurrent upper or lower respiratory tract infections occur throughout life.
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
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.
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
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.
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.
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
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
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
Treatment for all of the deep fungal diseases is with sequential amphotericin B & itraconazole or either voriconazole or fluconazole.
Treatment: Amphotericin B x 7-14 days Induction itraconazole
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%
Primary Prophylaxis: Itraconazole 200mg/day, effective in patients with CD4 count <100 cells/microL living in endemic areas
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