TRIPASS XR تري باس

 Viridans streptococci, including Streptococcus anginosus

group

Beta-hemolytic streptococci

Streptococcus pneumoniae

Staphylococcus aureus

Neisseria meningitidis

Mycoplasma spp.

Haemophilus influenzae

Haemophilus parainfluenzae

Moraxella catarrhalis

Candida albicans

Herpes simplex virus

Enterobacteriaceae

Mycobacterium spp.

Pseudomonas spp.

Burkholderia cepacia

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Filamentous fungi

Klebsiella ozaenae

Eikenella corrodens

Bacteroides spp.

Peptostreptococcus spp.

Actinomyces spp.

Capnocytophaga spp.

Actinobacillus spp., A. actinomycetemcomitans

Haemophilus aphrophilus

Entamoeba gingivalis

Trichomonas tenax

Rarely Pathogens

Nonhemolytic streptococci

Staphylococci

Micrococci

Corynebacterium spp.

Coagulase-negative staphylococci

Neisseria spp., other than N. gonorrhoeae and

N. meningitidis

Lactobacillus spp.

Veillonella spp.

Spirochetes

Rothia dentocariosa

Leptotrichia buccalis

Selenomonas

Wolinella

Stomatococcus mucilaginosus

Campylobacter spp.

Adherence. For any organism to cause disease, it must first gain a foothold within the respiratory tract to grow

to sufficient numbers to produce symptoms. Therefore, most etiologic agents of respiratory tract disease must

first adhere to the mucosa of the respiratory tract. The presence of normal flora and the overall state of the host

affect the ability of microorganisms to adhere. Surviving or growing on host tissue without causing overt

harmful effects is termed colonization. Except for those microorganisms inhaled directly into the lungs, all

etiologic agents of disease must first colonize the respiratory tract before they can cause harm.

Streptococcus pyogenes possess specific adherence factors such as fimbriae comprised of molecules such as

lipoteichoic acids and M proteins. These molecules appear as a thin layer of fuzz surrounding the bacteria.

Staphylococcus aureus and certain viridans streptococci are other bacteria that posses these lipoteichoic acid

adherence complexes. Many gram-negative bacteria (which do not have lipoteichoic acids), including

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Enterobacteriaceae, Legionella spp., Pseudomonas spp., Bordetella pertussis, and Haemophilus spp., also

adhere by means of proteinaceous finger-like surface fimbriae. Viruses possess either a hemagglutinin

(influenza and parainfluenza viruses) or other proteins that mediate their epithelial attachment.

(Table2): Respiratory Tract Pathogens:

Definite Respiratory Tract Pathogens:

Corynebacterium diphtheriae (toxin producing)

Mycobacterium tuberculosis

Mycoplasma pneumoniae

Chlamydia trachomatis

Chlamydia pneumoniae

Bordetella pertussis

Legionella spp.

Pneumocystis jiroveci (Pneumocystis carinii)

Nocardia spp.

Histoplasma capsulatum

Coccidioides immitis

Cryptococcus neoformans (may also be recovered from patients without disease)

Blastomyces dermatitidis

Viruses (respiratory syncytial virus, human metapneumovirus,

adenoviruses, enteroviruses, hantavirus, herpes simplex

virus, influenza and parainfluenza virus, rhinoviruses,severe acute respiratory syndrome)

Rare Respiratory Tract Pathogens:

Francisella tularensis

Bacillus anthracis

Yersinia pestis

Burkholderia pseudomallei

Coxiella burnetii

Chlamydia psittaci

Brucella spp.

Salmonella spp.

Pasteurella multocida

Klebsiella rhinoscleromatis

Varicella-zoster virus (VZV)

Parasites

Toxins. Certain microorganisms are almost always considered to be etiologic agents of disease if they are

present in any numbers in the respiratory tract because they possess virulence factors that are expressed in

every host. These organisms are listed in Table 2.

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The production of extracellular toxin was one of the first pathogenic mechanisms discovered among bacteria.

Corynebacterium diphtheriae is a classic example of a bacterium that produces disease through the action of an

extracellular toxin.

Once the organism colonizes the upper respiratory epithelium, it produces a toxin that is disseminated

systemically, adhering preferentially to central nervous system cells and muscle cells of the heart. Systemic

disease is characterized by myocarditis, peripheral neuritis, and local disease that can lead to respiratory

distress.Growth of C. diphtheriae causes necrosis and sloughing of the epithelial mucosa, producing a

“diphtheritic (pseudo) membrane,” which may extend from the anterior nasal mucosa to the bronchi or may be

limited to any area between—most often the tonsillar and peritonsillar areas. The membrane may cause sore

throat and interfere with respiration and swallowing. Although nontoxic strains of C. diphtheriae can cause

local disease, it is much milder than disease associated with toxigenic strains.

Some strains of Pseudomonas aeruginosa produce a toxin similar to diphtheria toxin. Whether this toxin

actually contributes to the pathogenesis of respiratory tract infection with P. aeruginosa has not been

established.

Bordetella pertussis, the agent of whooping cough, also produces toxins. The role of these toxins in production

of disease is not clear. They may act to inhibit the activity of phagocytic cells or to damage cells of the

respiratory tract. Staphylococcus aureus and beta-hemolytic streptococci

produce extracellular enzymes capable of damaging host cells or tissues. Extracellular products of

staphylococci aid in the production of tissue necrosis and the destruction of phagocytic cells and contribute to

the abscess formation associated with infection caused by this organism. Although S. aureus can be recovered

from throat specimens, it has not been proved to cause pharyngitis.

Enzymes of streptococci, including hyaluronidase, allow rapid dissemination of the bacteria.

Microorganism Growth. In addition to adherence and toxin production, pathogens cause disease by merely

growing in host tissue, interfering with normal tissue function, and attracting host immune effectors, such as

neutrophils and macrophages. Once these cells begin to attack the invading pathogens and repair the damaged

host tissue, an expanding reaction ensues with more nonspecific and immunologic factors being attracted to the

area, increasing the amount of host tissue damage. Respiratory viral infections usually progress in this manner,

as do many types of pneumonias, such as those caused by Streptococcus pneumoniae, S. pyogenes,

Staphylococcus aureus, Haemophilus influenzae, Neisseria meningitidis, Moraxella catarrhalis, Mycoplasma

pneumoniae, Mycobacterium tuberculosis, and most gram-negative bacilli.

Avoiding the Host Response. Another virulence mechanism present in various respiratory tract pathogens is

the ability to evade host defense mechanisms. S. pneumoniae, N. meningitidis, H. influenzae, Klebsiella

pneumoniae, mucoid P. aeruginosa, Cryptococcus neoformans, and others possess polysaccharide capsules that

serve both to prevent engulfment by phagocytic host cells and to protect somatic antigens from being exposed

to host immunoglobulins. The capsular material is produced in such abundance by certain bacteria, such as

pneumococci, that soluble polysaccharide antigen particles can bind

host antibodies, blocking them from serving as opsonins.

Vaccine consisting of capsular antigens provides host protection to infection, indicating tha

Vaccine consisting of capsular antigens provides host protection to infection, indicating that the capsular

polysaccharide is a major virulence mechanism of H. influenzae, S. pneumoniae, and N. meningitidis.

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Some respiratory pathogens evade the host immune system by multiplying within host cells. Chlamydia

trachomatis, Chlamydia psittaci, Chlamydia pneumoniae, and all viruses replicate within host cells. They have

evolved methods for being taken in by the “nonprofessional” phagocytic cells of the host to where they thrive

within the intracellular environment. Once within these cells, the organism is protected from host humoral

immune factors and other phagocytic cells. This protection lasts until the host cell becomes sufficiently

damaged that the organism is then recognized as foreign by the host and is attacked. A second group of

organisms that cause respiratory tract disease comprises organisms capable of survival within phagocytic host

cells (usually macrophages).

Once inside the phagocytic cell, these respiratory tract pathogens are able to multiply. Legionella, Pneumocystis

jiroveci (Pneumocystis carinii), and Histoplasma capsulatum are some of the more common intracellular

pathogens.

Mycobacterium tuberculosis is the classic representative of an intracellular pathogen. In primary tuberculosis,

the organism is carried to an alveolus in a droplet nucleus, a tiny aerosol particle containing tubercle bacilli.

Once phagocytized by alveolar macrophages, organisms are carried to the nearest lymph node, usually in the

hilar or other mediastinal chains. In the lymph node, the organisms slowly multiply within macrophages.

Ultimately,M. tuberculosis destroys the macrophage and is subsequently taken up by other phagocytic cells.

Tubercle bacilli multiply to a critical mass within the protected environment of the macrophages, which are

prevented from accomplishing phagosome-lysosome fusion capable of destroying the bacteria. Having reached

a critical mass, the organisms spill out of the destroyed macrophages,

through the lymphatics, and into the bloodstream, producing mycobacteremia and carrying tubercle bacilli to

many parts of the body. In most cases, the host immune system reacts sufficiently at this point to kill the bacilli;

however, a small reservoir of live bacteria may be left in areas of normally high oxygen concentration, such as

the apical (top) portion of the lung. These bacilli are walled off, and years later, an insult to the host, either

immunologic or physical, may cause breakdown of the focus of latent tubercle bacilli, allowing active

multiplicationvand disease (secondary tuberculosis). In certain patients with primary immune defects, the initial

bacteremia seeds bacteria throughout a compromised host, leading to disseminated or miliary tuberculosis.

Growth of the bacteria within host macrophages and histiocytes in the lung causes an influx of more effector

cells, including lymphocytes, neutrophils, and histiocytes, eventually resulting in granuloma formation, then

tissue destruction and cavity formation. The lesion consists of a semisolid, amorphous tissue mass resembling

semisoft cheese, from which it received the name caseating necrosis (death of cells or tissues). The infection

can extend into bronchioles and bronchi from which bacteria are disseminated via respiratory secretions and

coughing.Aerosolized droplets are produced by coughing and contain organisms that are inhaled by the next

susceptible host. Other portions of the patient’s lungs may become infected as well through aspiration

(inhalation of a fluid or solid).

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Diseases of the lower respiratory tract:

Bronchitis acute:

Acute bronchitis is characterized by acute inflammation of the tracheobronchial tree. This condition may be

part of, or preceded by, an upper respiratory tract infection such as influenza (the “flu”) or the common cold.

Most infections occur during the winter when acute respiratory tract infections are common.

The pathogenesis of acute bronchitis has no specific documented etiology but appears to be a mixture of viral

cytopathic events and a response by the host immune system. Regardless of the cause, the protective functions

of the bronchial epithelium are disturbed and excessive fluid accumulates in the bronchi. Depending on the

etiology, destruction of the bronchial epithelium may be either extensive (e.g., influenza virus) or minimal (e.g.,

rhinovirus colds).

Clinically, bronchitis is characterized by cough, variable fever, and sputum production. Sputum (pus from the

lungs) is often clear at the onset but may become purulent as the illness persists. Bronchitis may manifest as

croup (a clinical condition marked by a barking cough or hoarseness).

The value of microbiologic studies to determine the cause of acute bronchitis in otherwise healthy individuals

has not been established. Acute bronchitis is caused by viral agents, such as influenza and respiratory syncytial

virus (RSV). The bacterium Bordetella pertussis is often associated with bronchitis in infants and preschool

children(Table 3).

Chronic versus Acute:

Chronic bronchitis is a common condition affecting about 10% to 25% of adults. This disease is defined by

clinical symptoms in which excessive mucus production leads to coughing up sputum on most days during at

least 3 consecutive months for more than 2 successive years.

(Table3): Major Causes of Acute Bronchitis:

Bacteria Viruses

Influenza virus, adenovirus, rhinovirus,

coronavirus (other less common

viruses: respiratory syncytial virus,

human metapneumovirus,

coxsackie A21 virus)

Bordetella pertussis,

B. parapertussis,

Mycoplasma pneumoniae,

Chlamydia pneumoniae

(Table 3): Viral Agents That Cause Bronchiolitis:

Respiratory syncytial virus

Parainfluenza viruses, types 1-3

Rhinoviruses

Adenoviruses

Influenza viruses

Enteroviruses

Human metapneumovirus

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Patients with chronic bronchitis can suffer from acute flare-ups of infection, but determination of the cause of

the infection is difficult. Potentially pathogenic bacteria, such as nonencapsulated strains of Haemophilus

influenzae, Streptococcus pneumoniae, and Moraxella catarrhalis, are frequently cultured from the bronchi of

these patients.

Because of chronic colonization, it is difficult to incriminate one of these organisms as the specific cause of an

acute infection in patients with chronic bronchitis.

BRONCHIOLITIS:

Bronchiolitis, the inflammation of the smaller diameter bronchiolar epithelial surfaces, is an acute viral lower

respiratory tract infection that primarily occurs during the first 2 years of life.

The disease is primarily caused by viruses including a recently discovered virus, human metapneumovirus.

RSV accounts for 40% to 80% of cases of bronchiolitis and demonstrates a marked seasonality; the etiologic

agents of bronchiolitis are listed in (Table 4).

Initially, the virus replicates in the epithelium of the upper respiratory tract, but in the infant it rapidly spreads

to the lower tract airways. Early inflammation of the bronchial epithelium progresses to necrosis. Symptoms

such as wheezing may be related to the type of inflammatory

response to the virus as well as other host factors.

For the most part, patients are managed based on clinical parameters, with the laboratory having a role in cases

that require hospitalization; a specific viral etiology can be identified in a large number of infants by viral

isolation from respiratory secretions, preferably from a nasal wash.

Pneumonia:

Pneumonia (inflammation of the lower respiratory tract) is a major cause of illness and death. There are two

major categories of pneumonias: those considered communityacquired pneumonia (patients are believed to

have acquired their infection outside the hospital setting) and those including hospital- or ventilator-associated

(patients are believed to have acquired their infection within the hospital setting, usually at least 2 days

following admission) or health care–associated pneumonia (affects only patients hospitalized in an acute care

hospital for 2 or more days within 90 days of infection from a long-term care facility, or patients who have

received recent intravenous antibiotic therapy, chemotherapy, or wound care within 30 days of the current

infection, or who have attended a hospital or hemolysis clinic). Nevertheless, once a microorganism has

successfully invaded the lung, disease can follow affecting the alveolar spaces and their supporting structure,

the interstitium, and the terminal bronchioles.

Pathogenesis

Organisms can cause infection of the lung by four possible routes: by upper airway colonization or infection

that subsequently extends into the lung, by aspiration of organisms (thereby avoiding the upper airway

defenses), by inhalation of airborne droplets containing the organism, or by seeding of the lung via the blood

from a distant site of infection.

Viruses cause primary infections of the respiratory tract, as well as inhibit host defenses that, in turn, can lead

to a secondary bacterial infection. For example, viruses may destroy respiratory epithelium and disrupt normal

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ciliary activity. Presumably, the growth of viruses in host cells disrupts the function of the latter and encourages

the influx of nonspecific immune effector cells exacerbating the damage. Damage to host epithelial tissue by

virus infection is known to predispose patients to secondary bacterial infection.

Clinical Manifestations

The symptoms suggestive of pneumonia include fever, chills, chest pain, and cough. In the past, pneumonias

were classified into two major groups: (1) typical or acute pneumonias (e.g., Streptococcus pneumoniae) and

(2) atypical pneumonias, based on whether the cough was productive

or nonproductive of mucoid sputum. However, analysis of symptoms of pneumonia caused by the atypical

pneumonia pathogens (Mycoplasma pneumoniae, Legionella pneumophila, and Chlamydophila pneumoniae)

has revealed no significant differences from those symptoms of patients with typical bacterial pneumonias.

Because of this overlap in symptoms, it is important to consider all possible etiologies associated with the

patient’s clinical presentation.

Chronic Lower Respiratory Tract Infections:

Mycobacterium tuberculosis is the most likely etiologic agent of chronic lower respiratory tract infection, but

fungal infection and anaerobic pleuropulmonary infection may also run a subacute or chronic course.

Mycobacteria other than M. tuberculosis may also cause such disease, particularly M. avium complex and M.

kansasii. Although possible causes of acute, community-acquired lower respiratory tract infections, fungi and

parasites are more commonly isolated from patients with chronic disease. Actinomyces and Nocardia may also

be associated with gradual onset of symptoms. Actinomyces is usually associated with an infection of the pleura

or chest wall, and Nocardia may be isolated along with an infection caused by M. tuberculosis.

The pathogenesis of many of the infections caused by agents of chronic lower respiratory tract disease is

characterized by the requirement for breakdown of cellmediated immunity in the host or the ability of these

agents to avoid being destroyed by host cell-mediated immune mechanisms. This may be caused by an effect

on macrophages, the ability to mask foreign antigens, sheer size, or some other factor, allowing microbes to

grow within host tissues without eliciting an overwhelming local immune reaction.

Cystic fibrosis (CF) is a genetic disorder that leads to persistent bacterial infection in the lung, causing airway

wall damage and chronic obstructive lung disease. Eventually, a combination of airway secretions and damage

leads to poor gas exchange in the lungs, cardiac malfunction, and subsequent death. Patients with CF may

present as young adults with chronic respiratory tract disease or, more commonly, as children with

gastrointestinal problems and stunted growth. Staphylococcus aureus is the most prevalent opportunistic

bacterial pathogen infecting 55% of children 0–9 years of age with CF, with Pseudomonas aeruginosa the most

prevalent (81%) in older children. A very mucoid Pseudomonas, characterized by production of copious

amounts of extracellular capsular polysaccharide, can be isolated from the sputum of almost all patients with

CF who are older than 18 years of age, becoming more prevalent with increasing age after 5 years. Even if CF

has not been diagnosed, isolation of a mucoid Pseudomonas aeruginosa from sputum should alert the clinician

to the possibility of underlying disease.

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Microbiologists should always report this unusual morphologic feature. In addition to mucoid Pseudomonas

and Staphylococcus aureus, important pathogens in patients with CF are likely to harbor Haemophilus

influenzae, Streptococcus pneumoniae, Stenotrophomonas maltophilia, Achromobacter xylosoxidans, Ralsotnia

spp. Cupriavidus spp.,

Pandoraea spp., Escherichia coli, strains of Burkholderia cepacia complex, fast growing mycobacteria, RSV,

influenza and fungi including Aspergillu, Scedosporium spp., and Exophiala dermatidis. In addition, due to the

viscous mucous plugs associated with CF, several anaerobic organisms have been detected in the lungs of CF

patients including Prevotella, Bifidobacterium, Veillonella, Peptostreptococcus and Fusobacterium.

Using advanced diagnostic molecular methods, additional organisms have also been identified in chronic

polymicrobial CF infections including viridans streptococci, Streptococcus constellatus, Streptococcus

intermedius and Streptococcus anginosus.

Lung abscess is usually a complication of acute or chronic pneumonia. In these circumstances, organisms

infecting the lung cause localized destruction of the lung parenchyma (functional elements of the lung).

Symptoms associated with lung abscess are similar to those of acute and chronic pneumonia, except symptoms

fail to resolve with treatment.

Immunocompromised Patients: Patients with Neoplasms. Patients with cancer are at high risk to become

infected because of either granulocytopenia or other defects in phagocytic defenses, cellular or humoral

immune dysfunction, damage to mucosal surfaces and the skin, and various medical procedures such as blood

product transfusion.

Transplant Recipients. For successful organ transplantation,the recipient’s immune system must be suppressed.

As a result, these patients are predisposed to infection. Regardless of the type of organ transplant

(heart, renal, bone marrow, heart/lung, liver, pancreas), most infections occur within 4 months following

transplantation. Major infections can occur within the first month but are usually associated with infections

carried over from the pretransplant period. Pulmonary infections are of great importance in this patient

population. Some of the most common causes of pneumonia include S. aureus Streptococcus pneumoniae,

Haemophilus influenzae, Pneumocystis jiroveci, and cytomegalovirus. In addition, other organisms such as

Cryptococcus neoformans, Aspergillus spp., Candida spp., Nocardia sp. and over, can cause life-threatening

pulmonary infection.

HIV-Infected Patients. Patients who are infected with human immunodeficiency virus (HIV) are at high risk

for developing pneumonia. opportunistic infections as a result of severe immunodeficiency are a major cause

of illness and death among these patients.

In the United States, the most common opportunistic infection among patients with acquired immunodeficiency

syndrome is Pneumocystis jiroveci pneumonia. Although P. jiroveci remains a major pulmonary pathogen,

other organisms must be considered in this patient population, including Mycobacterium tuberculosis and

Mycobacterium avium complex, as well as common bacterial pathogens such as Streptococcus pneumonia and

Haemophilus influenzae. In addition to these common pathogens, many other organisms can cause lower

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respiratory tract infections, including Nocardia spp., Rhodococcus equi (a gram-positive, aerobic, pleomorphic

organism), and Legionella spp.

Pleural infections

As a result of an organism infecting the lung and subsequently gaining access to the pleural space via an

abnormal passage (fistula), the patient may develop an empyema (pus in a body cavity such as the pleural

cavity).

(Table 5): Examples of Infectious Agents Frequently Associated with Certain Malignancies:

Malignancy (site and type of infections) Pathogen

Enterobacteriaceae

Pseudomonas

Staphylococci

Corynebacterium jeikeium

Candida

Aspergillus

Mucor

Hepatitis C and other non-A, non-B

Acute nonlymphocytic

leukemia (pneumonia,

oral lesions, cutaneous

lesions, urinary tract

infections, hepatitis,

most often sepsis

without obvious focus

Streptococci (all types)

Pneumocystis jiroveci (P. carinii)

Herpes simplex virus

Cytomegalovirus

Varicella zoster vi

Acute lymphocytic leukemia

(pneumonia, cutaneous

lesions, pharyngitis,

disseminated disease

Brucella

Candida (mucocutaneous)

Cryptococcus neoformans

Herpes simplex virus (cutaneous)

Varicella zoster virus

Cytomegalovirus

Pneumocystis jiroveci (P. carinii)

Toxoplasma gondii

Listeria monocytogenes

Mycobacteria

Nocardia

Salmonella

Staphylococci

Enterobacteriaceae

Pseudomonas

Strongyloides stercoralis

Lymphoma (disseminated

disease, pneumonia,

urinary tract infections,

sepsis, cutaneous

lesions)

Multiple myeloma Haemophilus influenza

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Streptococcus pneumoniae

Neisseria meningitides

Enterobacteriaceae

Pseudomonas

Varicella zoster virus

Candida

Aspergillus

(pneumonia, cutaneous

lesions, sepsis

Symptoms in these patients are insidious because early in the course of disease they are related to the primary

infection in the lung. Once enough purulent exudate is formed, typical physical and radiographic findings

indicative of an empyema are produced.

Laboratory diagnosis of lower Respiratory tract infections:

Specimen collection and transport:

Although rapid determination of the etiologic agent is of paramount importance in managing pneumonia, the

responsible pathogen is not identified in as many as 50% of patients, despite extensive diagnostic testing.

Sputum

Expectorated. The examination of expectorated sputum has been the primary means of determining the causes

of bacterial pneumonia. However, lower respiratory tract secretions will be contaminated with upper respiratory

tract secretions, especially saliva, unless they are collected using an invasive technique. For this reason, sputum

is among the least clinically relevant specimens received for culture in microbiology laboratories, even though

it is one of the most numerous and time-consuming specimens.

Good sputum samples: depend on thorough health care worker education and patient understanding throughout

all phases of the collection process. Food should not have been ingested for 1 to 2 hours before expectoration

and the mouth should be rinsed with saline or water just before expectoration. Patients shouldbe instructed to

provide a deep-coughed specimen.

The material should be expelled into a sterile container, with an attempt to minimize contamination by saliva.

Specimens should be transported to the laboratory immediately. Even a moderate amount of time at room

temperature can result in the loss of viable infectious agents and the recovery of pathogens.

Induced. Patients unable to produce sputum may be assisted by respiratory therapists, who use postural

drainage and thoracic percussion to stimulate production of acceptable sputum. Before specimen collection,

patients should brush the buccal mucosa, tongue, and gums with a wet toothbrush. As an alternative, an aerosolinduced specimen may be collected for the isolation of mycobacterial or fungal agents. Induced sputum is also

recognized for its high diagnostic yield in cases of Pneumocystis jiroveci pneumonia. Aerosol-induced

specimens are collected by allowing the patient to breathe aerosolized droplets, using an ultrasonic nebulizer

containing 10% 0.85% NaCl or until a strong cough reflex is initiated.