Lower and Upper Respiratory Tract Bacteriology

Most respiratory specimens pass through heavily colonized airways before reaching the laboratory, so growth does not by itself identify a pathogen. Workup and reporting depend on whether the specimen represents the stated site and whether recovered organisms exceed expected colonization. Pathogens that do not grow on routine media require a specific request or molecular assay. General transport rules, Gram-stain mechanics, media, incubation, and the staged reporting cycle are covered in Specimen Collection, Transport, and Primary Processing in Microbiology.

Selecting lower respiratory specimens for culture

Sputum culture has limited value in mild community-acquired pneumonia, so it is targeted rather than routine. In hospitalized adults, a pretreatment lower respiratory Gram stain and culture is recommended for severe pneumonia, for patients being treated empirically for methicillin-resistant Staphylococcus aureus or Pseudomonas aeruginosa, for patients with prior respiratory isolation of either organism, and for patients hospitalized and given parenteral antimicrobials within the previous 90 days. When the patient is intubated, an endotracheal aspirate collected promptly after intubation gives better yield than expectorated sputum.¹ Negative results from these cultures support narrowing or stopping broad empiric coverage.¹

Lower respiratory specimens include expectorated or induced sputum, tracheal aspirate, bronchoalveolar lavage (BAL) fluid, protected-brush specimens, and bronchial washings.²,³

Expectorated sputum is best collected early in the morning before eating, after the patient rinses the mouth with water and produces a deep-cough specimen of 5 to 10 mL. A nonproductive cough can be induced with aerosolized saline. An induced specimen is thin and watery and can be mistaken for saliva on appearance alone, so the requisition identifies it as induced and the laboratory screens it accordingly.³

Sputum collected for mycobacterial culture follows different rules. At least three specimens are collected, 8 to 24 hours apart, with at least one taken early in the morning.⁴ The patient must not rinse the mouth with tap water first, because a water rinse can introduce environmental mycobacteria such as Mycobacterium gordonae or the M. avium-intracellulare complex and seed the specimen with organisms that imitate a true pathogen.³

Screening sputum for adequacy

Sputum passes through the oropharynx, so a screening Gram stain assesses whether it contains lower respiratory secretions or mostly saliva. More than 25 squamous epithelial cells per low-power field indicate significant salivary contamination, and the specimen is rejected as unrepresentative. Fewer than 25 squamous epithelial cells with more than 25 neutrophils per low-power field is acceptable. Report the rejection and its reason, and request a fresh specimen.²,³

Neutrophil numbers alone never decide acceptability. A neutropenic patient can have genuine bacterial pneumonia without the cell count to prove it.³

The screen applies to routine bacterial culture and not to every request on the same specimen. Mycobacterial, fungal, and Pneumocystis requests are processed regardless of the squamous cell count. For suspected legionellosis, a lower respiratory specimen should not be rejected because it appears contaminated or contains few leukocytes, since Legionella recovery does not depend on those features.⁵,³

Indigenous flora of the mouth and upper airway

Recognizing indigenous oral and upper-airway flora prevents colonizers from being worked up as pathogens. These organisms account for most growth on throat cultures.

Mixed flora of this kind is expected in specimens that pass through the mouth and does not alone make the specimen unacceptable. Squamous epithelial cells are the best marker of oral contamination. Numerous squamous cells with mixed flora and few or no neutrophils indicate saliva.³

Bronchoscopy specimens

BAL fluid and protected-brush specimens are used for acute bacterial pneumonia, for ventilator-associated pneumonia in patients not yet treated, for opportunistic pathogens in immunocompromised patients, and for mycobacterial infection when a patient cannot produce sputum.³

A protected-brush specimen is collected through a double-cannula catheter holding only 0.001 to 0.01 mL of secretions. A displaceable plug seals the outer cannula until it reaches the sampling site. The brush and inner cannula retract into it before withdrawal to prevent upper-airway flora from contaminating the brush during passage. Place the brush in 1 mL of sterile saline or broth for transport.³

BAL is performed by wedging the bronchoscope tip into an airway and instilling sterile saline in three or four aliquots, commonly more than 140 mL in total, which samples an estimated one million alveoli. Between 10 and 100 mL usually returns. The fluid should reach the laboratory within 30 minutes, because carryover from the procedure inhibits some bacteria; refrigeration limits that loss only partly when a delay is unavoidable.³

BAL fluid is vortexed for culture inoculation and cytocentrifuge preparations. Small tissue fragments are kept moist in sterile saline and processed separately. Viscous fluid suspected of harboring fungi, including Pneumocystis jirovecii, is treated with a mucolytic agent and centrifuged before staining. A Gram-stained cytospin showing one or more bacteria per oil-immersion field and no squamous epithelial cells strongly suggests acute bacterial pneumonia. A Papanicolaou-stained cytospin can show the cytopathic inclusions of cytomegalovirus pneumonia. Acid-fast and organism-specific antibody stains on cytospins extend testing to mycobacteria and targets such as Legionella species.³

Quantitative thresholds for lower respiratory cultures

Quantitative culture was introduced to raise specificity, but published trials in intubated patients have not shown better outcomes than qualitative or semiquantitative culture. Current guidance recommends noninvasive sampling with semiquantitative culture over invasive sampling with quantitative culture, so the method in use is set by local practice.⁶ Where quantitative culture is performed, plates are inoculated by serial dilution or calibrated loop and colony counts are compared with a threshold.

Growth below the applicable threshold is interpreted as airway colonization or upper-airway contamination even when a recognized respiratory pathogen is recovered.⁶,⁷ Antimicrobial therapy before collection can falsely lower the count. Contamination during passage through the endotracheal tube or bronchoscope can falsely raise it. Interpret the count with the Gram stain and clinical findings.⁶

Processing for mycobacteria, fungi, and Pneumocystis

Routine bacterial workup follows the general Gram stain and culture pathway. Mycobacterial workup adds decontamination and digestion to suppress faster-growing respiratory flora. All handling occurs in a biological safety cabinet, ideally in a negative-pressure room under biosafety level 3 practices.⁴,³ Fungal workup uses the same containment. Media may include blood enrichment and antimicrobial supplementation according to cost and the species expected in the local patient population.³

For P. jirovecii direct fluorescent antibody staining, a viscous specimen is first liquefied with a mucolytic agent such as N-acetyl-L-cysteine or dithiothreitol and vortexed vigorously, then centrifuged. The sediment is smeared, fixed according to the stain manufacturer’s instructions, and examined microscopically.³

Pathogens recovered on routine respiratory media

Streptococcus pneumoniae and Haemophilus influenzae are identified from respiratory specimens by the same methods used for blood isolates. Their characteristics, X and V factor differentiation, and related species are covered in Blood Cultures and Gram-Positive Blood Isolates and Gram-Negative, Fastidious, and Vector-Borne Agents of Bloodstream Infection.

Molecular targets such as lytA, plyA, penicillin-binding protein genes, pneumococcal surface protein A, and the DNA polymerase gene identify S. pneumoniae at the species level. In a respiratory specimen, however, a positive result cannot separate infection from asymptomatic colonization, which is especially common in children. A pneumococcal urinary antigen assay is used in some settings as a nonculture adjunct in adults with severe pneumococcal pneumonia.²,³

Moraxella catarrhalis is an encapsulated gram-negative diplococcus carried in the oropharynx of healthy children and adults. It adheres through outer-membrane pili and causes bronchitis, otitis media, sinusitis, and pneumonia, particularly in patients with chronic lung disease. Bacteremia, endocarditis, meningitis, and ophthalmia neonatorum are rare. On Gram stain, it is indistinguishable from Neisseria. It grows on plain blood agar, unlike N. gonorrhoeae, and does not oxidatively utilize carbohydrates. All sugar reactions are negative, in contrast to the glucose-positive Neisseria species, and the DNase reaction is positive. Nearly all isolates produce beta-lactamase, detectable with nitrocefin, and are presumed penicillin resistant.³

Pathogens missed by routine culture

Legionella species

Legionella species are obligately aerobic, faintly staining, small gram-negative bacilli first recognized in the 1976 Philadelphia pneumonia outbreak. More than 60 species are recognized, and L. pneumophila serogroup 1 causes most disease. The organisms persist in cooling towers, water heaters, warm-water spas, faucets, shower heads, and other water systems. They also survive inside environmental protozoa, including Acanthamoeba and Naegleria, which contributes to persistence between outbreaks. Aerosolized contaminated water transmits infection; person-to-person spread does not occur. Disease ranges from subclinical infection to severe fibrinopurulent pneumonia caused by intracellular infection of alveolar macrophages.³

Isolation requires buffered charcoal yeast extract (BCYE) agar supplemented with L-cysteine, ferric salt, and alpha-ketoglutarate. Selective supplements such as cefamandole, polymyxin B, and anisomycin, or polymyxin B, anisomycin, and vancomycin, suppress contaminating flora in nonsterile specimens. Weak-acid or heat pretreatment of sputum reduces contamination, but overtreatment also lowers Legionella recovery. Incubate plates for 5 to 14 days in a humid, low-carbon-dioxide atmosphere. Colonies are iridescent and sticky. Failure to grow after subculture to BCYE without cysteine or to blood agar confirms the absolute cysteine requirement.³ Routine respiratory media do not recover Legionella, so culture must be requested specifically.⁵

Current testing pairs a urinary antigen test with a lower respiratory specimen for culture or a molecular assay, collected concurrently and before antimicrobials when possible.

Assay performance varies with timing, specimen quality, prior therapy, and design. A negative urinary antigen result therefore does not exclude legionellosis when clinical suspicion is high; send a lower respiratory specimen for culture or a molecular assay.⁵

Routine susceptibility testing is not performed for Legionella. The organism is intracellular in vivo, growth-supporting media inactivate many antimicrobials, and no CLSI susceptibility method exists, so in vitro results do not predict clinical response. Macrolides and fluoroquinolones reach adequate intracellular concentrations and are the treatments of choice. Serology supports a retrospective diagnosis through a fourfold rise to a titer of 1:128 or more. A single titer of 1:256 or more is presumptive evidence of past infection, but the need for paired sera limits serology during acute illness.³

Mycoplasma pneumoniae

Mycoplasmas are the smallest self-replicating bacteria and lack a cell wall. They cannot synthesize peptidoglycan precursors and require cholesterol for membrane synthesis. The absent cell wall makes them inherently resistant to beta-lactams and other cell-wall-active agents, while growth in vitro requires complex media supplemented with cholesterol and nucleic acid precursors. M. pneumoniae attaches to respiratory epithelium through a terminal attachment organelle. Its P1 surface protein binds neuraminic-acid-containing glycoproteins, after which the organism evades phagocytosis and modulates the host response. A generation time near 6 hours and relatively low transmissibility usually produce slow spread. Point-source outbreaks still occur in confined populations such as schools and military recruits and recur roughly every 3 to 5 years.⁸

Tracheobronchitis is the most common presentation and occurs in about half of infected patients after an incubation period of several weeks. Pneumonia develops most often in children 5 to 15 years old. Extrapulmonary disease affects a minority of patients and can predominate when respiratory symptoms are mild. Manifestations include hemolytic anemia from high-titer cold agglutinins, dermatologic reactions that can resemble Stevens-Johnson syndrome, myocarditis, pericarditis, and encephalitis.⁸

Nucleic acid amplification is now the routine diagnostic method. Culture is slow and impractical, serology requires paired acute and convalescent specimens for reliable interpretation, and cold agglutinin titers lack sufficient sensitivity and specificity when used alone.⁸,²

Chlamydia pneumoniae and C. psittaci

C. pneumoniae, formerly Chlamydophila pneumoniae, is an obligate intracellular pathogen responsible for roughly 10% of community-acquired pneumonia. Infection is often mild or subclinical and may begin with pharyngitis and hoarseness before progressing to cough and a single subsegmental infiltrate. Older or chronically ill patients can have more severe disease. Culture is impractical in routine laboratories, and nucleic acid amplification of a respiratory specimen is preferred.⁹

C. psittaci causes psittacosis after inhalation of aerosols from the droppings, feathers, or secretions of infected birds, most often pet or agricultural birds. Person-to-person transmission has not been documented. After an incubation of 1 to 2 weeks, illness can include fever, dry cough, relative bradycardia, and severe headache; destructive endocarditis is rare. Diagnosis usually combines serology with a compatible bird-exposure history. Nucleic acid amplification is used where available. Culture is hazardous to laboratory personnel and is restricted to properly equipped laboratories.¹⁰

Bordetella pertussis and B. parapertussis

Both organisms are strictly aerobic, catalase-positive, small gram-negative coccobacilli that oxidize amino acids instead of fermenting sugars, and both spread by respiratory droplets. B. pertussis causes whooping cough and is considered a strictly human pathogen. B. parapertussis usually causes a milder, shorter pertussis-like illness. Pertussis toxin induces lymphocytosis and suppresses neutrophil and macrophage chemotaxis and oxidative killing. These effects suppress innate defenses at the epithelial attachment site. Other virulence factors include filamentous hemagglutinin, fimbriae, and pertactin. Testing requires a nasopharyngeal specimen. Susceptibility testing is not routine, and its methods are not standardized.³

Mycobacterium tuberculosis complex

Fluorochrome staining is more sensitive than Kinyoun or Ziehl-Neelsen carbol-fuchsin staining but still requires roughly 10⁴ organisms per milliliter. Lower organism burdens can therefore produce smear-negative disease. Nucleic acid amplification detects organisms directly in the specimen before culture becomes positive and is more sensitive than smear microscopy.⁴,³

Nasopharyngeal specimens

Nasopharyngeal specimens are used mainly for viral respiratory diagnosis by rapid molecular methods. The site is also sampled for B. pertussis, Chlamydia trachomatis, C. pneumoniae, and, rarely, Corynebacterium diphtheriae. Anterior-nares specimens screen for MRSA carriage. Endoscopically or surgically obtained sinus specimens are submitted for chronic or complicated sinusitis, which typically involves S. aureus, gram-negative bacilli, streptococci, anaerobes, or fungi.²,³

Aspirates and washings recover viruses better than swabs, but swabs are collected far more often for convenience. An aspirate is obtained through a small feeding-tube-style catheter attached to a 1-mL syringe or a mucus-trap suction catheter. A wash instills and withdraws 3 to 7 mL of sterile phosphate-buffered saline with a rubber suction bulb. A swab specimen is collected by clearing nasal mucus, passing a small flexible nasopharyngeal swab along the septum to the posterior pharynx, and rotating it against the mucosa. Swabs for molecular testing must have a plastic shaft and a polyester (Dacron), rayon, or nylon tip. Cotton and calcium alginate inhibit amplification, and cotton is toxic to B. pertussis.¹¹,³

Specimens collected for viral testing go into the appropriate transport medium and travel promptly, with brief refrigeration and packing in ice if a short delay cannot be avoided. When a molecular assay will be run, the manufacturer’s collection instructions govern the swab, the medium, and the holding conditions.³

Pertussis testing

The specimen must come from the posterior nasopharynx, not the throat or the anterior nares, and a flocked swab or an aspirate is preferred because it recovers more bacterial DNA. Polymerase chain reaction is faster and more sensitive than culture, while culture is the more specific method and is the only one that yields an isolate for susceptibility testing and molecular epidemiology. Culture sensitivity is highest within the first 2 weeks after cough onset, and PCR remains useful through about 3 to 4 weeks. After roughly 4 weeks of cough, or about 5 days of therapy, a negative result carries little weight and does not exclude pertussis.¹²,¹¹

Transport handling differs by method. For culture, the specimen is plated directly as soon as possible, or placed in half-strength Regan-Lowe transport medium, or in Amies charcoal gel when the receiving laboratory accepts it; plating should occur within 24 hours, and specimens are held and shipped at 2 to 8 degrees Celsius. For PCR alone, a dry sterile tube or the performing laboratory’s approved medium is used. Routine liquid transport media are discouraged, because DNA released from a contaminated swab shaft into the liquid produces false-positive results.¹²,¹¹

Cultures are plated onto Regan-Lowe or freshly prepared Bordet-Gengou agar, often with an antibiotic such as cephalexin to suppress contaminants, and incubated at least 7 days at 35 to 37 degrees Celsius in humid ambient air. B. pertussis colonies are small, smooth, and glistening, described as resembling mercury drops, and do not grow on blood agar. A positive catalase and oxidase reaction with a negative urease presumptively identifies B. pertussis, while B. parapertussis grows faster, shows variable growth on Columbia agar, and is oxidase negative with catalase and urease both positive.³ Direct fluorescent antibody staining of a nasopharyngeal smear returns a rapid result but carries meaningful false-positive and false-negative rates, and PCR has replaced it.³

IS481 is a multicopy insertion sequence with high analytical sensitivity but is not specific for B. pertussis because B. holmesii and B. bronchiseptica also carry it. IS1001 targets B. parapertussis, and the pertussis toxin promoter improves species discrimination. Multitarget assays are therefore preferred. Limit testing to symptomatic patients; do not test asymptomatic contacts to guide prophylaxis. A high cycle-threshold value indicates little target DNA and is more vulnerable to contamination, although it may still represent true infection. Interpret it with cough duration, therapy, vaccination history, and exposure history.¹¹

Other nasopharyngeal targets

A polyester-tipped nasopharyngeal swab supports either culture or a direct fluorescent antibody smear for C. trachomatis. For C. pneumoniae, the swab goes into transport medium and travels promptly, with brief refrigeration if needed, and nucleic acid amplification is the recommended detection method.⁹,³

For suspected diphtheria, swabbing multiple nasopharyngeal sites, including beneath any visible membrane, raises sensitivity. Specimens should reach the laboratory immediately or be held in semisolid Amies transport medium if a delay is unavoidable. Tinsdale medium, a tellurite-containing differential medium, gives the best yield but is expensive, has a short shelf life, and is not always available. Laboratories without experience in recovering and identifying C. diphtheriae refer these specimens rather than stock the medium.³

MRSA carriage screening uses a polyester-tipped swab of the anterior nares in a tube transport system, delivered promptly. Detection is by a commercial molecular assay, which returns a result in a few hours, or by culture on MRSA-selective chromogenic agar in 24 to 48 hours. When a molecular assay is used, the swab specified by the manufacturer is required.²,³

Throat specimens

Throat swabbing is contraindicated when epiglottitis is suspected, because of the risk of aspiration and airway obstruction.³

Group A streptococcus causes fewer than one-third of pharyngitis cases but is sought to prevent acute rheumatic fever and suppurative complications and to interrupt transmission. Other bacterial targets with a clear treatment benefit are C. diphtheriae and Neisseria gonorrhoeae. Groups C and G streptococci also cause pharyngitis, although the benefit of identifying them specifically is less established. Herpes simplex virus, cytomegalovirus, enteroviruses, and other viruses shed in oral secretions may be recovered without causing the pharyngitis. Testing is not indicated when cough, rhinorrhea, hoarseness, oral ulcers, conjunctivitis, or other findings point to a viral cause.¹³,¹⁴

For throat collection, depress the tongue and pass the swab between the tonsillar pillars and behind the uvula without touching the buccal mucosa. Swab the posterior pharynx back and forth. Bacterial culture swabs go into modified Stuart transport medium; viral specimens go into viral transport medium. N. gonorrhoeae requires a plastic-shafted Dacron, rayon, or nylon swab. Fatty acids in cotton and some calcium alginate lots kill gonococci, and calcium alginate also inhibits amplification.³

Detecting group A streptococcus

Culture on sheep or horse blood agar remains a sensitive method and shows complete beta-hemolysis, but it requires overnight incubation. Rapid antigen detection tests give a same-visit result with high specificity, so a positive result needs no confirmatory culture, but their sensitivity is lower. A negative rapid antigen test in a child 3 years or older is therefore backed up with culture or a validated molecular test, while adults do not need routine backup culture because their baseline risk of rheumatic fever is low.¹³,¹⁴ A validated nucleic acid amplification test is the most sensitive rapid option, and some platforms are waived under CLIA for point-of-care use. When such an assay is the primary test, a negative result generally stands without reflex culture.²,¹⁴

Other throat targets

Pharyngeal gonococcal infection is detected by nucleic acid amplification using an assay cleared or validated for that site, which is more sensitive than culture. Culture on a selective medium such as modified Thayer-Martin is still used where an isolate is needed for susceptibility testing, and the plate is inoculated as promptly as possible to maximize yield.¹⁵,³ For suspected diphtheria, both nasopharyngeal and throat swabs are collected and delivered immediately.³

Vincent’s angina, an acute necrotizing ulcerative tonsillitis caused by mixed oral fusobacteria and spirochetes, classically Fusobacterium nucleatum and Treponema vincentii, is diagnosed presumptively on a Gram-stained smear of the ulcerated lesion that shows fusiform gram-negative bacilli together with spirochetes. The dense mixed anaerobic flora normally present in the mouth makes culture unhelpful, so smear morphology carries the diagnosis. Blood cultures are reserved for systemic illness, and F. necrophorum sepsis is associated with Lemierre syndrome.¹⁶,³

Reading a throat culture selectively

Because throat flora is dense and mixed, the plate is read for specific organisms rather than identified colony by colony. It is examined for beta-hemolytic streptococci and, when the request or the colony morphology suggests them, for N. gonorrhoeae, C. diphtheriae, or Arcanobacterium haemolyticum. Growth of the expected mixed flora, with none of those organisms present in excess, is reported as normal respiratory or oral flora. Identifying every colony type to genus and species adds cost without changing patient care.³,¹³

Molecular detection targets

Matrix-assisted laser desorption/ionization time-of-flight mass spectrometry can identify mycobacteria after an isolate is available. The waxy cell wall requires additional preparation. Bead beating or boiling-water lysis also inactivates the culture and reduces aerosol risk. Ethanol extraction, drying, and resuspension in formic acid and acetonitrile prepare the sample before its spectrum is matched against a reference database.³

References

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2. Miller JM, Binnicker MJ, Campbell S, et al. Guide to utilization of the microbiology laboratory for diagnosis of infectious diseases: 2024 update by the Infectious Diseases Society of America and the American Society for Microbiology. Clin Infect Dis. Published online March 5, 2024. doi:10.1093/cid/ciae104
3. Carroll KC, Pfaller MA, Landry ML, McAdam AJ, Karlowsky JA, Patel R, Pritt BS, eds. Manual of Clinical Microbiology. 13th ed. ASM Press; 2023.
4. Lewinsohn DM, Leonard MK, LoBue PA, et al. Official American Thoracic Society/Infectious Diseases Society of America/Centers for Disease Control and Prevention clinical practice guidelines: diagnosis of tuberculosis in adults and children. Clin Infect Dis. 2017;64(2):e1-e33. doi:10.1093/cid/ciw694
5. Centers for Disease Control and Prevention. Laboratory testing for Legionella. Accessed August 30, 2026.
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7. Centers for Disease Control and Prevention. Pneumonia (ventilator-associated and non-ventilator-associated) event. In: National Healthcare Safety Network Patient Safety Component Manual. Accessed August 30, 2026.
8. Waites KB, Talkington DF. Mycoplasma pneumoniae and its role as a human pathogen. Clin Microbiol Rev. 2004;17(4):697-728. doi:10.1128/CMR.17.4.697-728.2004
9. Kumar S, Hammerschlag MR. Acute respiratory infection due to Chlamydia pneumoniae: current status of diagnostic methods. Clin Infect Dis. 2007;44(4):568-576. doi:10.1086/511076
10. Balsamo G, Maxted AM, Midla JW, et al. Compendium of measures to control Chlamydia psittaci infection among humans (psittacosis) and pet birds (avian chlamydiosis), 2017. J Avian Med Surg. 2017;31(3):262-282. doi:10.1647/217-265
11. Centers for Disease Control and Prevention. Best practices for use of polymerase chain reaction for diagnosing pertussis. Accessed August 30, 2026.
12. Centers for Disease Control and Prevention. Laboratory testing for pertussis. Accessed August 30, 2026.
13. Shulman ST, Bisno AL, Clegg HW, et al. Clinical practice guideline for the diagnosis and management of group A streptococcal pharyngitis: 2012 update by the Infectious Diseases Society of America. Clin Infect Dis. 2012;55(10):e86-e102. doi:10.1093/cid/cis629
14. Centers for Disease Control and Prevention. Clinical guidance for group A streptococcal pharyngitis. Accessed August 30, 2026.
15. Workowski KA, Bachmann LH, Chan PA, et al. Sexually transmitted infections treatment guidelines, 2021. MMWR Recomm Rep. 2021;70(RR-4):1-187. doi:10.15585/mmwr.rr7004a1
16. Riordan T. Human infection with Fusobacterium necrophorum (necrobacillosis), with a focus on Lemierre's syndrome. Clin Microbiol Rev. 2007;20(4):622-659. doi:10.1128/CMR.00011-07