Infections of the Respiratory System (2024)

Figure 93-1

Upper and lower respiratory tract infections.

Etiology

Common colds are the most prevalent entity of all respiratory infections and arethe leading cause of patient visits to the physician, as well as work and schoolabsenteeism. Most colds are caused by viruses. Rhinoviruses with more than 100serotypes are the most common pathogens, causing at least 25% of colds inadults. Coronaviruses may be responsible for more than 10% of cases.Parainfluenza viruses, respiratory syncytial virus, adenoviruses and influenzaviruses have all been linked to the common cold syndrome. All of these organismsshow seasonal variations in incidence. The cause of 30% to 40% of cold syndromeshas not been determined.

Pathogenesis

The viruses appear to act through direct invasion of epithelial cells of therespiratory mucosa (Fig. 93-2), butwhether there is actual destruction and sloughing of these cells or loss ofciliary activity depends on the specific organism involved. There is an increasein both leukocyte infiltration and nasal secretions, including large amounts ofprotein and immunoglobulin, suggesting that cytokines and immune mechanisms maybe responsible for some of the manifestations of the common cold (Fig. 93-3).

Clinical Manifestations

After an incubation period of 48–72 hours, classic symptoms of nasaldischarge and obstruction, sneezing, sore throat and cough occur in both adultsand children. Myalgia and headache may also be present. Fever is rare. Theduration of symptoms and of viral shedding varies with the pathogen and the ageof the patient. Complications are usually rare, but sinusitis and otitis mediamay follow.

Microbiologic Diagnosis

The diagnosis of a common cold is usually based on the symptoms (lack of fevercombined with symptoms of localization to the nasopharynx). Unlike allergicrhinitis, eosinophils are absent in nasal secretions. Although it is possible toisolate the viruses for definitive diagnosis, that is rarely warranted.

Prevention and Treatment

Treatment of the uncomplicated common cold is generally symptomatic.Decongestants, antipyretics, fluids and bed rest usually suffice. Restriction ofactivities to avoid infecting others, along with good hand washing, are the bestmeasures to prevent spread of the disease. No vaccine is commercially availablefor cold prophylaxis.

Etiology

Acute sinusitis most often follows a common cold which is usually of viraletiology. Vasomotor and allergic rhinitis may also be antecedent to thedevelopment of sinusitis. Obstruction of the sinusal ostia due to deviation ofthe nasal septum, presence of foreign bodies, polyps or tumors can predispose tosinusitis. Infection of the maxillary sinuses may follow dental extractions oran extension of infection from the roots of the upper teeth. The most commonbacterial agents responsible for acute sinusitis are Streptococcuspneumoniae, Haemophilus influenzae, and Moraxellacatarrhalis. Other organisms including Staphylococcusaureus, Streptococcus pyogenes, gram-negative organisms andanaerobes have also been recovered. Chronic sinusitis is commonly a mixedinfection of aerobic and anaerobic organisms.

Pathogenesis

Infections caused by viruses or bacteria impair the ciliary activity of theepithelial lining of the sinuses and increased mucous secretions. This leads toobstruction of the paranasal sinusal ostia which impedes drainage. Withbacterial multiplication in the sinus cavities, the mucus is converted tomucopurulent exudates. The pus further irritates the mucosal lining causing moreedema, epithelial destruction and ostial obstruction. When acute sinusitis isnot resolved and becomes chronic, mucosal thickening results and the developmentof mucoceles and polyps may ensue.

Clinical Manifestations

The maxillary and ethmoid sinuses are most commonly involved in sinusitis. Thefrontal sinuses are less often involved and the sphenoid sinuses are rarelyaffected. Pain, sensation of pressure and tenderness over the affected sinus arepresent. Malaise and low grade fever may also occur. Physical examinationusually is not remarkable with no more than an edematous and hyperemic nasalmucosa.

In uncomplicated chronic sinusitis, a purulent nasal discharge is the mostconstant finding. There may not be pain nor tenderness over the sinus areas.Thickening of the sinus mucosa and a fluid level are usually seen in x-ray filmsor magnetic resonance imaging.

Microbiologic Diagnosis

For acute sinusitis, the diagnosis is made from clinical findings. A bacterialculture of the nasal discharge can be taken but is not very helpful as therecovered organisms are generally contaminated by the resident flora from thenasal passage. In chronic sinusitis, a careful dental examination, with sinusx-rays may be required. An antral puncture to obtain sinusal specimens forbacterial culture is needed to establish a specific microbiologic diagnosis.

Prevention and Treatment

Symptomatic treatment with analgesics and moist heat over the affected sinus painand a decongestant to promote sinus drainage may suffice. For antimicrobialtherapy, a beta-lactamase resistant antibiotic such as amoxicillin-clavulanateor a cephalosporin may be used. For chronic sinusitis, when conservativetreatment does not lead to a cure, irrigation of the affected sinus may benecessary. Culture from an antral puncture of the maxillary sinus can beperformed to identify the causative organism for selecting antimicrobialtherapy. Specific preventive procedures are not available. Proper care ofinfectious and/or allergic rhinitis, surgical correction to relieve or avoidobstruction of the sinusal ostia are important. Root abscesses of the upperteeth should receive proper dental care to avoid secondary infection of themaxillary sinuses.

Etiology

For otitis externa, the skin flora such as Staphylococcus epidermidis,Staphylococcus aureus, diphtheroids and occasionally an anaerobicorganism, Propionibacterium acnes are major etiologic agents.In a moist and warm environment, a diffuse acute otitis externa (Swimmer's ear)may be caused by Pseudomonas aeruginosa, along with other skinflora. Malignant otitis externa is a severe necrotizing infection usually causedby Pseudomonas aeruginosa.

For otitis media, the commonest causative bacteria are Streptococcuspneumoniae, Hemophilus influenzae and beta-lactamase producingMoraxella catarrhalis. Respiratory viruses may play a rolein otitis media but this remains uncertain. Mycoplasmapneumoniae has been reported to cause hemorrhagic bullousmyringitis in an experimental study among nonimmune human volunteers inoculatedwith M pneumoniae. However, in natural cases of Mpneumoniae infection, clinical bullous myringitis or otitis mediais uncommon.

Pathogenesis

The narrow and tortuous auditory canal is lined by a protective surfaceepithelium. Factors that may disrupt the natural protective mechanisms, such ashigh temperature and humidity, trauma, allergy, tissue maceration, removal ofcerumen and an alkaline pH environment, favor the development of otitis externa.Prolonged immersion in a swimming pool coupled with frequent ear cleansingincreases the risk of otitis externa.

Acute otitis media commonly follows an upper respiratory infection extending fromthe nasopharynx via the eustachian tube to the middle ear. Vigorous nose blowingduring a common cold, sudden changes of air pressure, and perforation of thetympanic membrane also favor the development of otitis media. The presence ofpurulent exudate in the middle ear may lead to a spread of infection to theinner ear and mastoids or even meninges

Clinical Manifestations

Diagnosis

The diagnosis of both otitis externa and otitis media can be made from history,clinical symptomatology and physical examinations. Inspection of the tympanicmembrane is an indispensable skill for physicians and health care workers. Alldischarge, ear wax and debris must be removed and to perform an adequateotoscopy. In the majority of patients, routine cultures are not necessary, as anumber of good bacteriologic studies have shown consistently the same microbialpathogens mentioned in the section of etiology. If the patient isimmunocompromised or is toxic and not responding to initial antimicrobialtherapy tympanocentesis (needle aspiration) to obtain middle ear effusion formicrobiologic culture is indicated.

Prevention and Treatment

Etiology

Pharyngitis is an inflammation of the pharynx involving lymphoid tissues of theposterior pharynx and lateral pharyngeal bands. The etiology can be bacterial,viral and fungal infections as well as noninfectious etiologies such as smoking.Most cases are due to viral infections and accompany a common cold or influenza.Type A coxsackieviruses can cause a severe ulcerative pharyngitis in children(herpangina), and adenovirus and herpes simplex virus, although less common,also can cause severe pharyngitis. Pharyngitis is a common symptom ofEpstein-Barr virus and cytomegalovirus infections.

Group A beta-hemolytic streptococcus or Streptococcus pyogenesis the most important bacterial agent associated with acute pharyngitis andtonsillitis. Corynebacterium diphtheriae causes occasionalcases of acute pharyngitis, as do mixed anaerobic infections (Vincent's angina),Corynebacterium haemolyticum, Neisseria gonorrhoeae, andChlamydia trachomatis. Outbreaks of Chlamydiapneumoniae (TWAR agent) causing pharyngitis or pneumonitis haveoccurred in military recruits. Mycoplasma pneumoniae andMycoplasma hominis have been associated with acutepharyngitis. Candida albicans, which causes oral candidiasis orthrush, can involve the pharynx, leading to inflammation and pain.

Pathogenesis

As with common cold, viral pathogens in pharyngitis appear to invade the mucosalcells of the nasopharynx and oral cavity, resulting in edema and hyperemia ofthe mucous membranes and tonsils (Fig93-2). Bacteria attach to and, in the case of group A beta-hemolyticstreptococci, invade the mucosa of the upper respiratory tract. Many clinicalmanifestations of infection appear to be due to the immune reaction to productsof the bacterial cell. In diphtheria, a potent bacterial exotoxin causes localinflammation and cell necrosis.

Clinical Manifestations

Pharyngitis usually presents with a red, sore, or “scratchy”throat. An inflammatory exudate or membranes may cover the tonsils and tonsillarpillars. Vesicles or ulcers may also be seen on the pharyngeal walls. Dependingon the pathogen, fever and systemic manifestations such as malaise, myalgia, orheadache may be present. Anterior cervical lymphadenopathy is common inbacterial pharyngitis and difficulty in swallowing may be present.

Microbiologic Diagnosis

The goal in the diagnosis of pharyngitis is to identify cases that are due togroup A beta-hemolytic streptococci, as well as the more unusual and potentiallyserious infections. The various forms of pharyngitis cannot be distinguished onclinical grounds. Routine throat cultures for bacteria are inoculated onto sheepblood and chocolate agar plates. Thayer-Martin medium is used if Ngonorrhoeae is suspected. Viral cultures are not routinely obtainedfor most cases of pharyngitis. Serologic studies may be used to confirm thediagnosis of pharyngitis due to viral, mycoplasmal or chlamydial pathogens.Rapid diagnostic tests with fluorescent antibody or latex agglutination toidentify group A streptococci from pharyngeal swabs are available. Gene probeand polymerase chain reaction can be used to detect unusual organisms such asM pneumoniae, chlamydia or viruses but these procedures arenot routine diagnostic methods.

Prevention and Treatment

Symptomatic treatment is recommended for viral pharyngitis. The exception isherpes simplex virus infection, which can be treated with acyclovir ifclinically warranted or if diagnosed in immunocompromised patients. The specificantibacterial agents will depend on the causative organism, but penicillin G isthe therapy of choice for streptococcal pharyngitis. Mycoplasma and chlamydialinfections respond to erythromycin, tetracyclines and the new macrolides.

Etiology

Inflammation of the upper airway is classified as epiglottitis orlaryngotracheitis (croup) on the basis of the location, clinical manifestations,and pathogens of the infection. Haemophilus influenzae type bis the most common cause of epiglottitis, particularly in children age 2 to 5years. Epiglottitis is less common in adults. Some cases of epiglottitis inadults may be of viral origin. Most cases of laryngotracheitis are due toviruses. More serious bacterial infections have been associated with Hinfluenzae type b, group A beta-hemolytic streptococcus andC diphtheriae. Parainfluenza viruses are most common butrespiratory syncytial virus, adenoviruses, influenza viruses, enteroviruses andMycoplasma pneumoniae have been implicated.

Pathogenesis

A viral upper respiratory infection may precede infection with Hinfluenzae in episodes of epiglottitis. However, once Hinfluenzae type b infection starts, rapidly progressive erythemaand swelling of the epiglottis ensue, and bacteremia is usually present. Viralinfection of laryngotracheitis commonly begins in the nasopharynx and eventuallymoves into the larynx and trachea. Inflammation and edema involve theepithelium, mucosa and submucosa of the subglottis which can lead to airwayobstruction.

Clinical Manifestations

The syndrome of epiglottitis begins with the acute onset of fever, sore throat,hoarseness, drooling, dysphagia and progresses within a few hours to severerespiratory distress and prostration. The clinical course can be fulminant andfatal. The pharynx may be inflamed, but the diagnostic finding is a“cherry-red” epiglottis.

A history of preceding cold-like symptoms is typical of laryngotracheitis, withrhinorrhea, fever, sore throat and a mild cough. Tachypnea, a deep barking coughand inspiratory stridor eventually develop. Children with bacterial tracheitisappear more ill than adults and are at greater risk of developing airwayobstruction.

Haemophilus influenzae type b is isolated from the blood orepiglottis in the majority of patients with epiglottis; therefore a bloodculture should always be performed. Sputum cultures or cultures from pharyngealswabs may be used to isolate pathogens in patients with laryngotracheitis.Serologic studies to detect a rise in antibody titers to various viruses arehelpful for retrospective diagnosis. Newer, rapid diagnostic techniques, usingimmunofluorescent-antibody staining to detect virus in sputum, pharyngeal swabs,or nasal washings, have been successfully used. Enzyme-linked immunosorbentassay (ELISA), DNA probe and polymerase chain reaction procedures for detectionof viral antibody or antigens are now available for rapid diagnosis.

Prevention and Treatment

Epiglottitis is a medical emergency, especially in children. All children withthis diagnosis should be observed carefully and be intubated to maintain an openairway as soon as the first sign of respiratory distress is detected.Antibacterial therapy should be directed at H influenzae.Patients with croup are usually successfully managed with close observation andsupportive care, such as fluid, humidified air, and racemic epinephrine. Forprevention, Haemophilus influenzae type b conjugated vaccine isrecommended for all pediatric patients, as is immunization againstdiphtheria.

Etiology

Bronchitis and bronchiolitis involve inflammation of the bronchial tree.Bronchitis is usually preceded by an upper respiratory tract infection or formspart of a clinical syndrome in diseases such as influenza, rubeola, rubella,pertussis, scarlet fever and typhoid fever. Chronic bronchitis with a persistentcough and sputum production appears to be caused by a combination ofenvironmental factors, such as smoking, and bacterial infection with pathogenssuch as H influenzae and S pneumoniae.Bronchiolitis is a viral respiratory disease of infants and is caused primarilyby respiratory syncytial virus. Other viruses, including parainfluenza viruses,influenza viruses and adenoviruses (as well as occasionally Mpneumoniae) are also known to cause bronchiolitis.

Pathogenesis

When the bronchial tree is infected, the mucosa becomes hyperemic and edematousand produces copious bronchial secretions. The damage to the mucosa can rangefrom simple loss of mucociliary function to actual destruction of therespiratory epithelium, depending on the organisms(s) involved. Patients withchronic bronchitis have an increase in the number of mucus-producing cells intheir airways, as well as inflammation and loss of bronchial epithelium, Infantswith bronchiolitis initially have inflammation and sometimes necrosis of therespiratory epithelium, with eventual sloughing. Bronchial and bronchiolar wallsare thickened. Exudate made up of necrotic material and respiratory secretionsand the narrowing of the bronchial lumen lead to airway obstruction. Areas ofair trapping and atelectasis develop and may eventually contribute torespiratory failure.

Clinical Manifestations

Symptoms of an upper respiratory tract infection with a cough is the typicalinitial presentation in acute bronchitis. Mucopurulent sputum may be present,and moderate temperature elevations occur. Typical findings in chronicbronchitis are an incessant cough and production of large amounts of sputum,particularly in the morning. Development of respiratory infections can lead toacute exacerbations of symptoms with possibly severe respiratory distress.

Coryza and cough usually precede the onset of bronchiolitis. Fever is common. Adeepening cough, increased respiratory rate, and restlessness follow.Retractions of the chest wall, nasal flaring, and grunting are prominentfindings. Wheezing or an actual lack of breath sounds may be noted. Respiratoryfailure and death may result.

Microbiologic Diagnosis

Bacteriologic examination and culture of purulent respiratory secretions shouldalways be performed for cases of acute bronchitis not associated with a commoncold. Patients with chronic bronchitis should have their sputum cultured forbacteria initially and during exacerbations. Aspirations of nasopharyngealsecretions or swabs are sufficient to obtain specimens for viral culture ininfants with bronchiolitis. Serologic tests demonstrating a rise in antibodytiter to specific viruses can also be performed. Rapid diagnostic tests forantibody or viral antigens may be performed on nasopharyngeal secretions byusing fluorescent-antibody staining, ELISA or DNA probe procedures.

Prevention and Treatment

With only a few exceptions, viral infections are treated with supportivemeasures. Respiratory syncytial virus infections in infants may be treated withribavirin. Amantadine and rimantadine are available for chemoprophylaxis ortreatment of influenza type A viruses. Selected groups of patients with chronicbronchitis may receive benefit from use of corticosteroids, bronchodilators, orprophylactic antibiotics.

Pneumonia

Pneumonia is an inflammation of the lung parenchyma (Fig 93-4). Consolidation of the lung tissue may beidentified by physical examination and chest x-ray. From an anatomical point ofview, lobar pneumonia denotes an alveolar process involving an entire lobe ofthe lung while bronchopneumonia describes an alveolar process occurring in adistribution that is patchy without filling an entire lobe. Numerous factors,including environmental contaminants and autoimmune diseases, as well asinfection, may cause pneumonia. The various infectious agents that causepneumonia are categorized in many ways for purposes of laboratory testing,epidemiologic study and choice of therapy. Pneumonias occurring in usuallyhealthy persons not confined to an institution are classified ascommunity-acquired pneumonias. Infections arise while a patient is hospitalizedor living in an institution such as a nursing home are called hospital-acquiredor nosocomial pneumonias. Etiologic pathogens associated with community-acquiredand hospital-acquired pneumonias are somewhat different. However, many organismscan cause both types of infections.

Etiology

Pathogenesis and Clinical Manifestations

Infectious agents gain access to the lower respiratory tract by the inhalation ofaerosolized material, by aspiration of upper airway flora, or by hematogenousseeding. Pneumonia occurs when lung defense mechanisms are diminished oroverwhelmed. The major symptoms or pneumonia are cough, chest pain, fever,shortness of breath and sputum production. Patients are tachycardic. Headache,confusion, abdominal pain, nausea, vomiting and diarrhea may be present,depending on the age of the patient and the organisms involved.

Microbiologic Diagnosis

Etiologic diagnosis of pneumonia on clinical grounds alone is almost impossible.Sputum should be examined for a predominant organism in any patient suspected tohave a bacterial pneumonia; blood and pleural fluid (if present) should becultured. A sputum specimen with fewer than 10 while cells per high-power fieldunder a microscope is considered to be contaminated with oral secretions and isunsatisfactory for diagnosis. Acid-fast stains and cultures are used to identifyMycobacterium and Nocardia spp. Mostfungal pneumonias are diagnosed on the basis of culture of sputum or lungtissue. Viral infection may be diagnosed by demonstration of antigen insecretions or cultures or by an antibody response. Serologic studies can be usedto identify viruses, M pneumoniae, C. burnetii, Chlamydia species,Legionella, Francisella, and Yersinia. A rise inserum cold agglutinins may be associated with M pneumoniaeinfection, but the test is positive in only about 60% of patients with thispathogen.

Rapid diagnostic tests, as described in previous sections, are available toidentify respiratory viruses: the fluorescent-antibody test is used forLegionella. A sputum quellung test can specify Spneumoniae by serotype. Enzyme-linked immunoassay, DNA probe andpolymerase chain reaction methods are available for many agents causingrespiratory infections.

Some organisms that may colonize the respiratory tract are considered to bepathogens only when they are shown to be invading the parenchyma. Diagnosis ofpneumonia due to cytomegalovirus, herpes simplex virus,Aspergillus spp. or Candida spp requirespecimens obtained by transbronchial or open-lung biopsy. Pneumocystiscarinii can be found by silver stain of expectorated sputum.However, if the sputum is negative, deeper specimens from the lower respiratorytract obtained by bronchoscopy or by lung biopsy are needed for confirmatorydiagnosis.

Prevention and Treatment

Until the organism causing the infection is identified, decisions on therapy arebased upon clinical history, including history of exposure, age, underlyingdisease and previous therapies, past pneumonias, geographic location, severityof illness, clinical symptoms, and sputum examination. Once a diagnosis is made,therapy is directed at the specific organism responsible.

The pneumococcal vaccine should be given to patients at high risk for developingpneumococcal infections, including asplenic patients, the elderly and anypatients immunocompromised through disease or medical therapy. Yearly influenzavaccinations should also be provided for these particular groups. Anenteric-coated vaccine prepared from certain serotypes of adenoviruses isavailable, but is only used in military recruits. In AIDS patients,trimethoprim/sulfamethoxazole, aerosolized pentamidine or other antimicrobialscan be given for prophylaxis of Pneumocystis cariniiinfections.