Purushothama V. Dasaraju
1. Upper Respiratory Infections: Common Cold, Sinusitis, Pharyngitis, Epiglottitis and Laryngotracheitis:
Etiology: Most upper respiratory infections are of viral etiology. Epiglottitis and laryngotracheitis are exceptions with severe cases likely caused by Haemophilus influenzae type b. Bacterial pharyngitis is often caused by Streptococcus pyogenes (Table 1).
Pathogenesis: Organisms gain entry to the respiratory tract by inhalation of droplets and invade the mucosa. Epithelial destruction may ensue, along with redness, edema, hemorrhage and sometimes an exudate.
Clinical Manifestations: Initial symptoms of a cold are runny, stuffy nose and sneezing, usually without fever. Other upper respiratory infections may have fever. Children with epiglottitis may have difficulty in breathing, muffled speech, drooling and stridor. Children with serious laryngotracheitis (croup) may also have tachypnea, stridor and cyanosis.
Microbiologic Diagnosis: Common colds can usually be recognized clinically. Bacterial and viral cultures of throat swab specimens are used for pharyngitis, epiglottitis and laryngotracheitis. Blood cultures are also obtained in cases of epiglottitis.
Prevention and Treatment: Viral infections are treated symptomatically. Streptococcal pharyngitis and epiglottitis caused by H influenzae are treated with antibacterials. Haemophilus influenzae type b vaccine is commercially available and is now a basic component of childhood immunization program.
2. Lower Respiratory Infections: Bronchitis, Bronchiolitis and Pneumonia:
Etiology: Causative agents of lower respiratory infections are viral or bacterial. Viruses cause most cases of bronchitis and bronchiolitis. In community-acquired pneumonias, the most common bacterial agent is Streptococcus pneumoniae. Atypical pneumonias are cause by such agents as Mycoplasma pneumoniae, Chlamydia spp, Legionella, Coxiella burnetti and viruses. Nosocomial pneumonias and pneumonias in immunosuppressed patients have protean etiology with gram-negative organisms and staphylococci as predominant organisms.
Pathogenesis: Organisms enter the distal airway by inhalation, aspiration or by hematogenous seeding. The pathogen multiplies in or on the epithelium, causing inflammation, increased mucus secretion, and impaired mucociliary function; other lung functions may also be affected. In severe bronchiolitis, inflammation and necrosis of the epithelium may block small airways leading to airway obstruction.
Clinical Manifestations: Symptoms include cough, fever, chest pain, tachypnea and sputum production. Patients with pneumonia may also exhibit non-respiratory symptoms such as confusion, headache, myalgia, abdominal pain, nausea, vomiting and diarrhea.
Microbiologic Diagnosis: Sputum specimens are cultured for bacteria, fungi and viruses. Culture of nasal washings is usually sufficient in infants with bronchiolitis. Fluorescent staining technic can be used for legionellosis. Blood cultures and/or serologic methods are used for viruses, rickettsiae, fungi and many bacteria. Enzyme-linked immunoassay methods can be used for detections of microbial antigens as well as antibodies. Detection of nucleotide fragments specific for the microbial antigen in question by DNA probe or polymerase chain reaction can offer a rapid diagnosis.
Prevention and Treatment: Symptomatic treatment is used for most viral infections. Bacterial pneumonias are treated with antibacterials. A polysaccharide vaccine against 23 serotypes of Streptococcus pneumoniae is recommended for individuals at high risk.
Infections of the respiratory tract are grouped according to their symptomatology and anatomic involvement. Acute upper respiratory infections (URI) include the common cold, pharyngitis, epiglottitis, and laryngotracheitis (Fig. 93-1). These infections are usually benign, transitory and self-limited, altho ugh epiglottitis and laryngotracheitis can be serious diseases in children and young infants. Etiologic agents associated with URI include viruses, bacteria, mycoplasma and fungi (Table 93-1). Respiratory infections are more common in the fall and winter when school starts and indoor crowding facilitates transmission.
FIGURE 93-1 Upper and lower respiratory tract infections.
Common colds are the most prevalent entity of all respiratory infections and are the leading cause of patient visits to the physician, as well as work and school absenteeism. Most colds are caused by viruses. Rhinoviruses with more than 100 serotypes are the most common pathogens, causing at least 25% of colds in adults. Coronaviruses may be responsible for more than 10% of cases. Parainfluenza viruses, respiratory syncytial virus, adenoviruses and influenza viruses have all been linked to the common cold syndrome. All of these organisms show seasonal variations in incidence. The cause of 30% to 40% of cold syndromes has not been determined.
The viruses appear to act through direct invasion of epithelial cells of the respiratory mucosa (Fig. 93-2), but whether there is actual destruction and sloughing of these cells or loss of ciliary activity depends on the specific organism involved. There is an increase in both leukocyte infiltration and nasal secretions, including large amounts of protein and immunoglobulin, suggesting that cytokines and immune mechanisms may be responsible for some of the manifestations of the common cold (Fig. 93-3).
FIGURE 93-2 Pathogenesis of viral and bacterial mucosal respiratory infections.
FIGURE 93-3 Pathogenesis of upper respiratory tract infections.
After an incubation period of 48-72 hours, classic symptoms of nasal discharge and obstruction, sneezing, sore throat and cough occur in both adults and children. Myalgia and headache may also be present. Fever is rare. The duration of symptoms and of viral shedding varies with the pathogen and the age of the patient. Complications are usually rare, but sinusitis and otitis media may follow.
The diagnosis of a common cold is usually based on the symptoms (lack of fever combined with symptoms of localization to the nasopharynx). Unlike allergic rhinitis, eosinophils are absent in nasal secretions. Although it is possible to isolate the viruses for definitive diagnosis, that is rarely warranted.
Treatment of the uncomplicated common cold is generally symptomatic. Decongestants, antipyretics, fluids and bed rest usually suffice. Restriction of activities to avoid infecting others, along with good hand washing, are the best measures to prevent spread of the disease. No vaccine is commercially available for cold prophylaxis.
Sinusitis is an acute inflammatory condition of one or more of the paranasal sinuses. Infection plays an important role in this affliction. Sinusitis often results from infections of other sites of the respiratory tract since the paranasal sinuses are contiguous to, and communicate with, the upper respiratory tract.
Acute sinusitis most often follows a common cold which is usually of viral etiology. Vasomotor and allergic rhinitis may also be antecedent to the development of sinusitis. Obstruction of the sinusal ostia due to deviation of the nasal septum, presence of foreign bodies, polyps or tumors can predispose to sinusitis. Infection of the maxillary sinuses may follow dental extractions or an extension of infection from the roots of the upper teeth. The most common bacterial agents responsible for acute sinusitis are Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. Other organisms including Staphylococcus aureus, Streptococcus pyogenes, gram-negative organisms and anaerobes have also been recovered. Chronic sinusitis is commonly a mixed infection of aerobic and anaerobic organisms.
Infections caused by viruses or bacteria impair the ciliary activity of the epithelial lining of the sinuses and increased mucous secretions. This leads to obstruction of the paranasal sinusal ostia which impedes drainage. With bacterial multiplication in the sinus cavities, the mucus is converted to mucopurulent exudates. The pus further irritates the mucosal lining causing more edema, epithelial destruction and ostial obstruction. When acute sinusitis is not resolved and becomes chronic, mucosal thickening results and the development of mucoceles and polyps may ensue.
The maxillary and ethmoid sinuses are most commonly involved in sinusitis. The frontal sinuses are less often involved and the sphenoid sinuses are rarely affected. Pain, sensation of pressure and tenderness over the affected sinus are present. Malaise and low grade fever may also occur. Physical examination usually is not remarkable with no more than an edematous and hyperemic nasal mucosa.
In uncomplicated chronic sinusitis, a purulent nasal discharge is the most constant 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 films or magnetic resonance imaging.
For acute sinusitis, the diagnosis is made from clinical findings. A bacterial culture of the nasal discharge can be taken but is not very helpful as the recovered organisms are generally contaminated by the resident flora from the nasal passage. In chronic sinusitis, a careful dental examination, with sinus x-rays may be required. An antral puncture to obtain sinusal specimens for bacterial culture is needed to establish a specific microbiologic diagnosis.
Symptomatic treatment with analgesics and moist heat over the affected sinus pain and a decongestant to promote sinus drainage may suffice. For antimicrobial therapy, a beta-lactamase resistant antibiotic such as amoxicillin-clavulanate or a cephalosporin may be used. For chronic sinusitis, when conservative treatment does not lead to a cure, irrigation of the affected sinus may be necessary. Culture from an antral puncture of the maxillary sinus can be performed to identify the causative organism for selecting antimicrobial therapy. Specific preventive procedures are not available. Proper care of infectious and/or allergic rhinitis, surgical correction to relieve or avoid obstruction of the sinusal ostia are important. Root abscesses of the upper teeth should receive proper dental care to avoid secondary infection of the maxillary sinuses.
Infections of the ears are common events encountered in medical practice, particularly in young children. Otitis externa is an infection involving the external auditory canal while otitis media denotes inflammation of the middle ear.
For otitis externa, the skin flora such as Staphylococcus epidermidis, Staphylococcus aureus, diphtheroids and occasionally an anaerobic organism, 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 skin flora. Malignant otitis externa is a severe necrotizing infection usually caused by Pseudomonas aeruginosa.
For otitis media, the commonest causative bacteria are Streptococcus pneumoniae, Hemophilus influenzae and beta-lactamase producing Moraxella catarrhalis. Respiratory viruses may play a role in otitis media but this remains uncertain. Mycoplasma pneumoniae has been reported to cause hemorrhagic bullous myringitis in an experimental study among nonimmune human volunteers inoculated with M pneumoniae. However, in natural cases of M pneumoniae infection, clinical bullous myringitis or otitis media is uncommon.
The narrow and tortuous auditory canal is lined by a protective surface epithelium. Factors that may disrupt the natural protective mechanisms, such as high temperature and humidity, trauma, allergy, tissue maceration, removal of cerumen and an alkaline pH environment, favor the development of otitis externa. Prolonged immersion in a swimming pool coupled with frequent ear cleansing increases the risk of otitis externa.
Acute otitis media commonly follows an upper respiratory infection extending from the nasopharynx via the eustachian tube to the middle ear. Vigorous nose blowing during a common cold, sudden changes of air pressure, and perforation of the tympanic membrane also favor the development of otitis media. The presence of purulent exudate in the middle ear may lead to a spread of infection to the inner ear and mastoids or even meninges
Otitis externa: Furuncles of the external ear, similar to those in skin infection, can cause severe pain and a sense of fullness in the ear canal. When the furuncle drains, purulent otorrhea may be present. In generalized otitis externa, itching, pain and tenderness of the ear lobe on traction are present. Loss of hearing may be due to obstruction of the ear canal by swelling and the presence of purulent debris.
Malignant otitis externa tends to occur in elderly diabetic patients. It is characterized by severe persistent earache, foul smelling purulent discharge and the presence of granulation tissue in the auditory canal. The infection may spread and lead to osteomyelitis of the temporal bone or externally to involve the pinna with osteochondritis.
Otitis media: Acute otitis media occurs most commonly in young children. The initial complaint usually is persistent severe earache (crying in the infant) accompanied by fever, and, and vomiting. Otologic examination reveals a bulging, erythematous tympanic membrane with loss of light reflex and landmarks. If perforation of the tympanic membrane occurs, serosanguinous or purulent discharge may be present. In the event of an obstruction of the eustachian tube, accumulation of a usually sterile effusion in the middle ear results in serous otitis media. Chronic otitis media frequently presents a permanent perforation of the tympanic membrane. A central perforation of the pars tensa is more benign. On the other hand, an attic perforation of the pars placcida and marginal perforation of the pars tensa are more dangerous and often associated with a cholesteatoma.
The diagnosis of both otitis externa and otitis media can be made from history, clinical symptomatology and physical examinations. Inspection of the tympanic membrane is an indispensable skill for physicians and health care workers. All discharge, ear wax and debris must be removed and to perform an adequate otoscopy. In the majority of patients, routine cultures are not necessary, as a number of good bacteriologic studies have shown consistently the same microbial pathogens mentioned in the section of etiology. If the patient is immunocompromised or is toxic and not responding to initial antimicrobial therapy tympanocentesis (needle aspiration) to obtain middle ear effusion for microbiologic culture is indicated.
Otitis externa: Topical therapy is usually sufficient and systemic antimicrobials are seldom needed unless there are signs of spreading cellulitis and the patient appears toxic. A combination of topical antibiotics such as neomycin sulfate, polymyxin B sulfate and corticosteroids used as eardrops, is a preferred therapy. In some cases, acidification of the ear canal by applying a 2% solution of acetic acid topically may also be effective. If a furuncle is present in the external canal, the physician should allow it to drain spontaneously.
Otitis media: Amoxicillin is an effective and preferred antibiotic for treatment of acute otitis media. Since beta-lactamase producing H influenzae and M catarrhalis can be a problem in some communities, amoxicillin-clavulanate is used by many physicians. Oral preparations of trimethoprim/sulfamethoxazole, second and third generation cephalosporins, tetracyclines and macrolides can also be used. When there is a large effusion, tympanocentesis may hasten the resolution process by decreasing the sterile effusion. Patients with chronic otitis media and frequent recurrences of middle ear infections may be benefitted by chemoprophylaxis with once daily oral amoxicillin or trimethoprim/sulfamethoxazole during the winter and spring months. In those patients with persistent effusion of the middle ear, surgical interventions with myringotomy, adenoidectomy and the placement of tympanotomy tubes has been helpful.
Use of polyvalent pneumococcal vaccines has been evaluated for the prevention of otitis media in children. However, children under two years of age do not respond satisfactorily to polysaccharide antigens; further, no significant reduction in the number of middle ear infections was demonstrable. Newer vaccines composed of pneumococcal capsular polysaccharides conjugated to proteins may increase the immunogenicity and are currently under clinical investigation for efficacy and safety.
Pharyngitis is an inflammation of the pharynx involving lymphoid tissues of the posterior 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 of Epstein-Barr virus and cytomegalovirus infections.
Group A beta-hemolytic streptococcus or Streptococcus pyogenes is the most important bacterial agent associated with acute pharyngitis and tonsillitis. Corynebacterium diphtheriae causes occasional cases of acute pharyngitis, as do mixed anaerobic infections (Vincent's angina), Corynebacterium haemolyticum, Neisseria gonorrhoeae, and Chlamydia trachomatis. Outbreaks of Chlamydia pneumoniae (TWAR agent) causing pharyngitis or pneumonitis have occurred in military recruits. Mycoplasma pneumoniae and Mycoplasma hominis have been associated with acute pharyngitis. Candida albicans, which causes oral candidiasis or thrush, can involve the pharynx, leading to inflammation and pain.
As with common cold, viral pathogens in pharyngitis appear to
invade the mucosal cells of the nasopharynx and oral cavity,
resulting in edema and hyperemia of the mucous mem
branes and tonsils (Fig 93-2). Bacteria attach to and, in the case of group A beta-hemolytic streptococci, invade the mucosa of the upper respiratory tract. Many clinical manifestations of infection appear to be due to the immune reaction to products of the bacterial cell. In diphtheria, a potent bacterial exotoxin causes local inflammation and cell necrosis.
Pharyngitis usually presents with a red, sore, or "scratchy" throat. An inflammatory exudate or membranes may cover the tonsils and tonsillar pillars. Vesicles or ulcers may also be seen on the pharyngeal walls. Depending on the pathogen, fever and systemic manifestations such as malaise, myalgia, or headache may be present. Anterior cervical lymphadenopathy is common in bacterial pharyngitis and difficulty in swallowing may be present.
The goal in the diagnosis of pharyngitis is to identify cases that are due to group A beta-hemolytic streptococci, as well as the more unusual and potentially serious infections. The various forms of pharyngitis cannot be distinguished on clinical grounds. Routine throat cultures for bacteria are inoculated onto sheep blood and chocolate agar plates. Thayer-Martin medium is used if N gonorrhoeae is suspected. Viral cultures are not routinely obtained for most cases of pharyngitis. Serologic studies may be used to confirm the diagnosis of pharyngitis due to viral, mycoplasmal or chlamydial pathogens. Rapid diagnostic tests with fluorescent antibody or latex agglutination to identify group A streptococci from pharyngeal swabs are available. Gene probe and polymerase chain reaction can be used to detect unusual organisms such as M pneumoniae, chlamydia or viruses but these procedures are not routine diagnostic methods.
Symptomatic treatment is recommended for viral pharyngitis. The exception is herpes simplex virus infection, which can be treated with acyclovir if clinically warranted or if diagnosed in immunocompromised patients. The specific antibacterial agents will depend on the causative organism, but penicillin G is the therapy of choice for streptococcal pharyngitis. Mycoplasma and chlamydial infections respond to erythromycin, tetracyclines and the new macrolides.
Inflammation of the upper airway is classified as epiglottitis or laryngotracheitis (croup) on the basis of the location, clinical manifestations, and pathogens of the infection. Haemophilus influenzae type b is the most common cause of epiglottitis, particularly in children age 2 to 5 years. Epiglottitis is less common in adults. Some cases of epiglottitis in adults may be of viral origin. Most cases of laryngotracheitis are due to viruses. More serious bacterial infections have been associated with H influenzae type b, group A beta-hemolytic streptococcus and C diphtheriae. Parainfluenza viruses are most common but respiratory syncytial virus, adenoviruses, influenza viruses, enteroviruses and Mycoplasma pneumoniae have been implicated.
A viral upper respiratory infection may precede infection with H influenzae in episodes of epiglottitis. However, once H influenzae type b infection starts, rapidly progressive erythema and swelling of the epiglottis ensue, and bacteremia is usually present. Viral infection of laryngotracheitis commonly begins in the nasopharynx and eventually moves into the larynx and trachea. Inflammation and edema involve the epithelium, mucosa and submucosa of the subglottis which can lead to airway obstruction.
The syndrome of epiglottitis begins with the acute onset of fever, sore throat, hoarseness, drooling, dysphagia and progresses within a few hours to severe respiratory distress and prostration. The clinical course can be fulminant and fatal. 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, with rhinorrhea, fever, sore throat and a mild cough. Tachypnea, a deep barking cough and inspiratory stridor eventually develop. Children with bacterial tracheitis appear more ill than adults and are at greater risk of developing airway obstruction.
Haemophilus influenzae type b is isolated from the blood or epiglottis in the majority of patients with epiglottis; therefore a blood culture should always be performed. Sputum cultures or cultures from pharyngeal swabs may be used to isolate pathogens in patients with laryngotracheitis. Serologic studies to detect a rise in antibody titers to various viruses are helpful for retrospective diagnosis. Newer, rapid diagnostic techniques, using immunofluorescent-antibody staining to detect virus in sputum, pharyngeal swabs, or nasal washings, have been successfully used. Enzyme-linked immunosorbent assay (ELISA), DNA probe and polymerase chain reaction procedures for detection of viral antibody or antigens are now available for rapid diagnosis.
Epiglottitis is a medical emergency, especially in children. All children with this diagnosis should be observed carefully and be intubated to maintain an open airway 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 and supportive care, such as fluid, humidified air, and racemic epinephrine. For prevention, Haemophilus influenzae type b conjugated vaccine is recommended for all pediatric patients, as is immunization against diphtheria.
Infections of the lower respiratory tract include bronchitis, bronchiolitis and pneumonia (Fig 93-1). These syndromes, especially pneumonia, can be severe or fatal. Although viruses, mycoplasma, rickettsiae and fungi can all cause lower respiratory tract infections, bacteria are the dominant pathogens; accounting for a much higher percentage of lower than of upper respiratory tract infections.
Bronchitis and bronchiolitis involve inflammation of the bronchial tree. Bronchitis is usually preceded by an upper respiratory tract infection or forms part of a clinical syndrome in diseases such as influenza, rubeola, rubella, pertussis, scarlet fever and typhoid fever. Chronic bronchitis with a persistent cough and sputum production appears to be caused by a combination of environmental factors, such as smoking, and bacterial infection with pathogens such as H influenzae and S pneumoniae. Bronchiolitis is a viral respiratory disease of infants and is caused primarily by respiratory syncytial virus. Other viruses, including parainfluenza viruses, influenza viruses and adenoviruses (as well as occasionally M pneumoniae) are also known to cause bronchiolitis.
When the bronchial tree is infected, the mucosa becomes hyperemic and edematous and produces copious bronchial secretions. The damage to the mucosa can range from simple loss of mucociliary function to actual destruction of the respiratory epithelium, depending on the organisms(s) involved. Patients with chronic bronchitis have an increase in the number of mucus-producing cells in their airways, as well as inflammation and loss of bronchial epithelium, Infants with bronchiolitis initially have inflammation and sometimes necrosis of the respiratory epithelium, with eventual sloughing. Bronchial and bronchiolar walls are thickened. Exudate made up of necrotic material and respiratory secretions and the narrowing of the bronchial lumen lead to airway obstruction. Areas of air trapping and atelectasis develop and may eventually contribute to respiratory failure.
Symptoms of an upper respiratory tract infection with a cough is the typical initial presentation in acute bronchitis. Mucopurulent sputum may be present, and moderate temperature elevations occur. Typical findings in chronic bronchitis are an incessant cough and production of large amounts of sputum, particularly in the morning. Development of respiratory infections can lead to acute exacerbations of symptoms with possibly severe respiratory distress.
Coryza and cough usually precede the onset of bronchiolitis. Fever is common. A deepening cough, increased respiratory rate, and restlessness follow. Retractions of the chest wall, nasal flaring, and grunting are prominent findings. Wheezing or an actual lack of breath sounds may be noted. Respiratory failure and death may result.
Bacteriologic examination and culture of purulent respiratory secretions should always be performed for cases of acute bronchitis not associated with a common cold. Patients with chronic bronchitis should have their sputum cultured for bacteria initially and during exacerbations. Aspirations of nasopharyngeal secretions or swabs are sufficient to obtain specimens for viral culture in infants with bronchiolitis. Serologic tests demonstrating a rise in antibody titer to specific viruses can also be performed. Rapid diagnostic tests for antibody or viral antigens may be performed on nasopharyngeal secretions by using fluorescent-antibody staining, ELISA or DNA probe procedures.
With only a few exceptions, viral infections are treated with supportive measures. Respiratory syncytial virus infections in infants may be treated with ribavirin. Amantadine and rimantadine are available for chemoprophylaxis or treatment of influenza type A viruses. Selected groups of patients with chronic bronchitis may receive benefit from use of corticosteroids, bronchodilators, or prophylactic antibiotics.
Pneumonia is an inflammation of the lung parenchyma (Fig 93-4). Consolidation of the lung tissue may be identified by physical examination and chest x-ray. From an anatomical point of view, lobar pneumonia denotes an alveolar process involving an entire lobe of the lung while bronchopneumonia describes an alveolar process occurring in a distribution that is patchy without filling an entire lobe. Numerous factors, including environmental contaminants and autoimmune diseases, as well as infection, may cause pneumonia. The various infectious agents that cause pneumonia are categorized in many ways for purposes of laboratory testing, epidemiologic study and choice of therapy. Pneumonias occurring in usually healthy persons not confined to an institution are classified as community-acquired pneumonias. Infections arise while a patient is hospitalized or living in an institution such as a nursing home are called hospital-acquired or nosocomial pneumonias. Etiologic pathogens associated with community-acquired and hospital-acquired pneumonias are somewhat different. However, many organisms can cause both types of infections.
FIGURE 93-4 Pathogenesis of bacterial pneumonias.
Bacterial pneumonias: Streptococcus pneumoniae is the most common agent of community-acquired acute bacterial pneumonia. More than 80 serotypes, as determined by capsular polysaccharides, are known, but 23 serotypes account for over 90% of all pneumococcal pneumonias in the United States. Pneumonias caused by other streptococci are uncommon. Streptococcus pyogenes pneumonia is often associated with a hemorrhagic pneumonitis and empyema. Community-acquired pneumonias caused by Staphylococcus aureus are also uncommon and usually occur after influenza or from staphylococcal bacteremia. Infections due to Haemophilus influenzae (usually nontypable) and Klebsiella pneumoniae are more common among patients over 50 years old who have chronic obstructive lung disease or alcoholism.
The most common agents of nosocomial pneumonias are aerobic gram-negative bacilli that rarely cause pneumonia in healthy individuals. Pseudomonas aeruginosa, Escherichia coli, Enterobacter, Proteus, and Klebsiella species are often identified. Less common agents causing pneumonias include Francisella tularensis, the agent of tularemia; Yersinia pestis, the agent of plague; and Neisseria meningitidis, which usually causes meningitis but can be associated with pneumonia, especially among military recruits. Xanthomonas pseudomallei causes melioidosis, a chronic pneumonia in Southeast Asia.
Mycobacterium tuberculosis can cause pneumonia. Although the incidence of tuberculosis is low in industrialized countries, M tuberculosis infections still continue to be a significant public health problem in the United States, particularly among immigrants from developing countries, intravenous drug abusers, patients infected with human immunodeficiency virus (HIV), and the institutionalized elderly. Atypical Mycobacterium species can cause lung disease indistinguishable from tuberculosis.
Aspiration pneumonias: Aspiration pneumonia from anaerobic organisms usually occurs in patients with periodontal disease or depressed consciousness. The bacteria involved are usually part the oral flora and cultures generally show a mixed bacterial growth. Actinomyces, Bacteroides, Peptostreptococcus, Veilonella, Propionibacterium, Eubacterium, and Fusobacterium spp are often isolated.
Atypical pneumonias: Atypical pneumonias are those that are not typical bacterial lobar pneumonias. Mycoplasma pneumoniae produces pneumonia most commonly in young people between 5 and 19 years of age. Outbreaks have been reported among military recruits and college students.
Legionella species, including L pneumophila, can cause a wide range of clinical manifestations. The 1976 outbreak in Philadelphia was manifested as a typical serious pneumonia in affected individuals, with a mortality of 17% (see Ch. 40). These organisms can survive in water and cause pneumonia by inhalation from aerosolized tap water, respiratory devices, air conditioners and showers. They also have been reported to cause nosocomial pneumonias.
Chlamydia spp noted to cause pneumonitis are C trachomatis, C psittaci and C pneumoniae. Chlamydia trachomatis causes pneumonia in neonates and young infants. C psittaci is a known cause for occupational pneumonitis in bird handlers such as turkey farmers. Chlamydia pneumoniae has been associated with outbreaks of pneumonia in military recruits and on college campuses.
Coxiella burnetii the rickettsia responsible for Q fever, is acquired by inhalation of aerosols from infected animal placentas and feces. Pneumonitis is one of the major manifestations of this systemic infection.
Viral pneumonias are rare in healthy civilian adults. An exception is the viral pneumonia caused by influenza viruses, which can have a high mortality in the elderly and in patients with underlying disease. A serious complication following influenza virus infection is a secondary bacterial pneumonia, particularly staphylococcal pneumonia. Respiratory syncytial virus can cause serious pneumonia among infants as well as outbreaks among institutionalized adults. Adenoviruses may also cause pneumonia, serotypes 1,2,3,7 and 7a have been associated with a severe, fatal pneumonia in infants. Although varicella-zoster virus pneumonitis is rare in children, it is not uncommon in individuals over 19 years old. Morality can be as high as 10% to 30%. Measles pneumonia may occur in adults.
Other pneumonias and immunosuppression: Cytomegalovirus is well known for causing congenital infections in neonates, as well as the mononucleosis-like illness seen in adults. However, among its manifestations in immunocompromised individuals is a severe and often fatal pneumonitis. Herpes simplex virus also causes a pneumonia in this population. Giant-cell pneumonia is a serious complication of measles and has been found in children with immunodeficiency disorders or underlying cancers who receive live attenuated measles vaccine. Actinomyces and Nocardia spp can cause pneumonitis, particularly in immunocompromised hosts.
Among the fungi, Cryptococcus neoformans and Sporothrix schenckii are found worldwide, whereas Blastomyces dermatitidis, Coccidioides immitis, Histoplasma capsulatum and Paracoccidioides brasiliensis have specific geographic distributions. All can cause pneumonias, which are usually chronic and possible clinically inapparent in normal hosts, but are manifested as more serious diseases in immunocompromised patients. Other fungi, such as Aspergillus and Candida spp, occasionally are responsible for pneumonias in severely ill or immunosuppressed patients and neonates.
Pneumocystis carinii produces a life-threatening pneumonia among patients immunosuppressed by acquired immune deficiency syndrome (AIDS), hematologic cancers, or medical therapy. It is the most common cause of pneumonia among patients with AIDS when the CD4 cell counts drop below 200/mm3.
Infectious agents gain access to the lower respiratory tract by the inhalation of aerosolized material, by aspiration of upper airway flora, or by hematogenous seeding. Pneumonia occurs when lung defense mechanisms are diminished or overwhelmed. 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.
Etiologic diagnosis of pneumonia on clinical grounds alone is almost impossible. Sputum should be examined for a predominant organism in any patient suspected to have a bacterial pneumonia; blood and pleural fluid (if present) should be cultured. A sputum specimen with fewer than 10 while cells per high-power field under a microscope is considered to be contaminated with oral secretions and is unsatisfactory for diagnosis. Acid-fast stains and cultures are used to identify Mycobacterium and Nocardia spp. Most fungal pneumonias are diagnosed on the basis of culture of sputum or lung tissue. Viral infection may be diagnosed by demonstration of antigen in secretions or cultures or by an antibody response. Serologic studies can be used to identify viruses, M pneumoniae, C. burnetii, Chlamydia species, Legionella, Francisella,and Yersinia. A rise in serum cold agglutinins may be associated with M pneumoniae infection, but the test is positive in only about 60% of patients with this pathogen.
Rapid diagnostic tests, as described in previous sections, are available to identify respiratory viruses: the fluorescent-antibody test is used for Legionella. A sputum quellung test can specify S pneumoniae by serotype. Enzyme-linked immunoassay, DNA probe and polymerase chain reaction methods are available for many agents causing respiratory infections.
Some organisms that may colonize the respiratory tract are considered to be pathogens only when they are shown to be invading the parenchyma. Diagnosis of pneumonia due to cytomegalovirus, herpes simplex virus, Aspergillus spp. or Candida spp require specimens obtained by transbronchial or open-lung biopsy. Pneumocystis carinii can be found by silver stain of expectorated sputum. However, if the sputum is negative, deeper specimens from the lower respiratory tract obtained by bronchoscopy or by lung biopsy are needed for confirmatory diagnosis.
Until the organism causing the infection is identified, decisions on therapy are based upon clinical history, including history of exposure, age, underlying disease and previous therapies, past pneumonias, geographic location, severity of 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 developing pneumococcal infections, including asplenic patients, the elderly and any patients immunocompromised through disease or medical therapy. Yearly influenza vaccinations should also be provided for these particular groups. An enteric-coated vaccine prepared from certain serotypes of adenoviruses is available, but is only used in military recruits. In AIDS patients, trimethoprim/sulfamethoxazole, aerosolized pentamidine or other antimicrobials can be given for prophylaxis of Pneumocystis carinii infections.
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