Classification of adenoviral infection

(by Nosov S.D., Utchaykin V.F., 1990 y.)

Because the manifestations of adenovirus infections are protean, the major syndromes are discussed separately. The major syndromes are: (1) acute respiratory disease (ARD), (2) pharyngoconjunctival fever, (3) epidemic keratoconjunctivitis, (4) acute hemorrhagic cystitis, (5) gastroenteritis, and (5) adenoviral infections in immunocompromised hosts.

Given the range of manifestations, the varying levels and effects of immunosuppressive therapies, and rapid advances in molecular methods of detection, a comprehensive review of adenovirus infection in the immunosuppressed host is beyond the scope of this article; however, the author plans to report the most salient features and general updates here. The reader is encouraged to review the literature for more detail regarding infection in specific settings.

· Acute respiratory disease (predominantly serotypes 4 and 7)

o Similar to many other viral syndromes, ARD occurs with greater frequency in spring and winter months. Approximately half of adenovirus respiratory infections do not cause symptoms. Adenoviruses account for 10% of all childhood lower respiratory tract infections.

o Lower respiratory tract infections, including tracheobronchitis, bronchiolitis, and pneumonia, may mimic respiratory syncytial virus infection or influenza. Notably, conjunctivitis in the presence of bronchitis suggests adenoviral infection.

o Fatal pneumonia is uncommon, but it is more likely in neonates.

o Encephalitis is uncommon.

o Fever, rhinorrhea, cough, and sore throat usually lasting 3-5 days are typical symptoms of adenoviral ARD.

· Pharyngoconjunctival fever (predominantly serotypes 3, 4, and 7)

o This syndrome most often affects school-aged children. Contagious in nature, sporadic outbreaks of adenovirus infection occur in small groups, especially summer camps associated with an inadequately chlorinated water source such as a pool or lake. Interestingly, water sample cultures often are not confirmatory. Spread occurs via the re spiratory route and contact with ocular secretions during the acute illness.

o Acute conjunctivitis may occur both as a separate entity with or without pharyngitis or a respiratory syndrome. Encephalitis may occur but is rare.

o The classic presentation is characterized by fever, sore throat, coryza, and red eyes. Upper respiratory tract symptoms may precede ocular findings, or they may not be present.

o Conjunctivitis usually begins with one eye then spreads to the other, although both eyes may be affected simultaneously. Severe pain is atypical, but mild pain or discomfort, tearing, pruritus, and morning crusting are common.

o It usually is self-limited to 5 days (incubation period is 5 d).

o Uncommonly, an exanthem or diarrhea may occur.

· Epidemic keratoconjunctivitis (predominantly serotypes 8, 19, and 37)

o This is highly contagious, with approximately 10% transmission in household contacts via hands and fomites. Transmission has also been associated with instrumentation, industrial trauma (shipyard workers, welders, airborne particles), contaminated ophthalmic solutions, and the hands of health care workers. Corneal trauma facilitates infection.

o After an 8-day incubation period, an insidious onset of unilateral red eye occurs, which spreads to involve both eyes. Patients have photophobia, tearing, and pain (indicating corneal involvement). Children may have fever and lymphadenopathy.

o Malaise and headache are reported.

o Inflammation may persist for weeks, and residual scarring and visual impairment may occur.

· Acute hemorrhagic cystitis (serotypes 11 and 21)/nephritis

o Acute hemorrhagic cystitis usually affects children aged 5-15 years, but it also may affect adults who are immunosuppressed (eg, from kidney or bone marrow transplantation, AIDS). Boys are affected more often than girls.

o Dysuria, frequency, and grossly bloody urine are reported. Hematuria is self-limited to 3 days, and other symptoms resolve later. Symptoms may be more prolonged in recipients of hematopoietic stem cell transplants.

o Nephritis has occurred in hematopoietic stem cell transplant recipients and is associated with fever, hematuria, and flank pain.

· Gastroenteritis (most commonly associated with serotypes 40 and 41, but others may be involved)

o Enteric adenovirus infection is a common cause of infantile diarrhea in the daycare setting, but it is a less common cause than rotavirus infection and, in some settings, less than infection with astroviruses. Adenoviruses replicate readily in the human intestine and may be cultured from asymptomatic individuals; thus, their presence in the setting of a diarrheal syndrome may be incidental.

o Fever and watery diarrhea are usually limited to 1-2 weeks.

· General considerations

o Pulmonary infiltrates are often diffuse and reticulonodular, but they may be lobar.

o Hematuria may occur in the setting of nephritis or hemorrhagic cystitis.

o Abnormal transaminase levels, which may be dramatic, may indicate adenoviral hepatitis.

o Diarrhea may indicate adenoviral gastroenteritis.

Physical:

· Acute respiratory disease

o Pharyngitis, which may be exudative, is a finding. Conjunctivitis may occur in this setting.

o Patients have pulmonary rhonchi and rales.

· Pharyngoconjunctival fever

o Fever; coryza; pharyngitis, which may be exudative; follicular, bulbar, and palpebral conjunctivitis (typically mild granular appearance); and headache are reported.

o Cervical lymphadenopathy is a finding.

o The hallmark is preauricular lymphadenopathy (ie, Parinaud syndrome), with small lymph nodes palpable just anterior to the ear. This finding is not common; however, its presence in the setting of a viral conjunctivitis is very suggestive of adenovirus infection.

· Epidemic keratoconjunctivitis

o Severe follicular keratoconjunctivitis is reported. Palpebral conjunctiva may be granular.

o Palpebral edema is a finding.

o Preauricular lymphadenopathy is not common but is a pathognomonic finding with adenovirus infection.

o Hemorrhagic conjunctivitis may develop.

o Visual haziness or impairment resulting from keratitis develops and may persist for months to years.

· Acute hemorrhagic cystitis/nephritis

o No significant features are described in the setting of hemorrhagic cystitis, other than evidence of blood in the urine.

o Nephritis is characterized by flank pain.

o Patients with hemorrhagic cystitis are afebrile. Nephritis is characterized by fever.

· Gastroenteritis: If severe, the patient has signs of dehydration.

· Adenoviral infections in immunocompromised hosts: Features include dyspnea, dry cough, pulmonary rhonchi and rales, grossly bloody urine, and diarrhea.

Lab Studies:

· Adenovirus is stable in routine viral transport medium, including specimens of nasopharyngeal, rectal, and corneal secretions; urine; and unfixed biopsy tissue. Detection is enhanced if specimens are taken as early in the clinical course as possible and promptly shipped cold or frozen to the appropriate laboratory.

· Seroreactivity to adenovirus is common. By age 4 years, approximately half of all children have positive adenovirus titers. As a result, serology is less useful in the acute clinical setting. If a serologic diagnosis is pursued, serum should be obtained as early as possible in the clinical course, followed by a second titer 2-4 weeks later. A 4-fold rise in acute titers to convalescent titers is diagnostic.

· Indirect immunofluorescence assays may be used for direct examination of tissue specimens.

· Serotyping is generally in the domain of epidemiology and research and is not typically used in clinical practice. However, as specific syndromes are associated with specific serotypes and as molecular methods advance to allow rapid detection and typing, these assays may become clinically useful.

· The following laboratory studies are suggested in the given syndromes, both for diagnosis of adenoviral infections and to evaluate for other diagnoses in the differential of each syndrome.

o Acute respiratory disease

§ Nasopharyngeal swab for culture of respiratory viruses (eg, influenza virus, adenovirus) is suggested.

§ Consider Monospot assay or respiratory syncytial virus culture for Epstein-Barr virus and respiratory syncytial virus.

§ Consider rapid group A Streptococcus throat swab and culture.

o Pharyngoconjunctival fever

§ Nasopharyngeal swab for culture of respiratory viruses (eg, influenza virus, adenovirus) is suggested.

§ Consider Monospot assay or respiratory syncytial virus culture for Epstein-Barr virus and respiratory syncytial virus.

§ Consider rapid group A Streptococcus throat swab and culture.

o Epidemic keratoconjunctivitis: Viral and bacterial swab cultures of conjunctival secretions and scrapings are suggested.

o Acute hemorrhagic cystitis or nephritis: Urinalysis and cultures for bacterial and viral pathogens are suggested.

o Gastroenteritis: Consider stool Wright stain, ova and parasites examination, culture for bacterial enteric pathogens, rotavirus assay, and Clostridium difficile toxin assay.

Treatmrnt

Drug Category:

Antivirals -- These agents inhibit viral DNA and protein synthesis.

Further Inpatient Care:

· Patients with meningoencephalitis or severe respiratory disease, including pneumonia, or those who are immunosuppressed require hospitalization.

· Patients with severe keratitis who are suggested to have bacterial superinfection may require hospitalization.

Further Outpatient Care:

· Most disease is self-limited, and reassurance suffices; however, patients with keratoconjunctivitis or significant respiratory disease may need a follow-up evaluation within 2 weeks to monitor resolution. Immunosuppression often warrants hospitalization.

· Consultation with an ophthalmologist may be indicated in the setting of corneal opacities. Also, if hemorrhagic cystitis does not resolve within 5 days, consider noninfectious etiologies as the cause and refer the patient to a urologist or nephrologist, as appropriate.

Deterrence/Prevention:

· Effective isolation procedures, handwashing, and sterilization of instruments can prevent nosocomial infection.

o Hospitalized patients with adenoviral conjunctivitis require contact precautions. Adenoviral pneumonia requires both droplet and contact precautions.

o Health care workers with any adenoviral syndrome should be relieved of patient care duties and sent home until symptoms resolve. Health care workers should be educated to report to the employee health office if they develop symptoms suggesting conjunctivitis.

o Strict handwashing protocols should be emphasized, particularly in ophthalmologic care settings.

o Elimination of environmental reservoirs and fomites includes proper disinfection of tonometry and ophthalmologic instruments according to local infection control and manufacturer guidelines. Proper use and monitoring of open, multiple-use ophthalmic solutions (and timely discarding of these) according to local infection control and manufacturer guidelines is essential.

· Adequate chlorination of swimming pools may prevent waterborne outbreaks.

Complications:

· Meningoencephalitis occurs rarely, usually in association with pneumonia. No pathognomonic features distinguish adenovirus aseptic meningitis or meningoencephalitis from other causes.

· Immunosuppression in the host permits more severe manifestations. Pediatric liver transplantation, AIDS, and hematopoietic stem cell transplantation have been associated with protean adenovirus infections.

Prognosis:

· Overall, prognosis is good, except in cases of immunosuppressed patients with severe disease.

Parainfluenza Virus

Background:Parainfluenza viruses (PIVs) are paramyxoviruses. Over the last decade, both the nomenclature and the taxonomic relationships of human parainfluenza viruses (HPIVs) have changed considerably.

Reinfection with HPIV can occur throughout life, with elderly and immunocompromised persons being at a greater risk of serious complications of infections.

Pathophysiology:

Structural organization

HPIVs are pleomorphic viruses whose envelope is derived from the host cell they last infected. These viruses are 150-200 nm in diameter and possess a single-stranded, nonsegmented, negative-sense RNA genome with nucleoprotein P and L proteins. A lipid bilayer covered with glycoprotein spikes surrounds a helical nucleocapsid that measures 12-17 nm in diameter. These glycoproteins are hemagglutinin-neuraminidase (HN) and fusion (F) proteins, which play a major role in the pathogenesis of the disease caused by the viruses.

Epidemiology

Respiratory secretions from infected humans are the source of infection. Transmission is by respiratory droplets or by direct person-to-person contact with infected secretions. The inoculating dose is very small.

HPIVs are common community-acquired respiratory pathogens without ethnic, socioeconomic, gender, age, or geographic boundaries. Many factors have been found that predispose individuals to these infections, including malnutrition, overcrowding, vitamin A deficiency, lack of breastfeeding, and environmental smoke or toxins.

Mortality/Morbidity:

Mortality induced by HPIV is unusual in developed countries and occurs almost exclusively in young infants or people who are immunocompromised or elderly. However, the preschool population in developing countries is at considerable risk for HPIV-induced death. Whether because of primary viral disease or because of facilitating secondary bacterial infections in malnourished children, lower respiratory infection causes 25-30% of the death in this age group, and HPIV causes at least 10% of lower respiratory infections.

Age:

HPIV-1 can cause lower respiratory infection in young infants but is rare in those younger than 1 month. The full burden of HPIV-1 in adults and elderly persons has not been determined, but studies have shown that this virus causes yearly hospitalizations in healthy adults and may play a role in bacterial pneumonias and death in nursing-home residents.

HPIV-2 accounts for 60% of all infections that develop in children younger than 5 years, with peak incidence between ages 1 and 2 years.

Young infants (<6 mo) are particularly vulnerable to infection with HPIV-3. Unlike other HPIVs, 40% of HPIV-3 infections occur in the first year of life.
Clinical

The incubation period is generally 2-6 days.

Physical:

classification of parainfluenza

Mixt-infection.

A broad range of findings is observed and may include fever, nasal congestion, pharyngeal erythema, nonproductive to minimally productive cough, inspiratory stridor, rhonchi, rales, and wheezing.

· The epiglottis is sometimes grossly swollen and reddened because of viral infection. Severe airway obstruction may ensue, requiring emergency tracheotomy.

· In serious cases, children should be quickly hospitalized (generally within 3-24 h). In hosts who are immunocompromised, upper respiratory tract symptoms are similar to those observed in healthy hosts who are immunocompetent, but the incidence of lower respiratory tract symptoms and sinusitis is much higher. In these groups, especially bone marrow transplant recipients, lower respiratory tract infection can lead to respiratory failure and death.

Lab Studies:

· CBC count is usually within reference ranges. Lymphocytosis may be present.

· Virus antigen detection and isolation

o Collection and preparation of clinical specimens: Nasopharyngeal aspirations, nasal washings, and nasal aspirations are optimum specimens for collection. Throat swabs and nasal swabs can also be used. Specimens should be collected and placed in viral transport media (VTM), preferably at 4°C; if a delay of more than 24 hours is anticipated, specimens should be frozen.
Nonrespiratory specimens such as CSF, rectal swabs, and stool, though rare, can be used. Paired sera (acute and convalescent phase) should be collected, separated quickly, and stored at either -20°C or -70°C; both samples should be tested simultaneously.

o Direct examination for viruses: Human parainfluenza virus (HPIV) antigen can be detected with enzyme-linked immunoassay (ELISA), radioimmunoassay, fluoroimmunoassay, and immunofluorescent tests. The latter 2 tests are both rapid and specific. Shell vial assay is another method for rapid identification of HPIV. Detection of HPIV has been compared using shell vials and standard tissue culture, with sensitivities that average 84%.

o Virus isolation: HPIV has the best growth in primary monkey kidney (PMK) cells (rhesus MK cells, cynomolgus, and African green monkeys). LLC-MK2 is also excellent for continued passage and almost as good as PMK cells for primary isolation. LLC-MK2 cells need trypsin (2-3 g/mL) added to the maintenance medium to recover all HPIV serotypes.

Serologic diagnosis: A 4-fold rise or drop in titre is generally thought to signify acute infection if the testing is performed at the same time on paired acute- and convalescent-phase serum pimples.

Medical Care:

· Supportive care is mandatory. Antiviral agents are of uncertain benefit. Anecdotal reports of possible benefit have been published, but controlled studies are lacking.

· Treatment of croup

o Prehospital care

§ Controlling fever and relieving respiratory symptoms are paramount.

§ Respiratory symptoms are improved by exposing children to cool night air or by inhalation of vapor droplets to soothe inflamed airways.

§ Antipyretics may be administered to control fever.

§ Moderate or severe croup requires medical evaluation in the office or ED.

o ED care

§ Mild croup: Cool oxygen mist and control of fever are effective in the treatment of mild croup.

§ Moderate croup: Therapy includes cool oxygen mist and, possibly, orally administered glucocorticoids. If patients fail to improve, racemic epinephrine nebulization has been shown to be beneficial. Hydration must be maintained with oral fluids or with intravenous fluids when necessary.

§ Severe croup: In cases of impending respiratory failure, intensive-care monitoring is required in addition to repeat racemic epinephrine nebulization at 1- to 2-hour intervals. Endotracheal intubation followed by a tracheotomy may be required in patients with severe respiratory obstruction.

Drug Category:

Corticosteroids -- Prednisone, prednisolone, and dexamethasone are commonly used glucocorticoids. Dexamethasone, because of its high potency and prolonged intramuscular half-life, is the preferred anti-inflammatory drug for croup.

Drug Category:

Sympathomimetics -- Epinephrine is highly effective when delivered via nebulizer. Nebulizers are air- or oxygen-powered devices that deliver medications directly to mucosal surfaces of respiratory tract and smooth muscles.

Further Inpatient Care:

· Indications for hospitalization

o Development of respiratory distress

o Dehydration

o Stridor at rest, even after receiving therapy

Further Outpatient Care:

· Bed rest

· Use of vaporizers producing moist air

Complications:

· Adult respiratory distress syndrome and exacerbation of nephritic syndrome

· Serious morbidity in hosts who are immunocompromised (eg, transplant recipients)

· Rare complications, including Guillain-Barré syndrome and meningitis

Prognosis:

· HPIV infections in older children and adults are generally mild. Occasionally, bronchiolitis or viral pneumonia in children and tracheobronchitis in adults have been reported.

Mycoplasma Infections

Background

Mycoplasmal organisms are the smallest known free-living life forms. They are nearly ubiquitous in both the plant and animal kingdoms as colonizers and pathogens. They are prokaryotes but lack a cell wall. However, they have a unique cell membrane that contains sterols, which are not present in either bacteria or viruses. Mycoplasma organisms are small (150-250 nm) and have deformable membranes. The name Mycoplasma refers to the plasticity of the bacterial forms resembling fungal elements.

When they were first discovered, mycoplasmal organisms were believed to be viruses because they pass through filters that retain bacteria. However, unlike viruses, they are able to grow in cell-free media and contain both RNA and DNA. Mycoplasma species have also been mistakenly believed to be L-forms of bacteria, which also lack cell walls. Unlike mycoplasmal organisms, L-form bacteria do not have sterols in the cell membranes, and they can revert to their walled parental forms.

The general characteristics of Mycoplasma species include the following:

· Prokaryotic

· Size of 150-250 nm

· Lack of a cell wall

· Sterol-containing cell membrane

· Fastidious growth requirements

· Fried-egg or mulberry colonies on agar

Mycoplasma species differ from viruses in the following ways:

· They grow on cell-free media in vitro.

· They contain both RNA and DNA.

· They have both intracellular and extracellular parasitism in vivo.

Mycoplasma species differ from bacteria (including L-forms) in the following ways:

· They have sterols in the cell membrane.

· They share no DNA homology with known bacteria.

· They have low guanine levels plus cytosine content.

· Their genome has a low molecular weight.

· They exhibit no reversion to walled forms.

Pathophysiology

Mycoplasma organisms cause infection primarily as extracellular parasites, attaching to the surface of ciliated and nonciliated epithelial cells. The attachment site, or receptor, is a complex carbohydrate structurally akin to antigen I of red blood cells. The antibody response to this receptor results in production of the anti- antibody or cold agglutinin, which acts as an autoantibody. Following attachment, mycoplasmal organisms may cause direct cytotoxic damage to epithelial cells because of hydrogen peroxide generation or cytolysis via an inflammatory response mediated by mononuclear cells or antigen-antibody reactions.

Systemic spread of the bacterium is rare. Most Mycoplasma pneumoniae –associated illnesses are confined to the respiratory tract.

Mortality/Morbidity

Most M pneumoniae infections lead to clinically apparent disease involving the upper respiratory tract. In 5-10% of patients (with the rate depending on age), the infection progresses to tracheobronchitis or pneumonia and is usually self-limited. Pleural effusion (usually small) occurs in 5-20% of patients. Mycoplasmas have also been implicated in the pathogenesis of asthma, leading to acute and chronic wheezing in some individuals.

In individuals with sickle cell anemia, mycoplasmal infection may be severe. Unusually severe M pneumoniae infection has also been reported in children with Down syndrome.

Age

Children younger than 3 years primarily develop upper respiratory infection.

M pneumoniae infection is uncommon in the first year of life; however in neonates, it may cause severe disease.

M pneumoniae infection is common in school-aged children, with the highest rate of infection in individuals aged 5-20 years, in whom the tendency is to develop bronchitis and pneumonia.

Colonization of infants by genital Mycoplasma species usually occurs during passage through an infected birth canal, and genital mycoplasmal organisms have been isolated from the upper respiratory tract in 15% of infants. Colonization usually does not persist beyond 2 years.

Clinical

History

Symptoms of M pneumoniae infection are often nonspecific. The onset is usually insidious, with fever, malaise, headache, and cough. Cough is a hallmark of M pneumoniae infection. The frequency and severity of cough may increase over the few days after onset and may become debilitating.

In patients in whom the infection progresses to lower respiratory tract disease, the original symptoms persist, with a worsening and relatively nonproductive cough. On occasion, white or blood-flecked sputum and parasternal chest pain may be present as a result of muscle strain. Otitis media and sinusitis are uncommon. Postinfectious bronchitis may persist for weeks. M pneumoniae infection may complicate asthma, and acute asthma may be the first manifestation of infection.

Neonates may present with symptoms of cough, meningitis, or brain abscess.

Physical

Patients with M pneumoniae infection usually do not appear ill, and the illness often has been termed walking pneumonia. The pharynx may be erythematous without cervical adenopathy. Bullous myringitis is a classic but rare complication. Examination of the chest and lungs may yield little abnormality. A hallmark of M pneumoniae infection is the disparity between physical findings (relatively few) and radiographic evidence of pneumonia. Wheezing can occur, especially in patients with asthma. Rarely, fulminant pneumonia with respiratory failure can occur.

Extrarespiratory manifestations of M pneumoniae infection include the following:

Dermatologic manifestations (most common)

· Erythematous macular and/or morbilliform rash

· Erythema multiforme or Stevens-Johnson syndrome

· Erythema nodosum

· Urticarial manifestations

· Papulovesicular exanthem

· Raynaud phenomenon

Cardiac manifestations

· Arrhythmia and/or ECG abnormalities (conduction defects)

· Congestive failure

· Pericarditis

· Myocarditis

· Endocarditis

Neurologic manifestations

· Cranial neuropathy

· Aseptic meningitis or meningoencephalitis

· Transverse myelitis

· Brainstem dysfunction

· Dysfunction of the pyramidal or extrapyramidal tract

· Cerebellar dysfunction

· Cerebral infarction

· Guillain-Barré syndrome

· Peripheral neuropathy

· Musculoskeletal manifestations

· Polyarthralgias

· Acute arthritis (monoarticular or migratory)

· Digital necrosis

Hematologic manifestations – Immune hemolytic anemia

Causes

M pneumoniae causes infections leading to clinically apparent disease involving the upper respiratory tract. In 5-10% of patients, depending on age, the infection progresses to tracheobronchitis or pneumonia.

Differential Diagnoses

Chlamydial Infections, Q Fever, Influenza, Respiratory Syncytial Virus Infection, Legionella Infection, Rhinovirus Infection, Parainfluenza Virus Infections, Rickettsial Infection

Laboratory Studies

Tests for M pneumoniae

Bacterial culture is of little practical value because of fastidious growth requirements and slow growth.

Serologic diagnosis has been the mainstay of laboratory testing.

Enzyme-linked immunoassay is used to detect immunoglobulin M (IgM) and immunoglobulin G (IgG) directed against M pneumoniae. Specificity is greater than 99%, and sensitivity is 98% when both findings are obtained. The IgM result may be negative early (at 7-10 d) and may not be helpful in guiding initial therapy.

Direct antigen detection in sputum specimens is performed using antigen-capture indirect enzyme immunoassay. Relatively high specificity and sensitivity (91%) are achieved.

Seminested polymerase chain reaction (PCR) assay as a target and real-time PCR assays targeting the gene for P1 adhesion protein are available. Both techniques have high sensitivity and high specificity. Real-time PCR assays have the advantage of speed and the ability to analyze numerous samples.

Tests for genital mycoplasmal organisms

Imaging Studies

Chest radiographs demonstrate characteristic features of M pneumoniae infection:

· bilateral pulmonary involvement

· multifocal or diffuse disease

· reticular infiltrates.

Procedures

Because most infections tend to be mild, few diagnostic procedures need to be performed.

In severe lower respiratory infection caused by M pneumoniae, bronchoalveolar lavage with appropriate testing of the lavage fluid may be needed; antigen detection, PCR, and culturing are used.

Treatment

Medical Care

Antimicrobial therapy is not necessary for mycoplasmal infection of the upper respiratory tract.

Although pneumonia is self-limiting and is not life threatening in most patients, treat it with appropriate antimicrobials to shorten the duration of illness and perhaps reduce spread to contacts.

Medication

As a result of the lack of a cell wall, beta-lactams are ineffective; neither is the combined therapy of trimethoprim and sulfamethoxazole effective.

Macrolides are the agents of choice. Alternatively, tetracyclines may be used in patients older than 8 years. Fluoroquinolones may be considered if macrolides or tetracyclines are not suitable choices; however, most fluoroquinolones are not approved by the FDA for use in patients younger than 18 years.

Antibiotics

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. Whenever feasible, guide antibiotic selection using culture sensitivity.

Further Inpatient Care

Further inpatient care is usually necessary only if severe pneumonia or extrarespiratory complications occur.

Further Outpatient Care

Routine follow-up visits are usually not required because the response to therapy is generally excellent.

Prognosis

Prognosis for Mycoplasma infections is usually excellent; however, if complications occur, long-term sequelae may result.

Croup

Background:

Croup, also termed laryngotracheitis or laryngotracheobronchitis, is a viral respiratory tract infection. It is primarily a pediatric illness and, as its alternative names indicate, generally affects the larynx and trachea but may also extend to the bronchi. It is the most common etiology in the febrile infant.

Croup manifests as hoarseness and a seal-like barking cough. However, morbidity is secondary to narrowing of the larynx and trachea below the level of the glottis, causing the hallmark inspiratory stridor.

Stridor is a relatively common complaint; however, it can alarm parents enough to prompt an emergency department (ED) visit. Young children who present with stridor require a meticulous evaluation to determine the etiology and to exclude, most importantly, rare life-threatening causes. Although croup is usually a mild, self-limited disease, upper airway obstruction may result in respiratory distress and even death.

Pathophysiology:

Acute infectious croup is spread through inhalation of the responsible virus. It begins with the nasopharynx and eventually involves the larynx and trachea. While the lower respiratory tract may also be affected, some authors consider laryngotracheobronchitis a separate entity, with bacterial superinfection as the potential cause.

Of greatest clinical significance is inflammation and edema of the subglottic larynx and trachea, especially near the cricoid cartilage. This is the narrowest part of the pediatric airway. Accordingly, swelling can significantly reduce the diameter, limiting airflow. This narrowing leads to stridor. Decreased mobility of the vocal cords leads to the associated hoarseness. In severe disease, fibrinous exudates and pseudomembranes may develop, causing even greater airway obstruction.

Spasmodic croup may be a noninfectious variant of the disorder, with a clinical presentation similar to that of the acute disease. In such cases, subglottic edema occurs without the inflammation typical in viral disease. While viral illnesses may trigger spasmodic croup, the reaction may be allergic rather than a direct result of infection.

Mortality/Morbidity:

Hospitalizations vary widely among communities, with rates from 1.5-30% and typically averaging 2-5%. Fewer than 2% of hospitalized children require intubation. Although exact mortality is unknown, one 10-year study found a mortality rate of less than 0.5% in intubated patients.

Age:

Croup is primarily a disease of infants and toddlers, with most cases affecting children aged 6 months to 3 years. Incidence peaks in the second year. Although the disease is rare after age 6 years, it may be seen as late as age 12-15 years.

History:

Croup usually begins with nonspecific respiratory symptoms, including rhinorrhea, sore throat, and cough. Fever is generally low grade (38-39°C) but can exceed 40°C. Within 1-2 days, the characteristic signs of hoarseness, barking cough, and inspiratory stridor develop, often suddenly, along with a variable degree of respiratory distress. Most ED visits occur from 10 pm to 4 am, and symptoms are perceived as worse at night. Symptoms typically resolve within 3-7 days but can last as long as 2 weeks.

Spasmodic croup typically presents at night with the sudden onset of "croupy" cough and stridor. The child may have mild upper respiratory complaints but more often appears completely well prior to the onset of symptoms.

Physical:

The physical presentation of croup varies widely. Most children have no more than a croupy cough and hoarse cry. Some may have stridor only with activity or agitation, while others have audible stridor at rest and evidence of respiratory distress. Paradoxically, the severely affected child may have "quiet" stridor secondary to the degree of airway obstruction. The child with croup does not appear toxic.

Many authors have attempted to devise croup scores to assist the examiner in assessing the degree of respiratory compromise. One of the most commonly cited is the Westley score. Although widely used to evaluate treatment protocols, its clinical efficacy has not been extensively studied. According to the Westley scale, a score of less than 3 represents mild disease; 3-6, moderate disease; and greater than 6, severe disease.

The score uses the following 5 dimensions:

· Inspiratory stridor – None - 0 points; with agitation - 1 point; at rest - 2 points

· Retractions – Mild - 1 point; moderate - 2 points; severe - 3 points

· Air entry – Normal - 0 points; mild decrease - 1 point; marked decrease - 2 points

· Cyanosis – None - 0 points; with agitation - 4 points; at rest - 5 points

· Level of consciousness – Normal - 0 points; depressed - 5 points

· Mild disease consists of occasional barking cough, no stridor at rest, and mild or nonexistent suprasternal or subcostal retractions.

· Moderate disease includes frequent cough, audible stridor at rest, and visible retractions, but little distress or agitation.

· Severe disease consists of frequent cough, prominent inspiratory (and, occasionally, expiratory) stridor, conspicuous retractions, decreased air entry on auscultation, and significant distress and agitation.

· Lethargy, cyanosis, and decreasing retractions are harbingers of impending respiratory failure.

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