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Viral Pneumonia Clinical Presentation

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Viral Pneumonia Clinical Presentation


Author: Zab Mosenifar, MD; Chief Editor: Ryland P Byrd Jr, MD more...
Updated: Aug 11, 2014

History
The clinical manifestations of viral pneumonia vary because of the number of diverse etiologic agents. Their
presentations are described briefly below. Various viral pneumonias typically occur during specific times of the
year, among close populations or in populations with underlying cardiopulmonary or immunocompromising
disease.
The common constitutional symptoms of viral pneumonias are fever, chills, nonproductive cough, rhinitis,
myalgias, headaches, and fatigue. Symptoms of viral pneumonia are similar to that of bacterial pneumonia,
although studies have shown a lower probability of having chest pain and rigors in viral pneumonias.[3] Most
patients have cough, but in elderly persons, this may be only scant.
Ascertaining immunization status, travel history, and possible exposure is important. During outbreaks with the
usual respiratory viruses, the signs and symptoms can suggest the correct diagnosis in most cases. In very
elderly persons, the only complaint may be fever and change in mental status.
In immunocompromised patients, recognition of the clinical picture of viral pneumonia, risk factors, and new
changes in clinical parameters is important. All of these findings can indicate the need for further imaging or other
diagnostic procedures to make an etiologic diagnosis and to start early treatment.
The typical infection with influenza virus consists of a sudden onset of fever, chills, myalgia, arthralgia, cough, sore
throat, and rhinorrhea. The incubation period is 1-2 days, and symptoms normally last 3-5 days. These symptoms
are common to other respiratory viral infections but are highly suggestive of influenza virus infection when an
outbreak is occurring in the community. Influenza is usually seen in epidemics and pandemics in late winter and
early spring.
Peak attack rates for respiratory syncytial virus (RSV) occur in the winter in infants younger than six months.
Parainfluenza (PIV) infection most often occurs in the late fall or winter, although PIV-3 pneumonia is especially
common in the spring.

Physical Examination
The physical examination findings in viral pneumonia are similar to those of pyogenic pneumonia and are,
therefore, nonspecific. Physical examination demonstrates wheezing, crackles, increased fremitus, and bronchial
breath sounds over the involved regions of the lungs.
Some patients have few, if any, physical findings other than mild fever, whereas other patients may have
respiratory and/or multiorgan failure. Other findings include the following:
Fever and/or chills
Cough (with or without sputum production)
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Tachypnea and/or dyspnea


Tachycardia or bradycardia
Wheezing
Rhonchi
Rales
Sternal or intercostal retractions
Dullness to percussion
Decreased breath sounds
Pleurisy
Pleuarl friction rub
Cyanosis
Rash
Acute respiratory distress

Influenza virus
Influenza pneumonia especially affects the following groups of patients:
Children with cystic fibrosis or organ transplants
Adults with chronic cardiovascular or respiratory disease, diabetes mellitus, renal diseases,
hemoglobinopathies, or immunosuppression
Residents of nursing homes or chronic care facilities
Healthy adults older than 65 years.
The three clinical forms of influenza pneumonia are primary influenza pneumonia, secondary bacterial pneumonia,
and mixed viral and bacterial pneumonia.
Primary influenza pneumonia manifests with persistent symptoms of cough, sore throat, headache, myalgia, and
malaise for more than 3-5 days. The symptoms may worsen with time, and new respiratory symptoms, such as
dyspnea and cyanosis, may appear. This form is the least common but the most severe in terms of pulmonary
complications.
Secondary bacterial pneumonia is characterized by the relapse of high fever, cough with purulent sputum after
initial improvement, and radiographic evidence of new pulmonary infiltrates. The most common pathogen is
Streptococcus pneumoniae (48%), followed by Staphylococcus aureus,[52] Haemophilus influenzae, and Gramnegative pathogens.
Elderly persons may have a lower frequency of upper respiratory complaints. One study demonstrated that the
triad of cough, fever, and acute onset had only a 30% positive predictive value, in contrast to 78% in young adults.
Fever and altered mental status may be the only signs of influenza pneumonia in an older patient with chronic
cognitive impairment. Gastrointestinal complaints and myalgia are more common in influenza than in RSV
infection.[43, 53]
Avian influenza (H5N1) has an incubation period of 2-5 days, but it may be up to seven days after exposure. The
primary initial symptom is fever, and symptoms of cough, malaise, myalgia, headache, sore throat, abdominal
pain, vomiting, and diarrhea are also common. The gastrointestinal complaints may initially suggest
gastroenteritis. When pneumonia develops, cough, followed by dyspnea, tachypnea, and chest pain, are reported.
In severe cases, encephalitis/encephalopathy, cardiac failure, renal failure, multiorgan failure, and disseminated
intravascular coagulation can occur.[54]
H1N1 influenza presents similarly to seasonal influenza. Fever and cough are almost universal symptoms.
Shortness of breath (54%), fatigue/weakness (40%), chills (37%), myalgias (36%), rhinorrhea (36%), sore throat
(31%), headache (31%), vomiting (29%), wheezing (24%), and diarrhea (24%) are the most common other
symptoms.
Mixed viral and bacterial pneumonia is common and can manifest as a gradual progression of disease or as a
transiently improving condition followed by a worsening one. Both bacterial pathogens and an influenza virus are
isolated.
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Respiratory syncytial virus


Risk factors for RSV infection include age younger than six months, underlying lung disease (bronchopulmonary
dysplasia or cystic fibrosis), and congenital heart disease in children with asthma. Institutionalized elderly and
immunosuppressed patients (eg, those with severe combined immunodeficiency, leukemia, and/or transplant) are
also at risk.
RSV infections in adults are poorly characterized and rarely diagnosed. They are accompanied by long-lasting
upper respiratory tract infections and are more commonly associated with a prolonged productive or bronchitic
cough and wheezing than with other features. The findings tend to mimic the decompensated underlying
cardiopulmonary disease rather than the acute viral disease.
Various studies reported RSV pneumonia in recipients of solid organ transplants or HSCTs. The clinical
manifestations are usually severe, and supplemental oxygen and mechanical ventilation are required.
Severe cases of RSV giant-cell pneumonia have been reported in 4-10% of cases and also during concurrent viral
infections with EBV, CMV, or adenovirus.
In healthy hosts, RSV causes upper respiratory tract illness, tracheal bronchitis, bronchiolitis, and pneumonia.
Upper respiratory tract symptoms, such as coryza and pharyngitis, precede lower respiratory tract involvement.
Patients with RSV pneumonia typically present with fever, nonproductive cough, otalgia, anorexia, and dyspnea.
Wheezes, rales, and rhonchi are common physical findings.
Pneumonia and bronchiolitis often are difficult to differentiate, and both can be associated with wheezing, rales,
and hypoxemia. Dyspnea and cough are seen in 60-80% of cases. Compared with influenza, RSV is more often
associated with rhinorrhea, sputum production, and wheezing and less often associated with gastrointestinal
complaints and fever.[55, 1]
Immunocompromised hosts may have a range of respiratory involvement. These patients develop fever, cough,
rhinorrhea, sinus congestion, and respiratory difficulties; nearly half report wheezing. In these patients, the
symptoms range from mild dyspnea to severe respiratory distress and respiratory failure.
While most patients with RSV infection, including infants, have only upper respiratory symptoms, as many as 2540% develop bronchiolitis and/or pneumonia. Statistics demonstrate that as many as 20-25% of infants with
pneumonia who require hospitalization are infected with RSV.
Lower respiratory disease in infants is preceded by a prodrome of rhinorrhea and, perhaps, poor appetite. Lowgrade fever, cough, and wheezing usually occur. The chest examination reveals tachypnea, rales, and fine
wheezes. Disease from RSV in young, healthy adults is usually mild, although one study of community-acquired
pneumonia showed RSV to be the third most common pathogen,[55] after S pneumoniae and influenza viruses A
and B.
During their first RSV infection, 25-40% of infants and young children have signs or symptoms of bronchiolitis of
pneumonia, and 0.5-2% require hospitalization. Most pediatric patients hospitalized for RSV infection are younger
than six months.

Parainfluenza virus
Clinical manifestations of PIV infection can range from mild upper respiratory tract infections (mainly in
immunocompetent patients) to severe croup, bronchiolitis, or life-threatening pneumonia in the setting of
immunosuppression. Incubation is 1-3 days. The classic croup symptoms of barking cough, hoarseness, and
stridor commonly seen in children is less commonly seen in adults. In adults who are immunocompromised,
cough is the hallmark.
PIV-1 and PIV-2 produce croup in children that initially manifests as an upper respiratory tract infection followed by
a barking cough, dyspnea, stridor, and chest-wall retractions. PIV-2 infections tend to be milder than PIV-1
infections. PIV-4 causes mild upper respiratory tract infection in both adults and children.
PIV-3 is the main strain that causes pneumonia and bronchiolitis. The signs and symptoms are nonspecific, more
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prominent in children, and similar to, but milder than, those of RSV pneumonia. They include fever, cough, coryza,
dyspnea with rales, and wheezing.
Immunosuppression promotes the development of PIV pneumonia. Situations leading to immunosuppression
include the following: BMT, solid-organ transplantation (with mild forms), severe combined immunodeficiency in
children, or therapy with etanercept.
PIV infection may appear as giant-cell pneumonia. This form is most frequent in immunocompromised patients
(after BMT or umbilical-cord transfusion) and rarely associated with alveolar proteinosis. The mortality rate
approaches 100% in children, with a better prognosis than this in adults.
PIV pneumonia may mimic other lung infections most commonly encountered in an immunocompromised host.
Several clinical findings tend to distinguish PIV or RSV lung infection from CMV or other opportunistic forms of
pneumonia: upper respiratory infection before lung infection, clinical and imaging evidence of sinusitis, and
wheezing.
As many as one third of children with PIV infection can have bacterial superinfection. Even if long-term sequelae
are uncommon, cryptogenic organizing pneumonia is described after PIV infection.

Human metapneumovirus
Symptoms of human metapneumovirus (hMPV) infection are similar to those caused by other viruses: nasal
congestion and cough are present in 82-100% of cases. Other symptoms include rhinorrhea (69-82%), dyspnea
(69%), wheezing (62%), sputum production (55%), hoarseness (46-91%), and sore throat (23-45%). The
incubation period is 5-6 days.
In one study, hoarseness was more common in hMPV than in RSV infection. Hoarseness, dyspnea, and
wheezing were significantly more common among the elderly older than 65 years than among adults younger than
40 years.[16]
In different studies, cough was reported in 90% of patients; dyspnea, in 83%; coryza, in 88%; and fever, in 5292%. Among the physical signs, rales, wheezing, or stridor were found in one half of infected children. In children,
hMPV is an important cause of wheezing (9% in a 132 case series). Fever, cough, dyspnea, and sore throat are
commonly described in adults. In HSCT recipients, hMPV pneumonia is reported and tends to cause respiratory
failure.

Coronavirus
The incubation period is 2-5 days, with a mean of 3 days. Symptoms are similar to those from other respiratory
viruses, including cough, rhinorrhea, sore throat, headache, and malaise, although fever was only seen in 21-23%
of cases.

Varicella-zoster virus
The initial presenting symptoms of VZV infection are low-grade fever, malaise, and a rash that is typically
vesicular, starts on the trunk and face, spreads centrifugally to other parts of the body, and usually is in various
stages of evolution (from vesicles to crusted scabs) by the time of presentation. VZV pneumonia develops in 1 in
400 cases.
VZV pneumonia starts gradually within 1-6 days after the rash appears and manifests with fever, chest tightness,
tachypnea, dyspnea, dry cough, cyanosis, and (in rare cases) pleuritic chest pain and hemoptysis. Physical
examination reveals minimal findings, with rare rhonchi or wheezes. New chest symptoms are strongly associated
with radiologic findings. VZV pneumonia can develop as a mild disease, or it can be severe and rapidly fatal,
especially in immunocompromised individuals.
Some patients may be asymptomatic. One study in military personnel noted that only 25% of those with VZV
pneumonitis experienced cough and 10% had tachypnea.[56]
Risk factors related to VZV pneumonia are smoking, pregnancy (third trimester), immunosuppression, and male
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gender. The presence of more than 100 spots during the skin eruption, prolonged fever, a history of contact with an
index case, and chest symptoms at presentation are also reported risk factors.

Measles virus
The incubation period of measles is 10-14 days after exposure, after which a prodrome of fever, malaise, anorexia,
conjunctivitis, cough, and coryza ensue. Toward the end of the prodrome, Koplik spots (small white punctate
lesions) may appear on the buccal mucosa.
The rash is an erythematous, maculopapular eruption that may become confluent, beginning on the face, then
progressing down the body to involve the extremities last, including palms and soles.
Atypical measles occurs in patients who were immunized from 1963-1967 with a killed vaccine and are exposed to
measles virus or live measles virus vaccine. In these cases, the rash starts in the hands and feet rather than in a
central distribution.
Duration of the rash is approximately 5 days, after which it may desquamate. Duration of symptoms is usually 10
days, and the cough may be the last symptom to disappear.
In adults, 3% of measles cases are complicated by significant pneumonia requiring hospitalization, with 17% of
patients experiencing bronchospasm and 30%, bacterial superinfection. Bacterial superinfection most often occurs
5-10 days after the onset of the rash. The pulmonary findings parallel the cutaneous signs, and the severity of
pneumonia correlates with worsening rash.
Persons at risk for measles-virus pneumonia are those with T-cell immunosuppression (eg, those taking steroids),
BMT recipients, and those with HIV infection, lymphoma, leukemia, or Epstein-Barr virus infection. Others at risk
are children and the elderly, pregnant women, those with vitamin A deficiency, and persons not vaccinated or
those in whom primary vaccination failed.
Four types of measles-associated pneumonia are encountered. The first, measles-virus pneumonitis, usually
appears within a few days after the onset of rash. High levels of KL6 (a glycoprotein secreted by pneumocyte-2)
are markers for interstitial pneumonia and are associated with a poor prognosis.
The second form, bacterial superinfection, usually develops several days after rash appears. This type manifests
with cough, fever, purulent expectoration, tachycardia, and pleural pain.
Third, giant cell pneumonia typically develops before or with the peak of viral exanthema. In rare cases, it develops
after five months or longer. Rash may be absent. Cough may persist for 1-2 weeks during recovery. Lung biopsy
may be needed for final diagnosis.
Fourth, pneumonia of atypical measles is described in adults. These patients developed a potentially fatal illness,
with increased fever (7-14 d after exposure), minimal or absent rashes, headache, arthralgias, hepatitis, interstitial
or nodular infiltrates, hilar lymphadenopathy, and occasional pleural effusions.

Cytomegalovirus
CMV pneumonia is usually mild in otherwise healthy individuals. It starts as a mononucleosis-like syndrome (eg,
malaise, fever, myalgias) with mild hepatitis and no lymphadenopathy or splenomegaly.
In immunocompromised people, the clinical picture may vary. Most commonly, asymptomatic shedding affects
pulmonary secretions, blood, and urine, with no clinical significance and low mortality rates.
CMV syndrome manifests with self-limited fever and constitutional symptoms (fever, malaise, anorexia, myalgias,
arthralgias, fatigue). CMV syndrome precedes CMV pneumonitis by 1-2 weeks and usually has a sudden onset,
with respiratory complaints (cough, dyspnea, tachypnea), fever, an increased A-a gradient, and radiologic
infiltrates. The duration is less than two weeks. See the A-a Gradient calculator.
In allogeneic HSCT recipients, CMV disease presents post engraftment (30-99 d after transplantation) and late (
100 d) in those with graft versus host disease and/or on higher-dose immunosuppressive therapy. CMV pneumonia
is seen in 10-30% of such patients, and the median time to occurrence is 44 days after transplantation.
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Autologous HSCT recipients are at much lower risk for CMV pneumonia, seen in only 1-9% of cases, oftentimes
with milder symptoms.
Among solid organ transplant recipients, CMV pneumonia is most common in lung transplantations, ranging from
15-55% of cases. Typically, this pneumonia develops between day 15-60 post transplantation and is characterized
by fever, cough, and hypoxia. In CMV donor-positive/recipient-negative cases, the onset and progression can be
rapid.
Other solid organ transplantations are associated with low rates of CMV pneumonia: liver, 9.2%; heart, 0.8-6.6%;
and kidney less than 1%.
For BMT recipients, risk factors are pretreatment seropositivity, total-body irradiation, certain immunosuppressive
treatment, severe acute or chronic graft-versus-host disease, underlying disease (acute lymphoblastic leukemia
[ALL] or chronic lymphocytic leukemia [CLL]). Patients with primary CMV infection and allogeneic HSCT are at
increased risk for severe disease.
In HIV patients, the pathogenic significance of CMV is considered low, even in the condition of common
identification of viruses in bronchoalveolar lavage (BAL) and biopsy specimens. CMV pneumonia is found in HIV
patients with a CD4 count of less than 200 cells/L. CMV is thought to be a co-pathogen to Pneumocystis jiroveci
and a cause of alveolar hemorrhage in HIV patients (due to thrombotic microangiopathy).
Clinical outcomes range from mild, self-limited illness to rapidly fatal infection with multiorgan involvement (retinitis,
colitis, hepatitis). The mortality rate can be high.
CMV complicated by obstructive bronchiolitis in heart-lung and double-lung recipients affected 47% of 36 patients
in a study in France. Risk factors were CMV seropositivity among donors and CMV pneumonia or CMV
recurrence.

Herpes simplex virus


Herpes simplex virus causes pneumonia in only the most severely immunocompromised patients. HSV is not
usually isolated from immunocompetent patients, or even from BAL fluid from HIV-infected patients. The rate of
HSV pneumonia can be as high as 70-80% in HSCT recipients not receiving prophylaxis, and it can be decreased
to 5% with acyclovir prophylaxis.
HSV pneumonia often is preceded by oral mucocutaneous lesions or esophagitis. The presence of
mucocutaneous disease, esophagitis, or tracheitis, especially with endotracheal intubation, increases the
likelihood of this pneumonia. The spectrum of respiratory diseases due to HSV infection ranges from oral
pharyngitis to membranous tracheobronchitis and diffuse or localized pneumonia, which can proceed to ARDS.
In BMT recipients, the usual presentation of HSV pneumonitis consists of dyspnea, fever, cough, and hemoptysis
with associated dysphagia, liver, and CNS involvement. HSV pneumonia in organ-transplant recipients is reported.
In ICU patients, HSV pneumonia manifests as an unexplained dyspnea or as a failure of weaning the patient from
a ventilator. One study showed that most ICU patients had been intubated (95%) or had undergone thoracic
surgery (73%) at the time of diagnosis. Blood transfusions, use of corticosteroids and other immunosuppressants,
local trauma, smoking, and burns are risk factors.
Dyspnea, cough, fever, tachypnea, intractable wheezing, chest pain, and hemoptysis are common symptoms of
HSV pneumonia.

Hantavirus
Hantavirus pulmonary syndrome (HPS) has an incubation period of 9-35 days.
HPS is characterized by four clinical phases, as follows:
Prodrome
Noncardiogenic pulmonary edema/adult respiratory distress syndrome and shock
Diuresis
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Convalescence
Fever and myalgia are prominent in almost all phases and precede the onset of respiratory symptoms by 1-10
days. Cough and upper respiratory symptoms are uncommon, in contrast to many of the other viral prodromes to
pneumonia. These patients often complain of severe back and hip pain, and they develop nausea, vomiting,
abdominal pain, and diarrhea. Dry cough and shortness of breath herald the development of pulmonary edema.
Onset and rapid progression of cough, shortness of breath, fever, and hypotension herald the cardiopulmonary
phase of the disease. Progressive pulmonary edema and respiratory failure can occur in 80-90% of patients within
two days of hospitalization. The interval between the onset of dyspnea and respiratory failure requiring ventilatory
support may be a few hours. The earliest indication is hypoxemia.
In addition to the rapidly progressive, fulminant, and often fatal form of HPS, there is also a limited, less severe
form associated with mild interstitial edema and minimal airspace disease.

Adenovirus
Symptoms of adenovirus infection include fever, malaise, headache, sore throat, hoarseness, and cough. The
incubation period is 4-5 days. Keratoconjunctivitis and diarrhea may or may not be seen, depending on the
serotype (8, 19, 37 causing the former, and 2, 3, 5, 40, 41 causing the latter).
Serotype 14 pneumonia is associated most commonly with fever (89%) and cough (82%). Other common
symptoms include shortness of breath (58%), vomiting (42%), diarrhea (34%), headache (29%), myalgias (29%),
coryza (26%), chills (26%), sore throat (21%), and chest pain (16%).[12]
In adults who are immunocompromised, fever is predominant and gastrointestinal symptoms can be severe.
Although adenovirus is almost always isolated from the respiratory tract, pulmonary symptoms may not be
prominent and dissemination can occur without significant evidence of pneumonia (by symptoms or radiographs).
Dissemination can lead to gastroenteritis, hepatitis, and hemorrhagic cystitis.[35]

Avian influenza
Avian influenza has a fulminant course and a high mortality rate. The clinical symptoms of avian influenza depend
on the etiologic agent. Those infected with A/H7N7 have conjunctivitis and/or an influenzalike illness. In the 1997
outbreak of A/H5N5, 11 of 18 patients were younger than 14 years. Gastrointestinal symptoms of abdominal pain,
diarrhea, and vomiting were prominent. Seven recovered, but 11 progressed to pneumonia and six died of ARDS or
multiorgan failure.
In the 2004 outbreak, the young were affected more frequently, diarrhea was again prominent, fever was universally
present, and the main presenting syndrome was community-acquired pneumonia. Lymphopenia and
thrombocytopenia were common findings in all series of outbreaks and were prognostic indicators of ARDS and
death. The case-fatality rate ranged from 64-80%. The incidence of asymptomatic or mild infection is unknown.

Epstein-Barr virus
Lung involvement secondary to EBV infection is rare and can occur as a complication of infectious mononucleosis.
In healthy individuals, pulmonary manifestations, such as dyspnea and cough, are rare. Chronic interstitial lung
disease is reported in immunocompetent patients.
In children with cystic fibrosis, EBV can cause deterioration in pulmonary function that lasts longer than six
months after the infection is diagnosed.
In HIV patients, relatively few studies have been conducted to investigate EBV-related pulmonary disease. EBV
seems to be related to the development of AIDS-associated non-Hodgkin lymphoma. BAL fluid samples from 72
European patients with AIDS were positive for EBV in five. The patients had fever and low PaO2, with no
radiographic infiltrates, and recovery was the rule.
In BMT recipients, EBV-related lung manifestations are among widespread extrarenal manifestations of
posttransplant lymphatic disease. A fulminant presentation soon after transplantation is associated with a dire
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prognosis. Young age and primary infection are risk factors. Patients with EBV infection are at subsequent risk for
other viral lung superinfection (eg, severe RSV or Mycoplasma pneumoniae infection).

Human herpesvirus
HHV 6 (A and B) and HHV 7 have a limited clinical significance and prevalence as lung pathogens. HHV 6 appears
in healthy individuals or HIV-infected patients with a high CD4+ count, in whom it may result in further
immunosuppression. HHV 8 is an important pathogen in HIV patients with a 200 CD4+ count of less than 200
cells/L and has been associated with Kaposi sarcoma in the lungs, sometimes with alveolar hemorrhage.

Human immunodeficiency virus


HIV pneumonitis usually manifests as several months of mild cough and dyspnea and bilateral infiltrates on chest
radiograph. Transbronchial biopsy is usually required for diagnosis. The differential diagnosis includes
Pneumocystis pneumonia.

Human lymphotropic virus


HTLV-1related lung inflammatory disorders (eg, bronchopneumopathy associated with HTLV-1) encountered in
HTLV-1 carriers include lymphocytic interstitial pneumonia, diffuse panbronchiolitis, bronchiectasis, and bullous
lung disease.

Rhinovirus
Rhinoviruses are a common cause of upper respiratory tract infection, but in rare cases they can trigger lower
respiratory tract infections, too. Rhinoviruses commonly cause exacerbations of preexisting airway disease in
those with asthma, chronic obstructive pulmonary disease (COPD),[57] or cystic fibrosis.
Rhinovirus-induced lower respiratory infections in children include bronchiolitis or bronchitis (25.6%), pneumonia
(6.2%), and acute episodes of asthma (5.7%). Among 211 French children hospitalized with rhinovirus infection,
29% had ARDS. In addition, 9% of children had an associated bacterial infection, and 9% had a dual viral
involvement.
Rhinoviral infection can be complicated by S pneumoniae superinfection. This might be explained by increased
adherence of this virus to epithelial tracheal cells after rhinoviral infection.

Rotavirus
Rotavirus pneumonia is rare. In one study, rotaviruses were isolated in 27% of all tracheal aspirates from children
with pneumonia. One case of fatal rotaviral pneumonitis occurred with myocarditis in a two-year-old boy.
Two cases of fatal rotaviral pneumonitis were reported in adults. One patient was receiving long-term steroid
therapy and developed rapidly progressive respiratory distress that evolved into severe respiratory failure not
responsive to supportive measures. The other patient presented with massive pulmonary edema and pleural
effusions.

Transplantation-related pneumonia
In recipients of thoracic organ transplants, chest complications, though rare, may manifest as tracheobronchitis,
localized viral pneumonia, or diffuse and bilateral pneumonic infiltrates involving mainly the lower lobes. These
findings may develop secondary to bacterial pneumonia, bronchiolitis obliterans syndrome, or acute allograft
rejection. Mild clinical manifestations occur in 64% of lung transplant recipients with lung infection due to influenza
virus or PIV.

Contributor Information and Disclosures


Author
Zab Mosenifar, MD Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild
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Pulmonary Disease Institute, Professor and Executive Vice Chair, Department of Medicine, Cedars Sinai
Medical Center, University of California, Los Angeles, David Geffen School of Medicine
Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians,
American College of Physicians, American Federation for Medical Research, and American Thoracic Society
Disclosure: Nothing to disclose.
Coauthor(s)
Arthur Jeng, MD Assistant Professor of Clinical Medicine, University of California at Los Angeles School of
Medicine
Arthur Jeng, MD is a member of the following medical societies: Infectious Diseases Society of America
Disclosure: Nothing to disclose.
Nader Kamangar, MD, FACP, FCCP, FCCM, FAASM Associate Professor of Clinical Medicine, University of
California, Los Angeles, David Geffen School of Medicine; Chief, Division of Pulmonary and Critical Care
Medicine, Olive View-UCLA Medical Center; Associate Program Director, Multi-Campus Pulmonary and Critical
Care Fellowship Program, Cedars-Sinai/West Los Angeles Veterans Affairs/Los Angeles Kaiser
Permanente/Olive View-UCLA Medical Center
Nader Kamangar, MD, FACP, FCCP, FCCM, FAASM is a member of the following medical societies: American
Academy of Sleep Medicine, American Association of Bronchology, American College of Chest Physicians,
American College of Physicians, American Lung Association, American Medical Association, American
Thoracic Society, Association of Pulmonary and Critical Care Medicine Program Directors, Association of
Specialty Professors, Clerkship Directors in Internal Medicine, Society of Critical Care Medicine, and World
Association for Bronchology and Interventional Pulmonology
Disclosure: Nothing to disclose.
Chief Editor
Ryland P Byrd Jr, MD Professor of Medicine, Division of Pulmonary Disease and Critical Care Medicine,
James H Quillen College of Medicine, East Tennessee State University
Ryland P Byrd Jr, MD is a member of the following medical societies: American College of Chest Physicians
and American Thoracic Society
Disclosure: Nothing to disclose.
Additional Contributors
Shakeel Amanullah, MD Consulting Physician, Pulmonary, Critical Care, and Sleep Medicine, Lancaster
General Hospital
Shakeel Amanullah, MD is a member of the following medical societies: American College of Chest Physicians,
American Thoracic Society, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.
Michael S Beeson, MD, MBA, FACEP Professor of Emergency Medicine, Northeastern Ohio Universities
College of Medicine and Pharmacy; Attending Faculty, Akron General Medical Center
Michael S Beeson, MD, MBA, FACEP is a member of the following medical societies: American College of
Emergency Physicians, Council of Emergency Medicine Residency Directors, National Association of EMS
Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Paul Blackburn, DO, FACOEP, FACEP Attending Physician, Department of Emergency Medicine, Maricopa
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Medical Center
Paul Blackburn, DO, FACOEP, FACEP is a member of the following medical societies: American College of
Emergency Physicians, American College of Osteopathic Emergency Physicians, American Medical
Association, and Arizona Medical Association
Disclosure: Nothing to disclose.
Dan V Dinescu, MD Fellow in Pulmonary Medicine, Department of Internal Medicine, Memorial Sloan Kettering
Cancer Center
Dan V Dinescu, MD is a member of the following medical societies: American College of Chest Physicians,
American College of Physicians-American Society of Internal Medicine, American Medical Association,
American Thoracic Society, Medical Society of the State of New York, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.
Kavita Garg, MD Professor, Department of Radiology, University of Colorado School of Medicine
Kavita Garg, MD is a member of the following medical societies: American College of Radiology, American
Roentgen Ray Society, Radiological Society of North America, and Society of Thoracic Radiology
Disclosure: Nothing to disclose.
Gloria J Kuhn, DO, PhD, FACEP Professor, Vice-Chair of Academic Affairs, Dept of Emergency Medicine,
Wayne State University School of Medicine; Professor, Department of Internal Medicine, Section of Emergency
Medicine, Michigan State University College of Osteopathic Medicine
Gloria J Kuhn, DO, PhD, FACEP is a member of the following medical societies: American Osteopathic
Association
Disclosure: Nothing to disclose.
Robert E O'Connor, MD, MPH Professor and Chair, Department of Emergency Medicine, University of Virginia
Health System
Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of
Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives,
American Heart Association, American Medical Association, Medical Society of Delaware, National
Association of EMS Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.
Mark L Shapiro, MD Chief, Department of Radiology, Englewood Hospital and Medical Center
Mark L Shapiro, MD is a member of the following medical societies: American College of Radiology, American
Roentgen Ray Society, and Radiological Society of North America
Disclosure: Nothing to disclose.
Sat Sharma, MD, FRCPC Professor and Head, Division of Pulmonary Medicine, Department of Internal
Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital
Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep
Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal
Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and
Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical
Association
Disclosure: Nothing to disclose.
Satinder P Singh, MD, FCCP Professor of Radiology and Medicine, Chief of Cardiopulmonary Radiology,
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Director of Cardiac CT, Director of Combined Cardiopulmonary and Abdominal Radiology, Department of
Radiology, University of Alabama at Birmingham School of Medicine
Disclosure: Nothing to disclose.
Eric J Stern, MD Professor of Radiology, Adjunct Professor of Medicine, Adjunct Professor of Medical
Education and Biomedical Informatics, Adjunct Professor of Global Health, Vice-Chair, Academic Affairs,
University of Washington School of Medicine
Eric J Stern, MD is a member of the following medical societies: American Roentgen Ray Society, Association
of University Radiologists, European Society of Radiology, Radiological Society of North America, and Society
of Thoracic Radiology
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center
College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
Mark R Wallace, MD, FACP, FIDSA Clinical Professor of Medicine, Florida State University College of
Medicine; Head of Infectious Disease Fellowship Program, Orlando Regional Medical Center
Mark R Wallace, MD, FACP, FIDSA is a member of the following medical societies: American College of
Physicians, American Medical Association, American Society of Tropical Medicine and Hygiene, and Infectious
Diseases Society of America
Disclosure: Nothing to disclose.

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