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What Is an Upper Respiratory Infection?

Many people consider an upper respiratory infection (URI) and a common cold to be the same condition. This is not entirely true, however, since a cold virus is only one of many infectious agents that can cause an upper respiratory infection.

It is more accurate to describe an upper respiratory infection as any type of infection that affects the upper respiratory tract, namely the nose, sinuses, and throat. Learn more about the symptoms, causes, and treatment of URIs.

Upper Respiratory Infection Symptoms

Typical symptoms of URIs may include a combination of one or more of the following symptoms:

  • Nasal congestion
  • Sore throat
  • Sore muscles

Nausea, vomiting, or diarrhea may occur with a URI associated with influenza infection. If the URI progresses to sinusitis , symptoms may include a severe headache, face pain, thick green or yellow nasal discharge, or tooth pain.

It is possible to develop an ear infection after having an upper respiratory infection, and this is especially true in small children.

When to See a Healthcare Provider

You should see a healthcare provider to rule out strep throat if your sore throat is severe and you don't have typical symptoms of a cold virus such as a runny nose, sneezing, or coughing. You are also more likely to experience a bacterial infection that requires antibiotics if your symptoms have lasted 10 or more days.

You should seek emergency medical attention if you or your child experiences:

  • difficulty breathing including abnormal noises while breathing, rapid breathing, or blue lips or skin tone
  • excessive drooling or inability to swallow
  • extreme lethargy
  • little or no urine output

For a small child, little or no urine output means no wet diapers or very few wet diapers, especially if your child has not been eating or drinking well, has had diarrhea, or has been or vomiting.

Parents should not hesitate to consult expert medical help for any symptoms that seem atypical or worrisome.

An upper respiratory infection is likely to have one of the following causes:

  • one of hundreds of common cold viruses (including rhinoviruses, adenoviruses, coronaviruses, and coxsackieviruses)
  • influenza A and B
  • parainfluenza virus

This list is not comprehensive, but it does include some of the most common causes of URIs.

Are URIs Serious?

Most upper respiratory infections are caused by a cold virus and are not serious—most healthy individuals will fight off these infections on their own. There are a few exceptions, however. Strep throat can have serious complications if left untreated. If your sore throat is severe, you have abdominal pain, and you lack a runny nose or a cough, you may have strep throat.

Rarely, URIs can progress to more serious conditions such as epiglottis . This is more likely in small children. Viruses such as respiratory syncytial virus (RSV)—a respiratory tract infection in small children—can be serious and lead to hospitalization, especially in small infants.

Synagis (palivizumab) and Beyfortus (nirsevimab) are monoclonal antibodies that can help protect certain infants and children 24 months and younger who are at high risk of serious complications from RSV during their RSV season. Synagis and Beyfortus are not vaccines and cannot cure or treat a child diagnosed with RSV. If your child is at very high risk for RSV infection, your pediatrician may discuss this option with you.  

In many cases, especially in adults, upper respiratory infections do not require a diagnosis by a healthcare provider unless there are persistent, severe, or worrisome symptoms.

Most URIs are caused by rhinovirus and can be managed at home.

A diagnosis of an upper respiratory infection is usually not complicated. Your healthcare provider will usually ask you about your symptoms and other questions about your health history, such as when your symptoms started and what might make you feel better or worse.

Your healthcare provider will perform a physical examination in which she will look at the back of your throat, and into your ears.

If strep throat is suspected, a rapid strep test or a throat culture will be obtained. This involves swabbing the back of your throat and then testing it for strep bacteria. Occasionally, cultures from the nasal passageways may be taken and tested for a bacterial infection. However, this is usually only done with a nasopharyngeal swab diagnosis used for the flu and other pathogens (often performed in urgent care).

In some cases, other tests may be ordered to rule out conditions that cause similar symptoms such as allergies.

URIs caused by a virus can usually be managed at home. People with healthy immune systems can fight the virus off within a week or two. There are a variety of ways you can help your recovery and to treat bothersome symptoms.

Tips for Treating an Upper Respiratory Infection

  • Use a humidifier
  • Try decongestants and throat lozenges
  • Drink plenty of fluids
  • Take over-the-counter pain relievers
  • Stay home and rest
  • Keep your head elevated

Decongestants and OTC Drugs

Types of decongestants you might try include pseudoephedrine and oxymetazoline spray , which can be effective for managing symptoms but should not be used longer than three days in a row to avoid a condition called rebound congestion . In addition, you may also consider saline nasal sprays or nasal irrigation with a neti pot .

Decongestants and cough remedies are not usually recommended for small children and infants as they have not been proven effective. Talk to your pediatrician before using them. While over-the-counter (OTC) pain relievers such as ibuprofen and acetaminophen can help adults ease a sore throat, muscle aches, and headaches, children should not be given aspirin.

Over-the-counter upper respiratory infection medications for kids should be discussed thoroughly with and approved by your child's pediatrician.

If possible, do not attend work or school to avoid spreading illness. Additionally, keeping your head elevated can help with congestion and earaches.

Zinc and Vitamin C

There is limited evidence that taking zinc and vitamin C may shorten the duration of the common cold. However, since zinc can interact with other medications, you should check with your pharmacy if you are taking something in addition to zinc.

Antibiotics

Antibiotics are usually only prescribed in certain circumstances when a bacterial infection is confirmed or highly suspected. Overuse of antibiotics has contributed to the resistance of harmful bacteria, so your healthcare provider may not automatically prescribe something for you.

If you are prescribed an antibiotic, make sure you take it exactly as prescribed. Most bacterial infections start to respond to an appropriate antibiotic within 24 hours. Antibiotics may cause stomach problems including diarrhea. If you have problems with this, you may try eating yogurt with live active cultures and taking the antibiotic with food.

Good hygiene such as hand washing and covering your mouth and nose when you cough and sneeze is imperative when it comes to preventing the spread of upper respiratory infections. People who are sick should stay at home and avoid public places whenever possible.

It is also important to keep your immune system healthy by getting plenty of sleep, exercise, and eating a healthy diet. This will help your body fight off the germs it comes into contact with and also shortens the amount of time it takes to fight off illness.

Staying up to date on vaccinations and getting an annual flu shot is also an important factor when it comes to preventing URIs. Unfortunately, except for influenza, vaccines for most causes of URI haven’t been developed. Still, the influenza vaccine remains very important, because it prevents hundreds of thousands of cases and thousands of deaths of Americans each year.

A Word From Verywell

An upper respiratory infection is a condition that could be caused by a variety of factors, including a cold, the flu, or strep throat. It is important that you are proactive in treating your symptoms, which could involve using a humidifier or taking over-the-counter medications. It's crucial to get rest and stay home from activities when possible. If your symptoms worsen, be sure to contact your healthcare provider. Though most URIs are not a cause for concern, symptoms can sometimes lead to more severe conditions.

5 Tips: Natural Products for the Flu and Colds: What Does the Science Say? National Center for Complementary and Integrative Health. Updated December 2017.

Upper Respiratory Tract Infection. Medscape. Updated June 2018.

By Kristin Hayes, RN Kristin Hayes, RN, is a registered nurse specializing in ear, nose, and throat disorders for both adults and children.

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22.2: Bacterial Infections of the Respiratory Tract

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Learning Objectives

  • Identify the most common bacteria that can cause infections of the upper and lower respiratory tract
  • Compare the major characteristics of specific bacterial diseases of the respiratory tract

The respiratory tract can be infected by a variety of bacteria, both gram positive and gram negative. Although the diseases that they cause may range from mild to severe, in most cases, the microbes remain localized within the respiratory system. Fortunately, most of these infections also respond well to antibiotic therapy.

Streptococcal Infections

A common upper respiratory infection, streptococcal pharyngitis (strep throat) is caused by Streptococcus pyogenes . This gram-positive bacterium appears as chains of cocci, as seen in Figure \(\PageIndex{1}\). Rebecca Lancefieldserologically classified streptococci in the 1930s using carbohydrate antigens from the bacterial cell walls. S. pyogenes is the sole member of the Lancefield group A streptococci and is often referred to as GAS, or group A strep.

Micrograph of chains of spheres.

Similar to streptococcal infections of the skin, the mucosal membranes of the pharynx are damaged by the release of a variety of exoenzymes and exotoxins by this extracellular pathogen. Many strains of S. pyogenes can degrade connective tissues by using hyaluronidase, collagenase and streptokinase. Streptokinase activates plasmin, which leads to degradation of fibrin and, in turn, dissolution of blood clots, which assists in the spread of the pathogen. Released toxins include streptolysins that can destroy red and white blood cells. The classic signs of streptococcal pharyngitis are a fever higher than 38 °C (100.4 °F); intense pharyngeal pain; erythema associated with pharyngeal inflammation; and swollen, dark-red palatine tonsils, often dotted with patches of pus; and petechiae (microcapillary hemorrhages) on the soft or hard palate (roof of the mouth) (Figure \(\PageIndex{2}\)). The submandibular lymph nodes beneath the angle of the jaw are also often swollen during strep throat.

Some strains of group A streptococci produce erythrogenic toxin. This exotoxin is encoded by a temperate bacteriophage (bacterial virus) and is an example of phage conversion (see The Viral Life Cycle ). The toxin attacks the plasma membranes of capillary endothelial cells and leads to scarlet fever (or scarlatina), a disseminated fine red rash on the skin, and strawberry tongue, a red rash on the tongue (Figure \(\PageIndex{2}\)). Severe cases may even lead to streptococcal toxic shock syndrome (STSS), which results from massive superantigen production that leads to septic shock and death.

S. pyogenes can be easily spread by direct contact or droplet transmission through coughing and sneezing. The disease can be diagnosed quickly using a rapid enzyme immunoassay for the group A antigen. However, due to a significant rate of false-negative results (up to 30% 1 ), culture identification is still the gold standard to confirm pharyngitis due to S. pyogenes . S. pyogenes can be identified as a catalase-negative, beta hemolytic bacterium that is susceptible to 0.04 units of bacitracin. Antibiotic resistance is limited for this bacterium, so most β-lactams remain effective; oral amoxicillin and intramuscular penicillin G are those most commonly prescribed.

bright red inflammation at the back of the mouth.

Sequelae of S. pyogenes Infections

One reason strep throat infections are aggressively treated with antibiotics is because they can lead to serious sequelae, later clinical consequences of a primary infection. It is estimated that 1%–3% of untreated S. pyogenes infections can be followed by nonsuppurative (without the production of pus) sequelae that develop 1–3 weeks after the acute infection has resolved. Two such sequelae are acute rheumatic fever and acute glomerulonephritis.

Acute rheumatic fever can follow pharyngitis caused by specific rheumatogenic strains of S. pyogenes (strains 1, 3, 5, 6, and 18). Although the exact mechanism responsible for this sequela remains unclear, molecular mimicry between the M protein of rheumatogenic strains of S. pyogenes and heart tissue is thought to initiate the autoimmune attack. The most serious and lethal clinical manifestation of rheumatic fever is damage to and inflammation of the heart (carditis). Acute glomerulonephritis also results from an immune response to streptococcal antigens following pharyngitis and cutaneous infections. Acute glomerulonephritis develops within 6–10 days after pharyngitis, but can take up to 21 days after a cutaneous infection. Similar to acute rheumatic fever, there are strong associations between specific nephritogenic strains of S. pyogenes and acute glomerulonephritis, and evidence suggests a role for antigen mimicry and autoimmunity. However, the primary mechanism of acute glomerulonephritis appears to be the formation of immune complexes between S. pyogenes antigens and antibodies, and their deposition between endothelial cells of the glomeruli of kidney. Inflammatory response against the immune complexes leads to damage and inflammation of the glomeruli (glomerulonephritis).

Exercise \(\PageIndex{1}\)

  • What are the symptoms of strep throat?
  • What is erythrogenic toxin and what effect does it have?
  • What are the causes of rheumatic fever and acute glomerulonephritis?

Acute Otitis Media

An infection of the middle ear is called acute otitis media (AOM), but often it is simply referred to as an earache. The condition is most common between ages 3 months and 3 years. In the United States, AOM is the second-leading cause of visits to pediatricians by children younger than age 5 years, and it is the leading indication for antibiotic prescription. 2

AOM is characterized by the formation and accumulation of pus in the middle ear. Unable to drain, the pus builds up, resulting in moderate to severe bulging of the tympanic membrane and otalgia (ear pain). Inflammation resulting from the infection leads to swelling of the eustachian tubes, and may also lead to fever, nausea, vomiting, and diarrhea, particularly in infants. Infants and toddlers who cannot yet speak may exhibit nonverbal signs suggesting AOM, such as holding, tugging, or rubbing of the ear, as well as uncharacteristic crying or distress in response to the pain.

AOM can be caused by a variety of bacteria. Among neonates, S. pneumoniae is the most common cause of AOM, but Escherichia coli , Enterococcus spp., and group B Streptococcus species can also be involved. In older infants and children younger than 14 years old, the most common bacterial causes are S. pneumoniae , Haemophilus influenzae , or Moraxella catarrhalis . Among S. pneumoniae infections , encapsulated strains are frequent causes of AOM. By contrast, the strains of H. influenzae and M. cattarhalis that are responsible for AOM do not possess a capsule. Rather than direct tissue damage by these pathogens, bacterial components such as lipopolysaccharide (LPS) in gram-negative pathogens induce an inflammatory response that causes swelling, pus, and tissue damage within the middle ear (Figure \(\PageIndex{3}\)).

Any blockage of the eustachian tubes, with or without infection, can cause fluid to become trapped and accumulate in the middle ear. This is referred to as otitis media with effusion (OME). The accumulated fluid offers an excellent reservoir for microbial growth and, consequently, secondary bacterial infections often ensue. This can lead to recurring and chronic earaches, which are especially common in young children. The higher incidence in children can be attributed to many factors. Children have more upper respiratory infections, in general, and their eustachian tubes are also shorter and drain at a shallower angle. Young children also tend to spend more time lying down than adults, which facilitates drainage from the nasopharynx through the eustachian tube and into the middle ear. Bottle feeding while lying down enhances this risk because the sucking action on the bottle causes negative pressure to build up within the eustachian tube, promoting the movement of fluid and bacteria from the nasopharynx.

Diagnosis is typically made based on clinical signs and symptoms, without laboratory testing to determine the specific causative agent. Antibiotics are frequently prescribed for the treatment of AOM. High-dose amoxicillin is the first-line drug, but with increasing resistance concerns, macrolides and cephalosporins may also be used. The pneumococcal conjugate vaccine (PCV13) contains serotypes that are important causes of AOM, and vaccination has been shown to decrease the incidence of AOM. Vaccination against influenza has also been shown to decrease the risk for AOM, likely because viral infections like influenza predispose patients to secondary infections with S. pneumoniae . Although there is a conjugate vaccine available for the invasive serotype B of H. influenzae , this vaccine does not impact the incidence of H. influenzae AOM. Because unencapsulated strains of H. influenzae and M. catarrhalis are involved in AOM, vaccines against bacterial cellular factors other than capsules will need to be developed.

a) A close-up of the ear drum (tympanic membrane) which looks like a translucent, thin covering. Labels point out the malleus, incus, and tympanum. B) Without the tymphanic membrane, the region is red and swollen. The bones are deteriorating and yellow mucus builds up. Labels point to mucus, a torn membrane, and eroded inner ear bones.

Bacterial Rhinosinusitis

The microbial community of the nasopharynx is extremely diverse and harbors many opportunistic pathogens, so it is perhaps not surprising that infections leading to rhinitis and sinusitis have many possible causes. These conditions often occur as secondary infections after a viral infection, which effectively compromises the immune defenses and allows the opportunistic bacteria to establish themselves. Bacterial sinusitis involves infection and inflammation within the paranasal sinuses. Because bacterial sinusitis rarely occurs without rhinitis, the preferred term is rhinosinusitis. The most common causes of bacterial rhinosinusitis are similar to those for AOM, including S. pneumoniae , H. influenzae , and M. catarrhalis .

Exercise \(\PageIndex{2}\)

  • What are the usual causative agents of acute otitis media?
  • What factors facilitate acute otitis media with effusion in young children?
  • What factor often triggers bacterial rhinosinusitis?

The causative agent of diphtheria, Corynebacterium diphtheriae , is a club-shaped, gram-positive rod that belongs to the phylum Actinobacteria. Diphtheroids are common members of the normal nasopharyngeal microbiota. However, some strains of C. diphtheriae become pathogenic because of the presence of a temperate bacteriophage-encoded protein—the diphtheria toxin. Diphtheria is typically a respiratory infection of the oropharynx but can also cause impetigo-like lesions on the skin. Although the disease can affect people of all ages, it tends to be most severe in those younger than 5 years or older than 40 years. Like strep throat, diphtheria is commonly transmitted in the droplets and aerosols produced by coughing. After colonizing the throat, the bacterium remains in the oral cavity and begins producing the diphtheria toxin. This protein is an A-B toxin that blocks host-cell protein synthesis by inactivating elongation factor (EF)-2 (see Virulence Factors of Bacterial and Viral Pathogens ). The toxin’s action leads to the death of the host cells and an inflammatory response. An accumulation of grayish exudate consisting of dead host cells, pus, red blood cells, fibrin, and infectious bacteria results in the formation of a pseudomembrane. The pseudomembrane can cover mucous membranes of the nasal cavity, tonsils, pharynx, and larynx (Figure \(\PageIndex{4}\)). This is a classic sign of diphtheria. As the disease progresses, the pseudomembrane can enlarge to obstruct the fauces of the pharynx or trachea and can lead to suffocation and death. Sometimes, intubation, the placement of a breathing tube in the trachea, is required in advanced infections. If the diphtheria toxin spreads throughout the body, it can damage other tissues as well. This can include myocarditis (heart damage) and nerve damage that may impair breathing.

A gray, leathery blob in the back of a person’s mouth is shown and the label “pseudomembrane” points to it.

The presumptive diagnosis of diphtheria is primarily based on the clinical symptoms (i.e., the pseudomembrane) and vaccination history, and is typically confirmed by identifying bacterial cultures obtained from throat swabs. The diphtheria toxin itself can be directly detected in vitro using polymerase chain reaction (PCR)-based, direct detection systems for the diphtheria tox gene, and immunological techniques like radial immunodiffusion or Elek’s immunodiffusion test.

Broad-spectrum antibiotics like penicillin and erythromycin tend to effectively control C. diphtheriae infections. Regrettably, they have no effect against preformed toxins. If toxin production has already occurred in the patient, antitoxins (preformed antibodies against the toxin) are administered. Although this is effective in neutralizing the toxin, the antitoxins may lead to serum sickness because they are produced in horses (see Hypersensitivities ).

Widespread vaccination efforts have reduced the occurrence of diphtheria worldwide. There are currently four combination toxoid vaccines available that provide protection against diphtheria and other diseases: DTaP, Tdap, DT, and Td. In all cases, the letters “d,” “t,” and “p” stand for diphtheria, tetanus, and pertussis, respectively; the “a” stands for acellular. If capitalized, the letters indicate a full-strength dose; lowercase letters indicate reduced dosages. According to current recommendations, children should receive five doses of the DTaP vaccine in their youth and a Td booster every 10 years. Children with adverse reactions to the pertussis vaccine may be given the DT vaccine in place of the DTaP.

Exercise \(\PageIndex{3}\)

  • What effect does diphtheria toxin have?
  • What is the pseudomembrane composed of?

Bacterial Pneumonia

Pneumonia is a general term for infections of the lungs that lead to inflammation and accumulation of fluids and white blood cells in the alveoli. Pneumonia can be caused by bacteria, viruses, fungi, and other organisms, although the vast majority of pneumonias are bacterial in origin. Bacterial pneumonia is a prevalent, potentially serious infection; it caused more 50,000 deaths in the United States in 2014. 3 As the alveoli fill with fluids and white blood cells (consolidation), air exchange becomes impaired and patients experience respiratory distress (Figure \(\PageIndex{5}\)). In addition, pneumonia can lead to pleurisy, an infection of the pleural membrane surrounding the lungs, which can make breathing very painful. Although many different bacteria can cause pneumonia under the right circumstances, three bacterial species cause most clinical cases: Streptococcus pneumoniae , H . influenzae , and Mycoplasma pneumoniae . In addition to these, we will also examine some of the less common causes of pneumonia.

An X-ray that shows white bones on a black background. White regions within the lungs are labeled lesions.

Pneumococcal Pneumonia

The most common cause of community-acquired bacterial pneumonia is Streptococcus pneumoniae . This gram-positive, alpha hemolytic streptococcus is commonly found as part of the normal microbiota of the human respiratory tract. The cells tend to be somewhat lancet-shaped and typically appear as pairs (Figure \(\PageIndex{6}\)). The pneumococci initially colonize the bronchioles of the lungs. Eventually, the infection spreads to the alveoli, where the microbe’s polysaccharide capsule interferes with phagocytic clearance. Other virulence factors include autolysins like Lyt A, which degrade the microbial cell wall, resulting in cell lysis and the release of cytoplasmic virulence factors. One of these factors, pneumolysin O, is important in disease progression; this pore-forming protein damages host cells, promotes bacterial adherence, and enhances pro-inflammatory cytokine production. The resulting inflammatory response causes the alveoli to fill with exudate rich in neutrophils and red blood cells. As a consequence, infected individuals develop a productive cough with bloody sputum.

part a shows a micrograph of lancet (football) shaped cells, some of which have a clear ring around them. Part b shows two dumbbell shaped blue cells on an orange background.

Pneumococci can be presumptively identified by their distinctive gram-positive, lancet-shaped cell morphology and diplococcal arrangement. In blood agar cultures, the organism demonstrates alpha hemolytic colonies that are autolytic after 24 to 48 hours. In addition, S. pneumoniae is extremely sensitive to optochin and colonies are rapidly destroyed by the addition of 10% solution of sodium deoxycholate. All clinical pneumococcal isolates are serotyped using the quellung reaction with typing antisera produced by the CDC. Positive quellung reactions are considered definitive identification of pneumococci.

Antibiotics remain the mainstay treatment for pneumococci. β-Lactams like penicillin are the first-line drugs, but resistance to β-lactams is a growing problem. When β-lactam resistance is a concern, macrolides and fluoroquinolones may be prescribed. However, S. pneumoniae resistance to macrolides and fluoroquinolones is increasing as well, limiting the therapeutic options for some infections. There are currently two pneumococcal vaccines available: pneumococcal conjugate vaccine (PCV13) and pneumococcal polysaccharide vaccine (PPSV23). These are generally given to the most vulnerable populations of individuals: children younger than 2 years and adults older than 65 years.

Haemophilus Pneumonia

Encapsulated strains of Haemophilus influenzae are known for causing meningitis, but nonencapsulated strains are important causes of pneumonia. This small, gram-negative coccobacillus is found in the pharynx of the majority of healthy children; however, Haemophilus pneumonia is primarily seen in the elderly. Like other pathogens that cause pneumonia, H. influenzae is spread by droplets and aerosols produced by coughing. A fastidious organism, H. influenzae will only grow on media with available factor X (hemin) and factor V (NAD), like chocolate agar (Figure \(\PageIndex{7}\)). Serotyping must be performed to confirm identity of H. influenzae isolates.

Infections of the alveoli by H. influenzae result in inflammation and accumulation of fluids. Increasing resistance to β-lactams, macrolides, and tetracyclines presents challenges for the treatment of Haemophilus pneumonia. Resistance to the fluoroquinolones is rare among isolates of H. influenzae but has been observed. As discussed for AOM, a vaccine directed against nonencapsulated H. influenzae, if developed, would provide protection against pneumonia caused by this pathogen.

A micrograph of Haemophilus influenzae is shown. It looks like a brown disc with white streaks.

Tracy is a 6-year old who developed a serious cough that would not seem to go away. After 2 weeks, her parents became concerned and took her to the pediatrician, who suspected a case of bacterial pneumonia. Tests confirmed that the cause was Haemophilus influenzae . Fortunately, Tracy responded well to antibiotic treatment and eventually made a full recovery.

Because there had been several other cases of bacterial pneumonia at Tracy’s elementary school, local health officials urged parents to have their children screened. Of the children who were screened, it was discovered that greater than 50% carried H. influenzae in their nasal cavities, yet all but two of them were asymptomatic.

Why is it that some individuals become seriously ill from bacterial infections that seem to have little or no effect on others? The pathogenicity of an organism—its ability to cause host damage—is not solely a property of the microorganism. Rather, it is the product of a complex relationship between the microbe’s virulence factors and the immune defenses of the individual. Preexisting conditions and environmental factors such as exposure to secondhand smoke can make some individuals more susceptible to infection by producing conditions favorable to microbial growth or compromising the immune system. In addition, individuals may have genetically determined immune factors that protect them—or not—from particular strains of pathogens. The interactions between these host factors and the pathogenicity factors produced by the microorganism ultimately determine the outcome of the infection. A clearer understanding of these interactions may allow for better identification of at-risk individuals and prophylactic interventions in the future.

Mycoplasma Pneumonia (Walking Pneumonia)

Primary atypical pneumonia is caused by Mycoplasma pneumoniae . This bacterium is not part of the respiratory tract’s normal microbiota and can cause epidemic disease outbreaks. Also known as walking pneumonia, mycoplasma pneumonia infections are common in crowded environments like college campuses and military bases. It is spread by aerosols formed when coughing or sneezing. The disease is often mild, with a low fever and persistent cough. These bacteria, which do not have cell walls, use a specialized attachment organelle to bind to ciliated cells. In the process, epithelial cells are damaged and the proper function of the cilia is hindered (Figure \(\PageIndex{8}\)).

Mycoplasma grow very slowly when cultured. Therefore, penicillin and thallium acetate are added to agar to prevent the overgrowth by faster-growing potential contaminants. Since M. pneumoniae does not have a cell wall, it is resistant to these substances. Without a cell wall, the microbial cells appear pleomorphic. M. pneumoniae infections tend to be self-limiting but may also respond well to macrolide antibiotic therapy. β-lactams, which target cell wall synthesis, are not indicated for treatment of infections with this pathogen.

A micrograph showing a small oval cell binding to a much larger cell.

Chlamydial Pneumonias and Psittacosis

Chlamydial pneumonia can be caused by three different species of bacteria: Chlamydophila pneumoniae (formerly known as Chlamydia pneumoniae ), Chlamydophila psittaci (formerly known as Chlamydia psittaci ), and Chlamydia trachomatis . All three are obligate intracellular pathogens and cause mild to severe pneumonia and bronchitis. Of the three, Chlamydophila pneumoniae is the most common and is transmitted via respiratory droplets or aerosols. C. psittaci causes psittacosis, a zoonotic disease that primarily affects domesticated birds such as parakeets, turkeys, and ducks, but can be transmitted from birds to humans. Psittacosis is a relatively rare infection and is typically found in people who work with birds. Chlamydia trachomatis, the causative agent of the sexually transmitted disease chlamydia, can cause pneumonia in infants when the infection is passed from mother to baby during birth.

Diagnosis of chlamydia by culturing tends to be difficult and slow. Because they are intracellular pathogens, they require multiple passages through tissue culture. Recently, a variety of PCR- and serologically based tests have been developed to enable easier identification of these pathogens. Tetracycline and macrolide antibiotics are typically prescribed for treatment.

Health Care-Associated Pneumonia

A variety of opportunistic bacteria that do not typically cause respiratory disease in healthy individuals are common causes of health care-associated pneumonia. These include Klebsiella pneumoniae , Staphylococcus aureus , and proteobacteria such as species of Escherichia , Proteus , and Serratia . Patients at risk include the elderly, those who have other preexisting lung conditions, and those who are immunocompromised. In addition, patients receiving supportive therapies such as intubation, antibiotics, and immunomodulatory drugs may also be at risk because these interventions disrupt the mucociliary escalator and other pulmonary defenses. Invasive medical devices such as catheters, medical implants, and ventilators can also introduce opportunistic pneumonia-causing pathogens into the body. 4

Pneumonia caused by K. pneumoniae is characterized by lung necrosis and “currant jelly sputum,” so named because it consists of clumps of blood, mucus, and debris from the thick polysaccharide capsule produced by the bacterium. K. pneumoniae is often multidrug resistant. Aminoglycoside and cephalosporin are often prescribed but are not always effective. Klebsiella pneumonia is frequently fatal even when treated.

Pseudomonas Pneumonia

Pseudomonas aeruginosa is another opportunistic pathogen that can cause serious cases of bacterial pneumonia in patients with cystic fibrosis (CF) and hospitalized patients assisted with artificial ventilators. This bacterium is extremely antibiotic resistant and can produce a variety of exotoxins. Ventilator-associated pneumonia with P. aeruginosa is caused by contaminated equipment that causes the pathogen to be aspirated into the lungs. In patients with CF, a genetic defect in the cystic fibrosis transmembrane receptor (CFTR) leads to the accumulation of excess dried mucus in the lungs. This decreases the effectiveness of the defensins and inhibits the mucociliary escalator. P. aeruginosa is known to infect more than half of all patients with CF. It adapts to the conditions in the patient’s lungs and begins to produce alginate, a viscous exopolysaccharide that inhibits the mucociliary escalator. Lung damage from the chronic inflammatory response that ensues is the leading cause of mortality in patients with CF. 5

Exercise \(\PageIndex{4}\)

  • What three pathogens are responsible for the most prevalent types of bacterial pneumonia?
  • Which cause of pneumonia is most likely to affect young people?
  • In what contexts does Pseudomonas aeruginosa cause pneumonia?

Clinical Focus: Part 2

John’s chest radiograph revealed an extensive consolidation in the right lung, and his sputum cultures revealed the presence of a gram-negative rod. His physician prescribed a course of the antibiotic clarithromycin. He also ordered the rapid influenza diagnostic tests (RIDTs) for type A and B influenza to rule out a possible underlying viral infection. Despite antibiotic therapy, John’s condition continued to deteriorate, so he was admitted to the hospital.

Exercise \(\PageIndex{5}\)

What are some possible causes of pneumonia that would not have responded to the prescribed antibiotic?

Tuberculosis

Tuberculosis (TB) is one of the deadliest infectious diseases in human history. Although tuberculosis infection rates in the United States are extremely low, the CDC estimates that about one-third of the world’s population is infected with Mycobacterium tuberculosis , the causal organism of TB, with 9.6 million new TB cases and 1.5 million deaths worldwide in 2014. 6

M. tuberculosis is an acid-fast, high G + C, gram-positive, nonspore-forming rod. Its cell wall is rich in waxy mycolic acids, which make the cells impervious to polar molecules. It also causes these organisms to grow slowly. M. tuberculosis causes a chronic granulomatous disease that can infect any area of the body, although it is typically associated with the lungs. M. tuberculosis is spread by inhalation of respiratory droplets or aerosols from an infected person. The infectious dose of M. tuberculosis is only 10 cells. 7

After inhalation, the bacteria enter the alveoli (Figure \(\PageIndex{9}\)). The cells are phagocytized by macrophages but can survive and multiply within these phagocytes because of the protection by the waxy mycolic acid in their cell walls. If not eliminated by macrophages, the infection can progress, causing an inflammatory response and an accumulation of neutrophils and macrophages in the area. Several weeks or months may pass before an immunological response is mounted by T cells and B cells. Eventually, the lesions in the alveoli become walled off, forming small round lesions called tubercles. Bacteria continue to be released into the center of the tubercles and the chronic immune response results in tissue damage and induction of apoptosis (programmed host-cell death) in a process called liquefaction. This creates a caseous center, or air pocket, where the aerobic M. tuberculosis can grow and multiply. Tubercles may eventually rupture and bacterial cells can invade pulmonary capillaries; from there, bacteria can spread through the bloodstream to other organs, a condition known as miliary tuberculosis. The rupture of tubercles also facilitates transmission of the bacteria to other individuals via droplet aerosols that exit the body in coughs. Because these droplets can be very small and stay aloft for a long time, special precautions are necessary when caring for patients with TB, such as the use of face masks and negative-pressure ventilation and filtering systems.

Eventually, most lesions heal to form calcified Ghon complexes. These structures are visible on chest radiographs and are a useful diagnostic feature. But even after the disease has apparently ended, viable bacteria remain sequestered in these locations. Release of these organisms at a later time can produce reactivation tuberculosis (or secondary TB). This is mainly observed in people with alcoholism, the elderly, or in otherwise immunocompromised individuals (Figure \(\PageIndex{9}\)).

Diagram showing infectious cycle of tuberculosis. First a droplet nuclei containing tubercle bacilli are inhaled, enter the lungs and travel to the alveoli. Next, the tubercle bacilli multiply in the alveoli. Next, the immune cells form a barrier shell around the tubercle bacilli, called a granuloma. Finally, the granuloma shell breaks down and the tubercle bacilli escape and rapidly multiply forming more tubercles.

Because TB is a chronic disease, chemotherapeutic treatments often continue for months or years. Multidrug resistant (MDR-TB) and extensively drug-resistant (XDR-TB) strains of M. tuberculosis are a growing clinical concern. These strains can arise due to misuse or mismanagement of antibiotic therapies. Therefore, it is imperative that proper multidrug protocols are used to treat these infections. Common antibiotics included in these mixtures are isoniazid, rifampin, ethambutol, and pyrazinamide.

A TB vaccine is available that is based on the so-called bacillus Calmette-Guérin (BCG) strain of M. bovis commonly found in cattle. In the United States, the BCG vaccine is only given to health-care workers and members of the military who are at risk of exposure to active cases of TB. It is used more broadly worldwide. Many individuals born in other countries have been vaccinated with BCG strain. BCG is used in many countries with a high prevalence of TB, to prevent childhood tuberculous meningitis and miliary disease.

The Mantoux tuberculin skin test (Figure \(\PageIndex{10}\)) is regularly used in the United States to screen for potential TB exposure (see Hypersensitivities ). However, prior vaccinations with the BCG vaccine can cause false-positive results. Chest radiographs to detect Ghon complex formation are required, therefore, to confirm exposure.

a) a needle injects a small bubble into a person’s skin. B) a ruler is used to measure a red area on a person’s skin.

Exercise \(\PageIndex{6}\)

  • What characteristic of Mycobacterium tuberculosis allows it to evade the immune response?
  • What happens to cause miliary tuberculosis?
  • Explain the limitations of the Mantoux tuberculin skin test.

Pertussis (Whooping Cough)

The causative agent of pertussis, commonly called whooping cough, is Bordetella pertussis , a gram-negative coccobacillus. The disease is characterized by mucus accumulation in the lungs that leads to a long period of severe coughing. Sometimes, following a bout of coughing, a sound resembling a “whoop” is produced as air is inhaled through the inflamed and restricted airway—hence the name whooping cough. Although adults can be infected, the symptoms of this disease are most pronounced in infants and children. Pertussis is highly communicable through droplet transmission, so the uncontrollable coughing produced is an efficient means of transmitting the disease in a susceptible population.

Following inhalation, B. pertussis specifically attaches to epithelial cells using an adhesin, filamentous hemagglutinin. The bacteria then grow at the site of infection and cause disease symptoms through the production of exotoxins. One of the main virulence factors of this organism is an A-B exotoxin called the pertussis toxin (PT). When PT enters the host cells, it increases the cyclic adenosine monophosphate (cAMP) levels and disrupts cellular signaling. PT is known to enhance inflammatory responses involving histamine and serotonin. In addition to PT, B. pertussis produces a tracheal cytotoxin that damages ciliated epithelial cells and results in accumulation of mucus in the lungs. The mucus can support the colonization and growth of other microbes and, as a consequence, secondary infections are common. Together, the effects of these factors produce the cough that characterizes this infection.

A pertussis infection can be divided into three distinct stages. The initial infection, termed the catarrhal stage, is relatively mild and unremarkable. The signs and symptoms may include nasal congestion, a runny nose, sneezing, and a low-grade fever. This, however, is the stage in which B. pertussis is most infectious. In the paroxysmal stage, mucus accumulation leads to uncontrollable coughing spasms that can last for several minutes and frequently induce vomiting. The paroxysmal stage can last for several weeks. A long convalescence stage follows the paroxysmal stage, during which time patients experience a chronic cough that can last for up to several months. In fact, the disease is sometimes called the 100-day cough.

In infants, coughing can be forceful enough to cause fractures to the ribs, and prolonged infections can lead to death. The CDC reported 20 pertussis-related deaths in 2012, 9 but that number had declined to five by 2015. 10

During the first 2 weeks of infection, laboratory diagnosis is best performed by culturing the organism directly from a nasopharyngeal (NP) specimen collected from the posterior nasopharynx. The NP specimen is streaked onto Bordet-Gengou medium. The specimens must be transported to the laboratory as quickly as possible, even if transport media are used. Transport times of longer than 24 hours reduce the viability of B. pertussis significantly.

Within the first month of infection, B. pertussis can be diagnosed using PCR techniques. During the later stages of infection, pertussis-specific antibodies can be immunologically detected using an enzyme-linked immunosorbent assay (ELISA).

Pertussis is generally a self-limiting disease. Antibiotic therapy with erythromycin or tetracycline is only effective at the very earliest stages of disease. Antibiotics given later in the infection, and prophylactically to uninfected individuals, reduce the rate of transmission. Active vaccination is a better approach to control this disease. The DPT vaccine was once in common use in the United States. In that vaccine, the P component consisted of killed whole-cell B. pertussis preparations. Because of some adverse effects, that preparation has now been superseded by the DTaP and Tdap vaccines. In both of these new vaccines, the “aP” component is a pertussis toxoid.

Widespread vaccination has greatly reduced the number of reported cases and prevented large epidemics of pertussis. Recently, however, pertussis has begun to reemerge as a childhood disease in some states because of declining vaccination rates and an increasing population of susceptible children.

Exercise \(\PageIndex{7}\)

  • What accounts for the mucus production in a pertussis infection?
  • What are the signs and symptoms associated with the three stages of pertussis?
  • Why is pertussis becoming more common in the United States?

Legionnaires Disease

An atypical pneumonia called Legionnaires disease (also known as legionellosis) is caused by an aerobic gram-negative bacillus, Legionella pneumophila . This bacterium infects free-living amoebae that inhabit moist environments, and infections typically occur from human-made reservoirs such as air-conditioning cooling towers, humidifiers, misting systems, and fountains. Aerosols from these reservoirs can lead to infections of susceptible individuals, especially those suffering from chronic heart or lung disease or other conditions that weaken the immune system.

When L. pneumophila bacteria enter the alveoli, they are phagocytized by resident macrophages. However, L. pneumophila uses a secretion system to insert proteins in the endosomal membrane of the macrophage; these proteins prevent lysosomal fusion, allowing L. pneumophila to continue to proliferate within the phagosome. The resulting respiratory disease can range from mild to severe pneumonia, depending on the status of the host’s immune defenses. Although this disease primarily affects the lungs, it can also cause fever, nausea, vomiting, confusion, and other neurological effects.

Diagnosis of Legionnaires disease is somewhat complicated. L. pneumophila is a fastidious bacterium and is difficult to culture. In addition, since the bacterial cells are not efficiently stained with the Gram stain, other staining techniques, such as the Warthin-Starry silver-precipitate procedure, must be used to visualize this pathogen. A rapid diagnostic test has been developed that detects the presence of Legionella antigen in a patient’s urine; results take less than 1 hour, and the test has high selectivity and specificity (greater than 90%). Unfortunately, the test only works for one serotype of L. pneumophila (type 1, the serotype responsible for most infections). Consequently, isolation and identification of L. pneumophila from sputum remains the defining test for diagnosis.

Once diagnosed, Legionnaire disease can be effectively treated with fluoroquinolone and macrolide antibiotics. However, the disease is sometimes fatal; about 10% of patients die of complications. 11 There is currently no vaccine available.

Exercise \(\PageIndex{8}\)

  • Why is Legionnaires disease associated with air-conditioning systems?
  • How does Legionella pneumophila circumvent the immune system?

The zoonotic disease Q fever is caused by a rickettsia, Coxiella burnetii . The primary reservoirs for this bacterium are domesticated livestock such as cattle, sheep, and goats. The bacterium may be transmitted by ticks or through exposure to the urine, feces, milk, or amniotic fluid of an infected animal. In humans, the primary route of infection is through inhalation of contaminated farmyard aerosols. It is, therefore, largely an occupational disease of farmers. Humans are acutely sensitive to C. burnetii —the infective dose is estimated to be just a few cells. 12 In addition, the organism is hardy and can survive in a dry environment for an extended time. Symptoms associated with acute Q fever include high fever, headache, coughing, pneumonia, and general malaise. In a small number of patients (less than 5% 13 ), the condition may become chronic, often leading to endocarditis, which may be fatal.

Diagnosing rickettsial infection by cultivation in the laboratory is both difficult and hazardous because of the easy aerosolization of the bacteria, so PCR and ELISA are commonly used. Doxycycline is the first-line drug to treat acute Q fever. In chronic Q fever, doxycycline is often paired with hydroxychloroquine.

Bacterial Diseases of the Respiratory Tract

Numerous pathogens can cause infections of the respiratory tract. Many of these infections produce similar signs and symptoms, but appropriate treatment depends on accurate diagnosis through laboratory testing. The tables in Figure \(\PageIndex{11}\) and Figure \(\PageIndex{12}\) summarize the most important bacterial respiratory infections, with the latter focusing specifically on forms of bacterial pneumonia.

Table titled: Bacterial Infections of the Respiratory Tract. Columns: Disease, Pathogen, Signs and Symptoms, Transmission, Diagnostic Tests, Antimicrobial Drugs, Vaccine. Acute otitis media (AOM); Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis, others;  Earache, possible effusion; may cause fever, nausea, vomiting, diarrhea; Often a secondary infection; bacteria from respiratory tract become trapped in eustachian tube, cause infection; None; Cephalosporins, fluoroquinolones; None. Diphtheria; Corynebacterium diphtheria; Pseudomembrane on throat, possibly leading to suffocation and death; Inhalation of respiratory droplets or aerosols from infected person ; Identification of bacteria in throat swabs; PCR to detect diphtheria toxin in vitro; Erythromycin, penicillin, antitoxin produced in horses; DtaP, Tdap, DT, Td, DTP. Legionnaires disease; Legionella pneumophila; Cough, fever, muscle aches, headaches, nausea, vomiting, confusion; sometimes fatal; Inhalation of aerosols from contaminated water reservoirs; Isolation, using Warthin-Starry procedure, of bacteria in sputum; Fluoroquinolones, macrolides; None. Pertussis (whooping cough); Bordetella pertussis; Severe coughing with “whoop” sound; chronic cough lasting several months; can be fatal in infants; Inhalation of respiratory droplets from infected person; Direct culture of throat swab, PCR, ELISA Macrolides; DTaP, Tdap. Q fever; Coxiella burnetii; High fever, coughing, pneumonia, malaise; in chronic cases, potentially fatal endocarditis; Inhalation of aerosols of urine, feces, milk, or amniotic fluid of infected cattle, sheep, goats; PCR, ELISA; Doxycycline, hydroxychloroquine; None. Streptococcal pharyngitis, scarlet fever; Streptococcus pyogenes; Fever, sore throat, inflammation of pharynx and tonsils, petechiae, swollen lymph nodes; skin rash (scarlet fever), strawberry tongue; Direct contact, inhalation of respiratory droplets or aerosols from infected person Direct culture of throat swab, rapid enzyme immunoassay; β-lactams; None. Tuberculosis; Mycobacterium tuberculosis; Formation of tubercles in lungs; rupture of tubercles, leading to chronic, bloody cough; healed tubercles (Ghon complexes) visible in radiographs; can be fatal; Inhalation of respiratory droplets or aerosols from infected person Mantoux tuberculin skin test with chest radiograph to identify Ghon complexes; Isoniazid, rifampin, ethambutol, pyrazinamide; BCG.

Key Concepts and Summary

  • A wide variety of bacteria can cause respiratory diseases; most are treatable with antibiotics or preventable with vaccines.
  • Streptococcus pyogenes causes strep throat , an infection of the pharynx that also causes high fever and can lead to scarlet fever , acute rheumatic fever , and acute glomerulonephritis .
  • Acute otitis media is an infection of the middle ear that may be caused by several bacteria, including Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis . The infection can block the eustachian tubes, leading to otitis media with effusion .
  • Diphtheria , caused by Corynebacterium diphtheriae , is now a rare disease because of widespread vaccination. The bacteria produce exotoxins that kill cells in the pharynx, leading to the formation of a pseudomembrane ; and damage other parts of the body.
  • Bacterial pneumonia results from infections that cause inflammation and fluid accumulation in the alveoli. It is most commonly caused by S. pneumoniae or H. influenzae . The former is commonly multidrug resistant.
  • Mycoplasma pneumonia results from infection by Mycoplasma pneumoniae ; it can spread quickly, but the disease is mild and self-limiting.
  • Chlamydial pneumonia can be caused by three pathogens that are obligate intracellular parasites. Chlamydophila pneumoniae is typically transmitted from an infected person, whereas C. psittaci is typically transmitted from an infected bird. Chlamydia trachomatis , may cause pneumonia in infants.
  • Several other bacteria can cause pneumonia in immunocompromised individuals and those with cystic fibrosis.
  • Tuberculosis is caused by Mycobacterium tuberculosis . Infection leads to the production of protective tubercles in the alveoli and calcified Ghon complexes that can harbor the bacteria for a long time. Antibiotic-resistant forms are common and treatment is typically long term.
  • Pertussis is caused by Bordetella pertussis . Mucus accumulation in the lungs leads to prolonged severe coughing episodes (whooping cough) that facilitate transmission. Despite an available vaccine, outbreaks are still common.
  • Legionnaires disease is caused by infection from environmental reservoirs of the Legionella pneumophila bacterium. The bacterium is endocytic within macrophages and infection can lead to pneumonia, particularly among immunocompromised individuals.
  • Q fever is caused by Coxiella burnetii , whose primary hosts are domesticated mammals (zoonotic disease). It causes pneumonia primarily in farm workers and can lead to serious complications, such as endocarditis.
  • 1 WL Lean et al. “Rapid Diagnostic Tests for Group A Streptococcal Pharyngitis: A Meta-Analysis.” Pediatrics 134, no. 4 (2014):771–781.
  • 2 G. Worrall. “Acute Otitis Media.” Canadian Family Physician 53 no. 12 (2007):2147–2148.
  • 3 KD Kochanek et al. “Deaths: Final Data for 2014.” National Vital Statistics Reports 65 no 4 (2016).
  • 4 SM Koenig et al. “Ventilator-Associated Pneumonia: Diagnosis, Treatment, and Prevention.” Clinical Microbiology Reviews 19 no. 4 (2006):637–657.
  • 5 R. Sordé et al. “Management of Refractory Pseudomonas aeruginosa Infection in Cystic Fibrosis.” Infection and Drug Resistance 4 (2011):31–41.
  • 6 Centers for Disease Control and Prevention. “Tuberculosis (TB). Data and Statistics.” http://www.cdc.gov/tb/statistics/default.htm
  • 7 D. Saini et al. “Ultra-Low Dose of Mycobacterium tuberculosis Aerosol Creates Partial Infection in Mice.” Tuberculosis 92 no. 2 (2012):160–165.
  • 8 G. Kaplan et al. “ Mycobacterium tuberculosis Growth at the Cavity Surface: A Microenvironment with Failed Immunity.” Infection and Immunity 71 no.12 (2003):7099–7108.
  • 9 Centers for Disease Control and Prevention. “2012 Final Pertussis Surveillance Report.” 2015. http://www.cdc.gov/pertussis/downloa...eport-2012.pdf . Accessed July 6, 2016.
  • 10 Centers for Disease Control and Prevention. “2015 Provisional Pertussis Surveillance Report.” 2016. http://www.cdc.gov/pertussis/downloa...rovisional.pdf . Accessed July 6, 2016.
  • 11 Centers for Disease Control and Prevention. “ Legionella (Legionnaires’ Disease and Pontiac Fever: Diagnosis, Treatment, and Complications).” http://www.cdc.gov/legionella/about/diagnosis.html . Accessed Sept 14, 2016.
  • 12 WD Tigertt et al. “Airborne Q Fever.” Bacteriological Reviews 25 no. 3 (1961):285–293.
  • 13 Centers for Disease Control and Prevention. “Q fever. Symptoms, Diagnosis, and Treatment.” 2013. http://www.cdc.gov/qfever/symptoms/index.html . Accessed July 6, 2016.

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Upper respiratory tract infections

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Physician prescription practice of antibiotics for upper respiratory tract infection at kilimanjaro christian medical centre moshi, tanzania, 47 references, interventions for atrophic rhinitis., viral-bacterial interactions and risk of acute otitis media complicating upper respiratory tract infection, characteristics of atrophic rhinitis in thai patients at the siriraj hospital., diagnosis and treatment of streptococcal pharyngitis., postinfectious cough: accp evidence-based clinical practice guidelines., epiglottitis and croup., laryngeal candidiasis in the outpatient setting., the diagnosis and management of acute and chronic sinusitis., principles of appropriate antibiotic use for acute pharyngitis in adults, related papers.

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cold and flu health center / cold and flu a-z list / common cold article

Common Cold

  • Medical Author: Steven Doerr, MD
  • Medical Author: Sandra Gonzalez Gompf, MD, FACP
  • Medical Editor: William C. Shiel Jr., MD, FACP, FACR

What is the common cold?

What causes the common cold, what are the symptoms of the common cold, what are the stages of the common cold, common cold vs. flu (influenza), diagnosis of the common cold, what are the treatments and home remedies for the common cold, what is the prognosis for the common cold, what are complications of the common cold, is it possible to prevent the common cold.

The common cold progresses through four different stages.

  • The common cold is an upper respiratory tract infection caused by many different viruses .
  • The common cold is transmitted by virus-infected airborne droplets or by direct contact with infected secretions.
  • sore throat ,
  • sneezing, and
  • a runny nose.
  • Being in cold weather does not cause the common cold, but cold weather promotes close contact.
  • There are four stages of a common cold.
  • Over-the-counter medications may be used for the treatment of the common cold.
  • Antibiotics are not necessary for the common cold.
  • The common cold is a self-limited disease that can generally be managed at home.
  • Most people with a common cold recovered in about 7 to 10 days.
  • The common cold has no cure, and there is no available vaccine .

The common cold is a self-limited contagious disease that can be caused by a number of different types of viruses. The common cold is medically referred to as a viral upper respiratory tract infection. Symptoms of the common cold may include cough, sore throat , low-grade fever , nasal congestion , runny nose, and sneezing. More than 200 different types of viruses are known to cause the common cold, with rhinovirus causing approximately 30%-40% of all adult colds.

  • Rhinovirus multiplies best at temperatures found in the nose.
  • Rhinovirus infection rates peak from September to November and March to May.
  • Nevertheless, rhinovirus may cause disease at any time of year. During peak periods, up to 80% of colds may be due to rhinovirus.

Other commonly implicated viruses include coronavirus ( COVID-19 ), adenovirus , respiratory syncytial virus , and parainfluenza virus. Because so many different viruses can cause the common cold, and because new cold viruses constantly develop, the body never builds up resistance against all of them. For this reason, colds are a frequent and recurring problem. In fact, children in preschool and elementary school can have six to 12 colds per year while adolescents and adults typically have two to four colds per year.

  • The common cold occurs most frequently during the fall, winter, and spring.
  • The common cold is the most frequently occurring viral infection in the world, and it is a leading cause of doctor visits and missed days from school and work.
  • It is estimated that individuals in the United States suffer an estimated 1 billion colds per year, with approximately 22 million days of school absences recorded annually.
  • In the United States, the common cold is thought to account for approximately 75-100 million physician visits annually, with an economic impact of greater than $20 billion per year due to cold-related work loss.

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What are risk factors for the common cold?

There are various risk factors that may increase the chances of acquiring the common cold, including the following:

  • Age : Infants and young children are more likely to develop the common cold because they have not yet developed immunity to many of the implicated viruses.
  • Seasonal variation : Individuals more commonly acquire the common cold during the fall, winter, or rainy season (in warmer climates). This is felt to occur because people tend to stay indoors and are in closer proximity to one another.
  • Weakened immune system : Individuals with a poorly functioning immune system are more likely to develop the common cold. Also, individuals with excessive fatigue or emotional distress may be more susceptible to catching a common cold.

How does the common cold spread?

The common cold is spread either by direct contact with infected secretions from contaminated surfaces or by inhaling the airborne virus after individuals sneeze or cough. Person-to-person transmission often occurs when an individual has a cold blow or touches their nose and then touches someone or something else. A healthy individual who then makes direct contact with these secretions can subsequently become infected, often after their contaminated hands contact their own eyes, nose, or mouth.

A cold virus can live on frequently touched objects such as doorknobs, pens, books, cell phones, computer keyboards, and coffee cups for several hours and can thus be acquired from contact with these objects.

In general, the common cold can be contagious anywhere from one to two days before the symptoms begin up until the symptoms have completely resolved. However, the common cold is typically most contagious during the initial two to three days of illness.

Does the common cold have anything to do with exposure to cold weather?

Though the common cold usually occurs in the winter months, the cold weather itself does not cause the common cold. Rather, it is thought that during cold-weather months, people spend more time indoors near each other, thus facilitating the spread of the virus. For this same reason, children in daycare and school are particularly prone to acquiring the common cold.

The low humidity during these colder months is also felt to contribute to the increased prevalence of the common cold, as many of the implicated viruses seem to survive better in low-humidity conditions.

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Common cold symptoms typically begin two to three days after acquiring the infection (incubation period), though this may vary depending on the type of virus causing the infection. Individuals also tend to be most contagious during the initial two to three days of having symptoms. Cold viruses target mainly the upper respiratory tract (nose, sinuses, and throat). Symptoms and signs of the common cold may also vary depending on the virus responsible for the infection and may include

  • stuffy nose or nasal drainage,
  • sore or scratchy throat,
  • hoarseness ,
  • low-grade fever,
  • body aches,
  • loss of appetite, and

The signs and symptoms of the common cold in infants and children are similar to those seen in adults. The cold may begin with a runny nose with clear nasal discharge, which later may become yellowish or greenish in color. Infants and children may also become fussy and have decreased appetite.

Because the common cold can be caused by so many different viruses, the progression and severity of symptoms vary from individual to individual. In general, symptoms will develop two to three days after the virus is contracted. Some individuals will develop very mild symptoms whereas others will develop more severe symptoms. The type of symptoms will also vary, with some individuals developing only nasal congestion, while others may develop any or all of the symptoms described above. The symptoms that develop also depend on the underlying health of the person infected.

Most colds will resolve after seven to 10 days, though some individuals experience a shorter course and others a more prolonged illness, again depending on the particular virus involved, as well as the infected person's underlying health issues.

The four typical stages of a common cold are as follows:

  • Stage 1 (incubation period) : This refers to the stage between the infection by a cold virus and the development of symptoms. This stage may last for one to three days, although for some it may be as short as 10 to 12 hours. 
  • Stage 2 (appearance and progression of symptoms) : In this stage, symptoms begin and reach their peak intensity. The symptoms of a cold generally peak in one to three days. Typical cold symptoms include a sore throat, sneezing, cough, a stuffy nose, a runny nose (clear, watery discharge from the nose), feeling sick, headache , body ache, and fever. Fever is more commonly seen in children. 
  • Stage 3 (stage of remission) : This stage is marked by a decline and eventual fading of cold symptoms. The symptoms usually subside between 3 and 10 days. After two to three days of the appearance of symptoms, the discharge from the nose may appear white, yellow, or green. This color change is normal and does not mean that antibiotics are needed. 
  • Stage 4 (stage of recovery) : In this stage, the person feels normal and gets on their feet . There may be some lingering symptoms such as mild cough, stuffy nose, and scanty nasal discharge. Such mild symptoms may last up to two weeks in some people.

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Many people confuse the common cold with influenza (the flu ).

  • Flu is caused by the influenza virus, while the common cold generally is not.
  • While some of the symptoms of the common cold and flu may be similar, patients with the common cold typically have a milder illness than patients with the flu.
  • Patients with the flu usually appear more ill and have a more abrupt onset of illness wi th fever, chills, headache, substantial muscle and body aches, dry cough, and extreme weakness.

There is laboratory testing available to confirm the diagnosis of influenza, but health care professionals make a diagnosis of flu primarily based on classic flu symptoms rather than laboratory tests.

A general practitioner most often diagnoses and treats the common cold, in addition to family medicine physicians, internists, and pediatricians. If you visit an emergency department, an emergency medicine physician will likely treat you.

An infectious disease specialist may consult hospitalized individuals with very weakened immune systems, such as those who have had an organ or bone marrow transplant or have had recent chemotherapy for cancer .

A doctor or health care professional will generally diagnose the common cold based on the description of the symptoms and the findings during the physical exam. Laboratory testing and imaging studies are generally not necessary unless there are concerns about another underlying medical condition, such as a bacterial disease or potential complications of the common cold.

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There is no cure for the common cold. The common cold is a self-limiting illness that will resolve spontaneously with time and expectant management. Home remedies and medical treatments are directed at alleviating the symptoms associated with the common cold while the body fights off the infection.

Home treatment for upper respiratory infections includes getting rest and drinking plenty of fluids. In older children and adults, common over-the-counter drugs such as throat lozenges, throat sprays, cough drops, and cough syrups may help relieve symptoms, though they will not prevent or shorten the duration of the common cold. Gargling with warm salt water may help people with sore throats. Decongestant drugs such as pseudoephedrine ( Sudafed ) or antihistamines may be used for nasal symptoms, while saline nasal sprays may also be beneficial. It is important to note that over-the-counter medications may cause undesirable side effects, therefore they must be taken with care and as directed. Pregnant women should discuss the safety of common over-the-counter medications with their pharmacist or health care professional.

Acetaminophen ( Tylenol and others) and non-steroidal anti-inflammatory drugs such as ibuprofen ( Advil , Motrin ) are common over-the-counter medicines that can help with fever, sore throat, headache, and body aches.

The treatment for infants and small children with the common cold is supportive as well. It is especially important to allow rest and encourage plenty of fluids in order to prevent dehydration . Nasal drops and bulb suctioning may be used to clear nasal mucus from the nasal passages in infants. Medicines such as acetaminophen and ibuprofen may be taken for pain or fever based on the package recommendations for age and weight. Do not use aspirin or aspirin-containing medications in children or teenagers because it has been associated with a rare, potentially fatal condition called Reye's syndrome. Finally, over-the-counter cough and cold medications for infants and young children are not recommended. Medication manufacturers now recommend that over-the-counter cough and cold drugs not be used in children younger than 4 years of age because of serious and potentially life-threatening side effects.

Common alternative treatments to prevent or treat the common cold, such as vitamin C , zinc, echinacea , and other herbal remedies, have had mixed results in studies evaluating their effectiveness. Therefore, discuss these treatment options with a health care professional.

Do antibiotics treat the common cold?

No. Antibiotics play no role in treating the common cold. Antibiotics are effective only against illnesses caused by bacteria, and colds are caused by viruses. Not only do antibiotics not help, but they can rarely also cause severe allergic reactions that can sometimes be fatal. Furthermore, using antibiotics when they are not necessary has led to the growth of several strains of common bacteria that have become resistant to certain antibiotics. For these and other reasons, it is important to limit the use of antibiotics to situations in which they are medically indicated.

Occasionally, a bacterial infection such as sinusitis or a middle ear infection (acute otitis media ) can develop following the common cold, however, the decision to treat with antibiotics should be determined by a doctor or health care professional after a medical evaluation. About 30% of children with middle ear infections have rhinovirus. Because middle ear infection may be viral, some experts suggest treating acute otitis media in children with non-steroidal anti-inflammatory drugs and resorting to antibiotics only if there is worsening or no improvement.

Generally, the prognosis for the common cold is excellent. The common cold needs to run its natural course, and most people with the common cold will recover within seven to 10 days. However, certain viruses may take up to three weeks to completely resolve.

In general, the common cold can be treated at home and managed with over-the-counter medications. However, if more severe symptoms develop, such as

  • shaking chills,
  • high fever (greater than 102 F),
  • severe headache,
  • neck stiffness,
  • abdominal pain ,
  • difficulty breathing ,
  • chest pain ,
  • confusion, or failure to improve after 10 days,

Consult a health care professional immediately, if these severe symptoms occur. Infants 3 months of age or younger who develop a cold or fever should consult a health care professional as well.

Complications that may arise from the common cold include

  • the development of a bact erial middle ear infection (otitis media) or bacterial sinusitis .
  • In individuals with asthma or chronic obstructive pulmonary disease ( COPD ), the common cold can sometimes trigger an exacerbation of their illness, leading to shortness of breath and increased wheezing.
  • Though uncommon, pneumonia can sometimes develop as a secondary infection in individuals with the common cold. For example, coronaviruses, rhinoviruses, and several other cold-causing viruses can cause bronchitis and pneumonia in people with very weakened immune systems.

If a sore throat and a fever are present with no other cold symptoms, the individual should also be evaluated by a health care professional. This illness may be strep throat , a bacterial infection requiring treatment with antibiotics.

Finally, if there is facial pain , redness, or swelling associated with yellow/green drainage from the nose accompanied by a fever, it is possible that the individual has a bacterial sinus infection (sinusitis) that would benefit from a medical evaluation and a possible course of antibiotics.

Get an evaluation by a healthcare professional for any of these suspected complications.

The most important prevention measure for the common cold is to avoid contact with infected individuals. Other measures for prevention of the common cold include the following:

  • Frequent and thorough hand washing during flu and cold season are extremely important, as this can destroy viruses acquired from touching contaminated surfaces. In between using soap and water when hands are visibly dirty, use an alcohol -based hand sanitizer containing at least 60% alcohol.
  • Disinfect frequently touched surfaces or personal objects with a product that is effective against flu and cold-causing viruses (and safe for the type of surface).
  • Do not share personal belongings such as towels, handkerchiefs, or tissues.
  • Avoid sharing utensils and try to use disposable items (such as disposable cups) if someone in the family has a cold.
  • Encourage individuals to cover their nose and mouth when coughing or sneezing to prevent transmission of the virus. A sneeze can spray a fine mist of contagious droplets up to 6 feet.
  • Lifestyle modifications such as smoking cessation and stress management may decrease susceptibility to acquiring the common cold.
  • If the air in the home is very dry during the winter, a cool-mist humidifier or vaporizer may be helpful.

Currently, there is no effective vaccine against the common cold.

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Common Medical Abbreviations & Terms

Doctors, pharmacists, and other health-care professionals use abbreviations, acronyms, and other terminology for instructions and information in regard to a patient's health condition, prescription drugs they are to take, or medical procedures that have been ordered. There is no approved this list of common medical abbreviations, acronyms, and terminology used by doctors and other health- care professionals. You can use this list of medical abbreviations and acronyms written by our doctors the next time you can't understand what is on your prescription package, blood test results, or medical procedure orders. Examples include:

  • ANED: Alive no evidence of disease. The patient arrived in the ER alive with no evidence of disease.
  • ARF: Acute renal (kidney) failure
  • cap: Capsule.
  • CPAP: Continuous positive airway pressure. A treatment for sleep apnea.
  • DJD: Degenerative joint disease. Another term for osteoarthritis.
  • DM: Diabetes mellitus. Type 1 and type 2 diabetes
  • HA: Headache
  • IBD: Inflammatory bowel disease. A name for two disorders of the gastrointestinal (BI) tract, Crohn's disease and ulcerative colitis
  • N/V: Nausea or vomiting.
  • p.o.: By mouth. From the Latin terminology per os.
  • q.i.d.: Four times daily. As in taking a medicine four times daily.
  • RA: Rheumatoid arthritis
  • SOB: Shortness of breath.
  • T: Temperature. Temperature is recorded as part of the physical examination. It is one of the "vital signs."

essay on upper respiratory tract infection

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Sinus Surgery (Endoscopic) Procedure

essay on upper respiratory tract infection

Sore Throat

Sore throat (throat pain) usually is described as pain or discomfort in the throat area. A sore throat may be caused by bacterial infections, viral infections, toxins, irritants, trauma, or injury to the throat area. Common symptoms of a sore throat include a fever, cough, runny nose, hoarseness, earaches, sneezing, and body aches. Home remedies for a sore throat include warm soothing liquids and throat lozenges. OTC remedies for a sore throat include OTC pain relievers such as ibuprofen or acetaminophen. Antibiotics may be necessary for some cases of sore throat.

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Sore Throat Home Remedies

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Sore Throat or Strep Throat? How to Tell the Difference

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Swollen Lymph Nodes (Lymphadenopathy)

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Upper Respiratory Infection (URI)

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Effectiveness of honey for symptomatic relief in upper respiratory tract infections: a systematic review and meta-analysis

Affiliations.

  • 1 Oxford University Medical School, University of Oxford, Oxford, UK [email protected].
  • 2 Nuffield Department of Primary Care Health Sciences, University of Oxford, Oxford, UK.
  • PMID: 32817011
  • DOI: 10.1136/bmjebm-2020-111336

Background: Antibiotic over prescription for upper respiratory tract infections (URTIs) in primary care exacerbates antimicrobial resistance. There is a need for effective alternatives to antibiotic prescribing. Honey is a lay remedy for URTIs, and has an emerging evidence base for its use. Honey has antimicrobial properties, and guidelines recommended honey for acute cough in children.

Objectives: To evaluate the effectiveness of honey for symptomatic relief in URTIs.

Methods: A systematic review and meta-analysis. We searched Pubmed, Embase, Web of Science, AMED, Cab abstracts, Cochrane Library, LILACS, and CINAHL with a combination of keywords and MeSH terms.

Results: We identified 1345 unique records, and 14 studies were included. Overall risk of bias was moderate. Compared with usual care, honey improved combined symptom score (three studies, mean difference -3.96, 95% CI -5.42 to -2.51, I 2 =0%), cough frequency (eight studies, standardised mean difference (SMD) -0.36, 95% CI -0.50 to -0.21, I 2 =0%) and cough severity (five studies, SMD -0.44, 95% CI -0.64 to -0.25, I 2 =20%). We combined two studies comparing honey with placebo for relieving combined symptoms (SMD -0.63, 95% CI -1.44 to 0.18, I 2 =91%).

Conclusions: Honey was superior to usual care for the improvement of symptoms of upper respiratory tract infections. It provides a widely available and cheap alternative to antibiotics. Honey could help efforts to slow the spread of antimicrobial resistance, but further high quality, placebo controlled trials are needed.

Prospero registration no: Study ID, CRD42017067582 on PROSPERO: International prospective register of systematic reviews (https://www.crd.york.ac.uk/prospero/).

Keywords: general practice; public health.

© Author(s) (or their employer(s)) 2021. No commercial re-use. See rights and permissions. Published by BMJ.

PubMed Disclaimer

Conflict of interest statement

Competing interests: JL is a hobby beekeeper.

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Obstructive sleep apnea and acute lower respiratory tract infections: a narrative literature review.

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1. Introduction

2. literature search strategy, 3. obstructive sleep apnea and community-acquired pneumonia, 4. obstructive sleep apnea and influenza pneumonia, 5. obstructive sleep apnea and covid-19 pneumonia, 6. obstructive sleep apnea and lower respiratory tract infections: pathophysiology, 6.1. altered immunity, 6.2. risk of aspiration, 6.3. the role of obesity and other comorbidities, 7. obstructive sleep apnea and lower respiratory tract infections: treatment, 7.1. settings of care and empiric antibiotics, 7.2. specific risks guiding empiric antibiotic therapy, 7.3. antibiotic pharmacokinetics, side effects, and resistance, 8. discussion, 9. conclusions, supplementary materials, author contributions, institutional review board statement, informed consent statement, data availability statement, acknowledgments, conflicts of interest.

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(“Obstructive Sleep Apnea” OR “Sleep Apnea Syndromes” OR “Sleep-related breathing disorder” OR OSA) AND (pneumonia OR “acute pneumonia” OR “bacterial pneumonia” OR “community acquired pneumonia” OR CAP OR “lung infection” OR “respiratory infection” OR “bronchopneumonia”)
(“Obstructive Sleep Apnea” OR “Sleep Apnea Syndromes” OR “Sleep-related breathing disorder” OR OSA) AND (influenza OR “Influenza A” OR “Influenza B” OR “H1N1” OR “swine flu” OR “avian influenza” OR “H5N1” OR “seasonal influenza” OR “viral pneumonia” OR flu)
(“Obstructive Sleep Apnea” OR “Sleep Apnea Syndromes” OR “Sleep-related breathing disorder” OR OSA) AND (COVID-19 OR “SARS-CoV-2” OR “2019-nCoV” OR “coronavirus disease 2019” OR “novel coronavirus” OR “viral pneumonia”)
Author and DateDesignTotal N (OSA N)Inclusion and Exclusion CriteriaOutcomesKey FindingsLimitations
Keto et al., 2023 [ ]Case-control from Finland50,648 (25,324)I: ICD code for OSA. E: OSA in the two years preceding the index date.LRTI, recurring LRTI.↑ LRTI in the year preceding OSA RR 1.35, and during the year after OSA RR 1.39.No PSG data, no data on OSA treatment, no BMI data.
Grant et al., 2023 [ ]Retrospective cohort from healthcare plans database38.62M PY (1.29M PY)I: Minimum 1 year of enrollment in health plan. E: Death date before January 1st of the index year; Overlapping pneumonia inpatient admissions.All-cause pneumonia, invasive pneumococcal disease, pneumococcal pneumonia.OSA: ↑ pneumonia (18–49 y RR 3.6, 50–64 y RR 3.6, ≥65 y RR 3.4), ↑ invasive pneumococcal disease (18–49 y RR 5.7, 50–64 y RR 4.2, ≥65 y RR 4.2).No PSG data, no data on OSA treatment, no BMI data.
Lutsey et al., 2023 [ ]Post-hoc analysis of the multicentric prospective cohort1586 (772)I: Valid PSG data; Self-identify as White. E: CSA; Already had the outcome of interest at the time of visit.Hospitalization: with pneumonia; with respiratory infection; with any infection.OSA not linked to outcomes; T90 > 5% ↑ hospitalized pneumonia HR 1.59, ↑ hospitalized respiratory infection HR 1.53, ↑ hospitalized any infection HR 1.25.No data on OSA treatment, mostly White population.
Chiner et al., 2016 [ ]Single center case-control123
(85)
I: Cases: Hospitalized for CAP; Controls: Hospitalized for non-respiratory/non-ENT infection. E: Previous OSA diagnosis and CPAP.Pneumonia, PSI.AHI ≥ 10: ↑ pneumonia OR 2.86; AHI ≥ 30: ↑ pneumonia OR 3.184; AHI positively correlated with PSI.Small sample size, no data on OSA treatment.
Su et al., 2014 [ ]Retrospective cohort from Taiwan34,100 (6816)I: ICD codes for OSA; E: ICD codes for pneumonia, lung abscess, empyema.Pneumonia.OSA: ↑ pneumonia HR 1.19; OSA requiring CPAP: ↑ pneumonia HR 1.32.No PSG data, no BMI data.
Lindenauer et al., 2014 [ ]Multicenter, retrospective cohort 250,907 (15,569)I: ICD code for pneumonia; Chest radiography; Antibiotics within 48 h of admission. E: Transfers; Hospital LOS under 2 days; Cystic fibrosis; Pneumonia not present at admission.ICU, MV, hospital mortality, hospital LOS, costs.OSA: ↑ ICU OR 1.54, ↑ MV OR 1.68, ↑ hospital LOS RR 1.14, ↑ cost RR 1.22, ↓ mortality OR 0.90.No PSG data, no data on OSA treatment, no BMI data.
Beumer et al., 2019 [ ]Two center, retrospective cohort199 (9)I: Symptoms and positive influenza PCR; Transfers if not received antibiotics or antivirals.ICU, ICU mortality.OSA/CSA: ↑ ICU admission OR 9.73., not linked to mortality.Small sample size, no PSG data, no data on OSA treatment.
Boattini et al., 2023 [ ]Post-hoc analysis of a multicentric, retrospective cohort356 (23)I: Positive influenza or RSV PCR; Symptoms; Pulmonary infiltrate on imaging. E: Viral co-infections.NIV failure, hospital mortality.OSA/OHS: ↑ NIV failure OR 4.66, not linked to mortality.No PSG data, no data on OSA treatment, no BMI data, no adjustments for obesity.
Mok et al., 2020 [ ]Single center, retrospective cohort 53 (53)I: ICD codes for OSA, influenza. E: No PSG data; No OSA treatment data; CSA on PSG.Hospitalization, complications, hospital LOS.OSA non-CPAP vs. CPAP: ↑ hospitalization OR 4.7. Severity of OSA not linked to hospitalization in CPAP-non adherent.Small sample size, no adjustments for obesity and comorbidities.
Tsai et al., 2022 [ ]Retrospective cohort from Taiwan32,540 (6508)I: Cases: ICD codes for OSA; Controls: No OSA; Randomly selected, matched by income, gender, urbanization, and age. E: influenza pneumonia before OSA.Influenza-associated SARI.OSA: ↑ influenza-SARI HR 1.98, ↑ cumulative incidence of influenza-SARI.No PSG data, no data on OSA treatment, no BMI data.
Chen et al., 2021 [ ]Retrospective cohort from Taiwan27,501 (5483)I: Cases: ICD codes for OSA; Controls: No OSA; Randomly selected, matched by age, sex, index years, and comorbidities. E: UPPP; influenza before OSA.Influenza, composite (pneumonia, hospitalization).OSA: ↑ influenza HR 1.18, ↑ pneumonia or hospitalization 1.79.No PSG data, no data on OSA treatment, no BMI data.
Mashaqi et al., 2021 [ ]Multicentric, retrospective cohort 1738 (139)I: Hospitalized; ICD codes, PSG report, self-report, STOP-BANG for OSA; ICD codes COVID-19. E: ICD for CSA and unspecified sleep apnea.MV, ICU, hospital mortality, hospital LOS.OSA not linked to ICU admission, hospital LOS, MV, or mortality.No PSG data, no data on OSA treatment.
Maas et al., 2021 [ ]Multicentric, retrospective cohort 5544,884 (~44,877)I: All patient encounters; January to June 2020.COVID-19, hospitalization, respiratory failure.OSA: ↑ COVID-19, OR 8.6, ↑ hospitalization, OR 1.65, ↑ respiratory failure, OR 1.98.No PSG data, no data on OSA treatment.
Strausz et al., 2021 [ ]Retrospective cohort from FinnGen biobank445 (38)I: All positive COVID-19 PCR from FinnGen biobank.Hospitalization, COVID-19.OSA not linked with COVID-19, ↑ hospitalization, OR 2.93. Link attenuated after adjustment for BMI in meta-analysis.Small sample size, no PSG data, no data on OSA treatment.
Rögnvaldsson et al., 2022 [ ]Retrospective cohort from Iceland4756 (185)I: Positive COVID-19 PCR. E: Nursing home; COVID-19 during hospitalization or rehabilitation.Composite (hospitalization, mortality).OSA: ↑ composite outcome (hospitalization and mortality) OR 2.0. OSA and CPAP: ↑ composite outcome (hospitalization and mortality) OR 2.4.No PSG data for the control group, no BMI data for 30% of controls and 2% of the OSA group.
Cade et al., 2020 [ ]Multicentric, retrospective cohort4668 (443)I: Positive COVID-19 PCR; A minimum of two clinical notes, two encounters, and three ICD diagnoses.Mortality, composite (mortality, MV, ICU), hospitalization.OSA or CPAP not linked with mortality, MV, ICU, and hospitalization.No PSG data, no data on OSA treatment.
PenaOrbea et al., 2021 [ ]Multicentric, retrospective control and case-control5402 (2664)I: Positive COVID-19 PCR; PSG record available.COVID-19, WHO-designated COVID-19 clinical outcomes, composite (hospitalization, mortality).AHI, T90, SaO , ETCO and CPAP not linked with COVID-19. T90 and SaO : ↑ WHO-designated COVID-19 outcomes ↑ hospitalization, ↑ mortality.Included only patients who had indications for PSG.
Oh et al., 2021 [ ]Retrospective cohort from South Korea124,330 (550)I: ICD codes for COVID-19, chronic respiratory diseases. E: COVID-19 still hospitalized as of June 26, 2020.COVID-19; hospital mortality.OSA: ↑ COVID-19, OR 1.65, not linked to mortality.No PSG data, no data on OSA treatment, no BMI data.
Gottlieb et al., 2020 [ ]Retrospective cohort from Chicago, IL.8673 (288)I: Positive COVID-19 PCR. E: Interhospital transfers.Hospitalization, ICU.OSA not linked to hospitalization, ↑ ICU, OR 1.58.No PSG data, no data on OSA treatment.
Kendzerska et al., 2023 [ ]Retrospective cohort from Ontario, CA.4,912,229 (324,029)I: Alive at the start of the pandemic; Followed until March 31, 2021, or death.COVID-19, ED, hospitalization, ICU, 30-day mortality.OSA: ↑ COVID-19, csHR 1.17, ↑ ED, csHR 1.62, ↑ hospitalizations csHR 1.50, ↑ ICU csHR 1.53, not linked to mortality.No PSG data, no data on OSA treatment, no BMI data.
Peker et al., 2021 [ ]Multicenter, prospective, observational clinical trial320 (121)I: Positive COVID-19 PCR and/or clinical/radiologic.Clinical improvement, clinical worsening, hospitalization, oxygen, ICU.OSA: ↑ delayed clinical improvement, OR 0.42, ↑ oxygen OR 1.95, ↑ clinical worsening.No PSG data, no data on OSA treatment.
Girardin et al., 2021 [ ]Retrospective cohort from NYC and LI4446 (290)I: Positive COVID-19 PCR.Hospital mortality.OSA not linked to mortality.No PSG data, no data on OSA treatment, no BMI data.
Gimeno-Miguel et al., 2021 [ ]Retrospective cohort from Aragon, ES.68,913 (1231)I: Positive COVID-19 PCR/antigen; E: Patients diagnosed from March to May 2020.Composite (hospitalization, 30-day mortality)OSA: ↑ composite outcome (hospitalization and 30-day mortality) in women OR 1.43, but not in men.No PSG data, no data on OSA treatment, no BMI data.
Cariou et al., 2020 [ ]Multicentric, retrospective cohort 1317 (114)I: Positive COVID-19 PCR or clinical/radiological diagnosis, hospitalized, diabetics.Composite (MV, 7-day mortality), mortality on day 7, MV on day 7, ICU, discharge on day 7.OSA: ↑ mortality by day 7 OR 2.80, not linked to composite outcome (intubation and death within 7 days of admission).No PSG data, no data on OSA treatment, diabetic population.
Ioannou et al., 2020 [ ]Longitudinal cohort from VA registry.10,131 (2720)I: VA enrollees who had COVID-19 PCR test; E: VA employees.Hospitalization, MV, mortality.OSA: ↑ MV HR, 1.22, not linked to hospitalization, mortality.No PSG data, no data on OSA treatment, male veterans.
Izquierdo et al., 2020 [ ]Multicentric, retrospective cohort 10,504 (212)I: Positive COVID-19 PCR or clinical/radiological diagnosis.ICU.OSA not linked to ICU admission.No PSG data, no data on OSA treatment, no BMI data, no adjustments for obesity and comorbidities.
Lohia et al., 2021 [ ]Multicentric, retrospective cohort1871 (63)I: Adults; Positive COVID-19 PCR; E: Readmission; Ambulatory surgery, pregnant, transferred-for-ECMO patients.Mortality, MV, ICU.OSA ↑ mortality OR 2.59, ↑ ICU OR 1.95, ↑ MV OR 2.20.Small OSA sample size, no data on OSA treatment, mostly African Americans.
Prasad et al., 2024 [ ]Retrospective cohort from VA registry20,357 (6112)I: Tested for COVID-19 by PCR; Until 16 December 2023.COVID-19, LFNC, HFNC, NIV, MV, 30-day readmission; hospital LOS, ICU LOS, adapted WHO severity scale.OSA ↑ COVID-19 OR 1.37, ↑ NIV OR 1.83, not linked to LFNC, HFNC, MV, 30-day readmission. CPAP adherence not linked to outcomes.No PSG data.
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Nemet, M.; Vukoja, M. Obstructive Sleep Apnea and Acute Lower Respiratory Tract Infections: A Narrative Literature Review. Antibiotics 2024 , 13 , 532. https://doi.org/10.3390/antibiotics13060532

Nemet M, Vukoja M. Obstructive Sleep Apnea and Acute Lower Respiratory Tract Infections: A Narrative Literature Review. Antibiotics . 2024; 13(6):532. https://doi.org/10.3390/antibiotics13060532

Nemet, Marko, and Marija Vukoja. 2024. "Obstructive Sleep Apnea and Acute Lower Respiratory Tract Infections: A Narrative Literature Review" Antibiotics 13, no. 6: 532. https://doi.org/10.3390/antibiotics13060532

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Upper respiratory tract infections and academic attainment: A case study

Andrew p. smith.

Centre for Occupational and Health Psychology, School of Psychology, Cardiff University, Cardiff, Wales, United Kingdom

Background:

There has been extensive research showing that upper respiratory tract infections (URTIs), such as the common cold and influenza, can impair mental performance. Much of this research has involved studies of experimentally induced URTIs or laboratory studies of naturally occurring illnesses. The results from this research have implications for performance at work and in education.

The present article presents a case study of the association between URTIs and academic performance and reports the use of such information as an extenuating circumstance for poor performance.

The paper describes the poor performance of a primary school student taking the 11+ examination, which determines the choice of the future secondary school. Evidence suggested that it was plausible that the student was incubating an URTI at the time of the examination. Other possible infections, such as COVID, were ruled out. An appeal was made based on the possible association between incubating an URTI and unusually poor examination performance.

The appeal was supported by the adjudicating committee and the student was allowed a place in the preferred secondary school.

Conclusions:

This case study shows that information about the association between URTIs and mental performance can be used as an extenuating circumstance that can plausibly account for poor academic performance. This can form the basis of the future appeals and recommendations for the type of evidence needed to make such claims are made.

Relevance for Patients:

URTIs are frequent, common, and a cause of absence from education and work. They may also impair performance, with effects not being restricted to the time the person is symptomatic. They may also increase susceptibility to the negative effects of stress and fatigue.

1. Introduction

Over the past 30 years, there has been extensive research on the association between upper respiratory tract infections (URTIs) and mental performance [ 1 ]. This research initially started with the examination of the effects of experimentally induced URTIs on tests measuring underlying cognitive functions [ 2 ]. The results showed that viruses leading to the common cold led to psychomotor slowing, whereas influenza viruses impaired selective and sustained attention [ 3 , 4 ]. The effects of the URTIs were not restricted to the time that the person was symptomatic but were observed in those with sub-clinical infections [ 5 ], during the incubation period [ 5 ], and after the symptoms had gone [ 6 ]. Research investigating naturally occurring URTIs confirmed many of the results from the earlier research [ 7 , 8 ]. Furthermore, the research not only identified the direct effects of URTIs but showed that having an URTI made individuals more sensitive to other negative factors such as stress [ 9 ] or fatigue [ 10 ].

The above results have important implications for real-life activities such as driving and having an URTI has been shown to impair performance on driving simulators [ 11 , 12 ]. The results also suggest that impairments due to URTIs may be observed in occupational and educational settings. One of the best examples of the impact of influenza in the workplace is a case study of the after-effects of influenza on the skilled performance of a technician [ 13 ]. The person described in the study was a skilled technician who had been absent from work with influenza. When he returned to work, he made elementary mistakes in calibrating machinery and proceeded to collect incorrect data, which he only rejected several weeks later. There have also been epidemiological studies on the impact of URTI on the academic performance of university students [ 14 ]. This research studied nearly 5000 students for a 6-month period from November to the end of April. Over 45,000 days of illness due to URTIs were reported. Of those with URTIs, 27.8% did poorly on an examination, and 46.3% did poorly on coursework.

The present paper reports a case study of a primary school student who normally had very high academic grades and did very badly on the 11+ examination, which is used to determine the choice of secondary school. Evidence concerning the impact of an URTI was evaluated and, together with evidence on the behavioral effects of URTIs, was submitted as an extenuating circumstances appeal.

The author of the paper was approached by the parents of a 10-year-old student who had performed unusually badly in an 11+ examination. They had been aware of a decline in his health and asked for an opinion from an expert witness on whether the poor performance could plausibly be linked to an URTI. The next sections describe the student’s past performance and health at the time of the examination. The results section covers the information provided to the extenuating circumstances committee and their decision.

2.1. The past academic record of the student

The recent academic achievement scores for the student were made available. All areas showed that the student was either in line with National Age-related Expectations or above those expectations. Both the attitude to learning and pupil’s behavior were exceptionally high. The teacher judgment for specific domains (English, Maths, and Science) was above age-related expectations. The most relevant teacher comment was that “Student X --- is working 10–12% above the standardized equivalent for the 11+ pass mark.”

2.2. Events close to the 11+ examination

The following summary describes events before and after the 11+ examination.

The school term starts.

Evening walks with **** in an attempt to manage examination stress/anxiety.

**** sits Secondary Transfer Test (the 11+ Test).

**** starts to show symptoms in the evening with headache, runny nose, sneezing, and fatigue.

Symptoms worsen – a particularly bad cough and tiredness.

Symptoms become more severe – extreme fatigue and lethargy, coughing more persistent, breathing sounds wheezy, sleep is disturbed, and headache.

Symptoms persist. **** kept from school, and the school office was informed. A COVID PCR test is carried out.

**** kept home from school; a negative PCR test result was received.

**** is still too ill to return to the school; the school is notified.

**** is sufficiently recovered to return to lessons, but no PE.

2.3. Parents approach Professor Smith

On the October 21, 2021, the father of the student sent the following E-mail:

“ Dear Professor Smith ,

I have read with great interest reports of your article concerning the effects that a virus can have on cognitive function even before physical symptoms are showing .

I came across it whilst carrying out some research as our son’s school has asked us to consider what were the unusual circumstances around the time he sat his 11+ exam that may have caused his result to come out significantly lower than they had expected and below that predicted by various mock tests and his CAT scores .

We have looked back at the period and identified that on the evening after his examination, he started to feel unwell and deteriorated further, and then had to be kept off school the following week with a very bad cold, cough, flu, haziness, and fatigue symptoms. His PCR and lateral flow tests indicated, he was negative for COVID .

His headteacher had put him in the “Exceptionally able so very highly recommended’ and ‘Enjoys a challenge and is a highly motivated independent learner” categories in her recommendation to the local authority before the date of the examination. We’re considering the likelihood that he was already suffering symptoms as well as pre-exam anxiety and the possibility that this was negatively impacting the very qualities, he most needed to succeed in the examination .

We would be very grateful if you were available to discuss this in the context of your findings and perhaps to consult with you on any possible correlation?”

Following this E-mail, there were several telephone conversations and E-mail exchanges aimed at providing more detailed information. These were then reviewed and a letter was sent to the Selection Review Panel. The review process is entirely in writing. The panel consists of two grammar school headteachers and one junior school headteacher.

3.1. Professor Smith’s letter to the review panel

The following letter and supporting appendices were sent to the review panel. Appendix 1 has been outlined in section 2.2 of the paper. References to Appendix 2 [ 15 ], Appendx 3 [ 14 ], Appendix 4 [ 4 , 5 ] and Appendix 5 [ 9 ] are provided at the end of this article.

“ October 28, 2021

To whom it may concern

Re: Extenuating circumstances relating to the exam performance of ***

I have been asked by ****’s parents to review the extenuating circumstances relating to his underachievement in a recent examination. I have been asked to do this because I am an expert on the effects of URTIs and performance, a topic that I have researched for over 30 years .

The first issue I am going to cover is whether it is likely that **** was incubating an illness on the day of his examination. His parents have provided me with details of his subsequent illness (Appendix 1) which appears to be an URTI such as influenza or the common cold. These illnesses can take 24–96 h to develop after infection, making it likely that he was incubating the illness on the day of his examination. Data from Public Health England (Appendix 2) show that URTIS increased during this week due to children starting back to school .

The second issue to address is whether URTIs impair academic performance. A paper on this topic is shown in Appendix 3, and the results demonstrate that these illnesses can impair examination performance by up to 30% .

One must now ask whether performance during the incubation period is also impaired due to infection, even though the person is not symptomatic. One of the first studies we carried out at the MRC Common Cold Unit (Appendix 4) showed that performance was impaired during the incubation period, with the impairment being in the region of about 10%. Another finding from my research (Appendix 5) shows that URTIs can make the person more sensitive to stressful situations, and examinations would fall in this category .

Overall, my conclusion is that it is likely that Student X’s examination performance was impaired due to the developing infection. I hope that the panel will give this serious consideration when considering his appeal.”

3.2. The decision of the selection review panel

On the February 9, 2022, ****’s parents received the following E-mail from School Admission:

“We are writing to let you know the outcome of ****’s Selection Review. We are pleased to tell you that the review was successful .

What happens next?

This means that **** is now qualified for admission to any **** grammar school. The preferences that you expressed for these schools will be considered in the first allocation round. Your home local authority will let you know the outcome of your secondary school application on March 1, 2022.”

4. Discussion

It is very common for the authors of fundamental research to discuss the practical implications and applications of their results. Unfortunately, the translation process is often not achieved. The present case study shows that basic research on the behavioral effects of URTIs can be used to support extenuating circumstances appeals in education. The success of the present appeal depended on some crucial features of the supporting documentation. First, the suggested illness occurred when URTIs were prevalent. Second, subsequent symptoms suggested that at the time of the examination, the person was incubating and URTI. This is likely to have been a severe cold or influenza, as the PCR test for COVID was negative.

The supporting literature based on laboratory and epidemiological studies suggests that URTIs can impair academic performance. The laboratory research demonstrated that such effects can occur in the incubation period and that URTIs can make the individual more susceptible to the negative effects of stress. Taking an examination can be very stressful and this was confirmed here by the parents. Overall, the evidence presented was sufficiently strong for the Selection Review Panel to agree with the extenuating circumstances appeal. This could set a precedent for the future appeals. It should be pointed out that these are only likely to be successful if the relevant, plausible information is reported.

5. Conclusion

This case study demostrates that the research literature on URTIs and mental performance can be used as supporting evidence in extenuating circumstances appeals. It also outlines the nature of the evidence needed when such appeals are made.

Acknowledgments

The author would like to acknowledge all of the collaborators in research on the behavioral effects of URTIs, especially the late David Tyrrell, who allowed me to conduct my early studies at the MRC Common Cold Unit, Salisbury UK.

Conflict of Interest

The author declares no conflict of interest.

There was no funding associated with the present project.

Cambridge Dictionary

  • Cambridge Dictionary +Plus

Meaning of upper respiratory tract in English

  • The majority of cases involved the upper respiratory tract only.
  • These patients were less likely to have a cough and upper respiratory tract symptoms .
  • Infections of the upper respiratory tract , from the nose through the upper airways , are frequent causes of dry cough .
  • cardiopulmonary
  • cardiorespiratory
  • oxygen debt
  • respiratory system
  • respiratory tract
  • tracheobronchial
  • upper respiratory
  • vocal cords

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