Pneumococcal pneumonia

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Pneumococcal pneumonia
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Pneumococcal pneumonia is a type of bacterial pneumonia that is caused by Streptococcus pneumoniae (pneumococcus). [1] It is the most common bacterial pneumonia found in adults, the most common type of community-acquired pneumonia, and one of the common types of pneumococcal infection. The estimated number of Americans with pneumococcal pneumonia is 900,000 annually, with almost 400,000 cases hospitalized and fatalities accounting for 5-7% of these cases. [2]

Contents

Symptoms

The symptoms of pneumococcal pneumonia can occur suddenly, presenting as a severe chill, followed by a severe fever, cough, shortness of breath, rapid breathing, and chest pains. Other symptoms like nausea, vomiting, headache, fatigue, and muscle aches could also accompany initial symptoms. [1] The coughing can occasionally produce rusty or blood-streaked sputum. In 25% of cases, a parapneumonic effusion may occur. Chest X-rays will typically show lobar consolidation or patchy infiltrates. [3]

Treatment

In most cases, once pneumococcal pneumonia has been identified, doctors will prescribe antibiotics. These antibiotics usually help alleviate and eliminate symptoms between 12 and 36 hours after the initial dose. Despite most antibiotics' effectiveness in treating the disease, sometimes the bacteria can resist the antibiotics, causing symptoms to worsen. Age and health of the infected patient can also contribute to the effectiveness of the antibiotics. A vaccine has been developed for the prevention of pneumococcal pneumonia, recommended to children under age five as well as adults over the age of 65. [1]

Research advancements in the field

While it has been commonly known that the influenza virus increases one's chances of contracting pneumonia or meningitis caused by the streptococcus pneumonaie bacteria, new medical research in mice indicates that the flu is actually a necessary component for the transmission of the disease. Researcher Dimitri Diavatopoulo from the Radboud University Nijmegen Medical Centre in the Netherlands describes his observations in mice, stating that in these animals, the spread of the bacteria only occurs between animals already infected with the influenza virus, not between those without it. He says that these findings have only been inclusive in mice, however, he believes that the same could be true for humans. [4]

Mechanism of disease manifestation

Three stages can be used to categorize the infection process of pneumococcal pneumonia: transmission, colonization, and invasion. [5] The Streptococcus pneumoniae (S. pneumoniae) leave the colonized host via shedding in order to be transmissible to new hosts, and must survive in the environment until infection of a new host (unless direct transmission occurs). Animal models have allowed scientists to have an increased understanding of these stages of infection.

Transmission

In order for transmission to occur, there must be close contact with a carrier or amongst carriers. [5] The likelihood of this increases during colder, dryer months of the year.  The probability of transmission is shown to proliferate in coordination with other upper respiratory tract (URT) infections.

Animal models have allowed for an increased understanding of the transmission stage during infection.  A 2010 study examining co-infection of influenza in co-housed ferret pairs found that the influenza increased both incidence and severity of pneumococcal infection. [6]   These findings exhibited pneumococcal strain dependence. A separate 2010 study examining intra-litter transmission, with influenza co-infection in infant mice, found that the influenza co-infection is a facilitator for pneumococcal susceptibility, transmission, and disease via bacterial shedding. [7] A third study of note, from 2016, was able to examine pneumococcal transmission without co-infection of an URT infection. [8]   This study utilized intra-litter transmission in infant mice during bacterial mono-infection with pneumococcus.  The results of this study indicated higher rates of shedding for infections in younger mice. 

These studies, along with the animal models that they utilize have enhanced our understanding of the transmission of pneumococcus.  Inflammation induced by Influenza A Virus (IAV) stimulates the flow of mucus through the expression of glycoproteins, prompts secretion, and increases shedding. [5]   Streptococcus is found in the inflammation-generated mucus layers covering the URT and increased pneumococci are observed in nasal secretions with IAV co-infection.  Levels of shedding have correlations with IAV induced URT inflammation.  Pro-inflammatory effects are exhibited by the single pneumococcal toxin, pneumolysin (Ply); use of anti-Ply antibodies result in decreased inflammation. [9] Studies have found transmissible levels of bacterium only in young mice, exhibiting that shedding increases with incidences of contact and proximity[ failed verification (See discussion.)].  Shedding is shown to decrease in the presence of agglutinating antibodies such as IgG and IgA1 unless cleavage occurs via an IgA1-specific pneumococcal protease. [5]       

Transmission via the secretions of carriers can result from direct interpersonal contact or contact with a contaminated surface. [5]   Bacteria on contaminated surfaces can be easily cultured.  In conditions with sufficient nutrients, pneumococci can survive for 24 hours [10]  and avoid desiccation for multiple days. [11]  

Reduced transmission has been observed amongst children with Pneumococcal conjugate vaccine (PCV) immunization as acquisition of a new strain of S. pneumoniae is inhibited by pre-existing colonization. [5] Immunoglobulin G (IgG) immunization with high antibody concentration can also inhibit acquisition.  These antibodies require the agglutinating function of the Fc fragment

For successful acquisition in a new host, pneumococcus must successfully adhere to the mucous membrane of the new host's nasopharynx. [11] Pneumococcus is able to evade detection by the mucous membrane when there is a higher proportion of negatively charged capsules.  This clearance is mediated by Immunoglobulin A1 (IgA1) which is abundant on the URT mucosal surfaces. [5]

Colonization

Transparent and opaque colony morphology has been observed for pneumococci. [12]   Airway colonization is observed in transparent phenotypes of serotypes, while survival in bloodstreams is observed for opaque phenotypes.  Colonizable strains exhibit resistance against neutrophilic immune response.  

Successful colonization requires S. pnuemoniae to evade detection by the nasal mucus and attach to epithelial surface receptors. [5]   Asymptomatic colonization occurs when S. pneumoniae bind to N-acetyl-glucosamine on epithelium without inflammation. [13] However, co-infection with a pre-existing inflammatory URT infection results in an over-expression of the epithelial receptors utilized by S. pneumoniae, thus increasing the likelihood of colonization. Neuraminidase also increases instances of epithelial binding through its cleavage of N-acetylneuraminic acid, glycolipids, glycoproteins, and oligosaccharides. [13]    

Invasion

Initial colonization of the nasopharynx is typically asymptomatic, but invasion occurs when the bacteria spreads to other parts of the body including the lungs, blood, and brain. Interactions between Phosphorylcholine (ChoP) components on colonized epithelial cells allow for docking of choline binding proteins (CBPs), most notably CbpA.  Colonization of the respiratory tract, and thus pneumonia cannot occur without CpbA. [14]  

The pneumococcus moves across the mucosal barrier by integrating itself with the polymeric immunoglobulin receptor (pIgR), which is used by mucosal epithelial cells to transport IgA and IgM to the apical surface.  Following its cleavage at the apical surface, pIgR, and subsequently the pneumococcus, move back to the basolateral surface allowing invasion of the upper respiratory tract. [14]  

The pneumococcus then moves to invade the lower respiratory tract, evading the mucociliary escalator with the assistance of neuraminidase. [14]       

Related Research Articles

<i>Streptococcus</i> Genus of bacteria

Streptococcus is a genus of gram-positive coccus or spherical bacteria that belongs to the family Streptococcaceae, within the order Lactobacillales, in the phylum Bacillota. Cell division in streptococci occurs along a single axis, so as they grow, they tend to form pairs or chains that may appear bent or twisted. This differs from staphylococci, which divide along multiple axes, thereby generating irregular, grape-like clusters of cells. Most streptococci are oxidase-negative and catalase-negative, and many are facultative anaerobes.

<span class="mw-page-title-main">Pneumonia</span> Inflammation of the alveoli of the lungs

Pneumonia is an inflammatory condition of the lung primarily affecting the small air sacs known as alveoli. Symptoms typically include some combination of productive or dry cough, chest pain, fever, and difficulty breathing. The severity of the condition is variable.

<span class="mw-page-title-main">Frederick Griffith</span> British bacteriologist

Frederick Griffith (1877–1941) was a British bacteriologist whose focus was the epidemiology and pathology of bacterial pneumonia. In January 1928 he reported what is now known as Griffith's Experiment, the first widely accepted demonstrations of bacterial transformation, whereby a bacterium distinctly changes its form and function.

Atypical pneumonia, also known as walking pneumonia, is any type of pneumonia not caused by one of the pathogens most commonly associated with the disease. Its clinical presentation contrasts to that of "typical" pneumonia. A variety of microorganisms can cause it. When it develops independently from another disease, it is called primary atypical pneumonia (PAP).

<i>Streptococcus pneumoniae</i> Species of bacterium

Streptococcus pneumoniae, or pneumococcus, is a Gram-positive, spherical bacteria, alpha-hemolytic member of the genus Streptococcus. They are usually found in pairs (diplococci) and do not form spores and are non motile. As a significant human pathogenic bacterium S. pneumoniae was recognized as a major cause of pneumonia in the late 19th century, and is the subject of many humoral immunity studies.

<span class="mw-page-title-main">Lower respiratory tract infection</span> Medical term

Lower respiratory tract infection (LRTI) is a term often used as a synonym for pneumonia but can also be applied to other types of infection including lung abscess and acute bronchitis. Symptoms include shortness of breath, weakness, fever, coughing and fatigue. A routine chest X-ray is not always necessary for people who have symptoms of a lower respiratory tract infection.

<span class="mw-page-title-main">Bacterial pneumonia</span> Disease of the lungs

Bacterial pneumonia is a type of pneumonia caused by bacterial infection.

Community-acquired pneumonia (CAP) refers to pneumonia contracted by a person outside of the healthcare system. In contrast, hospital-acquired pneumonia (HAP) is seen in patients who have recently visited a hospital or who live in long-term care facilities. CAP is common, affecting people of all ages, and its symptoms occur as a result of oxygen-absorbing areas of the lung (alveoli) filling with fluid. This inhibits lung function, causing dyspnea, fever, chest pains and cough.

<span class="mw-page-title-main">Quellung reaction</span> Reaction in which antibodies bind to bacterial capsule

The quellung reaction, also called the Neufeld reaction, is a biochemical reaction in which antibodies bind to the bacterial capsule of Streptococcus pneumoniae, Klebsiella pneumoniae, Neisseria meningitidis, Bacillus anthracis, Haemophilus influenzae, Escherichia coli, and Salmonella. The antibody reaction allows these species to be visualized under a microscope. If the reaction is positive, the capsule becomes opaque and appears to enlarge.

<span class="mw-page-title-main">Pneumococcal vaccine</span> Vaccine to prevent infection by the bacteria Stretococcus pneumoniae

Pneumococcal vaccines are vaccines against the bacterium Streptococcus pneumoniae. Their use can prevent some cases of pneumonia, meningitis, and sepsis. There are two types of pneumococcal vaccines: conjugate vaccines and polysaccharide vaccines. They are given by injection either into a muscle or just under the skin.

Robert Austrian was an American infectious diseases physician and, along with Maxwell Finland, one of the two most important researchers into the biology of Streptococcus pneumoniae in the 20th century.

<span class="mw-page-title-main">Influenza</span> Infectious disease, often just "the flu"

Influenza, commonly known as "the flu", is an infectious disease caused by influenza viruses. Symptoms range from mild to severe and often include fever, runny nose, sore throat, muscle pain, headache, coughing, and fatigue. These symptoms begin from one to four days after exposure to the virus and last for about 2–8 days. Diarrhea and vomiting can occur, particularly in children. Influenza may progress to pneumonia, which can be caused by the virus or by a subsequent bacterial infection. Other complications of infection include acute respiratory distress syndrome, meningitis, encephalitis, and worsening of pre-existing health problems such as asthma and cardiovascular disease.

Pneumococcal infection is an infection caused by the bacterium Streptococcus pneumoniae.

<span class="mw-page-title-main">Acute exacerbation of chronic obstructive pulmonary disease</span> Medical condition

An acute exacerbation of chronic obstructive pulmonary disease, or acute exacerbations of chronic bronchitis (AECB), is a sudden worsening of chronic obstructive pulmonary disease (COPD) symptoms including shortness of breath, quantity and color of phlegm that typically lasts for several days.

<span class="mw-page-title-main">Austrian syndrome</span> Medical condition

Austrian syndrome, also known as Osler's triad, is a medical condition that was named after Robert Austrian in 1957. The presentation of the condition consists of pneumonia, endocarditis, and meningitis, all caused by Streptococcus pneumoniae. It is associated with alcoholism due to hyposplenism and can be seen in males between the ages of 40 and 60 years old. Robert Austrian was not the first one to describe the condition, but Richard Heschl or William Osler were not able to link the signs to the bacteria because microbiology was not yet developed.

<span class="mw-page-title-main">Classification of pneumonia</span> Medical condition

Pneumonia can be classified in several ways, most commonly by where it was acquired, but may also by the area of lung affected or by the causative organism. There is also a combined clinical classification, which combines factors such as age, risk factors for certain microorganisms, the presence of underlying lung disease or systemic disease and whether the person has recently been hospitalized.

Chronic Mycoplasma pneumonia and Chlamydia pneumonia infections are associated with the onset and exacerbation of asthma. These microbial infections result in chronic lower airway inflammation, impaired mucociliary clearance, an increase in mucous production and eventually asthma. Furthermore, children who experience severe viral respiratory infections early in life have a high possibility of having asthma later in their childhood. These viral respiratory infections are mostly caused by respiratory syncytial virus (RSV) and human rhinovirus (HRV). Although RSV infections increase the risk of asthma in early childhood, the association between asthma and RSV decreases with increasing age. HRV on the other hand is an important cause of bronchiolitis and is strongly associated with asthma development. In children and adults with established asthma, viral upper respiratory tract infections (URIs), especially HRVs infections, can produce acute exacerbations of asthma. Thus, Chlamydia pneumoniae, Mycoplasma pneumoniae and human rhinoviruses are microbes that play a major role in non-atopic asthma.

<span class="mw-page-title-main">Neonatal infection</span> Human disease

Neonatal infections are infections of the neonate (newborn) acquired during prenatal development or within the first four weeks of life. Neonatal infections may be contracted by mother to child transmission, in the birth canal during childbirth, or after birth. Neonatal infections may present soon after delivery, or take several weeks to show symptoms. Some neonatal infections such as HIV, hepatitis B, and malaria do not become apparent until much later. Signs and symptoms of infection may include respiratory distress, temperature instability, irritability, poor feeding, failure to thrive, persistent crying and skin rashes.

Necrotizing pneumonia (NP), also known as cavitary pneumonia or cavitatory necrosis, is a rare but severe complication of lung parenchymal infection. In necrotizing pneumonia, there is a substantial liquefaction following death of the lung tissue, which may lead to gangrene formation in the lung. In most cases patients with NP have fever, cough and bad breath, and those with more indolent infections have weight loss. Often patients clinically present with acute respiratory failure. The most common pathogens responsible for NP are Streptococcus pneumoniae, Staphylococcus aureus, Klebsiella pneumoniae. Diagnosis is usually done by chest imaging, e.g. chest X-ray, CT scan. Among these CT scan is the most sensitive test which shows loss of lung architecture and multiple small thin walled cavities. Often cultures from bronchoalveolar lavage and blood may be done for identification of the causative organism(s). It is primarily managed by supportive care along with appropriate antibiotics. However, if patient develops severe complications like sepsis or fails to medical therapy, surgical resection is a reasonable option for saving life.

<span class="mw-page-title-main">Daniela M. Ferreira</span> Brazilian immunologist

Daniela M. Ferreira is a Brazilian British immunologist. She is a specialist in bacterial infection, respiratory co-infection, mucosal immunology and vaccine responses. She is currently Professor of Respiratory Infection and Vaccinology at the Oxford Vaccine Group in the Department of Paediatrics at the University of Oxford and the Director of the Liverpool Vaccine Group at the Liverpool School of Tropical Medicine. She leads a team of scientists studying protective immune responses against pneumococcus and other respiratory pathogens such as SARS-CoV2. Her team has established a novel method of inducing pneumococcal carriage in human volunteers. They use this model to:

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