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Pneumonia bacteria name: What Is The Connection Between Influenza and Pneumonia?

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Learn About Pneumonia | American Lung Association

Pneumonia is a common lung infection caused by bacteria, a virus or fungi. It is often spread via coughing, sneezing, touching or even breathing, and those who don’t exhibit symptoms can also spread the illness.

What Is Pneumonia?

Pneumonia is an infection of the lungs that may be caused by bacteria, viruses, or fungi. The infection causes the lungs’ air sacs (alveoli) to become inflamed and fill up with fluid or pus. That can make it hard for the oxygen you breathe in to get into your bloodstream. The symptoms of pneumonia can range from mild to severe, and include cough, fever, chills, and trouble breathing.

Many factors affect how serious a case of pneumonia is, such as the type of germ causing the lung infection, the person’s age, and their overall health. The people most at risk are infants and young children, adults 65 or older, and people who have other health problems.

Pneumonia is a leading cause of hospitalization in both children and adults. Most cases can be treated successfully, although it can take weeks to fully recover. Tens of thousands of people in the U.S. die from pneumonia every year, most of them adults over the age of 65.

What Causes Pneumonia?

Pneumonia can be caused by a wide variety of bacteria, viruses and fungi in the air we breathe. Identifying the cause of your pneumonia can be an important step in getting the proper treatment.

Learn more about what causes pneumonia.

What Are the Risk Factors?

Anyone can get pneumonia, but many factors can increase your chances of getting sick and having a more severe illness. One of the most important factors is your age. People age 65 and over are at increased risk because their immune system is becoming less able to fight off infection as years go by. Infants and children two years of age or younger are also at increased risk because their immune systems are not yet fully developed.

Other risk factors can be grouped into three main categories: medical conditions, health behaviors, and environment.

Medical conditions

  • Chronic lung diseases such as COPD, bronchiectasis, or cystic fibrosis that make the lungs more vulnerable.
  • Other serious chronic illnesses, such as heart disease, diabetes and sickle cell disease.
  • A weakened immune system due to HIV/AIDs, an organ transplant, chemotherapy or long-term steroid use.
  • Difficulty swallowing, due to stroke, dementia, Parkinson’s disease, or other neurological conditions, which can result in aspiration of food, vomit or saliva into the lungs that then becomes infected.
  • Recent viral respiratory infection—a cold, laryngitis, influenza, etc.
  • Hospitalization, especially when in intensive care and using a ventilator to breathe.

Health behaviors

  • Cigarette smoking, which damages the lungs.
  • Drug and alcohol abuse, which increase the risk of aspiration pneumonia.

Environment

  • Exposure to certain chemicals, pollutants or toxic fumes, including secondhand smoke.

Pneumonia | Johns Hopkins Medicine

What is pneumonia?

Pneumonia is an infection of one or both of the lungs caused by bacteria, viruses, or fungi. It is a serious infection in which the air sacs fill with pus and other liquid.

What causes pneumonia?

There are more than 30 different causes of pneumonia, and they’re grouped by the cause. The main types of pneumonia are:

  • Bacterial pneumonia. This type is caused by various bacteria. The most common is Streptococcus pneumoniae. It usually occurs when the body is weakened in some way, such as by illness, poor nutrition, old age, or impaired immunity, and the bacteria are able to work their way into the lungs. Bacterial pneumonia can affect all ages, but you are at greater risk if you abuse alcohol, smoke cigarettes, are debilitated, have recently had surgery, have a respiratory disease or viral infection, or have a weakened immune system.

  • Viral pneumonia. This type is caused by various viruses, including the flu (influenza), and is responsible for about one-third of all pneumonia cases. You may be more likely to get bacterial pneumonia if you have viral pneumonia.

  • Mycoplasma pneumonia. This type has somewhat different symptoms and physical signs and is referred to as atypical pneumonia. It is caused by the bacterium Mycoplasma pneumoniae. It generally causes a mild, widespread pneumonia that affects all age groups.

  • Other pneumonias. There are other less common pneumonias that may be caused by other infections including fungi.

Who is at risk for pneumonia?

Anyone can get pneumonia. However, the following groups are at the highest risk:

What are the symptoms of pneumonia?

The symptoms of bacterial pneumonia include:

  • Bluish color to lips and fingernails

  • Confused mental state or delirium, especially in older people

  • Cough that produces green, yellow, or bloody mucus

  • Fever

  • Heavy sweating

  • Loss of appetite

  • Low energy and extreme tiredness

  • Rapid breathing

  • Rapid pulse

  • Shaking chills

  • Sharp or stabbing chest pain that’s worse with deep breathing or coughing

  • Shortness of breath that gets worse with activity

Early symptoms of viral pneumonia are the same as those of bacterial pneumonia, which may be followed by:

Mycoplasma pneumonia has somewhat different symptoms, which include a severe cough that may produce mucus.

How is pneumonia diagnosed?

Diagnosis is usually made based on your recent health history (such as surgery, a cold, or travel exposures) and the extent of the illness. Based on these factors, your healthcare provider may diagnose pneumonia simply on a thorough history and physical exam. The following tests may be used to confirm the diagnosis:

  • Chest X-ray. This test takes pictures of internal tissues, bones, and organs, including the lungs.

  • Blood tests. This test may be used to see whether infection is present and if infection has spread to the bloodstream (blood cultures). Arterial blood gas testing checks the amount of oxygen in your bloodstream.

  • Sputum culture. This test is done on the material that is coughed up from the lungs and into the mouth. It’s often used to see if there’s an infection in the lungs.

  • Pulse oximetry. An oximeter is a small machine that measures the amount of oxygen in the blood. A small sensor is taped or clipped onto a finger. When the machine is on, a small red light can be seen in the sensor. The test is painless and the red light does not get hot.

  • Chest CT scan. This imaging procedure uses a combination of X-rays and computer technology to produce sharp, detailed horizontal, or axial, images (often called slices) of the body. A CT scan shows detailed images of any part of the body, including the bones, muscles, fat, and organs. CT scans are more detailed than regular X-rays.

  • Bronchoscopy. This is direct exam of the bronchi (the main airways of the lungs) using a flexible tube (called a bronchoscope). It helps to evaluate and diagnose lung problems, assess blockages, and take out samples of tissue and/or fluid for testing,

  • Pleural fluid culture. In this test, a sample of a fluid sample is taken from the pleural space. This is the space between the lungs and chest wall. A long, thin needle is put through the skin between the ribs and into the pleural space. Fluid is pulled into a syringe attached to the needle. It is sent to the lab where it’s tested to find out which bacteria is causing the pneumonia.

How is pneumonia treated?

Treatment depends on the type of pneumonia you have. Most of the time, pneumonia is treated at home, but severe cases may be treated in the hospital. Antibiotics are used for bacterial pneumonia. Antibiotics may also speed recovery from mycoplasma pneumonia and some special cases. Most viral pneumonias don’t have specific treatment. They usually get better on their own.

Other treatment may include eating well, increasing fluid intake, getting rest, oxygen therapy, pain medicine, fever control, and maybe cough-relief medicine if cough is severe.

Can pneumonia be prevented?

Check with your healthcare provider about getting immunizations. The flu is a common cause of pneumonia. Because of that, getting a flu shot every year can help prevent both the flu and pneumonia.

There is also a pneumococcal vaccine. It will protect you from a common form of bacterial pneumonia. Children younger than age 5 and adults ages 65 and older should get this shot.

The pneumococcal shot is also recommended for all children and adults who are at increased risk of pneumococcal disease due to other health conditions.

What are the complications of pneumonia?

Most people with pneumonia respond well to treatment, but pneumonia can be very serious and even deadly.

You are more likely to have complications if you are an older adult, a very young child, have a weakened immune system, or have a serious medical problem like diabetes or cirrhosis. Complications may include:

  • Acute respiratory distress syndrome (ARDS). This is a severe form of respiratory failure.

  • Lung abscesses. These are pockets of pus that form inside or around the lung. They may need to be drained with surgery

  • Respiratory failure. This requires the use of a breathing machine or ventilator.

  • Sepsis. This is when the infection gets into the blood. It may lead to organ failure.

Key points about pneumonia

  • Pneumonia is an infection of one or both of the lungs caused by bacteria, viruses, or fungi.

  • There are more than 30 different causes of pneumonia, and they’re grouped by the cause. The main types of pneumonia are bacterial, viral, and mycoplasma pneumonia.

  • A cough that produces green, yellow, or bloody mucus is the most common symptom of pneumonia. Other symptoms include fever, shaking chills, shortness of breath, low energy, and extreme tiredness.

  • Pneumonia can often be diagnosed with a thorough history and physical exam. Tests used to look at the lungs, blood tests, and tests done on the sputum you cough up may also be used.

  • Treatment depends on the type of pneumonia you have. Antibiotics are used for bacterial pneumonia. It may also speed recovery from mycoplasma pneumonia and some special cases. Most viral pneumonias don’t have a specific treatment and just get better on their own. Other treatment may include a healthy diet, more fluids, rest, oxygen therapy, and medicine for pain, cough, and fever control.

  • Most people with pneumonia respond well to treatment, but pneumonia can cause serious lung and infection problems. It can even be deadly.

Typical Bacterial Pneumonia – StatPearls

Continuing Education Activity

The severe form of acute lower respiratory tract infection that affects the pulmonary parenchyma in one or both lungs is known as pneumonia. It is a common disease and a potentially serious infectious disease with considerable morbidity and mortality. Pneumonia is the sixth leading cause of death and the only infectious disease in the top ten causes of death in the United States. Community-acquired pneumonia is diagnosed in non-hospitalized patients or a previously ambulatory patient within 48 hours after admission to the hospital. CAP is further divided into “typical” and “atypical.” HAP develops more than 48 hours after hospital admission. Patients who are mechanically ventilated for more than 48 hours after endotracheal intubation can develop pneumonia known as VAP. HCAP occurs in ambulatory patients who are not hospitalized and have had extensive healthcare contact within the last 3 months. This activity reviews the evaluation and management of typical community-acquired pneumonia and highlights the role of interprofessional team members in collaborating to provide well-coordinated care and enhance patient outcomes.

Objectives:

  • Explain the causes of
    typical community-acquired pneumonia.

  • Describe the evaluation of a patient with typical community-acquired pneumonia.

  • Summarize the treatment options for typical community-acquired pneumonia.

  • Explore modalities to improve care coordination among interprofessional team members in order to improve outcomes for patients affected by typical community-acquired pneumonia.

Access free multiple choice questions on this topic.

Introduction

The severe form of acute lower respiratory tract infection that affects the pulmonary parenchyma in one or both lungs is known as pneumonia. It is a common disease and a potentially serious infectious disease with considerable morbidity and mortality. Pneumonia is the sixth leading cause of death and the only infectious disease in the top ten causes of death in the United States.

Pneumonia can be classified into 2 types based on how the infection is acquired:

  1. Community-acquired pneumonia (CAP): Most common type

  2. Nosocomial pneumonia  

  • Hospital-acquired pneumonia (HAP)

  • Ventilator-associated pneumonia (VAP)

  • Healthcare-associated pneumonia (HCAP)

Community-acquired pneumonia is diagnosed in non-hospitalized patients or a previously ambulatory patient within 48 hours after admission to the hospital. CAP is further divided into “typical” and “atypical.”

HAP develops more than 48 hours after hospital admission. Patients who are mechanically ventilated for more than 48 hours after endotracheal intubation can develop pneumonia known as VAP. HCAP occurs in ambulatory patients who are not hospitalized and have had extensive healthcare contact within the last 3 months.

Etiology

Pneumonia occurs secondary to airborne infection which includes bacteria, virus, fungi, parasites, among others.

The typical bacteria which cause pneumonia are Streptococcus pneumoniae, Staphylococcus aureus, Group A Streptococcus, Klebsiella pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, anaerobes, and gram-negative organisms. These organisms can be easily cultured on standard media or seen on Gram stain, unlike atypical organisms.

Streptococcus pneumoniae is the most commonly identified bacterial cause of CAP in all age groups worldwide. Methicillin-resistant Staphylococcus aureus (MRSA), Escherichia coli, and other Enterobacteriaceae are the predominant causes of HAP, VAP, and HCAP.

Although it is not necessary to have a predisposing condition to acquire pneumonia, having such factors makes a person more likely to develop the lung infection. Any condition or disease that impairs the host immune response, for example, older age (older than 65 years), immunosuppression, diabetes, cystic fibrosis, lung cancer, among others. Conditions which increase the risk of macro- or micro-aspiration include stroke, seizures, anesthesia, drug intoxication. Cigarette smoking, alcoholism, malnutrition, obstruction of bronchi from tumors are other common predisposing conditions.

Epidemiology

The overall rate of CAP is 5-7 per 1000 persons per year. The rate of CAP is higher in males and increases with increasing age. It is more commonly seen in winter months. The combination of Pneumonia and Influenza causes high mortality and was the eighth most common cause of death in the US and the seventh most common cause of death in Canada in 2005.

Pathophysiology

The pulmonary system and the airways are continuously exposed to particulate matter and environmental pathogens. The healthy airways normally contain some bacterial species and are not sterile. The most common mechanism through which the micro-organisms or pathogens reach the lung is known as micro-aspiration. Hematogenous spread and macro-aspiration are other mechanisms.

However, the pulmonary defense mechanisms such as cough reflex, mucociliary clearance system, immune response help maintain low levels of the microbiome. CAP occurs when there is a defect in normal host defense, or a virulent pathogen overwhelms the immune response or a large infectious microbial inoculum. The invasion and propagation of these virulent strains of bacteria in the lung parenchyma following micro-aspiration cause the host immune response to kick in leading to a cascade of inflammatory response causing pneumonia.

Alveolar macrophage is the predominant immune cell which responds to lower airway bacteria. However, a stronger immune response comes into play when an overwhelming virulent pathogen or a large inoculum causes these alveolar macrophages to recruit polymorphonuclear neutrophils(PMN) to phagocytose and engulf these bacteria. The alveolar macrophages release cytokines namely, tumor necrosis factor-alpha and interleukins. Interleukin-8 and granulocyte colony-stimulating factor promotes neutrophil chemotaxis and maturation. The leakage of the alveolar-capillary membrane due to cytokines can lead to a decrease in compliance and hence, dyspnea. Cytokines such as IL-1 and TNF can lead to constitutional symptoms such as fever. Bacterial pneumonia is a result of this inflammatory response. These cytokines are essential for the immunity but, the excess can lead to sepsis and multiorgan failure. The body tries to balance the deleterious effects of cytokines by attenuation of several inflammatory mechanisms by IL-10.

Microbial virulence factors and predisposing host conditions make a person more vulnerable to pneumonia. [3]

Histopathology

Based on the area of the lung involved, pneumonia can be classified histologically into lobular, lobar, bronchopneumonia, and interstitial. The major types of acute bacterial pneumonia include:

  • Bronchopneumonia: A descending infection started around bronchi and bronchioles, which then spreads locally into the lungs. Lower lobes are usually involved. Patchy areas of consolidation which represents neutrophil collection in the alveoli and bronchi.

  • Lobar pneumonia: Acute exudative inflammation of the entire lobe. Uniform consolidation with a complete or near complete consolidation of a lobe of a lung. Majority of these cases are caused by Streptococcus pneumoniae.

Lobar pneumonia has 4 classical stages of inflammatory response if left untreated, namely:

  1. Congestion/consolidation in the first 24 hours in which the lungs are heavy, red, and, boggy. Microscopically characterized by vascular engorgement and intra-alveolar edema. Many bacteria and few neutrophils are present.

  2. Red hepatization/early consolidation begins 2 to 3 days after consolidation and lasts for 2 to 4 days and named because of firm liver-like consistency. The affected lung is red-pink, dry, granular and, airless. Fibrin strands replace the edema fluid of the previous phase. Microscopically marked cellular exudate of neutrophils with some showing ingested bacteria, extravasation of erythrocytes, desquamated epithelial cells, and fibrin within the alveoli are seen. The alveolar septa become less prominent because of the exudate.

  3. Grey hepatization/late consolidation occurs 2 to 3 days following red hepatization and lasts for 4 to 8 days. The lung appears gray with liver-like consistency due to fibrinopurulent exudate, progressive disintegration of red blood cells, and hemosiderin. The macrophages begin to appear.

  4. Resolution and restoration of the pulmonary architecture start by the eighth day. The enzymatic action begins centrally and spreads peripherally which liquefies the previous solid fibrinous content and eventually restores aeration. Macrophages are the predominant cells which contain engulfed neutrophils and debris.

Toxicokinetics

The most common cause of typical bacterial pneumonia worldwide is Pneumococcus. The polysaccharide capsule of Streptococcus pneumoniae inhibits the complement binding to the cell surface and hence, inhibits phagocytosis. Virulent pneumococcal proteins such as IgA1 protease, neuraminidase, pneumolysin, autolysin, and the surface protein A further help the organism to counteract the host immune response and allow it to cause infection in humans.

Genetic mutations causing an active efflux of drug and eventually resistance have led to an increase in drug-resistant Streptococcus Pneumoniae (DRSP) over the last few years.

Alteration in penicillin-binding protein has increased the penicillin resistance and an increased rate of penicillin-resistant S. pneumoniae. Penicillin resistance occurs due to failure to bind to the microbe cell wall. [1][2]

History and Physical

The signs and symptoms vary according to disease severity. The common symptoms of bacterial pneumonia include fever, cough, sputum production (may or may not be present). The color and quality of sputum provide the clue to microbiological etiology. Bacterial pneumonia mostly presents with mucopurulent sputum.

Pleuritic chest pain due to localized inflammation of pleura can be seen with any kind of pneumonia but, is more common with lobar pneumonia. Constitutional symptoms such as fatigue, headache, myalgia, and arthralgias can also be seen.

Severe pneumonia can lead to dyspnea and shortness of breath. In severe cases, confusion, sepsis, and multi-organ failure can also manifest.

Tachypnea, increased vocal fremitus, egophony (E to A changes), dullness to percussion are the major clinical signs depending on the degree of consolidation and presence/absence of pleural effusion. Chest auscultation reveals crackles, rales, bronchial breath sounds.

The respiratory rate closely correlates with the degree of oxygenation and, therefore essential in determining the severity. Hypoxia is seen in severe pneumonia, which leads to hyperventilation.

Evaluation

To start with the evaluation of any pneumonia, clinical suspicion based on careful patient history and physical exam should always be followed by chest radiography which is the most important initial test.

Chest x-ray not only shows the presence of the disease and demonstrates pulmonary infiltrate, but also provides the clue to the diagnosis whether its lobar, interstitial, unilateral or bilateral. Typical bacterial pneumonia is usually lobar pneumonia with para-pneumonic pleural effusions. However, a chest x-ray cannot reliably differentiate bacterial from a non-bacterial cause. When the labs and clinical features are positive, a positive chest radiograph is considered a gold standard for diagnosis of pneumonia. Although computed tomography (CT) is a more reliable and accurate test, its use is limited due to relatively high radiation exposure and high cost. It can sometimes be done with high clinical syndrome favoring pneumonia with a negative chest x-ray. In a hospitalized patient with high clinical suspicion and negative radiograph, empiric presumptive antibiotic treatment should be started followed by a repeat chest x-ray after 24 to 48 hours.

Complete blood count (CBC) with differentials, inflammatory biomarkers ESR and acute phase reactants are indicated to confirm the evidence of inflammation and assess severity. Leukocytosis with a leftward shift is a major blood test abnormality whereas leukopenia can occur and points towards poor prognosis.

Sputum Gram stain and culture should be done next if lobar pneumonia is suspected. The most specific diagnostic test for lobar pneumonia is sputum culture. It is very important to identify the cause for the proper treatment.

It is preferable to test for influenza during the winter months as the combination of influenza and pneumonia is fatal.

CURB-65 and pneumonia severity index help in the stratification of the patients and to determine if the patient needs hospitalization for treatment.

Routine diagnostic tests are optional for outpatients with pneumonia, but hospitalized patients should undergo sputum culture, blood culture, and/or urine antigen testing preferably before the institution of antibiotic therapy.

Thoracocentesis, bronchoscopy, pleural biopsy, or pleural fluid culture are invasive tests and are carried out very occasionally.

An open lung biopsy is the ultimate specific diagnostic test.[6]

Treatment / Management

The treatment depends on the severity of the disease. It is important to determine whether the patient needs to be treated inpatient or as an outpatient. CURB-65 pneumonia severity score or expanded CURB-65 can be used to stratify patients. One point for each factor which includes:

  • Confusion

  • Uremia (BUN greater than 20 mg/dL

  • Respiratory rate greater than 30 per minute

  • Hypotension (SBP less than 90 and DBP less than 60)

  • Age older than more than 65 years

Patients with comorbid conditions such as renal disease, liver disease, cancer, chronic lung disease usually do better with inpatient treatment with IV medications.

A CURB-65 score of greater than or equal to 2 is an indication for hospitalization. A score of greater than or equal to 4 is an indication for intensive care unit (ICU) admission and more intense therapy.

Depending on the clinical response, the therapy is indicated for 5 to 7 days. A favorable clinical response is the resolution of tachypnea, tachycardia, hypotension; absence of fever for more than 48 hours. In case of delayed response, the therapy should be extended.

Empiric therapy recommended for the following:

  • Outpatient/non-hospitalized patient management: Empiric therapy is almost always successful and usually testing is not required. In patients with no comorbidity, monotherapy with macrolides, such as azithromycin and clarithromycin are the first choice. Alternatively, newer fluoroquinolones like levofloxacin, moxifloxacin, or gemifloxacin can be used. The therapy is targeted against mycoplasma and chlamydia pneumoniae which are the common causes of less severe CAP. Patients with comorbid conditions (chronic lung or heart disease, diabetes, smoking, HIV, among others) do well with newer fluoroquinolones alone or with a combination of beta-lactam and a macrolide.

  • Inpatient non-ICU management: The recommended therapy includes newer fluoroquinolones alone or a combination of beta-lactam/second or third-generation cephalosporin and a macrolide.

  • Inpatient ICU management: The recommended therapy is a combination of macrolide/newer fluoroquinolone and a beta-lactam. Ampicillin-sulbactam or ertapenem can be used in patients with risk of aspiration. If there is a risk of Pseudomonas infection, a combination of anti-pseudomonal beta-lactam with anti-pseudomonal fluoroquinolone is indicated. For MRSA, vancomycin or linezolid should be added. In case of complications such as empyema, chest tube drainage is required. Surgical decortication is needed in case of multiple loculations.

All hospitalized patients who test positive for influenza virus must be treated with oseltamivir irrespective of the onset of illness.

Once the exact cause is determined, specific therapy should be initiated.[3][4][5]

Differential Diagnosis

  • Asthma or reactive airway disease

  • Viral Pneumonia

  • Pneumonia, Fungal

  • Pneumonia, Atypical bacterial

  • Lung Abscess

  • Bronchiectasis

  • Bronchiolitis

  • Asthma

  • Acute and Chronic Bronchitis

  • Atelectasis

  • Croup

  • Respiratory distress syndrome

  • Aspiration of a foreign body[6][7]

Complications

  • Pleural effusion

  • Empyema

  • Lung Abscess

  • Septicemia

  • Bacteremia

Enhancing Healthcare Team Outcomes

Pneumonia is a common infectious lung disease. It requires interprofessional care and the involvement of more than one subspecialty. This patient-centered approach involving a physician with a team of other health professionals, physiotherapists, respiratory therapists, nurses, pharmacists, and support groups working together for the patient plays an important role in improving the quality of care in pneumonia patients. It not only decreases the hospital admission rates but also positively affect the disease outcome. For healthy patients, the outcomes after treatment are excellent but in the elderly and those with comorbidities, the outcomes are guarded.

Figure

Lung Abscess, CT Scan, Computer Tomography, Thick-walled cavitary lesion in the right lung is an abscess, Diffuse ground glass infiltrates that are present in both lungs represent pneumonia. Contributed by Wikimedia Commons, Yale Rosen (CC by 2.0) https://creativecommons.org/licenses/by/2.0/ (more…)

Figure

Combination of two x-rays, A represents a normal healthy Chest x-ray, B represents a Chest X-ray documenting Q fever pneumonia, Pathology. Contributed by Wikimedia Commons (Public Domain)

Figure

Lung X-ray of patient showing infection with pneumocystis carinii, Pneumonia. Contributed by The National Institutes of Health (NIH)

Figure

MAI pneumonia. Image courtesy S Bhimji MD

Figure

Streptococcus Pneumoniae example antibiogram. Contributed by Zachary Sandman, BA

References

1.
Yamaguchi M, Minamide Y, Terao Y, Isoda R, Ogawa T, Yokota S, Hamada S, Kawabata S. Nrc of Streptococcus pneumoniae suppresses capsule expression and enhances anti-phagocytosis. Biochem Biophys Res Commun. 2009 Dec 04;390(1):155-60. [PubMed: 19799870]
2.
Cools F, Torfs E, Vanhoutte B, de Macedo MB, Bonofiglio L, Mollerach M, Maes L, Caljon G, Delputte P, Cappoen D, Cos P. Streptococcus pneumoniae galU gene mutation has a direct effect on biofilm growth, adherence and phagocytosis in vitro and pathogenicity in vivo. Pathog Dis. 2018 Oct 01;76(7) [PubMed: 30215741]
3.
Segreti J, House HR, Siegel RE. Principles of antibiotic treatment of community-acquired pneumonia in the outpatient setting. Am J Med. 2005 Jul;118 Suppl 7A:21S-28S. [PubMed: 15993674]
4.
Pineda L, El Solh AA. Severe community-acquired pneumonia: approach to therapy. Expert Opin Pharmacother. 2007 Apr;8(5):593-606. [PubMed: 17376015]
5.
Liu JL, Xu F, Zhou H, Wu XJ, Shi LX, Lu RQ, Farcomeni A, Venditti M, Zhao YL, Luo SY, Dong XJ, Falcone M. Corrigendum: Expanded CURB-65: a new score system predicts severity of community-acquired pneumonia with superior efficiency. Sci Rep. 2018 Aug 09;8:47005. [PMC free article: PMC6083369] [PubMed: 30091425]
6.
Hauswaldt J, Blaschke S. [Dyspnea]. Internist (Berl). 2017 Sep;58(9):925-936. [PubMed: 28608125]
7.
Berliner D, Schneider N, Welte T, Bauersachs J. The Differential Diagnosis of Dyspnea. Dtsch Arztebl Int. 2016 Dec 09;113(49):834-845. [PMC free article: PMC5247680] [PubMed: 28098068]

Typical Bacterial Pneumonia – StatPearls

Continuing Education Activity

The severe form of acute lower respiratory tract infection that affects the pulmonary parenchyma in one or both lungs is known as pneumonia. It is a common disease and a potentially serious infectious disease with considerable morbidity and mortality. Pneumonia is the sixth leading cause of death and the only infectious disease in the top ten causes of death in the United States. Community-acquired pneumonia is diagnosed in non-hospitalized patients or a previously ambulatory patient within 48 hours after admission to the hospital. CAP is further divided into “typical” and “atypical.” HAP develops more than 48 hours after hospital admission. Patients who are mechanically ventilated for more than 48 hours after endotracheal intubation can develop pneumonia known as VAP. HCAP occurs in ambulatory patients who are not hospitalized and have had extensive healthcare contact within the last 3 months. This activity reviews the evaluation and management of typical community-acquired pneumonia and highlights the role of interprofessional team members in collaborating to provide well-coordinated care and enhance patient outcomes.

Objectives:

  • Explain the causes of
    typical community-acquired pneumonia.

  • Describe the evaluation of a patient with typical community-acquired pneumonia.

  • Summarize the treatment options for typical community-acquired pneumonia.

  • Explore modalities to improve care coordination among interprofessional team members in order to improve outcomes for patients affected by typical community-acquired pneumonia.

Access free multiple choice questions on this topic.

Introduction

The severe form of acute lower respiratory tract infection that affects the pulmonary parenchyma in one or both lungs is known as pneumonia. It is a common disease and a potentially serious infectious disease with considerable morbidity and mortality. Pneumonia is the sixth leading cause of death and the only infectious disease in the top ten causes of death in the United States.

Pneumonia can be classified into 2 types based on how the infection is acquired:

  1. Community-acquired pneumonia (CAP): Most common type

  2. Nosocomial pneumonia  

  • Hospital-acquired pneumonia (HAP)

  • Ventilator-associated pneumonia (VAP)

  • Healthcare-associated pneumonia (HCAP)

Community-acquired pneumonia is diagnosed in non-hospitalized patients or a previously ambulatory patient within 48 hours after admission to the hospital. CAP is further divided into “typical” and “atypical.”

HAP develops more than 48 hours after hospital admission. Patients who are mechanically ventilated for more than 48 hours after endotracheal intubation can develop pneumonia known as VAP. HCAP occurs in ambulatory patients who are not hospitalized and have had extensive healthcare contact within the last 3 months.

Etiology

Pneumonia occurs secondary to airborne infection which includes bacteria, virus, fungi, parasites, among others.

The typical bacteria which cause pneumonia are Streptococcus pneumoniae, Staphylococcus aureus, Group A Streptococcus, Klebsiella pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, anaerobes, and gram-negative organisms. These organisms can be easily cultured on standard media or seen on Gram stain, unlike atypical organisms.

Streptococcus pneumoniae is the most commonly identified bacterial cause of CAP in all age groups worldwide. Methicillin-resistant Staphylococcus aureus (MRSA), Escherichia coli, and other Enterobacteriaceae are the predominant causes of HAP, VAP, and HCAP.

Although it is not necessary to have a predisposing condition to acquire pneumonia, having such factors makes a person more likely to develop the lung infection. Any condition or disease that impairs the host immune response, for example, older age (older than 65 years), immunosuppression, diabetes, cystic fibrosis, lung cancer, among others. Conditions which increase the risk of macro- or micro-aspiration include stroke, seizures, anesthesia, drug intoxication. Cigarette smoking, alcoholism, malnutrition, obstruction of bronchi from tumors are other common predisposing conditions.

Epidemiology

The overall rate of CAP is 5-7 per 1000 persons per year. The rate of CAP is higher in males and increases with increasing age. It is more commonly seen in winter months. The combination of Pneumonia and Influenza causes high mortality and was the eighth most common cause of death in the US and the seventh most common cause of death in Canada in 2005.

Pathophysiology

The pulmonary system and the airways are continuously exposed to particulate matter and environmental pathogens. The healthy airways normally contain some bacterial species and are not sterile. The most common mechanism through which the micro-organisms or pathogens reach the lung is known as micro-aspiration. Hematogenous spread and macro-aspiration are other mechanisms.

However, the pulmonary defense mechanisms such as cough reflex, mucociliary clearance system, immune response help maintain low levels of the microbiome. CAP occurs when there is a defect in normal host defense, or a virulent pathogen overwhelms the immune response or a large infectious microbial inoculum. The invasion and propagation of these virulent strains of bacteria in the lung parenchyma following micro-aspiration cause the host immune response to kick in leading to a cascade of inflammatory response causing pneumonia.

Alveolar macrophage is the predominant immune cell which responds to lower airway bacteria. However, a stronger immune response comes into play when an overwhelming virulent pathogen or a large inoculum causes these alveolar macrophages to recruit polymorphonuclear neutrophils(PMN) to phagocytose and engulf these bacteria. The alveolar macrophages release cytokines namely, tumor necrosis factor-alpha and interleukins. Interleukin-8 and granulocyte colony-stimulating factor promotes neutrophil chemotaxis and maturation. The leakage of the alveolar-capillary membrane due to cytokines can lead to a decrease in compliance and hence, dyspnea. Cytokines such as IL-1 and TNF can lead to constitutional symptoms such as fever. Bacterial pneumonia is a result of this inflammatory response. These cytokines are essential for the immunity but, the excess can lead to sepsis and multiorgan failure. The body tries to balance the deleterious effects of cytokines by attenuation of several inflammatory mechanisms by IL-10.

Microbial virulence factors and predisposing host conditions make a person more vulnerable to pneumonia. [3]

Histopathology

Based on the area of the lung involved, pneumonia can be classified histologically into lobular, lobar, bronchopneumonia, and interstitial. The major types of acute bacterial pneumonia include:

  • Bronchopneumonia: A descending infection started around bronchi and bronchioles, which then spreads locally into the lungs. Lower lobes are usually involved. Patchy areas of consolidation which represents neutrophil collection in the alveoli and bronchi.

  • Lobar pneumonia: Acute exudative inflammation of the entire lobe. Uniform consolidation with a complete or near complete consolidation of a lobe of a lung. Majority of these cases are caused by Streptococcus pneumoniae.

Lobar pneumonia has 4 classical stages of inflammatory response if left untreated, namely:

  1. Congestion/consolidation in the first 24 hours in which the lungs are heavy, red, and, boggy. Microscopically characterized by vascular engorgement and intra-alveolar edema. Many bacteria and few neutrophils are present.

  2. Red hepatization/early consolidation begins 2 to 3 days after consolidation and lasts for 2 to 4 days and named because of firm liver-like consistency. The affected lung is red-pink, dry, granular and, airless. Fibrin strands replace the edema fluid of the previous phase. Microscopically marked cellular exudate of neutrophils with some showing ingested bacteria, extravasation of erythrocytes, desquamated epithelial cells, and fibrin within the alveoli are seen. The alveolar septa become less prominent because of the exudate.

  3. Grey hepatization/late consolidation occurs 2 to 3 days following red hepatization and lasts for 4 to 8 days. The lung appears gray with liver-like consistency due to fibrinopurulent exudate, progressive disintegration of red blood cells, and hemosiderin. The macrophages begin to appear.

  4. Resolution and restoration of the pulmonary architecture start by the eighth day. The enzymatic action begins centrally and spreads peripherally which liquefies the previous solid fibrinous content and eventually restores aeration. Macrophages are the predominant cells which contain engulfed neutrophils and debris.

Toxicokinetics

The most common cause of typical bacterial pneumonia worldwide is Pneumococcus. The polysaccharide capsule of Streptococcus pneumoniae inhibits the complement binding to the cell surface and hence, inhibits phagocytosis. Virulent pneumococcal proteins such as IgA1 protease, neuraminidase, pneumolysin, autolysin, and the surface protein A further help the organism to counteract the host immune response and allow it to cause infection in humans.

Genetic mutations causing an active efflux of drug and eventually resistance have led to an increase in drug-resistant Streptococcus Pneumoniae (DRSP) over the last few years.

Alteration in penicillin-binding protein has increased the penicillin resistance and an increased rate of penicillin-resistant S. pneumoniae. Penicillin resistance occurs due to failure to bind to the microbe cell wall. [1][2]

History and Physical

The signs and symptoms vary according to disease severity. The common symptoms of bacterial pneumonia include fever, cough, sputum production (may or may not be present). The color and quality of sputum provide the clue to microbiological etiology. Bacterial pneumonia mostly presents with mucopurulent sputum.

Pleuritic chest pain due to localized inflammation of pleura can be seen with any kind of pneumonia but, is more common with lobar pneumonia. Constitutional symptoms such as fatigue, headache, myalgia, and arthralgias can also be seen.

Severe pneumonia can lead to dyspnea and shortness of breath. In severe cases, confusion, sepsis, and multi-organ failure can also manifest.

Tachypnea, increased vocal fremitus, egophony (E to A changes), dullness to percussion are the major clinical signs depending on the degree of consolidation and presence/absence of pleural effusion. Chest auscultation reveals crackles, rales, bronchial breath sounds.

The respiratory rate closely correlates with the degree of oxygenation and, therefore essential in determining the severity. Hypoxia is seen in severe pneumonia, which leads to hyperventilation.

Evaluation

To start with the evaluation of any pneumonia, clinical suspicion based on careful patient history and physical exam should always be followed by chest radiography which is the most important initial test.

Chest x-ray not only shows the presence of the disease and demonstrates pulmonary infiltrate, but also provides the clue to the diagnosis whether its lobar, interstitial, unilateral or bilateral. Typical bacterial pneumonia is usually lobar pneumonia with para-pneumonic pleural effusions. However, a chest x-ray cannot reliably differentiate bacterial from a non-bacterial cause. When the labs and clinical features are positive, a positive chest radiograph is considered a gold standard for diagnosis of pneumonia. Although computed tomography (CT) is a more reliable and accurate test, its use is limited due to relatively high radiation exposure and high cost. It can sometimes be done with high clinical syndrome favoring pneumonia with a negative chest x-ray. In a hospitalized patient with high clinical suspicion and negative radiograph, empiric presumptive antibiotic treatment should be started followed by a repeat chest x-ray after 24 to 48 hours.

Complete blood count (CBC) with differentials, inflammatory biomarkers ESR and acute phase reactants are indicated to confirm the evidence of inflammation and assess severity. Leukocytosis with a leftward shift is a major blood test abnormality whereas leukopenia can occur and points towards poor prognosis.

Sputum Gram stain and culture should be done next if lobar pneumonia is suspected. The most specific diagnostic test for lobar pneumonia is sputum culture. It is very important to identify the cause for the proper treatment.

It is preferable to test for influenza during the winter months as the combination of influenza and pneumonia is fatal.

CURB-65 and pneumonia severity index help in the stratification of the patients and to determine if the patient needs hospitalization for treatment.

Routine diagnostic tests are optional for outpatients with pneumonia, but hospitalized patients should undergo sputum culture, blood culture, and/or urine antigen testing preferably before the institution of antibiotic therapy.

Thoracocentesis, bronchoscopy, pleural biopsy, or pleural fluid culture are invasive tests and are carried out very occasionally.

An open lung biopsy is the ultimate specific diagnostic test.[6]

Treatment / Management

The treatment depends on the severity of the disease. It is important to determine whether the patient needs to be treated inpatient or as an outpatient. CURB-65 pneumonia severity score or expanded CURB-65 can be used to stratify patients. One point for each factor which includes:

  • Confusion

  • Uremia (BUN greater than 20 mg/dL

  • Respiratory rate greater than 30 per minute

  • Hypotension (SBP less than 90 and DBP less than 60)

  • Age older than more than 65 years

Patients with comorbid conditions such as renal disease, liver disease, cancer, chronic lung disease usually do better with inpatient treatment with IV medications.

A CURB-65 score of greater than or equal to 2 is an indication for hospitalization. A score of greater than or equal to 4 is an indication for intensive care unit (ICU) admission and more intense therapy.

Depending on the clinical response, the therapy is indicated for 5 to 7 days. A favorable clinical response is the resolution of tachypnea, tachycardia, hypotension; absence of fever for more than 48 hours. In case of delayed response, the therapy should be extended.

Empiric therapy recommended for the following:

  • Outpatient/non-hospitalized patient management: Empiric therapy is almost always successful and usually testing is not required. In patients with no comorbidity, monotherapy with macrolides, such as azithromycin and clarithromycin are the first choice. Alternatively, newer fluoroquinolones like levofloxacin, moxifloxacin, or gemifloxacin can be used. The therapy is targeted against mycoplasma and chlamydia pneumoniae which are the common causes of less severe CAP. Patients with comorbid conditions (chronic lung or heart disease, diabetes, smoking, HIV, among others) do well with newer fluoroquinolones alone or with a combination of beta-lactam and a macrolide.

  • Inpatient non-ICU management: The recommended therapy includes newer fluoroquinolones alone or a combination of beta-lactam/second or third-generation cephalosporin and a macrolide.

  • Inpatient ICU management: The recommended therapy is a combination of macrolide/newer fluoroquinolone and a beta-lactam. Ampicillin-sulbactam or ertapenem can be used in patients with risk of aspiration. If there is a risk of Pseudomonas infection, a combination of anti-pseudomonal beta-lactam with anti-pseudomonal fluoroquinolone is indicated. For MRSA, vancomycin or linezolid should be added. In case of complications such as empyema, chest tube drainage is required. Surgical decortication is needed in case of multiple loculations.

All hospitalized patients who test positive for influenza virus must be treated with oseltamivir irrespective of the onset of illness.

Once the exact cause is determined, specific therapy should be initiated.[3][4][5]

Differential Diagnosis

  • Asthma or reactive airway disease

  • Viral Pneumonia

  • Pneumonia, Fungal

  • Pneumonia, Atypical bacterial

  • Lung Abscess

  • Bronchiectasis

  • Bronchiolitis

  • Asthma

  • Acute and Chronic Bronchitis

  • Atelectasis

  • Croup

  • Respiratory distress syndrome

  • Aspiration of a foreign body[6][7]

Complications

  • Pleural effusion

  • Empyema

  • Lung Abscess

  • Septicemia

  • Bacteremia

Enhancing Healthcare Team Outcomes

Pneumonia is a common infectious lung disease. It requires interprofessional care and the involvement of more than one subspecialty. This patient-centered approach involving a physician with a team of other health professionals, physiotherapists, respiratory therapists, nurses, pharmacists, and support groups working together for the patient plays an important role in improving the quality of care in pneumonia patients. It not only decreases the hospital admission rates but also positively affect the disease outcome. For healthy patients, the outcomes after treatment are excellent but in the elderly and those with comorbidities, the outcomes are guarded.

Figure

Lung Abscess, CT Scan, Computer Tomography, Thick-walled cavitary lesion in the right lung is an abscess, Diffuse ground glass infiltrates that are present in both lungs represent pneumonia. Contributed by Wikimedia Commons, Yale Rosen (CC by 2.0) https://creativecommons.org/licenses/by/2.0/ (more…)

Figure

Combination of two x-rays, A represents a normal healthy Chest x-ray, B represents a Chest X-ray documenting Q fever pneumonia, Pathology. Contributed by Wikimedia Commons (Public Domain)

Figure

Lung X-ray of patient showing infection with pneumocystis carinii, Pneumonia. Contributed by The National Institutes of Health (NIH)

Figure

MAI pneumonia. Image courtesy S Bhimji MD

Figure

Streptococcus Pneumoniae example antibiogram. Contributed by Zachary Sandman, BA

References

1.
Yamaguchi M, Minamide Y, Terao Y, Isoda R, Ogawa T, Yokota S, Hamada S, Kawabata S. Nrc of Streptococcus pneumoniae suppresses capsule expression and enhances anti-phagocytosis. Biochem Biophys Res Commun. 2009 Dec 04;390(1):155-60. [PubMed: 19799870]
2.
Cools F, Torfs E, Vanhoutte B, de Macedo MB, Bonofiglio L, Mollerach M, Maes L, Caljon G, Delputte P, Cappoen D, Cos P. Streptococcus pneumoniae galU gene mutation has a direct effect on biofilm growth, adherence and phagocytosis in vitro and pathogenicity in vivo. Pathog Dis. 2018 Oct 01;76(7) [PubMed: 30215741]
3.
Segreti J, House HR, Siegel RE. Principles of antibiotic treatment of community-acquired pneumonia in the outpatient setting. Am J Med. 2005 Jul;118 Suppl 7A:21S-28S. [PubMed: 15993674]
4.
Pineda L, El Solh AA. Severe community-acquired pneumonia: approach to therapy. Expert Opin Pharmacother. 2007 Apr;8(5):593-606. [PubMed: 17376015]
5.
Liu JL, Xu F, Zhou H, Wu XJ, Shi LX, Lu RQ, Farcomeni A, Venditti M, Zhao YL, Luo SY, Dong XJ, Falcone M. Corrigendum: Expanded CURB-65: a new score system predicts severity of community-acquired pneumonia with superior efficiency. Sci Rep. 2018 Aug 09;8:47005. [PMC free article: PMC6083369] [PubMed: 30091425]
6.
Hauswaldt J, Blaschke S. [Dyspnea]. Internist (Berl). 2017 Sep;58(9):925-936. [PubMed: 28608125]
7.
Berliner D, Schneider N, Welte T, Bauersachs J. The Differential Diagnosis of Dyspnea. Dtsch Arztebl Int. 2016 Dec 09;113(49):834-845. [PMC free article: PMC5247680] [PubMed: 28098068]

Typical Bacterial Pneumonia – StatPearls

Continuing Education Activity

The severe form of acute lower respiratory tract infection that affects the pulmonary parenchyma in one or both lungs is known as pneumonia. It is a common disease and a potentially serious infectious disease with considerable morbidity and mortality. Pneumonia is the sixth leading cause of death and the only infectious disease in the top ten causes of death in the United States. Community-acquired pneumonia is diagnosed in non-hospitalized patients or a previously ambulatory patient within 48 hours after admission to the hospital. CAP is further divided into “typical” and “atypical.” HAP develops more than 48 hours after hospital admission. Patients who are mechanically ventilated for more than 48 hours after endotracheal intubation can develop pneumonia known as VAP. HCAP occurs in ambulatory patients who are not hospitalized and have had extensive healthcare contact within the last 3 months. This activity reviews the evaluation and management of typical community-acquired pneumonia and highlights the role of interprofessional team members in collaborating to provide well-coordinated care and enhance patient outcomes.

Objectives:

  • Explain the causes of
    typical community-acquired pneumonia.

  • Describe the evaluation of a patient with typical community-acquired pneumonia.

  • Summarize the treatment options for typical community-acquired pneumonia.

  • Explore modalities to improve care coordination among interprofessional team members in order to improve outcomes for patients affected by typical community-acquired pneumonia.

Access free multiple choice questions on this topic.

Introduction

The severe form of acute lower respiratory tract infection that affects the pulmonary parenchyma in one or both lungs is known as pneumonia. It is a common disease and a potentially serious infectious disease with considerable morbidity and mortality. Pneumonia is the sixth leading cause of death and the only infectious disease in the top ten causes of death in the United States.

Pneumonia can be classified into 2 types based on how the infection is acquired:

  1. Community-acquired pneumonia (CAP): Most common type

  2. Nosocomial pneumonia  

  • Hospital-acquired pneumonia (HAP)

  • Ventilator-associated pneumonia (VAP)

  • Healthcare-associated pneumonia (HCAP)

Community-acquired pneumonia is diagnosed in non-hospitalized patients or a previously ambulatory patient within 48 hours after admission to the hospital. CAP is further divided into “typical” and “atypical.”

HAP develops more than 48 hours after hospital admission. Patients who are mechanically ventilated for more than 48 hours after endotracheal intubation can develop pneumonia known as VAP. HCAP occurs in ambulatory patients who are not hospitalized and have had extensive healthcare contact within the last 3 months.

Etiology

Pneumonia occurs secondary to airborne infection which includes bacteria, virus, fungi, parasites, among others.

The typical bacteria which cause pneumonia are Streptococcus pneumoniae, Staphylococcus aureus, Group A Streptococcus, Klebsiella pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, anaerobes, and gram-negative organisms. These organisms can be easily cultured on standard media or seen on Gram stain, unlike atypical organisms.

Streptococcus pneumoniae is the most commonly identified bacterial cause of CAP in all age groups worldwide. Methicillin-resistant Staphylococcus aureus (MRSA), Escherichia coli, and other Enterobacteriaceae are the predominant causes of HAP, VAP, and HCAP.

Although it is not necessary to have a predisposing condition to acquire pneumonia, having such factors makes a person more likely to develop the lung infection. Any condition or disease that impairs the host immune response, for example, older age (older than 65 years), immunosuppression, diabetes, cystic fibrosis, lung cancer, among others. Conditions which increase the risk of macro- or micro-aspiration include stroke, seizures, anesthesia, drug intoxication. Cigarette smoking, alcoholism, malnutrition, obstruction of bronchi from tumors are other common predisposing conditions.

Epidemiology

The overall rate of CAP is 5-7 per 1000 persons per year. The rate of CAP is higher in males and increases with increasing age. It is more commonly seen in winter months. The combination of Pneumonia and Influenza causes high mortality and was the eighth most common cause of death in the US and the seventh most common cause of death in Canada in 2005.

Pathophysiology

The pulmonary system and the airways are continuously exposed to particulate matter and environmental pathogens. The healthy airways normally contain some bacterial species and are not sterile. The most common mechanism through which the micro-organisms or pathogens reach the lung is known as micro-aspiration. Hematogenous spread and macro-aspiration are other mechanisms.

However, the pulmonary defense mechanisms such as cough reflex, mucociliary clearance system, immune response help maintain low levels of the microbiome. CAP occurs when there is a defect in normal host defense, or a virulent pathogen overwhelms the immune response or a large infectious microbial inoculum. The invasion and propagation of these virulent strains of bacteria in the lung parenchyma following micro-aspiration cause the host immune response to kick in leading to a cascade of inflammatory response causing pneumonia.

Alveolar macrophage is the predominant immune cell which responds to lower airway bacteria. However, a stronger immune response comes into play when an overwhelming virulent pathogen or a large inoculum causes these alveolar macrophages to recruit polymorphonuclear neutrophils(PMN) to phagocytose and engulf these bacteria. The alveolar macrophages release cytokines namely, tumor necrosis factor-alpha and interleukins. Interleukin-8 and granulocyte colony-stimulating factor promotes neutrophil chemotaxis and maturation. The leakage of the alveolar-capillary membrane due to cytokines can lead to a decrease in compliance and hence, dyspnea. Cytokines such as IL-1 and TNF can lead to constitutional symptoms such as fever. Bacterial pneumonia is a result of this inflammatory response. These cytokines are essential for the immunity but, the excess can lead to sepsis and multiorgan failure. The body tries to balance the deleterious effects of cytokines by attenuation of several inflammatory mechanisms by IL-10.

Microbial virulence factors and predisposing host conditions make a person more vulnerable to pneumonia. [3]

Histopathology

Based on the area of the lung involved, pneumonia can be classified histologically into lobular, lobar, bronchopneumonia, and interstitial. The major types of acute bacterial pneumonia include:

  • Bronchopneumonia: A descending infection started around bronchi and bronchioles, which then spreads locally into the lungs. Lower lobes are usually involved. Patchy areas of consolidation which represents neutrophil collection in the alveoli and bronchi.

  • Lobar pneumonia: Acute exudative inflammation of the entire lobe. Uniform consolidation with a complete or near complete consolidation of a lobe of a lung. Majority of these cases are caused by Streptococcus pneumoniae.

Lobar pneumonia has 4 classical stages of inflammatory response if left untreated, namely:

  1. Congestion/consolidation in the first 24 hours in which the lungs are heavy, red, and, boggy. Microscopically characterized by vascular engorgement and intra-alveolar edema. Many bacteria and few neutrophils are present.

  2. Red hepatization/early consolidation begins 2 to 3 days after consolidation and lasts for 2 to 4 days and named because of firm liver-like consistency. The affected lung is red-pink, dry, granular and, airless. Fibrin strands replace the edema fluid of the previous phase. Microscopically marked cellular exudate of neutrophils with some showing ingested bacteria, extravasation of erythrocytes, desquamated epithelial cells, and fibrin within the alveoli are seen. The alveolar septa become less prominent because of the exudate.

  3. Grey hepatization/late consolidation occurs 2 to 3 days following red hepatization and lasts for 4 to 8 days. The lung appears gray with liver-like consistency due to fibrinopurulent exudate, progressive disintegration of red blood cells, and hemosiderin. The macrophages begin to appear.

  4. Resolution and restoration of the pulmonary architecture start by the eighth day. The enzymatic action begins centrally and spreads peripherally which liquefies the previous solid fibrinous content and eventually restores aeration. Macrophages are the predominant cells which contain engulfed neutrophils and debris.

Toxicokinetics

The most common cause of typical bacterial pneumonia worldwide is Pneumococcus. The polysaccharide capsule of Streptococcus pneumoniae inhibits the complement binding to the cell surface and hence, inhibits phagocytosis. Virulent pneumococcal proteins such as IgA1 protease, neuraminidase, pneumolysin, autolysin, and the surface protein A further help the organism to counteract the host immune response and allow it to cause infection in humans.

Genetic mutations causing an active efflux of drug and eventually resistance have led to an increase in drug-resistant Streptococcus Pneumoniae (DRSP) over the last few years.

Alteration in penicillin-binding protein has increased the penicillin resistance and an increased rate of penicillin-resistant S. pneumoniae. Penicillin resistance occurs due to failure to bind to the microbe cell wall. [1][2]

History and Physical

The signs and symptoms vary according to disease severity. The common symptoms of bacterial pneumonia include fever, cough, sputum production (may or may not be present). The color and quality of sputum provide the clue to microbiological etiology. Bacterial pneumonia mostly presents with mucopurulent sputum.

Pleuritic chest pain due to localized inflammation of pleura can be seen with any kind of pneumonia but, is more common with lobar pneumonia. Constitutional symptoms such as fatigue, headache, myalgia, and arthralgias can also be seen.

Severe pneumonia can lead to dyspnea and shortness of breath. In severe cases, confusion, sepsis, and multi-organ failure can also manifest.

Tachypnea, increased vocal fremitus, egophony (E to A changes), dullness to percussion are the major clinical signs depending on the degree of consolidation and presence/absence of pleural effusion. Chest auscultation reveals crackles, rales, bronchial breath sounds.

The respiratory rate closely correlates with the degree of oxygenation and, therefore essential in determining the severity. Hypoxia is seen in severe pneumonia, which leads to hyperventilation.

Evaluation

To start with the evaluation of any pneumonia, clinical suspicion based on careful patient history and physical exam should always be followed by chest radiography which is the most important initial test.

Chest x-ray not only shows the presence of the disease and demonstrates pulmonary infiltrate, but also provides the clue to the diagnosis whether its lobar, interstitial, unilateral or bilateral. Typical bacterial pneumonia is usually lobar pneumonia with para-pneumonic pleural effusions. However, a chest x-ray cannot reliably differentiate bacterial from a non-bacterial cause. When the labs and clinical features are positive, a positive chest radiograph is considered a gold standard for diagnosis of pneumonia. Although computed tomography (CT) is a more reliable and accurate test, its use is limited due to relatively high radiation exposure and high cost. It can sometimes be done with high clinical syndrome favoring pneumonia with a negative chest x-ray. In a hospitalized patient with high clinical suspicion and negative radiograph, empiric presumptive antibiotic treatment should be started followed by a repeat chest x-ray after 24 to 48 hours.

Complete blood count (CBC) with differentials, inflammatory biomarkers ESR and acute phase reactants are indicated to confirm the evidence of inflammation and assess severity. Leukocytosis with a leftward shift is a major blood test abnormality whereas leukopenia can occur and points towards poor prognosis.

Sputum Gram stain and culture should be done next if lobar pneumonia is suspected. The most specific diagnostic test for lobar pneumonia is sputum culture. It is very important to identify the cause for the proper treatment.

It is preferable to test for influenza during the winter months as the combination of influenza and pneumonia is fatal.

CURB-65 and pneumonia severity index help in the stratification of the patients and to determine if the patient needs hospitalization for treatment.

Routine diagnostic tests are optional for outpatients with pneumonia, but hospitalized patients should undergo sputum culture, blood culture, and/or urine antigen testing preferably before the institution of antibiotic therapy.

Thoracocentesis, bronchoscopy, pleural biopsy, or pleural fluid culture are invasive tests and are carried out very occasionally.

An open lung biopsy is the ultimate specific diagnostic test.[6]

Treatment / Management

The treatment depends on the severity of the disease. It is important to determine whether the patient needs to be treated inpatient or as an outpatient. CURB-65 pneumonia severity score or expanded CURB-65 can be used to stratify patients. One point for each factor which includes:

  • Confusion

  • Uremia (BUN greater than 20 mg/dL

  • Respiratory rate greater than 30 per minute

  • Hypotension (SBP less than 90 and DBP less than 60)

  • Age older than more than 65 years

Patients with comorbid conditions such as renal disease, liver disease, cancer, chronic lung disease usually do better with inpatient treatment with IV medications.

A CURB-65 score of greater than or equal to 2 is an indication for hospitalization. A score of greater than or equal to 4 is an indication for intensive care unit (ICU) admission and more intense therapy.

Depending on the clinical response, the therapy is indicated for 5 to 7 days. A favorable clinical response is the resolution of tachypnea, tachycardia, hypotension; absence of fever for more than 48 hours. In case of delayed response, the therapy should be extended.

Empiric therapy recommended for the following:

  • Outpatient/non-hospitalized patient management: Empiric therapy is almost always successful and usually testing is not required. In patients with no comorbidity, monotherapy with macrolides, such as azithromycin and clarithromycin are the first choice. Alternatively, newer fluoroquinolones like levofloxacin, moxifloxacin, or gemifloxacin can be used. The therapy is targeted against mycoplasma and chlamydia pneumoniae which are the common causes of less severe CAP. Patients with comorbid conditions (chronic lung or heart disease, diabetes, smoking, HIV, among others) do well with newer fluoroquinolones alone or with a combination of beta-lactam and a macrolide.

  • Inpatient non-ICU management: The recommended therapy includes newer fluoroquinolones alone or a combination of beta-lactam/second or third-generation cephalosporin and a macrolide.

  • Inpatient ICU management: The recommended therapy is a combination of macrolide/newer fluoroquinolone and a beta-lactam. Ampicillin-sulbactam or ertapenem can be used in patients with risk of aspiration. If there is a risk of Pseudomonas infection, a combination of anti-pseudomonal beta-lactam with anti-pseudomonal fluoroquinolone is indicated. For MRSA, vancomycin or linezolid should be added. In case of complications such as empyema, chest tube drainage is required. Surgical decortication is needed in case of multiple loculations.

All hospitalized patients who test positive for influenza virus must be treated with oseltamivir irrespective of the onset of illness.

Once the exact cause is determined, specific therapy should be initiated.[3][4][5]

Differential Diagnosis

  • Asthma or reactive airway disease

  • Viral Pneumonia

  • Pneumonia, Fungal

  • Pneumonia, Atypical bacterial

  • Lung Abscess

  • Bronchiectasis

  • Bronchiolitis

  • Asthma

  • Acute and Chronic Bronchitis

  • Atelectasis

  • Croup

  • Respiratory distress syndrome

  • Aspiration of a foreign body[6][7]

Complications

  • Pleural effusion

  • Empyema

  • Lung Abscess

  • Septicemia

  • Bacteremia

Enhancing Healthcare Team Outcomes

Pneumonia is a common infectious lung disease. It requires interprofessional care and the involvement of more than one subspecialty. This patient-centered approach involving a physician with a team of other health professionals, physiotherapists, respiratory therapists, nurses, pharmacists, and support groups working together for the patient plays an important role in improving the quality of care in pneumonia patients. It not only decreases the hospital admission rates but also positively affect the disease outcome. For healthy patients, the outcomes after treatment are excellent but in the elderly and those with comorbidities, the outcomes are guarded.

Figure

Lung Abscess, CT Scan, Computer Tomography, Thick-walled cavitary lesion in the right lung is an abscess, Diffuse ground glass infiltrates that are present in both lungs represent pneumonia. Contributed by Wikimedia Commons, Yale Rosen (CC by 2.0) https://creativecommons.org/licenses/by/2.0/ (more…)

Figure

Combination of two x-rays, A represents a normal healthy Chest x-ray, B represents a Chest X-ray documenting Q fever pneumonia, Pathology. Contributed by Wikimedia Commons (Public Domain)

Figure

Lung X-ray of patient showing infection with pneumocystis carinii, Pneumonia. Contributed by The National Institutes of Health (NIH)

Figure

MAI pneumonia. Image courtesy S Bhimji MD

Figure

Streptococcus Pneumoniae example antibiogram. Contributed by Zachary Sandman, BA

References

1.
Yamaguchi M, Minamide Y, Terao Y, Isoda R, Ogawa T, Yokota S, Hamada S, Kawabata S. Nrc of Streptococcus pneumoniae suppresses capsule expression and enhances anti-phagocytosis. Biochem Biophys Res Commun. 2009 Dec 04;390(1):155-60. [PubMed: 19799870]
2.
Cools F, Torfs E, Vanhoutte B, de Macedo MB, Bonofiglio L, Mollerach M, Maes L, Caljon G, Delputte P, Cappoen D, Cos P. Streptococcus pneumoniae galU gene mutation has a direct effect on biofilm growth, adherence and phagocytosis in vitro and pathogenicity in vivo. Pathog Dis. 2018 Oct 01;76(7) [PubMed: 30215741]
3.
Segreti J, House HR, Siegel RE. Principles of antibiotic treatment of community-acquired pneumonia in the outpatient setting. Am J Med. 2005 Jul;118 Suppl 7A:21S-28S. [PubMed: 15993674]
4.
Pineda L, El Solh AA. Severe community-acquired pneumonia: approach to therapy. Expert Opin Pharmacother. 2007 Apr;8(5):593-606. [PubMed: 17376015]
5.
Liu JL, Xu F, Zhou H, Wu XJ, Shi LX, Lu RQ, Farcomeni A, Venditti M, Zhao YL, Luo SY, Dong XJ, Falcone M. Corrigendum: Expanded CURB-65: a new score system predicts severity of community-acquired pneumonia with superior efficiency. Sci Rep. 2018 Aug 09;8:47005. [PMC free article: PMC6083369] [PubMed: 30091425]
6.
Hauswaldt J, Blaschke S. [Dyspnea]. Internist (Berl). 2017 Sep;58(9):925-936. [PubMed: 28608125]
7.
Berliner D, Schneider N, Welte T, Bauersachs J. The Differential Diagnosis of Dyspnea. Dtsch Arztebl Int. 2016 Dec 09;113(49):834-845. [PMC free article: PMC5247680] [PubMed: 28098068]

Typical Bacterial Pneumonia – StatPearls

Continuing Education Activity

The severe form of acute lower respiratory tract infection that affects the pulmonary parenchyma in one or both lungs is known as pneumonia. It is a common disease and a potentially serious infectious disease with considerable morbidity and mortality. Pneumonia is the sixth leading cause of death and the only infectious disease in the top ten causes of death in the United States. Community-acquired pneumonia is diagnosed in non-hospitalized patients or a previously ambulatory patient within 48 hours after admission to the hospital. CAP is further divided into “typical” and “atypical.” HAP develops more than 48 hours after hospital admission. Patients who are mechanically ventilated for more than 48 hours after endotracheal intubation can develop pneumonia known as VAP. HCAP occurs in ambulatory patients who are not hospitalized and have had extensive healthcare contact within the last 3 months. This activity reviews the evaluation and management of typical community-acquired pneumonia and highlights the role of interprofessional team members in collaborating to provide well-coordinated care and enhance patient outcomes.

Objectives:

  • Explain the causes of
    typical community-acquired pneumonia.

  • Describe the evaluation of a patient with typical community-acquired pneumonia.

  • Summarize the treatment options for typical community-acquired pneumonia.

  • Explore modalities to improve care coordination among interprofessional team members in order to improve outcomes for patients affected by typical community-acquired pneumonia.

Access free multiple choice questions on this topic.

Introduction

The severe form of acute lower respiratory tract infection that affects the pulmonary parenchyma in one or both lungs is known as pneumonia. It is a common disease and a potentially serious infectious disease with considerable morbidity and mortality. Pneumonia is the sixth leading cause of death and the only infectious disease in the top ten causes of death in the United States.

Pneumonia can be classified into 2 types based on how the infection is acquired:

  1. Community-acquired pneumonia (CAP): Most common type

  2. Nosocomial pneumonia  

  • Hospital-acquired pneumonia (HAP)

  • Ventilator-associated pneumonia (VAP)

  • Healthcare-associated pneumonia (HCAP)

Community-acquired pneumonia is diagnosed in non-hospitalized patients or a previously ambulatory patient within 48 hours after admission to the hospital. CAP is further divided into “typical” and “atypical.”

HAP develops more than 48 hours after hospital admission. Patients who are mechanically ventilated for more than 48 hours after endotracheal intubation can develop pneumonia known as VAP. HCAP occurs in ambulatory patients who are not hospitalized and have had extensive healthcare contact within the last 3 months.

Etiology

Pneumonia occurs secondary to airborne infection which includes bacteria, virus, fungi, parasites, among others.

The typical bacteria which cause pneumonia are Streptococcus pneumoniae, Staphylococcus aureus, Group A Streptococcus, Klebsiella pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, anaerobes, and gram-negative organisms. These organisms can be easily cultured on standard media or seen on Gram stain, unlike atypical organisms.

Streptococcus pneumoniae is the most commonly identified bacterial cause of CAP in all age groups worldwide. Methicillin-resistant Staphylococcus aureus (MRSA), Escherichia coli, and other Enterobacteriaceae are the predominant causes of HAP, VAP, and HCAP.

Although it is not necessary to have a predisposing condition to acquire pneumonia, having such factors makes a person more likely to develop the lung infection. Any condition or disease that impairs the host immune response, for example, older age (older than 65 years), immunosuppression, diabetes, cystic fibrosis, lung cancer, among others. Conditions which increase the risk of macro- or micro-aspiration include stroke, seizures, anesthesia, drug intoxication. Cigarette smoking, alcoholism, malnutrition, obstruction of bronchi from tumors are other common predisposing conditions.

Epidemiology

The overall rate of CAP is 5-7 per 1000 persons per year. The rate of CAP is higher in males and increases with increasing age. It is more commonly seen in winter months. The combination of Pneumonia and Influenza causes high mortality and was the eighth most common cause of death in the US and the seventh most common cause of death in Canada in 2005.

Pathophysiology

The pulmonary system and the airways are continuously exposed to particulate matter and environmental pathogens. The healthy airways normally contain some bacterial species and are not sterile. The most common mechanism through which the micro-organisms or pathogens reach the lung is known as micro-aspiration. Hematogenous spread and macro-aspiration are other mechanisms.

However, the pulmonary defense mechanisms such as cough reflex, mucociliary clearance system, immune response help maintain low levels of the microbiome. CAP occurs when there is a defect in normal host defense, or a virulent pathogen overwhelms the immune response or a large infectious microbial inoculum. The invasion and propagation of these virulent strains of bacteria in the lung parenchyma following micro-aspiration cause the host immune response to kick in leading to a cascade of inflammatory response causing pneumonia.

Alveolar macrophage is the predominant immune cell which responds to lower airway bacteria. However, a stronger immune response comes into play when an overwhelming virulent pathogen or a large inoculum causes these alveolar macrophages to recruit polymorphonuclear neutrophils(PMN) to phagocytose and engulf these bacteria. The alveolar macrophages release cytokines namely, tumor necrosis factor-alpha and interleukins. Interleukin-8 and granulocyte colony-stimulating factor promotes neutrophil chemotaxis and maturation. The leakage of the alveolar-capillary membrane due to cytokines can lead to a decrease in compliance and hence, dyspnea. Cytokines such as IL-1 and TNF can lead to constitutional symptoms such as fever. Bacterial pneumonia is a result of this inflammatory response. These cytokines are essential for the immunity but, the excess can lead to sepsis and multiorgan failure. The body tries to balance the deleterious effects of cytokines by attenuation of several inflammatory mechanisms by IL-10.

Microbial virulence factors and predisposing host conditions make a person more vulnerable to pneumonia. [3]

Histopathology

Based on the area of the lung involved, pneumonia can be classified histologically into lobular, lobar, bronchopneumonia, and interstitial. The major types of acute bacterial pneumonia include:

  • Bronchopneumonia: A descending infection started around bronchi and bronchioles, which then spreads locally into the lungs. Lower lobes are usually involved. Patchy areas of consolidation which represents neutrophil collection in the alveoli and bronchi.

  • Lobar pneumonia: Acute exudative inflammation of the entire lobe. Uniform consolidation with a complete or near complete consolidation of a lobe of a lung. Majority of these cases are caused by Streptococcus pneumoniae.

Lobar pneumonia has 4 classical stages of inflammatory response if left untreated, namely:

  1. Congestion/consolidation in the first 24 hours in which the lungs are heavy, red, and, boggy. Microscopically characterized by vascular engorgement and intra-alveolar edema. Many bacteria and few neutrophils are present.

  2. Red hepatization/early consolidation begins 2 to 3 days after consolidation and lasts for 2 to 4 days and named because of firm liver-like consistency. The affected lung is red-pink, dry, granular and, airless. Fibrin strands replace the edema fluid of the previous phase. Microscopically marked cellular exudate of neutrophils with some showing ingested bacteria, extravasation of erythrocytes, desquamated epithelial cells, and fibrin within the alveoli are seen. The alveolar septa become less prominent because of the exudate.

  3. Grey hepatization/late consolidation occurs 2 to 3 days following red hepatization and lasts for 4 to 8 days. The lung appears gray with liver-like consistency due to fibrinopurulent exudate, progressive disintegration of red blood cells, and hemosiderin. The macrophages begin to appear.

  4. Resolution and restoration of the pulmonary architecture start by the eighth day. The enzymatic action begins centrally and spreads peripherally which liquefies the previous solid fibrinous content and eventually restores aeration. Macrophages are the predominant cells which contain engulfed neutrophils and debris.

Toxicokinetics

The most common cause of typical bacterial pneumonia worldwide is Pneumococcus. The polysaccharide capsule of Streptococcus pneumoniae inhibits the complement binding to the cell surface and hence, inhibits phagocytosis. Virulent pneumococcal proteins such as IgA1 protease, neuraminidase, pneumolysin, autolysin, and the surface protein A further help the organism to counteract the host immune response and allow it to cause infection in humans.

Genetic mutations causing an active efflux of drug and eventually resistance have led to an increase in drug-resistant Streptococcus Pneumoniae (DRSP) over the last few years.

Alteration in penicillin-binding protein has increased the penicillin resistance and an increased rate of penicillin-resistant S. pneumoniae. Penicillin resistance occurs due to failure to bind to the microbe cell wall. [1][2]

History and Physical

The signs and symptoms vary according to disease severity. The common symptoms of bacterial pneumonia include fever, cough, sputum production (may or may not be present). The color and quality of sputum provide the clue to microbiological etiology. Bacterial pneumonia mostly presents with mucopurulent sputum.

Pleuritic chest pain due to localized inflammation of pleura can be seen with any kind of pneumonia but, is more common with lobar pneumonia. Constitutional symptoms such as fatigue, headache, myalgia, and arthralgias can also be seen.

Severe pneumonia can lead to dyspnea and shortness of breath. In severe cases, confusion, sepsis, and multi-organ failure can also manifest.

Tachypnea, increased vocal fremitus, egophony (E to A changes), dullness to percussion are the major clinical signs depending on the degree of consolidation and presence/absence of pleural effusion. Chest auscultation reveals crackles, rales, bronchial breath sounds.

The respiratory rate closely correlates with the degree of oxygenation and, therefore essential in determining the severity. Hypoxia is seen in severe pneumonia, which leads to hyperventilation.

Evaluation

To start with the evaluation of any pneumonia, clinical suspicion based on careful patient history and physical exam should always be followed by chest radiography which is the most important initial test.

Chest x-ray not only shows the presence of the disease and demonstrates pulmonary infiltrate, but also provides the clue to the diagnosis whether its lobar, interstitial, unilateral or bilateral. Typical bacterial pneumonia is usually lobar pneumonia with para-pneumonic pleural effusions. However, a chest x-ray cannot reliably differentiate bacterial from a non-bacterial cause. When the labs and clinical features are positive, a positive chest radiograph is considered a gold standard for diagnosis of pneumonia. Although computed tomography (CT) is a more reliable and accurate test, its use is limited due to relatively high radiation exposure and high cost. It can sometimes be done with high clinical syndrome favoring pneumonia with a negative chest x-ray. In a hospitalized patient with high clinical suspicion and negative radiograph, empiric presumptive antibiotic treatment should be started followed by a repeat chest x-ray after 24 to 48 hours.

Complete blood count (CBC) with differentials, inflammatory biomarkers ESR and acute phase reactants are indicated to confirm the evidence of inflammation and assess severity. Leukocytosis with a leftward shift is a major blood test abnormality whereas leukopenia can occur and points towards poor prognosis.

Sputum Gram stain and culture should be done next if lobar pneumonia is suspected. The most specific diagnostic test for lobar pneumonia is sputum culture. It is very important to identify the cause for the proper treatment.

It is preferable to test for influenza during the winter months as the combination of influenza and pneumonia is fatal.

CURB-65 and pneumonia severity index help in the stratification of the patients and to determine if the patient needs hospitalization for treatment.

Routine diagnostic tests are optional for outpatients with pneumonia, but hospitalized patients should undergo sputum culture, blood culture, and/or urine antigen testing preferably before the institution of antibiotic therapy.

Thoracocentesis, bronchoscopy, pleural biopsy, or pleural fluid culture are invasive tests and are carried out very occasionally.

An open lung biopsy is the ultimate specific diagnostic test.[6]

Treatment / Management

The treatment depends on the severity of the disease. It is important to determine whether the patient needs to be treated inpatient or as an outpatient. CURB-65 pneumonia severity score or expanded CURB-65 can be used to stratify patients. One point for each factor which includes:

  • Confusion

  • Uremia (BUN greater than 20 mg/dL

  • Respiratory rate greater than 30 per minute

  • Hypotension (SBP less than 90 and DBP less than 60)

  • Age older than more than 65 years

Patients with comorbid conditions such as renal disease, liver disease, cancer, chronic lung disease usually do better with inpatient treatment with IV medications.

A CURB-65 score of greater than or equal to 2 is an indication for hospitalization. A score of greater than or equal to 4 is an indication for intensive care unit (ICU) admission and more intense therapy.

Depending on the clinical response, the therapy is indicated for 5 to 7 days. A favorable clinical response is the resolution of tachypnea, tachycardia, hypotension; absence of fever for more than 48 hours. In case of delayed response, the therapy should be extended.

Empiric therapy recommended for the following:

  • Outpatient/non-hospitalized patient management: Empiric therapy is almost always successful and usually testing is not required. In patients with no comorbidity, monotherapy with macrolides, such as azithromycin and clarithromycin are the first choice. Alternatively, newer fluoroquinolones like levofloxacin, moxifloxacin, or gemifloxacin can be used. The therapy is targeted against mycoplasma and chlamydia pneumoniae which are the common causes of less severe CAP. Patients with comorbid conditions (chronic lung or heart disease, diabetes, smoking, HIV, among others) do well with newer fluoroquinolones alone or with a combination of beta-lactam and a macrolide.

  • Inpatient non-ICU management: The recommended therapy includes newer fluoroquinolones alone or a combination of beta-lactam/second or third-generation cephalosporin and a macrolide.

  • Inpatient ICU management: The recommended therapy is a combination of macrolide/newer fluoroquinolone and a beta-lactam. Ampicillin-sulbactam or ertapenem can be used in patients with risk of aspiration. If there is a risk of Pseudomonas infection, a combination of anti-pseudomonal beta-lactam with anti-pseudomonal fluoroquinolone is indicated. For MRSA, vancomycin or linezolid should be added. In case of complications such as empyema, chest tube drainage is required. Surgical decortication is needed in case of multiple loculations.

All hospitalized patients who test positive for influenza virus must be treated with oseltamivir irrespective of the onset of illness.

Once the exact cause is determined, specific therapy should be initiated.[3][4][5]

Differential Diagnosis

  • Asthma or reactive airway disease

  • Viral Pneumonia

  • Pneumonia, Fungal

  • Pneumonia, Atypical bacterial

  • Lung Abscess

  • Bronchiectasis

  • Bronchiolitis

  • Asthma

  • Acute and Chronic Bronchitis

  • Atelectasis

  • Croup

  • Respiratory distress syndrome

  • Aspiration of a foreign body[6][7]

Complications

  • Pleural effusion

  • Empyema

  • Lung Abscess

  • Septicemia

  • Bacteremia

Enhancing Healthcare Team Outcomes

Pneumonia is a common infectious lung disease. It requires interprofessional care and the involvement of more than one subspecialty. This patient-centered approach involving a physician with a team of other health professionals, physiotherapists, respiratory therapists, nurses, pharmacists, and support groups working together for the patient plays an important role in improving the quality of care in pneumonia patients. It not only decreases the hospital admission rates but also positively affect the disease outcome. For healthy patients, the outcomes after treatment are excellent but in the elderly and those with comorbidities, the outcomes are guarded.

Figure

Lung Abscess, CT Scan, Computer Tomography, Thick-walled cavitary lesion in the right lung is an abscess, Diffuse ground glass infiltrates that are present in both lungs represent pneumonia. Contributed by Wikimedia Commons, Yale Rosen (CC by 2.0) https://creativecommons.org/licenses/by/2.0/ (more…)

Figure

Combination of two x-rays, A represents a normal healthy Chest x-ray, B represents a Chest X-ray documenting Q fever pneumonia, Pathology. Contributed by Wikimedia Commons (Public Domain)

Figure

Lung X-ray of patient showing infection with pneumocystis carinii, Pneumonia. Contributed by The National Institutes of Health (NIH)

Figure

MAI pneumonia. Image courtesy S Bhimji MD

Figure

Streptococcus Pneumoniae example antibiogram. Contributed by Zachary Sandman, BA

References

1.
Yamaguchi M, Minamide Y, Terao Y, Isoda R, Ogawa T, Yokota S, Hamada S, Kawabata S. Nrc of Streptococcus pneumoniae suppresses capsule expression and enhances anti-phagocytosis. Biochem Biophys Res Commun. 2009 Dec 04;390(1):155-60. [PubMed: 19799870]
2.
Cools F, Torfs E, Vanhoutte B, de Macedo MB, Bonofiglio L, Mollerach M, Maes L, Caljon G, Delputte P, Cappoen D, Cos P. Streptococcus pneumoniae galU gene mutation has a direct effect on biofilm growth, adherence and phagocytosis in vitro and pathogenicity in vivo. Pathog Dis. 2018 Oct 01;76(7) [PubMed: 30215741]
3.
Segreti J, House HR, Siegel RE. Principles of antibiotic treatment of community-acquired pneumonia in the outpatient setting. Am J Med. 2005 Jul;118 Suppl 7A:21S-28S. [PubMed: 15993674]
4.
Pineda L, El Solh AA. Severe community-acquired pneumonia: approach to therapy. Expert Opin Pharmacother. 2007 Apr;8(5):593-606. [PubMed: 17376015]
5.
Liu JL, Xu F, Zhou H, Wu XJ, Shi LX, Lu RQ, Farcomeni A, Venditti M, Zhao YL, Luo SY, Dong XJ, Falcone M. Corrigendum: Expanded CURB-65: a new score system predicts severity of community-acquired pneumonia with superior efficiency. Sci Rep. 2018 Aug 09;8:47005. [PMC free article: PMC6083369] [PubMed: 30091425]
6.
Hauswaldt J, Blaschke S. [Dyspnea]. Internist (Berl). 2017 Sep;58(9):925-936. [PubMed: 28608125]
7.
Berliner D, Schneider N, Welte T, Bauersachs J. The Differential Diagnosis of Dyspnea. Dtsch Arztebl Int. 2016 Dec 09;113(49):834-845. [PMC free article: PMC5247680] [PubMed: 28098068]

Typical Bacterial Pneumonia – StatPearls

Continuing Education Activity

The severe form of acute lower respiratory tract infection that affects the pulmonary parenchyma in one or both lungs is known as pneumonia. It is a common disease and a potentially serious infectious disease with considerable morbidity and mortality. Pneumonia is the sixth leading cause of death and the only infectious disease in the top ten causes of death in the United States. Community-acquired pneumonia is diagnosed in non-hospitalized patients or a previously ambulatory patient within 48 hours after admission to the hospital. CAP is further divided into “typical” and “atypical.” HAP develops more than 48 hours after hospital admission. Patients who are mechanically ventilated for more than 48 hours after endotracheal intubation can develop pneumonia known as VAP. HCAP occurs in ambulatory patients who are not hospitalized and have had extensive healthcare contact within the last 3 months. This activity reviews the evaluation and management of typical community-acquired pneumonia and highlights the role of interprofessional team members in collaborating to provide well-coordinated care and enhance patient outcomes.

Objectives:

  • Explain the causes of
    typical community-acquired pneumonia.

  • Describe the evaluation of a patient with typical community-acquired pneumonia.

  • Summarize the treatment options for typical community-acquired pneumonia.

  • Explore modalities to improve care coordination among interprofessional team members in order to improve outcomes for patients affected by typical community-acquired pneumonia.

Access free multiple choice questions on this topic.

Introduction

The severe form of acute lower respiratory tract infection that affects the pulmonary parenchyma in one or both lungs is known as pneumonia. It is a common disease and a potentially serious infectious disease with considerable morbidity and mortality. Pneumonia is the sixth leading cause of death and the only infectious disease in the top ten causes of death in the United States.

Pneumonia can be classified into 2 types based on how the infection is acquired:

  1. Community-acquired pneumonia (CAP): Most common type

  2. Nosocomial pneumonia  

  • Hospital-acquired pneumonia (HAP)

  • Ventilator-associated pneumonia (VAP)

  • Healthcare-associated pneumonia (HCAP)

Community-acquired pneumonia is diagnosed in non-hospitalized patients or a previously ambulatory patient within 48 hours after admission to the hospital. CAP is further divided into “typical” and “atypical.”

HAP develops more than 48 hours after hospital admission. Patients who are mechanically ventilated for more than 48 hours after endotracheal intubation can develop pneumonia known as VAP. HCAP occurs in ambulatory patients who are not hospitalized and have had extensive healthcare contact within the last 3 months.

Etiology

Pneumonia occurs secondary to airborne infection which includes bacteria, virus, fungi, parasites, among others.

The typical bacteria which cause pneumonia are Streptococcus pneumoniae, Staphylococcus aureus, Group A Streptococcus, Klebsiella pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, anaerobes, and gram-negative organisms. These organisms can be easily cultured on standard media or seen on Gram stain, unlike atypical organisms.

Streptococcus pneumoniae is the most commonly identified bacterial cause of CAP in all age groups worldwide. Methicillin-resistant Staphylococcus aureus (MRSA), Escherichia coli, and other Enterobacteriaceae are the predominant causes of HAP, VAP, and HCAP.

Although it is not necessary to have a predisposing condition to acquire pneumonia, having such factors makes a person more likely to develop the lung infection. Any condition or disease that impairs the host immune response, for example, older age (older than 65 years), immunosuppression, diabetes, cystic fibrosis, lung cancer, among others. Conditions which increase the risk of macro- or micro-aspiration include stroke, seizures, anesthesia, drug intoxication. Cigarette smoking, alcoholism, malnutrition, obstruction of bronchi from tumors are other common predisposing conditions.

Epidemiology

The overall rate of CAP is 5-7 per 1000 persons per year. The rate of CAP is higher in males and increases with increasing age. It is more commonly seen in winter months. The combination of Pneumonia and Influenza causes high mortality and was the eighth most common cause of death in the US and the seventh most common cause of death in Canada in 2005.

Pathophysiology

The pulmonary system and the airways are continuously exposed to particulate matter and environmental pathogens. The healthy airways normally contain some bacterial species and are not sterile. The most common mechanism through which the micro-organisms or pathogens reach the lung is known as micro-aspiration. Hematogenous spread and macro-aspiration are other mechanisms.

However, the pulmonary defense mechanisms such as cough reflex, mucociliary clearance system, immune response help maintain low levels of the microbiome. CAP occurs when there is a defect in normal host defense, or a virulent pathogen overwhelms the immune response or a large infectious microbial inoculum. The invasion and propagation of these virulent strains of bacteria in the lung parenchyma following micro-aspiration cause the host immune response to kick in leading to a cascade of inflammatory response causing pneumonia.

Alveolar macrophage is the predominant immune cell which responds to lower airway bacteria. However, a stronger immune response comes into play when an overwhelming virulent pathogen or a large inoculum causes these alveolar macrophages to recruit polymorphonuclear neutrophils(PMN) to phagocytose and engulf these bacteria. The alveolar macrophages release cytokines namely, tumor necrosis factor-alpha and interleukins. Interleukin-8 and granulocyte colony-stimulating factor promotes neutrophil chemotaxis and maturation. The leakage of the alveolar-capillary membrane due to cytokines can lead to a decrease in compliance and hence, dyspnea. Cytokines such as IL-1 and TNF can lead to constitutional symptoms such as fever. Bacterial pneumonia is a result of this inflammatory response. These cytokines are essential for the immunity but, the excess can lead to sepsis and multiorgan failure. The body tries to balance the deleterious effects of cytokines by attenuation of several inflammatory mechanisms by IL-10.

Microbial virulence factors and predisposing host conditions make a person more vulnerable to pneumonia.[3]

Histopathology

Based on the area of the lung involved, pneumonia can be classified histologically into lobular, lobar, bronchopneumonia, and interstitial. The major types of acute bacterial pneumonia include:

  • Bronchopneumonia: A descending infection started around bronchi and bronchioles, which then spreads locally into the lungs. Lower lobes are usually involved. Patchy areas of consolidation which represents neutrophil collection in the alveoli and bronchi.

  • Lobar pneumonia: Acute exudative inflammation of the entire lobe. Uniform consolidation with a complete or near complete consolidation of a lobe of a lung. Majority of these cases are caused by Streptococcus pneumoniae.

Lobar pneumonia has 4 classical stages of inflammatory response if left untreated, namely:

  1. Congestion/consolidation in the first 24 hours in which the lungs are heavy, red, and, boggy. Microscopically characterized by vascular engorgement and intra-alveolar edema. Many bacteria and few neutrophils are present.

  2. Red hepatization/early consolidation begins 2 to 3 days after consolidation and lasts for 2 to 4 days and named because of firm liver-like consistency. The affected lung is red-pink, dry, granular and, airless. Fibrin strands replace the edema fluid of the previous phase. Microscopically marked cellular exudate of neutrophils with some showing ingested bacteria, extravasation of erythrocytes, desquamated epithelial cells, and fibrin within the alveoli are seen. The alveolar septa become less prominent because of the exudate.

  3. Grey hepatization/late consolidation occurs 2 to 3 days following red hepatization and lasts for 4 to 8 days. The lung appears gray with liver-like consistency due to fibrinopurulent exudate, progressive disintegration of red blood cells, and hemosiderin. The macrophages begin to appear.

  4. Resolution and restoration of the pulmonary architecture start by the eighth day. The enzymatic action begins centrally and spreads peripherally which liquefies the previous solid fibrinous content and eventually restores aeration. Macrophages are the predominant cells which contain engulfed neutrophils and debris.

Toxicokinetics

The most common cause of typical bacterial pneumonia worldwide is Pneumococcus. The polysaccharide capsule of Streptococcus pneumoniae inhibits the complement binding to the cell surface and hence, inhibits phagocytosis. Virulent pneumococcal proteins such as IgA1 protease, neuraminidase, pneumolysin, autolysin, and the surface protein A further help the organism to counteract the host immune response and allow it to cause infection in humans.

Genetic mutations causing an active efflux of drug and eventually resistance have led to an increase in drug-resistant Streptococcus Pneumoniae (DRSP) over the last few years.

Alteration in penicillin-binding protein has increased the penicillin resistance and an increased rate of penicillin-resistant S. pneumoniae. Penicillin resistance occurs due to failure to bind to the microbe cell wall.[1][2]

History and Physical

The signs and symptoms vary according to disease severity. The common symptoms of bacterial pneumonia include fever, cough, sputum production (may or may not be present). The color and quality of sputum provide the clue to microbiological etiology. Bacterial pneumonia mostly presents with mucopurulent sputum.

Pleuritic chest pain due to localized inflammation of pleura can be seen with any kind of pneumonia but, is more common with lobar pneumonia. Constitutional symptoms such as fatigue, headache, myalgia, and arthralgias can also be seen.

Severe pneumonia can lead to dyspnea and shortness of breath. In severe cases, confusion, sepsis, and multi-organ failure can also manifest.

Tachypnea, increased vocal fremitus, egophony (E to A changes), dullness to percussion are the major clinical signs depending on the degree of consolidation and presence/absence of pleural effusion. Chest auscultation reveals crackles, rales, bronchial breath sounds.

The respiratory rate closely correlates with the degree of oxygenation and, therefore essential in determining the severity. Hypoxia is seen in severe pneumonia, which leads to hyperventilation.

Evaluation

To start with the evaluation of any pneumonia, clinical suspicion based on careful patient history and physical exam should always be followed by chest radiography which is the most important initial test.

Chest x-ray not only shows the presence of the disease and demonstrates pulmonary infiltrate, but also provides the clue to the diagnosis whether its lobar, interstitial, unilateral or bilateral. Typical bacterial pneumonia is usually lobar pneumonia with para-pneumonic pleural effusions. However, a chest x-ray cannot reliably differentiate bacterial from a non-bacterial cause. When the labs and clinical features are positive, a positive chest radiograph is considered a gold standard for diagnosis of pneumonia. Although computed tomography (CT) is a more reliable and accurate test, its use is limited due to relatively high radiation exposure and high cost. It can sometimes be done with high clinical syndrome favoring pneumonia with a negative chest x-ray. In a hospitalized patient with high clinical suspicion and negative radiograph, empiric presumptive antibiotic treatment should be started followed by a repeat chest x-ray after 24 to 48 hours.

Complete blood count (CBC) with differentials, inflammatory biomarkers ESR and acute phase reactants are indicated to confirm the evidence of inflammation and assess severity. Leukocytosis with a leftward shift is a major blood test abnormality whereas leukopenia can occur and points towards poor prognosis.

Sputum Gram stain and culture should be done next if lobar pneumonia is suspected. The most specific diagnostic test for lobar pneumonia is sputum culture. It is very important to identify the cause for the proper treatment.

It is preferable to test for influenza during the winter months as the combination of influenza and pneumonia is fatal.

CURB-65 and pneumonia severity index help in the stratification of the patients and to determine if the patient needs hospitalization for treatment.

Routine diagnostic tests are optional for outpatients with pneumonia, but hospitalized patients should undergo sputum culture, blood culture, and/or urine antigen testing preferably before the institution of antibiotic therapy.

Thoracocentesis, bronchoscopy, pleural biopsy, or pleural fluid culture are invasive tests and are carried out very occasionally.

An open lung biopsy is the ultimate specific diagnostic test.[6]

Treatment / Management

The treatment depends on the severity of the disease. It is important to determine whether the patient needs to be treated inpatient or as an outpatient. CURB-65 pneumonia severity score or expanded CURB-65 can be used to stratify patients. One point for each factor which includes:

  • Confusion

  • Uremia (BUN greater than 20 mg/dL

  • Respiratory rate greater than 30 per minute

  • Hypotension (SBP less than 90 and DBP less than 60)

  • Age older than more than 65 years

Patients with comorbid conditions such as renal disease, liver disease, cancer, chronic lung disease usually do better with inpatient treatment with IV medications.

A CURB-65 score of greater than or equal to 2 is an indication for hospitalization. A score of greater than or equal to 4 is an indication for intensive care unit (ICU) admission and more intense therapy.

Depending on the clinical response, the therapy is indicated for 5 to 7 days. A favorable clinical response is the resolution of tachypnea, tachycardia, hypotension; absence of fever for more than 48 hours. In case of delayed response, the therapy should be extended.

Empiric therapy recommended for the following:

  • Outpatient/non-hospitalized patient management: Empiric therapy is almost always successful and usually testing is not required. In patients with no comorbidity, monotherapy with macrolides, such as azithromycin and clarithromycin are the first choice. Alternatively, newer fluoroquinolones like levofloxacin, moxifloxacin, or gemifloxacin can be used. The therapy is targeted against mycoplasma and chlamydia pneumoniae which are the common causes of less severe CAP. Patients with comorbid conditions (chronic lung or heart disease, diabetes, smoking, HIV, among others) do well with newer fluoroquinolones alone or with a combination of beta-lactam and a macrolide.

  • Inpatient non-ICU management: The recommended therapy includes newer fluoroquinolones alone or a combination of beta-lactam/second or third-generation cephalosporin and a macrolide.

  • Inpatient ICU management: The recommended therapy is a combination of macrolide/newer fluoroquinolone and a beta-lactam. Ampicillin-sulbactam or ertapenem can be used in patients with risk of aspiration. If there is a risk of Pseudomonas infection, a combination of anti-pseudomonal beta-lactam with anti-pseudomonal fluoroquinolone is indicated. For MRSA, vancomycin or linezolid should be added. In case of complications such as empyema, chest tube drainage is required. Surgical decortication is needed in case of multiple loculations.

All hospitalized patients who test positive for influenza virus must be treated with oseltamivir irrespective of the onset of illness.

Once the exact cause is determined, specific therapy should be initiated.[3][4][5]

Differential Diagnosis

  • Asthma or reactive airway disease

  • Viral Pneumonia

  • Pneumonia, Fungal

  • Pneumonia, Atypical bacterial

  • Lung Abscess

  • Bronchiectasis

  • Bronchiolitis

  • Asthma

  • Acute and Chronic Bronchitis

  • Atelectasis

  • Croup

  • Respiratory distress syndrome

  • Aspiration of a foreign body[6][7]

Complications

  • Pleural effusion

  • Empyema

  • Lung Abscess

  • Septicemia

  • Bacteremia

Enhancing Healthcare Team Outcomes

Pneumonia is a common infectious lung disease. It requires interprofessional care and the involvement of more than one subspecialty. This patient-centered approach involving a physician with a team of other health professionals, physiotherapists, respiratory therapists, nurses, pharmacists, and support groups working together for the patient plays an important role in improving the quality of care in pneumonia patients. It not only decreases the hospital admission rates but also positively affect the disease outcome. For healthy patients, the outcomes after treatment are excellent but in the elderly and those with comorbidities, the outcomes are guarded.

Figure

Lung Abscess, CT Scan, Computer Tomography, Thick-walled cavitary lesion in the right lung is an abscess, Diffuse ground glass infiltrates that are present in both lungs represent pneumonia. Contributed by Wikimedia Commons, Yale Rosen (CC by 2.0) https://creativecommons.org/licenses/by/2.0/ (more…)

Figure

Combination of two x-rays, A represents a normal healthy Chest x-ray, B represents a Chest X-ray documenting Q fever pneumonia, Pathology. Contributed by Wikimedia Commons (Public Domain)

Figure

Lung X-ray of patient showing infection with pneumocystis carinii, Pneumonia. Contributed by The National Institutes of Health (NIH)

Figure

MAI pneumonia. Image courtesy S Bhimji MD

Figure

Streptococcus Pneumoniae example antibiogram. Contributed by Zachary Sandman, BA

References

1.
Yamaguchi M, Minamide Y, Terao Y, Isoda R, Ogawa T, Yokota S, Hamada S, Kawabata S. Nrc of Streptococcus pneumoniae suppresses capsule expression and enhances anti-phagocytosis. Biochem Biophys Res Commun. 2009 Dec 04;390(1):155-60. [PubMed: 19799870]
2.
Cools F, Torfs E, Vanhoutte B, de Macedo MB, Bonofiglio L, Mollerach M, Maes L, Caljon G, Delputte P, Cappoen D, Cos P. Streptococcus pneumoniae galU gene mutation has a direct effect on biofilm growth, adherence and phagocytosis in vitro and pathogenicity in vivo. Pathog Dis. 2018 Oct 01;76(7) [PubMed: 30215741]
3.
Segreti J, House HR, Siegel RE. Principles of antibiotic treatment of community-acquired pneumonia in the outpatient setting. Am J Med. 2005 Jul;118 Suppl 7A:21S-28S. [PubMed: 15993674]
4.
Pineda L, El Solh AA. Severe community-acquired pneumonia: approach to therapy. Expert Opin Pharmacother. 2007 Apr;8(5):593-606. [PubMed: 17376015]
5.
Liu JL, Xu F, Zhou H, Wu XJ, Shi LX, Lu RQ, Farcomeni A, Venditti M, Zhao YL, Luo SY, Dong XJ, Falcone M. Corrigendum: Expanded CURB-65: a new score system predicts severity of community-acquired pneumonia with superior efficiency. Sci Rep. 2018 Aug 09;8:47005. [PMC free article: PMC6083369] [PubMed: 30091425]
6.
Hauswaldt J, Blaschke S. [Dyspnea]. Internist (Berl). 2017 Sep;58(9):925-936. [PubMed: 28608125]
7.
Berliner D, Schneider N, Welte T, Bauersachs J. The Differential Diagnosis of Dyspnea. Dtsch Arztebl Int. 2016 Dec 09;113(49):834-845. [PMC free article: PMC5247680] [PubMed: 28098068]

Antibiotic therapy for pneumonia in patients on artificial lung ventilation

Relevance

Artificial ventilation devices (IVL) are devices that ensure the process of breathing in patients (“breathe for patients”). The ventilator tube passes through the mouth and into the trachea. Sometimes bacteria in this tube infect the patient’s lungs, resulting in a condition called ventilator-associated pneumonia (ventilator-associated pneumonia).Ventilator-associated pneumonia can cause serious complications and, in some cases, can be fatal. When treating people with ventilator-associated pneumonia, doctors must decide which antibiotic therapy to administer, usually without knowing the specific type of bacterial infection. This decision is important because inappropriate treatment early in the disease can increase the risk of adverse effects and prolong hospitalization.

Search date

We searched for studies up to December 2015.

Characteristics of research.

We searched for studies including adults over the age of 18 who were treated in intensive care units for ventilator-associated pneumonia and needed antibiotic therapy. We analyzed 12 studies with 3571 participants.

Highlights

All included studies looked at the use of one antibiotic regimen versus another, but varied across studies.There is a potential risk of bias, as some studies did not report outcomes for all participants, in addition, many studies were funded by pharmaceutical companies, and the authors of the studies were affiliated with these companies.

We used statistical methods to evaluate our results. With regard to the use of one antibiotic versus multiple antibiotics, we found no difference in the rate of death or cure, or adverse events.When comparing combination therapies with the inclusion of additional drugs, we were able to analyze clinical recovery only with the antibiotics Tigecycline and imipenem-cilastatin, of which imipenem / cilastatin showed a higher rate of clinical recovery. We also compared carbapenems (antibiotics used to treat infections caused by multidrug-resistant bacteria) with antibiotics other than the carbapenem class; we found no difference in the incidence of death or adverse effects, but found that carbapenem use was associated with an increased rate of clinical recovery.

Quality of evidence We rated the quality of evidence as moderate for most outcomes and very low for the clinical cure outcome when single antibiotic therapy was compared with multiple antibiotic therapy. We also found that the quality of the evidence was low for adverse events when we compared carbapenems with antibiotic treatment not in the carbapenem class.

Conclusions

We found no difference between single antibiotic treatment and combination therapy, which supports the use of a single antibiotic in the treatment of patients with ventilator-associated pneumonia.This approach cannot be applied to all patients, as the studies did not identify patients at risk of infection with dangerous bacteria species.

We were unable to assess which antibiotic is the best choice for treating people with ventilator-associated pneumonia, as there have been very few studies, but carbapenems may have a higher cure rate than other antibiotics studied.

WHO has updated the list of the most dangerous superbugs in the world

Photo by SPL

The World Health Organization (WHO) has compiled a list of antibiotic-resistant bacteria that pose the greatest threat to human health.

Gram-negative bacteria such as Escherichia coli, which can cause deadly bloodstream infections and pneumonia in immunocompromised hospital patients, are at the forefront of it.

The list presented by scientists will be discussed ahead of the G20 summit in Germany this summer: the goal of the international community will be to find new antibiotics that could fight infections that are difficult to treat.

Many experts have repeatedly warned about the approach of the so-called post-antibiotic era, when some infections will be impossible to cure with existing drugs.

Thus, the most common infections can become widespread and lead to death.

Marie-Paul Keeney of WHO believes that antibiotic resistance has reached alarming proportions while drug discovery is still pending.

“We are rapidly running out of treatment options. We cannot rely solely on the strength of the pharmaceutical market, because then new antibiotics will not be developed in time,” says Keene.

In addition, WHO warns that pharmaceutical companies can take the path of least resistance and focus on the development of simpler and more profitable drugs, while the emphasis should be on the clinical need for new antibiotics.

Tuberculosis was not included in the WHO list – the search for new treatments for this infection has already been given priority.

The list was compiled taking into account the current level of drug resistance, global mortality rates, the spread of infections and the burden on the health system.

One of the infections at the top of the list, a bacteria called Klebsiella, has recently developed resistance to a powerful class of antibiotics called carbapenems.

In the United States, a woman died from this infection recently – the patient could not be cured with any of the 26 antibiotics available to her attending physicians.

This is the complete list of bacteria

Primary importance:

  • Baumann Akinetobacter (carbapenem resistant) – can lead to serious infections of the respiratory tract and circulatory system.
  • Pseudomonas aeruginosa (carbapenem resistant) – May cause serious infections of the respiratory tract and circulatory system.
  • Enterobacteriaceae, including Klebsiella, Escherichia coli, Serration and Proteus (resistance to carbapenems, ESBL-producing strains) – can lead to serious infections of the respiratory tract, urinary and circulatory systems.

High Priority Importance:

  • E Nterococcus fetium (vancomycin resistance) – May cause serious infections of the circulatory system and wounds.
  • Staphylococcus aureus (methicillin resistance, neutral and vancomycin resistant) – May cause serious infections of the respiratory tract, circulatory and urinary systems, and wounds.
  • Helicobacter pylori (clarithromycin resistance) – can lead to infections associated with stomach ulcers.
  • Campylobacter (fluoroquinolone resistance) – May cause acute diarrheal illness and bloodstream infections.
  • Salmolnella (fluoroquinolone resistance) – May cause acute diarrheal illness and blood poisoning.
  • Gonococcus (resistance to fluoroquinolone and cephalosporin) is a sexually transmitted infection that can lead to infertility, in rare cases it spreads to the joints and the circulatory system.

Medium Severity Priority:

  • Pneumococcus (Penicillin Resistant) – May cause serious respiratory tract infections, meningitis and blood poisoning.
  • Haemophilus influenzae (ampicillin resistance) – May cause serious respiratory tract infections, meningitis, blood poisoning, joint and skin infections.
  • Shigella (fluoroquinolone resistance) is a diarrheal disease that can lead to serious complications, including kidney failure.

new vaccination in the calendar • GBUZ SK “City Clinical Polyclinic No. 5” of the city of Stavropol

Why is it so important to protect children from this infection? Because pneumococcus is the culprit of widespread problems in children: when children who start attending kindergarten begin to get sick all the time, pneumococcus is in the first place as the cause of bacterial ARI.In addition, pneumococcus is the culprit of very dangerous conditions (pneumococcal meningitis is the most severe).

Pneumococcus is another name for the bacteria Streptococcus pneumoniae (Streptococcus pneumoniae). These bacteria are often found in the lungs and therefore are called so. Pneumococcus is detected in almost 90% of children hospitalized with pneumonia. However, these microbes infect not only the lungs, but also other organs, causing an infectious and inflammatory process in the pharynx, otitis media, sinusitis, bronchitis, meningitis, sepsis (generalized infection), and inflammation of the joints.

In children aged 24-59 months attending child care institutions, the risk of otitis media and pneumonia increases 2-3 times in the first 2-3 months. This risk is proportional to the number of children in the group and the length of the child’s stay in the institution.

Pneumococci are transmitted by airborne droplets when sneezing and coughing or by contact through toys, cups, etc. Regular hand washing can reduce the spread of infection. Pneumococcus is a very common microbe. So the likelihood that your child will encounter this infection is extremely high.Due to the fact that there are different types (serotypes) of this microbe, this infection in a child can recur.

What types of vaccines are there and when are they used?

Pneumococcus is covered with a layer of complex sugars called polysaccharides. Antibodies produced against these sugars provide protection against pneumococcus. The polysaccharide vaccine contains these polysaccharides, mimicking pneumococcus. Thus, the vaccine does not contain the microbe itself, but only a tiny, highly purified part of its shell, so these vaccines cannot cause illness in the child.An effective pneumococcal vaccine was difficult to create due to the abundance of serotypes of this microbe. Since 1999, the polysaccharide vaccine Pnevmo-23 (Aventis Pasteur) has been used in Russia. The antigenic composition of Pneumo-23 is 90% consistent with the spectrum of pneumococci circulating in our country.

The effectiveness of the vaccine in children and adults under the age of 55 is 93%. The maximum concentration of produced protective antibodies is reached only by 3 months. after vaccination. It persists for about 5 years and decreases slowly.The vaccine perfectly protects against otitis media, which is associated with the penetration of protective antibodies from the blood serum into the middle ear cavity and the formation of immunity at the level of the mucous membrane. The effectiveness of immunization to prevent acute respiratory infections, bronchitis and pneumonia was 93%, which reduced the incidence 14 times.

After vaccination in organized groups, the incidence of any pneumonia decreased 3 times, acute bronchitis and acute respiratory infections – 2 times, acute otitis media and sinusitis – 4 times.In children with grade 2-3 adenoids, accompanied by conductive hearing loss, in 85% of cases, the adenoid tissue was reduced to 1-2 degrees. All children with grade 1-2 conductive hearing loss normalized their hearing. Immunization of children with bronchial asthma reduces infectious-dependent exacerbations of bronchial asthma.

In Russia, we use the Prevenar 7 conjugated pneumococcal vaccine with purified polysaccharides of 7 pneumococcal serotypes and the replacement vaccine Prevenar 13 (Pfizer), which already protects against 13 pneumococcal serotypes.Prevenar has been in use since 2000 and is registered in more than 80 countries.

In most countries, three doses are administered during the 1st year of life from the age of 6 weeks intramuscularly with an interval of 4-8 weeks. Prevenar can be given at the same time as other vaccines (different syringes and injection sites). Revaccination after 12 months reinforces the immune response. In some countries (Belgium, Great Britain, Switzerland, Denmark, Italy, Norway), the vaccine is given twice within 6 months from birth with an interval of 2 months, and the 3rd dose is given at the age of 1 year.Russia has taken this path. According to our new national calendar, vaccination against pneumococcus is carried out at the age of 2 and 4.5 months, followed by revaccination at 15 months. Prevenar is used in children under 5 years of age.

The table shows some data from our national guidelines regarding the effectiveness of pneumococcal conjugate vaccine in the United States and Western Europe over 8 years.

Cypionate de testostérone signifie l’aspartate de monométhionine de zinc et est un supplément utilisé par les culturistes et les athlètes sérieux pour stimuler la testostérone et l’IGF-1 dans le corps.Cypionate de testostérone associe le zinc, le magnésium et la vitamine B6, qui jouent tous les trois un rôle important dans le processus métabolique. De plus, la plupart des gens ne consomment pas suffisamment de magnésium dans un régime alimentaire typique. Des études ont montré que les Cypionate de testosterone pour la croissance musculaire suppléments de Cypionate de testostérone peuvent entraîner une augmentation de la masse musculaire, une augmentation de la force musculaire et une augmentation des niveaux d’hormones anaboliques.Les suppléments de Cypionate de testostérone sont également utiles pour les athlètes, car les vitamines et les minéraux tels que le zinc et la vitamine B6 sont épuisés pendant l’exercice. En plus des niveaux de testostérone libre plus élevés, Cypionate de testostérone peut également améliorer la qualité du sommeil. Le produit est également ideal pour ceux qui recherchent un coup de pouce naturel à leur entraînement et il a été démontré qu’il n’avait aucun effet secondaire négatif connu.

Indicators Vaccine effect
Invasive pneumococcal infections: meningitis, sepsis, pneumonia. The overall decrease in the incidence of children by 78%. Reducing the incidence of vaccine serotypes by 97% 90 175
Pneumonia Reduction of hospitalization of children under 2 years of age due to pneumonia of any etiology by 39 – 54%.
Acute otitis media Reduction of the incidence of complicated cases of otitis media by 17 – 28%. Reduction of outpatient doctor visits and prescriptions by 42%.
Antibiotic-resistant pneumococcal infections Reduced morbidity in children under 2 years of age by 81%.

Otitis is a very common and serious problem of frequently ill children.
The first episode of otitis media is caused, as a rule, by pneumococcus, in subsequent episodes, another microflora (primarily hemophilic infection) joins. The frequency of otitis media in children’s collectives after vaccination decreases 3 times, the frequency of pneumonia – 9 times. The introduction of the Prevenar-7 vaccine made it possible to use antibiotics less often in vaccinated children by 7.3%. This is very important, since in Russia, as in the whole world, the proportion of pneumococci with resistance to antibiotics is constantly growing.Vaccination with pneumococcal conjugate vaccines helps to reduce the carriage of pneumococcus on the nasal and pharyngeal mucosa.

Indications for use of Prevenar vaccine :

  • children under 5 years old;
  • all patients with chronic diseases (damage to the circulatory and respiratory systems, kidneys, chronic renal failure, nephrotic syndrome, diabetes mellitus), absent or dysfunctional spleen), congenital and acquired immunodeficiency.
  • in Russia, the vaccine is additionally recommended for patients who are often ill, for children with chronic foci of infection, otitis media, hearing loss, for those infected with tuberculosis and for people with latent tuberculosis.

Contraindications to the use of Prevenar vaccine:

  • acute infectious and non-infectious diseases, exacerbations of chronic diseases;
  • Hypersensitivity to previous drug administration;
  • hypersensitivity to the components that make up the vaccine.

Acute infectious and non-infectious diseases, as well as exacerbations of a chronic disease – temporary contraindications; in this case, vaccination is carried out 2-4 weeks after recovery during the period of convalescence or remission. With a mild clinical course ARI , as well as intestinal infectious diseases, it is allowed to carry out immunization immediately after the normalization of body temperature and condition.

Thus, now in Russia there is an opportunity to protect a child from a very common and serious infection from the first year, so that our children, communicating with their peers, are less sick.

90,000 Doctors of St. Petersburg State Pediatric Medical University told what is important to know about pneumonia

World Pneumonia Day is celebrated on 12 November, and Antibiotic Awareness Week kicks off on 13 November. These dates are inextricably linked, because to this day, antibiotic therapy is the main thing in the treatment of this disease.

There is probably no need to explain what pneumonia is: almost every one of us has heard this diagnosis at least once in our life. About 450 million people fall ill with pneumonia every year.About 7 million cases are fatal.

About what pneumonia there are, whether vaccination against this disease helps, and whether it is necessary to take antibiotics prophylactically, we asked Svetlana Petrova, associate professor of the Department of Faculty Pediatrics, St.

Pneumonia is an inflammation of the lung tissue, alveoli. There are many criteria by which experts classify this disease, and one of the most important is the conditions of occurrence.

Community-acquired pneumonia (and there are about 80-90% of them), as the name implies, begins outside the hospital. Hospital pneumonia, on the contrary, occurs already in a medical institution – as a rule, in people with suppressed immunity. And the third group is pneumonia directly related to medical manipulations – they are called nosocomial.

It is important to understand that this disease does not occur “out of the blue”: there are always certain triggers provoking it.

– First of all, this is a decrease in the immune-resistant characteristics of the body.For example, a child is overcooled or has had an acute respiratory viral infection and then the disease continues with complications, the temperature rises, his somatic state changes, and the doctor may suspect that the child is developing pneumonia Natalya Solomatina believes.

According to experts, official science does not divide pneumonia into viral and bacterial.

The so-called viral pneumonias are atypical pneumonias, which have a special course, – says Svetlana Petrova .

In a normal situation, viruses and bacteria in pneumonia act together: the former reduce our immune response, and the latter skillfully take advantage of the situation. Sometimes even the body’s own flora “raises its head” and rebelles against us.

We have our own flora everywhere, but when we are healthy, our immunity copes with it, and where we get sick and our immune response weakens, – explains Svetlana Petrova.

Most often, the disease is caused by a microorganism such as pneumococcus.At the same time, doctors prescribe antibiotic therapy – one that will directly fight the pathogen.

We recommend vaccinating children against this pathogen. This is especially important for babies from birth to 5 years old. In this age group, the highest percentage of deaths from pneumonia caused by pneumococcal infection, – Natalia Solomatina is confident.

Recall that since 2014 this vaccination has been included in the national calendar.

Memo for parents:

The decision to prescribe an antibiotic for any complication can only be made by a doctor.

In no case should the antibacterial preparation be used prophylactically! This is ineffective and can lead to more severe illness. Antibiotics can have a direct toxic effect and worsen the course of any chronic pathology in a child.

You can suspect pneumonia in children by the following signs:

  • persistent temperature rise
  • no effect from the therapy prescribed by the doctor
  • lethargy, feeling unwell, drowsiness
  • refusal to eat
  • rapid breathing
  • cough

If a child’s temperature lasts for more than 5 days with ARVI, the child still feels unwell, it is imperative to call a doctor!

Date of publication: 13.11.2020

Vaccination against pneumonia for adults and children

Vaccination against pneumonia

Pneumonia is one of the infectious diseases, the risk of which can be reduced by timely vaccination. What is it, how does it work and can it protect against pneumonia against the background of COVID-19?

Pneumococcus and its danger

Pneumonia, along with some other dangerous diseases, can be associated with pneumococcus infection.This is a gram-positive bacterium, a representative of the conditionally pathogenic flora of humans. It can be present in the airways, sinuses, and nasal cavities in normal, healthy people without causing symptoms. However, with a decrease in immune defense, especially in childhood and old age, pneumococcus can become pathogenic (1).

According to the World Health Organization, pneumococcal infection is considered the most dangerous of all vaccine-preventable diseases.It causes a number of diseases, including (1):

  • pneumonia – it is pneumococcus that plays a primary role in the development of pneumonia and is considered the most common cause of bacterial forms of the disease;
  • meningitis – inflammation of the lining of the brain associated with pneumococcal infection is very dangerous: the mortality rate in such cases is 5-7 times higher than in meningococcal meningitis;
  • Acute otitis media is one of the most common diseases of the ENT organs in babies, often caused by pneumococcal infection;
  • acute sinusitis – pneumococcus is considered the leading causative agent of acute inflammation of the paranasal sinuses;
  • acute conjunctivitis – along with Staphylococcus aureus, Haemophilus influenzae pneumococcus is one of the main causative agents of acute inflammation of the conjunctiva of the eye in childhood.

Timely vaccination helps to prevent the development of all these diseases.

Pneumococcal vaccine

Vaccine administration is the only way to significantly reduce the incidence of pneumococcal infections, which is why the “pneumococcal vaccine”, as it is sometimes called, is included in national immunization programs. The maximum degree of protection is achieved with the routine administration of the vaccine to all children under 2 years of age (1).

There are two types of pneumococcal vaccines available today: the 23-valent polysaccharide and the 13-valent conjugate vaccine.

Polysaccharide vaccine contains 23 purified pneumococcal polysaccharides. Its disadvantage is the low efficiency of the immune response in babies under 2 years of age (1). Therefore, this vaccine is recommended for all children over 2 years of age and adults who have additional risk factors – chronic lung diseases, diabetes mellitus, heart disease, liver disease and some others (1).

Pneumococcal conjugate vaccine contains 13 purified pneumococcal capsular polysaccharides. It forms a powerful immune response, including in young children. It is this vaccine that is included in the National Vaccination Schedule – it is shown to all children according to the vaccination schedule, as well as to all adults 65 years of age and older.

One of the main contraindications to the administration of these vaccines is severe allergies after previous doses or to vaccine components.

Does ‘pneumonia vaccine’ help with COVID-19?

The causative agent of the new coronavirus infection is known to be the SARS-CoV-2 coronavirus, and pneumonia is one of its most famous complications.With COVID-19, it is not associated with a bacterial infection, including pneumococcal infection: the virus becomes the causative agent. Therefore, vaccination against pneumococcus does not affect the risk of developing pneumonia in patients with new coronavirus infection.

However, it should be borne in mind that in about 7% of cases, a bacterial one joins the viral infection with COVID-19 (2). In this situation, the pneumococcal vaccine may reduce the risk of pneumococcal pneumonia associated with pneumococcal disease.

If the characteristic symptoms of the disease appear – cough, shortness of breath, weakness – you should immediately consult a doctor.

References

1. Baranov A. A. et al. Vaccine prevention of pneumococcal infection in children // Pediatric Pharmacology, 2015. T. 12. No. 5.

2. Langford B. J. et al. Bacterial co-infection and secondary infection in patients with COVID-19: a living rapid review and meta-analysis // Clinical Microbiology and Infection. 2020.

3. Noale M. et al. The association between influenza and pneumococcal vaccinations and SARS-Cov-2 infection: Data from the EPICOVID19 web-based survey // Vaccines.2020; 8 (3): 471.

* This information is for informational purposes only and does not replace a doctor’s consultation

Azithromycin is an important drug

As you know, the spread of COVID-19 took the healthcare system by surprise. There is no specific and definite treatment for this disease, it is not for nothing that a dangerous virus paralyzed the whole world. Traditional antiviral drugs and the well-known antibiotic azithromycin turned out to be ineffective in its treatment.There is an explanation for this: this is a drug that is not only an antibiotic, but also has a pronounced anti-inflammatory effect, thanks to which it was included in the coronavirus treatment protocol. Eraliev Sattar Molybekovich, a pulmonologist, a member of the European Respiratory Society (ERS), told us more about the drug.

– And why was azithromycin included in the COVID-19 treatment protocol?

– COVID-19 came unexpectedly, so at first the doctors tried to use different drugs: antimalarial drugs, drugs for the treatment of HIV (after all, it is also a viral disease).As you know, antibiotics do not work on viruses, but azithromycin, which we know as an antibacterial drug, was included in the original treatment protocol for COVID-19, because it, like its closest relative clarithromycin, also has anti-inflammatory properties.

There is a rare disease – the so-called diffuse panbronchiolitis, when the bronchi continuously secrete a huge amount of mucus that clogs them, and the person gradually dies. Most of the inhabitants of Southeast Asia suffer from it, and until recently it was considered an incurable disease.Japanese doctors, who first discovered the anti-inflammatory properties of azithromycin, used it to treat this disease and obtained excellent results in most patients. Or there is such a pulmonary problem – chronic obstructive pulmonary disease (COPD). Sometimes, in a number of patients, this disease does not respond to treatment, the so-called. basic drugs, according to the decision of the expert council, these patients are prescribed azithromycin for a year. Also, a number of studies have shown that azithromycin still has an immunomodulatory effect, although it is mild.

Therefore, azithromycin was included in the COVID-19 treatment protocol, but, unfortunately, with covid, it turned out to be ineffective, like all other drugs. Nevertheless, antibiotics, including the same azithromycin, are indicated for covid when signs of a secondary bacterial infection appear, which are layered on a viral infection. But I want to note that biomarkers of bacterial pneumonia (C-reactive protein, procalcitonin), it turns out, can increase with COVID-19. This is the insidiousness of coronavirus infection, when the traditional markers for determining where the virus is, where the bacteria are, stopped working.Therefore, in spite of the uncontrolled use of antibiotics, which we, pulmonologists, do not stop fighting with, it is important to consult a doctor in a timely manner. Only their professional approach to the treatment of patients with covid determines a favorable outcome of treatment.

It is important to note that azithromycin, along with other classes of antibiotics, is the drug of first choice in the empiric treatment of bacterial pneumonia. It is used in the initial therapy of atypical pneumonia caused by intracellular pathogens such as chlamydia, mycoplasma.Because azithromycin, unlike many antibiotics, penetrates into the cell, where the causative agent of the disease has “hidden”.

– What contraindications for the use of azithromycin would you single out?

– This is definitely an intolerance to the drug, as well as severe dysfunctions of the liver and kidneys, which often remove drugs from the body.

– Can azithromycin be called safer for humans than other antibiotics?

In general, yes.Antibacterial drugs are divided into more and less safe conditionally. However, there are specially approved groups of first-line and second-line antibiotics for the doctor. There are also reserve drugs (usually more toxic), which are used when the antibiotics of choice are ineffective or intolerant, which is more common in severe stationary infections. Azithromycin and a number of its relatives – macrolide antibiotics – along with amoxicillin are the first-line drugs of choice in the treatment of bacterial pulmonological diseases.But antibiotics of the fluoroquinolone group, although very effective, belong to the second row because of their relative toxicity. They are categorically contraindicated in pregnancy, as they have a teratogenic effect, and for nursing mothers.

Therefore, I want to emphasize once again how dangerous the uncontrolled use of antibiotics, in other words, to the right and to the left, is. Unfortunately, since the days of the USSR, antibiotics could be bought in the pharmacy freely without a prescription. It is precisely because of this that we have irrevocably lost a number of antibiotics and antibacterial drugs.And now in the post-Soviet space, antibiotic resistance, although it is a global problem, is very acute. The weak side of macrolide antibiotics, which includes azithromycin, is precisely the development of rapid resistance to them, therefore it is extremely important that azithromycin, like all macrolides, is used strictly as intended.

– Can you tell us more about the side effects of the drug?

– A reaction from the liver and nervous system is possible, however, it is rarely manifested.In principle, any drug has a side effect. And this does not always lead to drug withdrawal. If, say, it is mild nausea, then you can continue treatment, keeping the symptoms under control. If it is vomiting, then, of course, we cancel the drug. For us, allergic reactions can be a more dangerous manifestation than side effects, and primarily anaphylactic shock. Therefore, before using the drug, it is necessary to conduct a biological test.

Although side effects can also be dangerous for the patient.You’ve probably heard about the effects of azithromycin on the heart, causing rhythm disturbances. For some reason, our media wrote extensively about this. Yes, in 2011, an article by American researchers was published that when using azithromycin, severe arrhythmias can occur, which theoretically can lead to fatal consequences. Subsequent studies in Canada and the Scandinavian countries did not confirm these findings. However, the American Food and Drug Administration (FDA) has recommended that azithromycin manufacturers include a warning in their instructions for use: be careful who has arrhythmia.But there is no supporting evidence that the drug causes death, otherwise the drug would be immediately banned for release.

– Many doctors prescribe probiotics along with antibiotics to prevent dysbiosis. And after azithromycin, is it necessary to restore the intestinal microflora?

– When using azithromycin, the intestinal microbiome may be disturbed. In order to prevent this situation, we prescribe probiotics. While there is no clear evidence that probiotics protect the intestinal flora from the harmful effects of antibiotics, it is better than taking antifungal antibiotics.The occurrence of a fungal infection of the intestine after taking antibiotics has not been described. The most formidable consequence of disturbed intestinal microflora is pseudomembranous colitis, when we sometimes lose patients. Thank God, this is a rare complication and, oddly enough, it is also treated with an antibiotic – vancomycin.

– How is azithromycin combined with other drugs?

– Yes with almost all antibiotics, although care must be taken with antibiotics, which are also excreted through the liver (bile), like azithromycin.We have an unofficial gold standard in pulmonology – the combination of azithromycin with cephalosporin antibiotics. By doing this, we achieve coverage of the widest possible spectrum of pathogenic microbes, in particular in severe pneumonia. Secondly, when during therapy it is necessary to combine 2 drugs, we reduce the dose of each, and the manifestation of side effects sometimes depends on the dose of the drug being administered. At the same time, we exclude a combination with drugs that can provoke arrhythmia.

– What needs to be looked at to find out if azithromycin treatment has affected heart function?

– Violation of the heart rhythm has its own clinic, therefore, we focus on the patient’s complaints.If there is a suspicion that the patient has arrhythmia, we recommend taking an ECG or Holter monitoring.

– Should the liver be checked?

– Of course. The best indicator is the level of liver enzymes.

– Can azithromycin be used by pregnant and breastfeeding women, minors?

– It is possible for lactating and pregnant women, but at the same time, each doctor should take into account – only when the benefits of the medicine outweigh the risk of side effects.Children are allowed from 12 years old, there is a special dosage different from adults. But again I want to note that children and adults often get sick with ARVI, and, no matter how regrettable it is to realize, many begin to use antibiotics on their own, which is categorically unacceptable. Antibiotics are foods that are made to kill other bacteria, reclaiming their place in the environment. And a virus is not a bacterium, it is a completely different class of microorganisms, and antibiotics do not work on them!

– Is azithromycin used in the postcoid period?

– Yes, it does.After a person recovers, the coronavirus leaves a mark, dramatically reducing the immunity of many who have recovered. Therefore, in the postcoid period, there are some bacterial acute infections or exacerbation of chronic infections, in particular the respiratory tract. Here is just the indication for the use of azithromycin.

– Is there a significant difference between the original and the generic of this drug?

– Generics are practically not inferior to the original, this also applies to other antibiotics. In 2016, WHO experts released a bulletin on the rational use of antibiotics, where they emphasized that generic antibiotics are the solution to the problem for developing countries, since the general population cannot afford the original drug.The problem of medicine is the so-called pseudo-genetics, which contain a sub-optimal dose of the drug. Therefore, any generic antibiotic must have an international quality certificate and a registration certificate confirming the effectiveness, safety and admissibility of using the drug on the territory of the Republic of Kazakhstan. For example, the domestic company SANTO has these certificates and registration certificates.

In general, all of the above suggests that the state should regulate the pharmaceutical sector.The patient should not take antibiotics without a doctor’s prescription.

90,000 Plague killed a quarter of the inhabitants of the Earth due to a random mutation

The accidental appearance of just one extra gene in the DNA of the plague bacillus turned it from a harmless bacterium that causes minor digestive problems into a deadly microorganism that has caused the death of more than 100 million people around the world and continues to kill to this day.

The bacterium Yersinia pestis, better known as the plague bacillus, is the cause of several types of plague – bubonic, septic, and pulmonary, which is also called plague pneumonia.It was these three forms of the disease that caused the death of a huge number of people during the epidemics of the 6th-8th and 14th centuries, which went down in history under the names of Justinian’s plague and the black death.

Justinian’s plague manifested itself in the form of separate epidemics over two centuries and claimed about 100 million lives. British historian Philip Ziegler in 1969 estimated the number of victims of the black death at 20-25 million people, which was about a third of the population of Europe at that time.With regard to the estimated number of deaths worldwide, according to the Cambridge Encyclopedia of Paleopathology,

their number exceeded 60 million people, that is, 25% of the world’s population.

Do not think that with the attenuation of the last plague epidemic, the disease disappeared: every year, about 2 thousand people become victims of the bacterium Yersinia pestis , most of whom die. For many years, researchers have been studying the mechanisms of the spread of the plague bacillus, its effect on the body of surviving people, as well as possible ways of treating the disease.

On June 30, Nature Communications magazine published a article by a group of researchers led by Daniel Zimbler of Northwestern University (Illinois, USA), who for the first time in the world managed to find out exactly how the plague bacillus acquired its deadly qualities and turned from a harmless microorganism into a cause deaths of more than hundreds of millions of people.

It turned out that the responsibility for this lies with just one gene, which arose in the bacterial DNA as a result of an accidental mutation.

It is worth noting that the genome of the plague bacillus, which existed about 1.5 thousand years ago, was deciphered by an international group of scientists led by David Wagner from Northern Arizona University, as reported by last year by Lancet Infectious Diseases. Samples of the bacteria were taken from the teeth of two Bavarian residents who died from the Justinian plague in 541-543.

Using experiments on mice, the researchers studied the strains of the plague bacillus, which are the “ancestors” of the bacteria that cause the deadly plague pneumonia.It turned out that the earlier variant of Yersinia pestis affects the lungs, but does not cause either pneumonia, much less pneumonic plague.

This meant that the original, even more ancient strain of the bacterium could be completely safe for humans.

Further research showed that the original version of the plague bacillus Yersinia pseudotuberculosis, which was distributed about 10 thousand years ago, was only capable of provoking minor disorders of the gastrointestinal tract (despite the name, this bacterium has nothing to do with tuberculosis ).Scientists managed to find out that the properties of the bacterium have changed dramatically due to the appearance in its DNA of a gene called Pla. After that, Yersinia pseudotuberculosis turned into Yersinia pestis, capable of infecting the lungs.

Then one amino acid was replaced by the protein encoded by the Pla gene.This was enough for

, more and more strains of the plague bacillus began to develop, each of which was more dangerous than the previous ones and spread rapidly, infecting more and more people and becoming a source of plague pneumonia.

Oddly enough, experts studying the impact of the consequences of plague epidemics on society say that the disease had not only a negative, but also a positive effect on people. So, in 2014, PLoS ONE magazine published a article by the researcher Sharon de Witte from the University of South Carolina, who found out that people who survived the black death epidemic had much better health than people who lived before the outbreak of the plague.

In the course of the work, the remains of more than a thousand people were analyzed – men, women and children who died before the plague epidemic of the XIV century, during and after it. Sharon de Witte paid special attention to the causes of death of people, as well as the condition of their teeth and bones, by which it was possible to judge the state of health of a person during his lifetime. The work results showed:

people who survived the black death epidemic, as well as their descendants quite often lived to be 70–80 years old and generally had much better health than those who lived before the outbreak of the plague.

The author of the work notes that the Black Death was one of the first outbreaks of the medieval plague, so people who lived after it were also at risk of contracting the bacteria Yersinia pestis, , not to mention other diseases typical of that time. Despite this, the body of the average European resident of that time began to withstand the tests that fell to its lot much better.

Nevertheless, the human body has never learned to cope with Yersinia pestis on its own. Modern treatment for plague includes the use of antibiotics such as streptomycin, tetracycline, gentamicin. Despite this, antibiotics are not always able to cope with the disease, and the patient needs support for the respiratory or circulatory system. If this does not help, then the disease is fatal. Scientists believe that a repetition of the black death should not be expected, since there are no reasons or suitable conditions for this.

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