BIO216 Respiratory System Infections - PDF
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Dr. Abdel-Samad
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These are lecture notes for a course on respiratory system infections. It covers topics such as the components of the mucociliary escalator, bacterial and viral infections of the upper and lower respiratory tract, and common conditions and causative agents. It also demonstrates how antigenic variations affect the epidemiology of influenza.
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CHAPTER 14 – RESPIRATORY SYSTEM INFECTIONS BIO216 – Introduction to Microbiology Dr. Abdel-Samad 14-Respiratory System Infections 1 Learning outcomes Outline the st...
CHAPTER 14 – RESPIRATORY SYSTEM INFECTIONS BIO216 – Introduction to Microbiology Dr. Abdel-Samad 14-Respiratory System Infections 1 Learning outcomes Outline the structures of the upper and lower respiratory tracts and describe their functions Describe the components of the mucociliary escalator and explain its importance. Recognize bacterial and viral infections of the upper and lower respiratory tract Compare the distinctive characteristics of strep throat and diphtheria List the strategies helpful in avoiding common colds Recognize the causative agents of bacterial pneumonia Discuss how antigenic variations affect the epidemiology of influenza 14-Respiratory System Infections 2 Upper and lower respiratory tract Major function: gas exchange alsohelpstalk smell The upper respiratory tract include the nose, nasal cavity, pharynx, larynx, epiglottis. s cavity epiglottis Paget The lower respiratory tract includes the trachea (windpipe), bronchi, lungs. cavityopentotheoutside linedwithmucusmembranes 14-Respiratory System Infections 3 Mucous membrane and mucociliary escalator Mucous membranes line the respiratory tract. They are mostly formed by ciliated cells. Coated with mucus (glycoprotein) Traps airborne dust, other particles, microorganisms Mucus is produced by specialized cells called goblet cells, scattered among the cells of the membrane. produce release a The mucociliary escalator is an important defense mechanism: The cilia beat synchronously, continually propelling mucus away from the lungs. The mucus (along with any trapped microbes) is then swallowed and digested Goal Not let infections organisms int thelungs 14-Respiratory System Infections 4 Infections of the upper and lower respiratory tract 2Type Type Bacterial infections Viral infections Upper RTI Upper RTI – Pharyngitis (Strep throat) – Pharyngitis (viral sore throat) – Tonsilitis – Common cold – Diphtheria – Pertussis (whooping cough) Lower RTI Lower RTI – Bronchitis – Viral Bronchitis – Pneumonia – Viral Pneumonia – Tuberculosis – Influenza (Flu) 14-Respiratory System Infections 5 Streptococcal pharyngitis (“Strep throat”) staptthroat One of the most common reasons that people in the US seek medical care Signs and Symptoms Sore throat, difficulty swallowing, fever Red throat, patches of pus and scattered tiny hemorrhages Enlarged lymph nodes in the neck Most patients recover spontaneously after about a week Many infected people have only mild or no symptoms at all Causative agent: Streptococcus pyogenes Blood agar Gram-positive bacteria Spherical shape, grows in chains On blood agar, β-hemolysis completedestruction of RBC's 14-Respiratory System Infections 6 Streptococcal pharyngitis (2) Pathogenesis Virulence factors: t.itiit iEEiataciaottreimmmsyst M protein => adhesion Fibronectin-binding proteins (FBPs) => attach to fibrin Production of enzymes => break down of cellular connections to allow the organism to spread rapidly to other cells Hyaluronic acid capsule => prevents phagocytosis M protein prevents attachment of C3b => prevents phagocytosis Release of C5a peptidase => prevents phagocytosis Transmission Direct contact and respiratory droplet infection Contaminated food all the virulencefactors allowthe bacteria to attach andfiftyally 14-Respiratory System Infections 7 Streptococcal pharyngitis (3) Complications (sequelae) Treatment and prevention 14-Respiratory System Infections 8 Diphtheria (1) Signs and symptoms Begins with a mild sore throat and slight fever, accompanied by extreme fatigue and malaise. In many cases, a whitish-gray pseudomembrane forms on tonsils and throat or in nose; it is a tough layer of dead cells and debris accumulated on the epithelial surface. In severe cases, lymph nodes and surrounding neck tissue can swell dramatically, resulting in the characteristic bull-neck appearance. Heart and kidney failure and paralysis may occur later. Causative agent Corynebacterium diphtheriae Non-motile, non-spore forming, Gram- positive bacteria Stains irregularly because of the presence of storage granules that stain darkly 14-Respiratory System Infections 9 Diphtheria (2) Pathogenesis Little invasive ability, rarely enters the blood or tissues. Disease caused by diphtheria exotoxin releases by the bacteria growing in the throat. The pseudomembrane that forms is made up of deal epithelial cells (killed by the exotoxin) and clotted blood, along with fibrin and leukocytes that accumulate during inflammation. The pseudomembrane may come loose and obstruct the airways, causing the patient to suffocate. The toxin may be absorbed into the bloodstream: access and damage heart, nerve, and kidney tissues. Diphtheria toxin is an A-B toxin: the B subunit attaches to specific receptors on a host cell membrane, and the entire toxin molecule is taken into the cell by endocytosis. The A subunit then separates from the B subunit and stops protein synthesis => cell death 14-Respiratory System Infections 10 Diphtheria (3) Transmission: Humans are the primary reservoir for Corynebacterium diphtheriae. Typically spread by air from infected people. Acquired either by inhalation or from fomites. Treatment and prevention: Injection with antiserum against diphtheria toxin. IMMEDIATELY once disease suspected: the toxin is so powerful that delaying treatment to wait for culture results can be fatal. Antibiotics can prevent further transmission, but have no effect on toxin that has already been absorbed. Even with treatment, about 10% of diphtheria patients die. Can be prevented by immunization with toxoid: vaccine prepared with an inactive form of the toxin. Childhood vaccination DTaP consists of diphtheria and tetanus toxoids along with components of the bacteria causing pertussis (whooping cough). 14-Respiratory System Infections 11 Diphtheria (4) 14-Respiratory System Infections 12 Common Cold (1) It is the most frequent infectious disease in humans It accounts for more than half of upper respiratory tract infections every year. Leading cause of absences from school; and results in an estimate of 150 million workdays missed per year in the US. Signs and symptoms: Colds begin 1 to 2 days after infection and start with malaise, followed by a runny nose, sneezing, coughing, a mildly sore throat, and hoarseness. Nasal secretions initially profuse and watery, but may thicken and become cloudy as cold progresses. Typically no fever, unless secondary bacterial infection occurs. Symptoms typically last about a week, but a mild cough may continue a bit longer. 14-Respiratory System Infections 13 Common Cold (2) Causative agent: Viruses that cause common cold are often called “cold viruses”. Between 30% and 50% of colds are caused by the 100 or more types of human rhinoviruses (“rhino” means “nose”). Rhinoviruses are non-enveloped viruses with a single-stranded RNA genome. Rhinoviruses can usually be grown in cell culture under conditions that mimic the URT (33˚C and a slightly acid pH) They are inactivated at pH < 5.3 => destroyed in stomach. Many other viruses, and some bacterial species can also produce signs and symptoms of the common cold. Why do you think there are no vaccines to prevent the common cold? Such a large number of immunologically different viruses cause colds 14-Respiratory System Infections 14 Common Cold (3) Pathogenesis: Rhinoviruses bind to and infect nasal epithelial cells and may cause the cells to die and slough off. Infection causes cells to release pro-inflammatory cytokines that recruit neutrophils to the area. Other chemical mediators result in sneezing, increased nasal secretions, tissue swelling. Infection can spread to ears, sinuses, or LRT before it is stopped by the immune response. Transmission: Humans are the only source Spread when airborne virus-containing droplets are inhaled or secretions rubbed into eyes or nose. Treatment and prevention: No proven treatment (viruses not affected by antibiotics) Analgesics (painkillers) and antipyretics (fever-reducers) can help reduce symptoms Most important way to prevent the spread of rhinoviruses is handwashing to physically remove viruses. Keep hands away from face, avoid crowded places when respiratory diseases are prevalent. 14-Respiratory System Infections 15 Common Cold (4) 14-Respiratory System Infections 16 Pneumococcal Pneumonia (1) important Pneumonia is a disease of the LRT caused by bacterial, viral, or fungal infection of the lungs. An inflammatory response to the infection generally results in the alveoli of the lungs filling with fluids such as pus and blood. Pneumonia is the leading cause of death due to infectious disease in the United States. Bacterial infections of the LRT are less common than those of the URT, but more fatal. Signs and symptoms of Pneumococcal Pneumonia: After an incubation period of 1 to 3 days, begin abruptly with fever and shaking chills. Severe chest pain, aggravated by each breath or cough; blood from the lungs makes sputum pinkish Most patients improve after 3 to 5 days of antimicrobial treatment, but full recovery can take weeks. Causative agent: causes premonia to Pneumococcal pneumonia is caused by Streptococcus pneumoniae, a Gram-positive diplococcus known as pneumococcus. Inpairs Thick polysaccharide capsule. fromphagocytosis protects escator mucusciliate 14-Respiratory System Infections mentioned 17 Pneumococcal Pneumonia (2) Pathogenesis: a number of virulence factors: opsinization Capsule interferes with C3b => prevents phagocytosis Production of pneumolysin, a membrane-damaging toxin when bacteria die. This potent cytotoxin kills eukaryotic cells and also activates the inflammatory response. finior Fluid As with most severe pneumonias, the inflammatory response leads to an accumulation of fluid and phagocytic cells in the lung alveoli => abnormal shadows on chest X rays of patients. Pneumococci may enter the bloodstream from the inflamed lungs (if patient doesn’t produce enough anti-capsular antibodies), causing three often fatal complications: Sepsis (due to bloodstream infection) Endocarditis (due to an infection of the heart valves) 1 Meningitis (due to an infection of the membranes covering the brain and spinal cord) 14-Respiratory System Infections 18 Pneumococcal Pneumonia (3) Epidemiology: Many healthy people carry encapsulated pneumococci in their throat Bacteria seldom reach the lungs because the mucociliary escalator effectively removes them When mucociliary escalator is impaired, risk of pneumococcal pneumonia rises dramatically Treatment and prevention: Penicillin if given early in the illness highresistance Strains of pneumococci resistant to one or more antibiotics are becoming increasingly common Effective vaccines contain capsular polysaccharides from different pneumococcal serotypes. Pneumonia can be caused by different bacteria: Klebsiella pneumonia by Klebsiella species Mycoplasmal pneumonia (walking pneumonia) caused by Mycoplasma pneumoniae Klebsiella pneumoniae colonies Mycoplasma pneumoniae colonies 19 Influenza Influenza is a good example of the constantly changing interaction between people and infectious agents. Antigenic changes in the influenza viruses are responsible for serious annual epidemics of the disease: almost 20% of the world population gets infected with a flu virus every year. Causative agent: influenza A virus, member of Orthomyxoviruses (RNA viruses) (B, C, D also exist) Influenza viruses are classified into subtypes based on hemagglutinin (HA) and neuraminidase (NA) types. 16 HA and 9 NA antigenic forms are known Ex: H5N1 (Bird Flu), H1N1 (Spanish Flu) New HA/NA influenza subtypes are produced as they make new combinations of these HA and NA proteins 14-Respiratory System Infections 20 Influenza antigenic variation of antigenic Bothantigenicdrift shift are examples variation The antigenic drift is caused by minor changes that occur naturally in influenza virus antigens as a result of mutation => seasonal influenza The antigenic shift is caused by major changes in the antigenic composition of influenza viruses that result from reassortment of viral RNA during infection of the same host cell by different viral strains => pandemic influenza Why is influenza never completely prevented by vaccines? 14-Respiratory System Infections 21 Influenza characteristics mm 22 Review questions Why are upper respiratory tract infections more common than lower respiratory tract infections? What is the infectious agent of streptococcal pharyngitis? Describe its mechanism of pathogenesis. What are some characteristic symptoms of diphtheria? How can you compare treatments of bacterial infections to those of viral infections? What is the most characteristic clinical sign of pneumonia? What is the most common viral infection in the US? How can it be prevented? Define the antigenic variation of the influenza virus and explain how it affects the use of vaccines. 14-Respiratory System Infections 23