Function of the Respiratory System
Gas exchange. Each breath brings in O2, replenished supply in blood, and releases CO2, waste product in cellular metabolism. Movement of vocal cords makes sound and sensors in nose detect odors. Mouth is considered part of digestive tract.

2 general parts of the respiratory system
Upper and lower respiratory tract. Including eyes and ears even though not part of respiratory tract, eyes and nose are important from microbiological standpoint because they serve as 2 main portals of entry to body.

Upper Respiratory Tract
Includes nose and nasal cavity, pharynx, and epiglottis. Mucous membranes line the respiratory tract and are coated with mucus, slimy glycoprotein material that raps air borne dust and other particles. Mucus is produced by goblet cells. Ciliated epithelium lines mucous membranes and have cilia- tiny hairlike projections- along exposed boarder. Cilia beat constantly propelling mucus film out of respiratory tract. Mucus, along with anything captured, is swallowed and digested. This is called mucociliary escalator, which normally keeps lower respiratory tract free of organisms. Smoking, alcohol, narcotic abuse, viral infections impair ciliary movement.
Tonsils are secondary lymphoid organs, located so they come in contact with microbes entering upper respiratory tract.
Table 21.1 shows bacteria that are opportunists and cause disease when defenses are impaired.

Table 21.1 Normal Microbiota of the Upper Respiratory System
Genus – Staphylococcus
Characteristics – Gram positive cocci in clusters
Comments – Facultative anaerobes. Commonly includes potential pathogen Staphylococcus aureus, Inhabits nostrils

Genus – Corynebacterium
Characteristics – Pleomorphic, Gram positive rods; nonmotile; nonspore forming
Comments – Aerobic or facultatively anaerobic. Diphtheroids include anaerobic and aerotolerant organisms.

Genus – Moraxella
Characteristics – Gram negative diplococci and diplobacilli
Comments – Aerobic. Some microscopically resemble pathogenic Neisseria species such as N. meningitidis.

Genus – Haemophilius
Characteristics – Small, gram negative rods
Comments – Facultative anaerobes. Commonly include potential pathogen H. influenzae.

Genus – Bacteroides
Characteristics – Small, pleomorphic, gram negative rods
Comments – Obligate anerobes

Genus – Streptococcus
Characteristics – Gram positive cocci in chains
Comments – Aerotolerant (obligate fermenters). alpha (green hemolysis), beta (clear hemolysis), and gamma (nonhemolytic) types; potential pathogen S. pneumoniae is often present

The Nose and Nasal Cavity
Air enters respiratory system at nostrils and flows into nasal cavity. Cold air enters the nose, blood flows to tissues there immediately increases due to nervous reflexes, warming air to near body temperature and saturating it with water vapor. Nasal entrance contains pathogens and other healthy microbiota. Inside nasal passages, normal microbiota are similar to that of the throat. Infection of nasal passages, usually by viruses, results in rhinitis; inflammation of nasal tissues causes runny nose.

Pharynx (Throat) and Epiglottis
Past the nose, air moves down the pharynx. Inflammation of the throat is pharyngitis, and commonly result of viral infection. Throat is part of respiratory and digestive system.
Small muscular flap, the epiglottis, covers the opening to the lower respiratory tract during swallowing, preventing material from entering. Inflammation of epiglottis, epiglottitis, can be life threatening emergency because the swollen flap can block the airway.
Streptococci, including viridans streptococci (alpha hemolytic) and non hemolytic species are common members of normal microbiota.

Surface of eyes and lining of eyelids are covered by mucus membranes called conjunctiva. Infection is called conjunctivitis. Tear ducts connect eyes to nasal chamber. Infection of tear ducts called dacryocystitis.
Eye is constantly exposed to large number of microorganisms, conjunctiva of healthy people have few bacteria because eye is bathed with lysozyme rich tears and cleaned by eyelids blinking reflux, which wipes eye surface. If unable to colonize, gets swept into tear ducts and nasopharynx. Bacteria found on conjunctiva usually originate from skin and generally unable to colonize respiratory system.

3 parts ; external, middle, and inner ear. External ear protected from microbes by cerumen (ear wax). Middle ear is sterile and connected by eustachian tubes to nasopharynx. Tubes equalize pressure in middle ear and drain mucus secretions, but is also way for bacteria to enter leading to otitis media. Enlargement of adenoids can contribute to middle ear infection by interfering with normal drainage from eustachian tubes. The inner ear, fluid filled, also microbe free. Viruses or bacteria can enter, often following URI, causing labyrinthitis. Skull also has air filled chambers, called sinuses and mastoid air cells. Infections of these called sinusitis and mastoiditis.

Lower Respiratory Tract
Includes larynx (voice box), trachea, bronchi, and lungs. Inflammation of larynx is called laryngitis, and manifest as hoarseness. Trachea (windpipe) is continuation of larynx and branches into two bronchi. Inflammation of bronchi is bronchitis, commonly result of viral infection or smoking. Bronchi branch repeatedly, becoming bronchioles, site of important viral infection called bronchiolitis. Smallest branches of bronchioles end in alveoli, or tiny tin walled air sacs that make up bulk of lung tissue. Inflammation of lungs is called pneumonitis. Pneumotitis that causes alveoli to fill with pus and fluid is called Pneumonia.
Lung tissues have lots macrophages that move in to alveoli and airways to engulf infectious agents, helping prevent pneumonia. Lungs are surrounded by 2 members called pleura; One adheres to lung and other to chest wall and diaphragm. Pleura normally slide against each other as lung expands and contracts. Inflammation of pleura is pleurisy, characterized by severe chest pain. Lower respiratory tract is usually sterile with no normal microbiota.

Bacterial infections of the Upper Respiratory System;
Streptococcal Pharyngitis, Post-Streptococcal Sequelae, Diphtheria, Pinkeye, Earache, and Sinus Infections
Some bacteria can infect the upper respiratory tract. Some generally do not require treatment because bacteria are quickly eliminated by immune system. Others cause infections that require treatment because they are not easily eliminated and cause serious complications.

Streptococcal Pharyngitis aka
Strep Throat
Sore throats are very common and can be because of Streptococcal pharyngitis. A concern about streptococcal infections is risk of post-streptococcal sequelae, which are complications developed after infection.

Streptococcal Pharyngitis – Signs and symptoms
Characterized by sore throat, difficulty swallowing, fever. Throat is red with patches of pus and scattered hemorrhages. Lymph nodes in neck are enlarged. Abdominal pain or headache can occur. Usually there is no cough, runny nose, or weepy eyes. Most recover after a week and most have only mild symptoms.

Streptococcal Pharyngitis – Causative agent
Caused by Streptococcus pyogenes, gram positive coccus grows in chains. Can be differentiated by colonizing it on blood agar – characterized by clear zone of beta-hemolysis. Most species of Streptococcus are alpha-hemolytic producing green clearing colonize on blood, or non hemolytic. Group A streptococcus GAS using Lancefield grouping using antibodies to distinguish the cell wall carbohydrates. Different strains within GAS are distinguished by variations of surface antigen called M proteins, an important virulence factor.

Streptococcal Pharyngitis – Pathogenesis
Streptococcal Pharyngitis has many virulence factors in table 21.2. Proteins in the cell wall allows the bacteria to attach to host cells.

Virulence Factors of Streptococcus pyogenes – M Protiens
M Proteins – Interferes with phagocytosis by causing breakdown of complement C3b, an opsonin.
Important adhesion involved in attachment, antibodies that bind to it prevent infection. There are more than 80 antigenic types of M protein and antibodies to one does not prevent infection by a different type.M protein also interferes with phagocytosis by preventing complement C3b (which would increase phagocytosis) from being deposited on bacterial cell wall.

Virulence Factors of Streptococcus pyogenes – Protien F
Responsible for attachment to host cell. Mediates attachment of S. pyogenes to cells of the throat by adhering to fibrin, protein found on epithelial cells.

Virulence Factors of Streptococcus pyogenes – Tissue degrading enzymes aka DNase, hyaluronidase and proteases
Enhance spread of bacteria by breaking down DNA, proteins, blood clots, tissue, hyauronic acid.

Virulence Factors of Streptococcus pyogenes – Hyaluronic acid capsule
Inhibits phagocytosis
A cloaking device as hyaluronic acid is normal component of human tissue.

Virulence Factors of Streptococcus pyogenes – Protein G
Binds to Fc portion of antibody, thereby interfering with opsonization.
Binds to Fc portion of IgG preventing opsonization by antibodies.

Virulence Factors of Streptococcus pyogenes – C5a peptidase and Streptolysins O and S
Inhibits recruitment of phagocytes by destroying complement C5a.
C5a is normally responsible for attracting phagocytes to site of bacterial infection.

Enzymes that destroy erythrocytes and leukocytes by making holes in cell membranes. Leukocyte destruction inhibits immune response. Erythrocytes destruction causes beta hemolysis.

Virulence Factors of Streptococcus pyogenes – Streptococcal pyogenic exotoxins SPEs
Superantigens responsible for scarlet fever, toxic shock, “flesh eating” faciitis.
SPEs are encoded by bacteriophages. These toxins cause massive activation of T cells resulting in uncontrolled release of cytokines. Many SPE producing strains of S. pyogenes have additional virulence factors allowing them to cause severe invasive disease.

Scarlet fever
Few S. pyogenes strains produce streptococcal pyogenic exotoxins and may develop scarlet fever which causes high fever, roughening of skin texture, pink rash. Rash is found on head, neck, chest and thights and causes the tongue to look ripe like a strawberry, read and spotted. Both skin and tongue may pee..

Epidemiology of Streptococcus pyogenes
Infects only humans. Strains are spread by respiratory droplets and also via food contamination. Carriers can be via nasal and anal and person may be asymptomatic carrier for weeks if they are not treated. People can be long term carriers where infecting strain becomes deficient in M protein and is not a threat to the carrier or others.

Treatment and Prevention of Streptococcus pyogenes
People with fever sore throat should get a throat swab and can be treated in 10 days with penicillin or erythromycin. Treatment within 9 days after onset prevents post streptococcal sequelae. Ventilation and avoiding crowded situations help control and there is no vaccine yet.

Strep Throat Table 21.3
1) S. pyogenes enters by inhalation or ingestion.
2) Pharyngitis, fever, enlarged lymph nodes; sometimes tonsillitis, abscess; scarlet fever with strains with SPEs. Symptoms go away
3) S. pyogenes exits by nose and mouth. Late complications appear
4) Glomerulonephritis
5) Rheumatic fever
6) Neurological abnormalities. Complications subside.
7) Damaged heart valves leak, heart failure develops.
Signs and symptoms – Sore, red throat, with pus and tiny hemorrhages, enlargement and tenderness of lymph nodes in neck; less frequently, abscess formation involving tonsils; occasionally rheumatic fever and glomerulonephritis as sequelae.
Incubation period – 2 to 5 days
Causative agent – S. pyogenes; lancefield group A beta-hemolytic streptococci.
Pathogenesis – Virulence associated with hyaluronic acid capsule and M protien; both which inhibit phagocytosis; protein G binds Fc segment of IgG, protein F for mucosal attachment; multiple enzymes.
Epidemiology – Direct contact and droplet infection; ingestion of contaminated food.
Treatment and prevention – Prevention, avoiding crowds, adequate ventilation, daily penicillin to prevent recurrent infection in those with history of rheumatic heart disease.

Post – Streptococcal Sequelae
Complications that develop after strep throat or other streptococcal infections. Thought of as immune responses to S. pyogenes. Includes acute rheumatic fever and Acute post streptococcal glomerulonephritis.

Acute Rheumatic Fever
Begins approx 3 weeks after recovery from strep.
Signs and symptoms – fever, joint paints, chest pains, rash, nodules under skin. Uncontrollable body movements (chorea) can occur. Carditis, most serious complication, develops in 1/3 of pts and can lead to chronic rheumatic heart disease where one or more heart valves are damage causing leakage resulting in heart failure. Damaged valves are prone to infection, usually by bacterial from normal skin and mouth microbiota, resulting in subacute bacterial endocarditis. Only develops in people who are predisposed to the disease – some MHC class alleles are involved.
Pathogenesis – Unsure, but thought to be autoimmune response involving both humoral and cell mediated immunity. Sometimes, antibodies cross react with host tissue antigens that are similar to pathogen antigens, cause molecular mimicry. Ex; In chronic rheumatic heart disease, molecular mimicry between cardiac myosin and epitopes of strep M protein may result in production of antibodies that bind to both M protein and cardiac myosin. Tissue is then targeted for attack by host own effector T helper cells. T cells release proinflammatory cytokines, causing inflammation leading to permanent damage to local tissues, particularly heart valves.
Outbreaks still occur, but declines because of quick treatment of strep with antibiotics and decreased prevalaence of strains associated with disease. Signs and symptoms subside with rest and anti inflammatory meds. People with acute rheumatic fever damage take penicillin daily for years to prevent reoccurance.

Acute Post Streptococcal Glomerulonephritis
Happens after strep or more likely strep skin infection. Begins 7-21 days after initial infection.
Signs and symptoms – Fever, fluid retention, high bp, blood and protein in urine (looks brownish). There is no bacteria in urine or diseased kidney tissues – it has been eliminated from throat by bodys immune response by time symptoms occur. Damage to kidneys is due to inflammatory reaction by streptococcal antigens that accumulate in kidney glomeruli. Antibodies are bound to antigens causing immune complexes to activate complement system.

Deadly toxin mediated disease. Relatively rare because childhood immunizations.

Signs and symptoms – Diphtheria
Begins with mild sore throat, fever, with extreme fatigue and malaise. Dramatic swelling of neck occurs. White-grey pseudomembrane forms on tonsils and throat or in nasal cavity. Heart and kidney failure and paralysis may occur.

Causative Agent – Diphtheria
Corynebacterium diphtheriae, pleomorphic, nonmotile, nonspore forming, gram positive rod. Are club shapes and occur side by side. Most strains release diphtheria toxin, powerful exotoxin responsible for serious symptoms of disease. Gene for toxin carried by specific lysogenic bacteriophage. Identification involves medium with special chemical that causes bacteria to form black colonies.

Pathogenesis – Diphtheria
Has little invasive ability and rarely enters blood or tissues. Caused by exotoxin released by bacteria growing in throat. Pseudomembrane forms and made of dead epithelial cells and clotted blood, along with fibrin and leukocytes that accumulate with inflammation. Membrane can be loose and obstruct airway causing pt to suffocate. Toxin can be absorbed in blood allowing access to heart, nerves and kidneys.
Is an A-B toxin. B subunit attaches to specific receptors on host cell membrane and entire toxin molecule taken into cell by endocytosis. Some tissues do not have receptors and others do which explains why some are not affected by toxin. When toxin is in the cell, A separates from B and A becomes active enzyme and catalyses chemical reaction that inactivates elongation factor 2 EF-2, which is required for movement of eukaryotic ribosome on mRNA. This stops protein synthesis and cell dies. A is not used up so one or 2 molecules can inactivate nearly all cells EF-2.

Epidemiology – Diphtheria
Humans are primary reservoir. Typically spread by air form infected people. Acquired via inhalation or formites. Can cause cutaneous diphtheria and chronic skin ulcers.

Treatment and Prevention – Diphtheria
Treated with antiserum against diphtheria toxin ASAP. Delayed treatment can be fatal. Bacteria are sensitive to antibiotics like penicillin or erythromycin, but treatment only stops transmission of disease and has no effect of toxin that is absorbed. Caused by toxin as opposed to bacterial invation, can be prevented by immunization with toxoid. Toxid causes body to produce antibodies that neutralize toxin.

Diphtheria Table 21.4
1) Corynebacterium diphtheriae enters by inhalation
2) Infection established in nasal cavity and/or throat
3) Toxin release, pseudomembrane forms
4) Toxin causes paralysis, damages heart muscle, kidney, nerves
5) Membrane may come loose and obstruct breathing
6) Exit from body by respiratory secretions.
Signs and symptoms – Sore throat, fever, fatigue, malaise; pseudomembrane forms on tonsils and throat or in nose; paralysis, heart and kidney failure.
Incubation period – 2 to 6 days
Causative agent – Corynebacterium diphtheriae, an A-B toxin producing, nonspore forming , gram positive rod
Pathogenesis – Infection in UR tract; exotoxin release and absorbed in blood, toxin kills cell by interfering with protein synthesis; effect is on cells that have receptors for toxin- mainly heart, kidney and nerve tissue
Epidemiology – Inhalation of infectious droplets, direct contact with pt or carrier, indirect contact with contaminated articles
Treatment and prevention – Treat is antitoxin, erythromycin to prevent transmission. Prevent by immunization with diphtheria toxoid

Pinkeye, Earache, and Sinus infections
Infections of eye surface (conjunctivitis), middle ear , (otitis media), and sinuses (sinusitis), are common and often occur together with same causative agent. Media is common in children. Pinkeye is spread easily. Sinusitis is common in adults and children.

Signs and symptoms – Pinkeye, Earache, and Sinus infections
Pinkeye – tears, redness of conjunctiva, swollen eyelids, sensitivity to bright light, large amounts of pus.
Otitis media – severe earache. Intense pain often causes vomiting. Fever is mild or absent.
Sinusitis – Facial pain and pressure sensation in region of involved sinus. Headache and severe malaise. Thick green nasal discharge may contain pus and blood can develop.

Causative Agents – Pinkeye, Earache, and Sinus infections
All caused by 2 common bacterial pathogens 1) Haemophilus influenzae, tiny gram neg rod or 2) Streptococcus pneumoniae, gram pos encapsulated diplococcus.
Strains that infect eye have adhesion that allow to attach to epithelium. Conjunctivitis can be caused by different bacteria and some can be caused by environmental microbes that contaminate eye medications and contact lens solutions.
Otitis media and sinusitis can be caused by other bacteria and 1/3 cases are caused by respiratory viruses, explaining why some infections do not respond to antibiotics, which has no effect on viruses.

Pathogenesis – Pinkeye, Earache, and Sinus infections
Conjunctivitis – unknown but organisms probably inoculated directly onto conjunctiva from airborne respiratory droplets or rubbed from contaminated hands. They resist lysozymes. Attachment aided sometimes by degradation of mucin, protective component of epithelial surface mucus. After attachment, bacteria release proteases, collagenases, and coagulases, combined with toxins that further damage tissue.
Otitis media and sinusitis – Preceded by infection of nasal chamber and nasopharynx that probably spread to eustachian tube. Infection damages ciliated cells, causing inflammation and swelling. Because damaged eustachian tube cannot move secretions from middle eye, fluid and pus collect behind eardrum, increases pressure, causing ear ache. Drum may perforate,discharging blood or pus. With treatment, holes in eardrum heal quickly. Pressure in middle ear may force infected material into mastoid air cells, causing mastoiditis. Fluid behind eardrum can impair hearing. Both infections can spread to brain coverings, causing meningitis.

Epidemiology – Pinkeye, Earache, and Sinus infections
Ecological factors in appearance and spread of infections caused by H. influenzae and S. pneumoniae are unknown. Virulence of bacteria, crowding, and presence of respiratory virus are important factors in epidemics. Preceding or simultaneous viral illness is common in otitis media and sinusitis; virus likely damages mucocilary mechanism that normally protects against infection. Conditions that cause inflammation of nasal mucosa, viral infections, nasal allergies, exposure to air pollution and cigarette smoke, play a role in infections. Sinusitits affects adults and older children with more developed sinuses.

Treatment and Prevention – Pinkeye, Earache, and Sinus infections
Conjunctivitis is treated with eyedrops or ointments contain antibacterial meds. Amoxicillin is effective against otitis media and sinusitis. When antibiotics used properly, can reduce mastoiditis and meningitis. Decongestants and antihistamines are ineffective and can be harmful as they reduce inflammatory response. Conjuncitivits is highly contagious. Otitis media can be decreased if given flu vaccine. Surgical removal of enlarged adenoids improves drainage from eustachian tubes and can help prevent recurrent infections. Chronically malfunctioning eustachian tubes and hearing loss, tiny plastic tubes are inserted through eardrum so pressure can equalize.

Viral infections of Upper respiratory system – Common Cold
Most frequent infectious disease in humans.
Signs and symptoms – Malaise, scratchy or mild sore throat, runny nose, cough, hoarseness. Nasal secretions initially profuse and watery, the thicken to be cloudy and greenish. No fever unless secondary bacterial infection occurs. Gone within week, but mild cough sometimes longer.

Causative agents – Common Cold
Referred to as cold viruses. 30 to 50% of colds caused by 100 or more types of human rhinoviruses. Members of picornavirus family (small RNA viruses), group of naked viruses that have single stranded RNA genome. Rhinoviruses cannot tolerated low pH so are destroyed in the stomach.

Pathogenesis – Common Cold
Attach to specific receptors on respiratory epithelial cells and infect those cells. Replication cycle produces tons of virons and released to infect other cells. Ciliary motion in infected cells stops and cells may die and slough of. Damage causes release of pro inflammatory cytokines and stimulates nervous reflexes, resulting in increased nasal secretions, tissue swelling that partially or completely obstructs airways and sneezing. Later in inflammatory response, blood vessels dilate, allowing plasma to ooze out and leukocytes to migrate to infected area. Secretions from area may contain pus and blood. Infection stopped by innate and adaptive responded, but may spread to ears, sinuses, or even lower respiratory tract.

Epidemiology – Common Cold
Humans only source of cold virus. Contracted when airborne virus containing droplets inhaled or rubbed onto eyes or nose. Virus introduce in eye quickly enters into nasal passage. Lots of symptoms = more contagious. Emotional stress can double risk of cold, but cold temperatures show no relationship with developing a cold

Treatment and Prevention – Common Cold
No proven treatments for cold. Pain killers and fever reducers like aspirin and ibuprofen can reduce symptoms, but evidence shows these prolong symptoms and delay antibody production. Prevent by washing hands, keep hands away from face, avoiding crowds, avoid people with colds.

The Common Cold Table 21.5
Signs and Symptoms – Scratchy throat, nasal discharge, malaise, headache, cough
Incubation period – 1 to 2 days
Causative agent – Mainly rhinoviruses, more than 100 types, some bacteria
Pathogenesis – Viruses attach to respiratory epithelium, starting infection that spreads to adjacent cells; ciliary action ceases and cells slough; mucus secretion increases, and inflammatory reaction occurs; infection stopped by interferon release, cell mediated and humoral immunity.
Epidemiology – Inhalation of infected droplets, transfer of infectious mucus to nose or eye by contaminated fingers; children initiate many outbreaks in families because lack of care with nasal secretions
Treatment and prevention – No generally accepted treatment except for control of symptoms. Handwashing; avoiding people with colds and touching face

Adenoviral Respiratory Tract Infections
Signs and symptoms – Fever, very sore throat, severe cough, swollen lymph nodes of neck, pus on tonsils and throat, sometimes conjunctivitis; less frequently pneumonia
Incubation period – 5 to 10 days
Causative agent – Adenoviruses more than 45 types. Viruses are nonenveloped with double stranded DNA.
Pathogenesis – Virus multiplies in host cells; cell destruction and inflammation occur; Virus attaches receptors near basement membrane and genome transports into host cell nucleus for multiplying. Has mechanisms to avoid host defenses including delaying apoptosis, blocking interferon function and interfering with antigen presentation by MHC class I molecules.
Epidemiology – Inhalation of infected droplets; possible spread from gastrointestinal tract. Can survive in environment.
Treatment and Prevention – No treatment except relief of symptoms. No vaccine. Avoided by handwashing, avoiding people with symptoms.

Bacterial infections of lower respiratory system
Less common than in upper respiratory because they are stopped by immune defenses at portal of entry. Generally more life threatening.

Pneumococcal Pneumonia
Signs and Symptoms – cough, fever, single shaking chill, rust colored sputum from degraded blood, shortness of breath, chest pain
Incubation period – 1 to 3 days
Causitive Agent – Streptococcus pneumoniae, gram positive diplococcus. It has thick polysaccharide capsule, which is responsible for organisms virulence.
Pathogenesis – Inhalation of encapsulated pneumococci, multiply and cause inflammatory response. Response affects nerve endings in pleura, causing pain or pleurisy. Bacteria are resistant to phagocytosis because capsule interferes with C3b. Pneumococcal surface protein (PspA) also interferes with C3b action. Also produces pneumolysin, membrane damaging toxin that destroys ciliated epithelium. Inflammatory response leads to accumulation of serum and phagocytic cells in lung alveoli, causing DIB. Sputum coughed from lungs increases in amount and contains pus, blood and many pneumococci. Can enter blood from inflamed lungs cuasing sepsis, endocarditis, and meningitis.
Epidemiology – 30% healthy carry encapsulated pneumococci in throat and seldom reach lungs because mucociliary escalator removes them. Infection increases when defense impaired with alcohol, narctoics, and viral respiratory infections.
Treatment and Prevention – Most cured with Penicillin or erythromycin if given early. Vaccine

Klebsiella Pneumonia
Signs and symptoms – Chills, fever, cough, chest pain, grossly bloody, mucoid sputum
Incubation period – 1 to 3 days
Causative Agent – Klebsiella pneumoniae, an enterobacterium
Pathogenesis – Aspiration of colonized mucus droplets form throat. Specific adhesins aid colonization and capsule is essential virulent factor, interfering with action of complement system component C3b. Destruction of lung tissue and abscess formation common; infection spreads via blood to other bloody tissues.
Epidemiology – Often resistant to antibiotics, and colonize individuals who are taking them. Klebsiella sp. and other gram neg rods are common causes of fatal healthcare associated pneumonias.
Treatment and prevention – Treated with a cephalosporin with an aminoglycoside. Many strains produse beta lactamase (resistant to beta lactam meds). Strains are also extended spectrum lactamases ESBLs making resistant to many cephalosporins. No vaccine available.

Mycoplasma Pneumonia or Walking Pneumonia
Signs and symptoms – gradual onset of cough, fever, sputum production, headache, fatigue, and muscle aches
Incubation period – 2 to 3 weeks
Causative agent – Mycoplasma pneumoniae; lacks cell wall
Pathogenesis – Cells attach to specific receptors on respiratory epithelium; inhibition of ciliary motion and destruction of cells follow. Inflammation response characterized by accumulation of lymphocytes and macrophages causes the walls of bronchial tubes and alveoli to thicken.
Epidemiology – Inhalation of infected droplets; mild infections common and foster the spread of disease.
Treatment and prevention – Treated with tetracycline or erythromycin. No vaccine available; avoiding of crowding in schools and military facilities advisable.

Pertussis aka Whooping Cough
Signs and symptoms – 3 stages Catarrhal stage or inflammation of mucus membranes includes runny nose, sneezing, low fever and cough.
Paroxysmal stage or sudden attack has frequent burst of violent uncontrollable coughing. Coughing spasm followed by forecull attempts to inhale. Inspired air is gasped in causing characteristic whoop of disease.
Convalescent stage – No longer contagious. Coughing attacks become less frequent and person slowly recovers.
Incubation period – 7 to 21 days
Causative agent – Bordetella pertussis, tiny gram neg rod
Pathogenesis – Colonization of surfaces of upper respiratory tract and tracheobronchial system . Colonization aided by filamentous hemagglutinin FHA, a pilus that extends from the bacterial surface and pertussis toxin PTx, a protein that functions as adhesin and toxic effects. Pertussis toxin is A-B exotoxin. B attaches to receptors on host cell, A moves through cytoplasmic membrane of host cell. It activates membrane bound regulatory protein that controls production of cAMP leading to high cAMP which interferes with cell signaling pathways. Ciliary action slowed; toxins released by B. pertussis cause death of epithelial cells and increased cAMP; fever, excessive mucus output, and rise in number of lymphocytes in bloodstream. Tracheal cytotoxin is a fragment of peptidoglycan that pertussis releases in growth cuasing host cell to release fever inducing cytokine , interlukin- 1. Its toxic to ciliated epithelial cells cuasing decline ciliary action and death. Combo of inc mucus and dec ciliary action results in cough.
Epidemiology – Inhalation of infected droplets highly contagious; older children and adults have mild symptoms.
Treatment and prevention – Erythromycin, somewhat effective if given before coughing spasms start, eliminates B. pertussis. Acellular vaccine DTaP, for immunizations of infants and children.

Tuberculosis – Pathogenesis
1) Airborne Mycobacterium tuberculosis cells are inhaled and lodge in the lungs
2) The bacteria are phagocytized by lung macrophages and multiply within them, protected by lipid containing cell walls and other mechanisms. ( Alveolar macrophages ingest bacteria, bacteria survive and multiply. Additionally macrophages and lymphocytes recruits and foamy macrophages develop. Fibrous capsule surrounds macrophages, excluding lymphocytes. Infected macrophages die, releasing mycobactera creating caseous necrosis. Tubercle ruptures, releasing live bacteria into airway) Lymphocytes wall off area from surronding tissue. Granulomas is bodys response to substance that resist destruction and removal by phagocytosis and are called tubercles in tuberculosis.
3) Infected macrophages are carried to various parts of the body such as the kidneys, brain, lungs, and lymph nodes; release of M. tuberculosis occurs.
4) Delayed hypersensitivity develops; wherever infected M. tuberculosis has lodged, an intense inflammatory reaction develops.
5) The bacteria are surrounded by macrophages and lymphocytes; growth of the bacteria ceases.
6) Intense inflammatory reaction and release of enzymes can cause caseation necrosis and cavity formation.
7) With uncontrolled or reactive infection, M. tuberculosis exits the body through the mouth with coughing.

Tuberculosis continued
Signs and symptoms – Chronic fever, weight loss, cough, sputum production. Typically is asymptomatic immune response, but not eliminated entirely so healthy person is left healthy but with latent tuberculosis infection LTBI. Later in life person may develop acute tuberculosis disease ATBD.
Incubation periods – 2 to 10 weeks
Causative agent – Mycobacterium tuberculosis; unusual cell wall with high lipid content. Very slow growth.
Pathogenesis – Colonization of the alveoli incites inflammatory response; ingestion by macrophages follows; organisms survive ingestion, cause inflammatory response for more macrophages aka more reproduction and are carried to lymph nodes, lungs, and other body tissues; tubercle bacilli multiply; granulomas form.
Epidemiology – Inhalation of airborne organisms; latent infections can reactivate.
Treatment and prevention – Treatment; two or more antitubercular medications given simultaneously long term, such as isoniazid (INH) and rifampin; DOTS; BCG vaccination preventive but not used in the United States; tuberculin (Mantoux) skin test for detection of infection, allows early therapy of cases; treatment of all high risk cases including young people with positive tests and individuals whose skin test converts from negative to positive.

Leginonaires; Disease
Signs and symptoms – Muscle aches, headache, fever, cough, shortness of breath, chest and abdominal pain, diarrhea
Incubation period – 2 to 10 days
Causative agent – Lagionella pneumophila, gram neg bacterium that stains poorly in clinical specimens
Pathogenesis – Organism multiplies within phagocytes.heir surface protein, macrophage invasion potentiator Mip, aids entry into macrophages and cells also bind to C3b.Survive in macrophage by preventing phagosome-lysosome fusion. Released with death of cell; necrosis of cells lining alveoli; inflammation and formation of microabscesses
Epidemiology – Orginates maily from warm water contaminated with other microorganisms, such as found in air conditioning systems.
Treatment and prevention – Treatment ; erythromycin and rifampin. Avoidance of contaminated water aerosols; regular cleaning and disinfection of humidifying devices.

Viruses of lower respiratory tract – Influenza
1) Influenza virus is inhaled and carried into lungs
2) Viral hemagglutinin attaches to specific receptors on ciliated epithelial cells, the viral envelop fuses with epithelial cell, and virus enters by endocytosis.
3) Host cell synthesis is diverted to synthesizing new virus
4) Newly formed virons bud from infected cells; they are released by viral neuraminidase and infect ciliated epithelium, mucus secreting, and alveolar cells.
5) Infected cells ultimately die and slough off; recover of mucociliary escalator may take weeks
6) Secondary bacterial infection of lungs, ears , and sinuses are common
7) Virus exits with coughing

Influenza aka Flu
Signs and symptoms – Fever, muscle aches, lack of energy, headache, sore throat, nasal congestion, cough
Incubation period – 1 to 2 days
Causative agent – Influenza virus, an orthomyxovirus. Contains 2 glycoproein spikes Hemagglutinin antigen HA and neuraminidase antigen NA, which have role in viral pathogenesis. HA allows virus to recognize and attach to receptors on epithelial cells. These cause hemagglutination. NA is enzyme that helps in release of newly formed virions from host cell. Virons bud out of cell but remain bound to surface receptors and NA destroys them allowing virions to leave infected cell to spread. Subtypes are given numbers of different subtypes of HA and NA spikes ex H1N1
Pathogenesis – Infection of respiratory epithelium; cells destroyed and virus released to infect other cells. Secondary bacterial infection results from damaged mucociliary escalator.
Epidemiology – Antigenic drift and antigenic shift prevent immunity
Treatment and prevention – Amatadine and rimantadine are sometimes effective for preventing type A but not type B virus disease; neuraminidase inhibitors effective against both A and B virus. These meds somewhat effective for treatment when given early. Vaccines are 80 to 90% effective.

Antigenic drift and Antigenic shift
Caused by minor mutations in genes that code for HA and NA antigens. Mutations happen during normal viral replications often causing change in 1 AA but occur frequently.

Uncommon but more dramatic change occurs as result of viral genome reassortment. Genome is segmented, meaning viral proteins are encoded on 8 different RNA segments. if 2 different strains infect a cell at the same time, progeny produced can have RNA segments from either viruses. Can be a problem because virus can emerge with segment from different infection strand so pig and human.

Respiratory Syncytial Virus (RSV) infections
Signs and symptoms – Runny nose, cough, fever, wheezing, difficulty breathing, dusky color
Incubation period – 1 to 4 days
Causative agent – RSV, a paramyxovirus that produces syncytia, clumps of fused cells
Pathogenesis – Sloughing of respiratory epithelium and inflammatory response plug bronchioles, cause bronchiolitis; pneumonia results from bronchiolar and alveolar inflammation, or secondary infection.
Epidemiology – Yearly epidemics during cool months, readily spread by otherwise healthy older children and adults who often have mild symptoms, no lasting immunity
Treatment and Prevention – No satisfactory antiviral treatment. No vaccine. Preventable by injections of immune serumglobulin or monoclonal antibody.

Hantavirus Pulmonary Syndrome
Signs and symptoms – Fever, muscle aches, vomiting, diarrhea, cough, shortness of breath, shock
Incubation period – 3 days to 6 weeks
Causative agent – Sin Nombre and related hantaviruses of the bunyavirus family
Pathogenesis – Viral antigen localizes in capillary walls in lungs; inflammation. Inflammatory response causes capillaries to leak large amounts of plasma into lungs, suffocating the pt and causing bp to drop.
Epidemiology – Zoonosis likely to involve humans in proximity to increasing mouse populations; generally no person to person spread
Treatment and Prevention – Avoid contact with rodents; seal access to houses, food supplies; good ventilation, avoid dust, use disinfectants in cleaning rodent contaminated areas. No proven antiviral treatment.

Fungal infections of the lung – Coccidioidomycosis aka Valley Fever
Signs and symptoms – fever, cough , chest pain, loss of appetite and weight; less frequently, painful nodules on extremities, pain in joints; skin , mucous membranes, brain, and internal organs sometimes involved.
Incubation period – 2 days to 3 weeks
Causative agent – Coccidioides immitis, dimorphic fungus
Pathogenesis – After lodging in lung, arthrospores develop into spherules that mature and discharge endospores, each of which then develops into another spherule; inflammatory response damages tissue; hypersensitivity to fungal antigens causes painful nodules and joint pain.
Epidemiology – Inhalation of airborne C. immitis spores with dust from soil growing the organism. Occurs only in certain semi arid regions of western hemisphere
Treatment and prevention – Treatment is amphotericin B and Fluconazol or Itraconazol. Prevention by dust control methods such as grass planting and watering.

Histoplasmosis aka Spelunkers Disease
Signs and symptoms – Mild respiratory symptoms; less frequently, fever , chest pain cough, chronic sores
Incubation period – 5 to 8 days
Causative agent – Histoplasma capsulatum, dimorphic fungus
Pathogenesis – Spores inhales, chage to yeast phase, multiply in macrophages; granulomas form; disease spreads in individuals with AIDS or immunodeficiencies
Epidemiology – Fungus prefers to grow in soil contaminated by birds or bat droppings. Spotty distribution in many countries.
Treatment and Prevention – Treatment; amphotericin B and Itraconazole for serious infections. Prevented by avoiding soils contaminated with chicken, bird, or bat droppings.

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