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.
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
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.
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.
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.
Streptococcal Pharyngitis, Post-Streptococcal Sequelae, Diphtheria, Pinkeye, Earache, and Sinus Infections
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.
A cloaking device as hyaluronic acid is normal component of human tissue.
Binds to Fc portion of IgG preventing opsonization by antibodies.
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.
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.
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
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.
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.
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.
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.
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
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.
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.
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.
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.
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
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.
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
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.
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.
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.
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.
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.
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.
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
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.
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.
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.
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.
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.
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.