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Upper Respiratory Tract Infections BACTERIAL AND FUNGAL: Location of Infection Causative Agent ORAL INFECTION Oral Anaerobes Virulence Factors Lymphocyte Activators: induce inflammatory response Etiology Caused by normal flora Polymicrobic Complement activation/PMN content release: tissue damage Form localized abscesses Pathogenesis Chronic Marginal Gingivitis: between teeth and gums -PMNs/lymphocytes enter CT attached to tooth (inflammation) -No bacterial invasion -Can occur in 2 weeks w/o tooth care Periodontitis: teeth and supp. tissue -Progressive gingivitis (bone resorption, loss of ligament, loss of entire tooth) -Bacterial invasion may occur Actinomyces israelii -- Normal flora: colonizes mucosal surfaces (oropharynx to lower intestine) Endogenous infection: only occurs upon penetration of epithelial barrier (low O2 tension) Viridans Streptococci Candida albicans Glucans: polysaccharides that permit attachment to teeth Adhesion: mannoprotein binds fibronectin receptors Invasion: -Invasive hyphae bind fibronectin, collagen, and laminin -Proteases and elastases Normal flora: of oral and nasopharyngeal cavity Predisposing Factors: -Abx (diminish normal flora) -Compromised immune system -Disruption of mucosa (ie. catheter or cancer chemotherapy) -Diabetes (increased glucose and surface R) Acute Necrotizing Ulcerative Gingivitis (Trench Mouth): -Ulceration of gingiva (bone resportion and tooth loss) -Bacterial invasion occurs Follows mouth trauma: -Inflammatory sinuses fill with pus and bacteria from initial site of infection -Slow progressing Thoracic Actinomycosis: may occur if sinus extension or aspiration occurs Polymicrobic infection: also GNRs in sinuses Dental Cavities: S.mutans Subacute Bacterial Endocarditis: tooth extraction leads to transient bacteremia and colonization of damaged heart valves Stomatitis: inflammation of the oral cavity -Oral Thrush: multiple white plaques loosely adherent to tongue or palate -Inflammatory patches on esophagus Clinical ID Diagnosis: via Sx Mixed anaerobes not differentiated Abscesses may be sampled: must be cultured in anaerobic conditions -Mostly G(-) rods and PMNs Shape: G(+) filamentous rod- looks like fungi Culture: -Sulfur granules (yellow granules- diagnostic) -Anaerobic or microaerophilic -Slow growth Shape: G(+) cocci Biochemical: -Catalase (-) -No Lancefield group Specimen: scrapings of infected mucosa -KOH or Gram stain shows budding round yeast with hyphae -Germ tube formation EAR/SINUS INFECTION Streptococcus pneumoniae Polysaccharide Capsule: primary VF -Anti-phagocytic -Prevents complement deposition -Abs to it confer immunity Cell Wall TA and PG: inflammation Predisposition for URTIs: -High carriage rate Predisposition for Acute Otitis Media: -Viral infection -Allergies -Infant (short/pliant Eustachian tubes) Acute Otitis Media: middle ear inf. -Eustachian tube inflammation -Bacteria enters middle ear from nasopharynx Sinus Infection: acute and chronic sinusitis in all ages Needle Aspiration: difficult cases -OM: pus behind tympanic membrane -S: sinus wall puncture or catheterization Predisposition for Sinusitis: -Viral Infection -Allergies -Anatomical blockage Haemophilus influenzae Polysaccharide Capsule: primary VF -Antiphagocytic -Antigenic variation -Polyribitol phosphate capsule with 6 serotypes (a-f) IgA Protease: colonization Non-Pilus Adhesins: tissue tropism (direct to mucosal surfaces) PHARYNX INFECTION Streptococcus pyogenes (GAS) Facilitating Immune Evasion: M protein: -Anti-phagocytic -80 different serotypes -Antigenic variation Protein G: -Binds Fc portion IgG Abs Hyaluronic Acid Capsule: -Antiphagocytic Facilitating Colonization: Protein F: -Bind nasopharyngeal epithelium -Regulated by O2 levels M Protein: -Binds epidermis (impetigo) Normal Flora: high carriage rate in URT -Most have no capsule (nontypeable) Predisposing Factors for Otitis Media/Sinusitis: -Viral infection -Displacement of flora to sterile sites Transmission: person to person spread via droplets Diagnosis: clinical exam -OM: swollen tympanic membrane (pus formation) -S: symptoms and radiography Otitis Media and Sinusitis: -Most causes of OM are non-typeable (therefore, not affected by Hib vaccine) -Common in kids under 5 -If caused by Hib, can lead to meningitis Shape: G(+) lancet shaped diplococcic Biochemical: -No Lancefield group -Optochin sensitive Diagnosis: clinical exam Needle aspirate: in difficult cases (as above) Shape: G(-) coccobacillus Growth: fastidious (needs factor X and V) Most common bacterial cause of pharyngitis: but usually due to viruses Scarlet Fever: may occur with pharyngitis (due to Spe) -Rash (Face trunk and extremities) -Strawberry tongue Post-Streptococcal Sequelae: -Rheumatic Heart Disease (~3 weeks after pharyngitis) -Acute Glomerulonephritis (more commonly following skin infection) Capsular serotyping Throat swab of tonsils and pharynx: -Culture on BAP for Bhemolysis -Aggulitination test for Lancefield group A (rapid) Biochemical Tests: -Catalase (-) -Bacitracin sensitive High titers anti-SLO Abs: in patients with rheumatic fever Corynebacterium diphtheria Exotoxins: SLO: oxygen labile SLS: oxygen stable -B-hemolysis -Form pores in cell membranes Spe A-C (Erythrogenic/Scarlet Fever Toxins): -SpeA only produced by some lysogenized GAS -Superantigens (similar to Staph exotoxins) -Cytokine release -Toxic Shock Like Syndrome Diphtheria Toxin: only VF -AB toxin (polypeptide with nicked chain between A and B) -B binds EGF precursor on cell membrane -A is enzymatic subunit (ADPribosylates elongation factor 2 to halt translation) Tox Genes: -Carried by bacteriophages -Synthesis negatively regulated by iron (production is on when iron is low, such as in human host) Bordetella pertussis (Whooping Cough) Filamentous Hemagglutinin (FHA) and Pili: -Adhesin for binding mucosal epithelial cells -Directs organism to MØ -Agglutinates RBCs Pertussis Toxin (Ptx): -AB toxin -B subunit made of 5 non-identical subunits (binding) -A subunit (enzymatic) ADPribosylates Gi, preventing Gs from being turned off (increase cAMP) Invasive Adenylate Cyclase: -Enters cell directly to ↑ cAMP -Requires calmodulin Rare in US: due to immunization Bacterial Toxinosis with NO invasion: -DT responsible for ALL pathogenesis Diagnosis: based on clinical symptoms Only lysogenized strains produce DT: required for pathogenesis (can lysogenize in vivo and convert to toxin producing strain) Manifestations of DT Cytotoxicity: -Pseudomembrane formation (can cause suffocation) -Systemic manifestations (organ damage to heart and CNS) Throat swab: difficult because it is a normal resident flora in many people Transmission: droplet spread or contact with cutaneous infection/fomite -Can have asymptomatic carriers of toxinogenic strains Only infects humans: often seen in infants and preschoolers Transmission: HIGHLY contagious; droplet spread -Adults can be carriers and a source of infection for unvaccinated newborns Shape: G(+) club shaped rods (remain attached after division-“Chinese Letters”) Whooping Cough: acute bronchitis with violent/paroxysmal cough -Can also cause edema and hemorrhages in the brain Deep Nasopharyngeal Cultures: needs to be cultured immediately (does not survive well) Pathogenesis: -FHA directs organism to adhere to bronchial epithelium -Toxins kill ciliated cells and interfere with phagocytosis -Systemic effects due to TOXIN -Local inflammatory response to BACTERIA in bronchi leads to cough Growth: -CAP with cephalosporins (to inhibit G positive) Shape: G(-) coccobacillus (resembles H.flu) Direct fluorescent Ab detection: should still confirm with culture Lower Respiratory Tract Infections BACTERIAL AND FUNGAL: Causative Agent Virulence Factors Streptococcus pneumoniae Polysaccharide capsule: primary VF -Over 90 serotypes -Anti-phagocytic -Prevents complement deposition -Evasion of lung surfactant -Abs to it confer immunity Pneumolysin: sulfhydryl activated cytolysin -Damages membranes (like SLO) -Binds cholesterol on cell membrane -Acts on several cell types (PMN, monocytes, pulmonary epithelium) -Several functions (immune evasion, spread to bloodstream, inflammation via complement activation) Etiology Human pathogen only: many asymptomatic carriers Transmission: person to person (droplet) Most common cause of acute bacterial pneumonia: in all age groups Polysaccharide Capsule: -Anti-phagocytic -Antigenic variation -Serotype B most virulent Normal Flora: common in URT -Both encapsulated and nonencapsulated (more common) Transmission: person to person (droplet) Common Age: 2-5 years old Legionella pneumophilia Existence inside amoeba: -More resistant to disinfectants -Can survive winter inside cyst of amoeba Clinical ID Sputum Gram Stain: issue because of contamination with polymicrobic saliva Acute Pneumonia: infection of lung parenchyma -Cough with productive sputum (purulent and rusty red color) -Inflammation ↑ vascular permeability fluid accumulation suffocation Radiology: bronchopneumonia or lobar consolidation Secondary Complications: -Bacteremia (due to inflammation and damage to endothelial cells) -Acute Purulent Meningitis Cell Wall TA/PG: inflammation -Causes fever and lung damage -Activate alternative complement pathway -Production of IL1 and TNF Haemophilus influenzae Pathogenesis Organism establishes in LRT: -Aspiration from middle RT -Compromised cough reflex permits entry (stroke, alcoholism, viral infection, anesthesia) -Alveolar Abs NORMAY clear it Parasite of freshwater and soil protozoa: found in cooling towers, AC systems, plumbing, respiratory equipment etc. Transmission: inhalation (no person-to-person spread) Generally low virulence in humans: most people have Abs because of ubiquity Pneumonia: Encapsulated: similar to pneumococcal pneumonia -Higher virulence/blood culture more likely (+) with Hib infection -Less common as normal flora Non-encapsulated: less virulent -Predisposing factors include chronic bronchitis, emphysema, COPD Acute Epiglottitis: also possible Legionnaire’s Disease: severe pneumonia with high mortality rate -2 to 10 day IP Pontiac Fever: nonpneumonic febrile illness (mild flu-like symptoms); may be due to inhalation of dead or low virulence strains -1 to 2 day IP Disseminated Disease: rare Blood Culture: detects bacteremia -Latex agglutination for Abs Shape: G(+) lancet shaped diplococcic Biochemical: -Alpha hemolytic -No Lancefield grouping -Capsular serotyping -Quelling reaction -Optochin sensitive -Bile soluble (distinguish from viridians strep) Samples: -Sputum -Blood cultures (positive in 10-15% of patients; higher with Hib) Shape: G(+) coccbacilli Growth: fastidious (requires X and V) Urine EIA test for soluble Ag Does not Gram stain well: -Silver stain (thin, pleiomorphic G(-) rod with filamentous forms) Growth (slow): requires L-cysteine, amino acids, and ferric ions; also needs buffered medium (pH rest.) Organism rarely found in sputum Disease Process: -Tropism for lung alveoli and bronchioles -Surface protein binds C3 to enhance its own phagocytosis (“coiling”); can also have bacteria-induced phagocytosis (no C3 bound) -Intracellular parasite in monocytes and macrophages (multiplication normally inhibited in activated MØ) Acinetobacter spp. Mycoplasma pneumoniae Antibiotic Resistance: innately resistant to many classes of antibiotics Adhesin: binds sialic acid containing glycolipids or glycoprotens on bronchial epithelial cells Hydrogen peroxide: damages tissue Superoxide: damages tissue AutoAb generation: may occur; reactive to lymphocytes, smooth muscle, brain and lung tissue Environmental organism: lives in soil, water and on the skin of healthy people (esp. health care workers) Frequent cause of nosocomial infections Common in teenagers Transmission: droplet spread (low ID) Protein Expression in MØ: -Prevent phagolysosome fusion -Prevent acidification of endocytotic vesicle -Induce accumulation of ribosomes and mitochondria around phagosome -Facilitate iron scavenging from transferrin Pathogenesis (in immunocompromise): -Pneumonia -Serious blood or wound infections Walking Pneumonia: less severe than other bacterial pneumonia Disease Process: -Colonization of bronchial epithelium interferes with ciliary action -Inflammation and exudates contribute to pathogenesis Secondary infection site: otitis media (nonpurlent) Chlamydia pneumoniae Life Cycle: -Elementary body (infectious stage) -Reticulate body (metabolically active and replicates in the cell) Humans are only host: over ½ of adults are seropositive but reinfection can occur Sequelae: immunopathology results due to cross reactive Abs -Hemolytic anemia -Aseptic meningitis -Pancreatitis Pharyngitis Bronchitis Atypical/Walking Pneumonia: school aged children and young adults Similar clinical picture to M.pneumoniae Shape: G(-) coccobacillus No Cell Wall: -No Gram stain -No B-Lactam treatment Bound by triple membrane containing sterols No organism in sputum Diagnosis: -Circulating Ag -Complement fixing Ag (ELISA) Shape: G(-) outer membrane with no cell wall; coccobacillus Glycogen (-) inclusions Detection: immunofluorescence of outer membrane proteins or PCR Staphylococcus aureus Causes infection secondary to some other lung insult: for example, a viral infection Acute Pneumonia Empyema: purulent infection of the pleural space (spread from infected lung) Lung Abscess: complication of acute or chronic pneumonia Samples: -Sputum -Lung abscess aspirate (may also use radiology to diagnose) -Blood culture (if disseminated) Shape: G(+) cocci in clusters Biochemical: -Catalase and coagulase (+) Mycobacterium tuberculosis Mycolic Acid (Cord Factor): -Resistance to drying/disinfectants -Promotes hypersensitivity granuloma -Promotes inflamm. response/tissue damage Lipoarabinomamman: cell wall glycolipid -Suppresses T cell proliferation -Prevents MØ activation Incidence highest amongst AIDS patients and immigrants XDR TB: ~1% are extensively drug resistant Transmission: aerosol inhalation Primary Infection: Gohn complex formation (granuloma) and enlarged LNs -unapparent most of the time Progressive Primary TB: ~5% of primary infections; infection does not resolve and disseminates (bloodborne or miliary) Reactivation TB: commonly reactivates at the apex of the lung (highest O2) -Increased risk with age, alcoholism, diabetes or decrease immune function) Sulfolipids: inhibit MØ phagosome-lysosome fusion Antibiotic susceptibilities required Tuberculin Skin Test: -Inject PPD (autolyzed bacteria, lipid, polysaccharides and NSs) -Causes DTH reaction (local induration and erythema) if (+) PPD+: -Current infection (granuloman formation) -Previous exposure (but not necessarily disease) -BCG vaccine Catalase: degrades hydrogen peroxide Disseminated TB: either due to progressive primary or reactivated -Via lymph or erosion of necrotic tubercle in lung -Infects liver, spleen, kidney, bone, or meninges Ammonia Production: prevents acidification in phagolysosome PPD-: -No exposure -Prehypersensitivity stage (within 6 weeks of exposure) -Loss of sensitivity (disappearance of Ag from primary complex) -Anergy (immunocompromise) Specimen Collection: sputum, biopsy or blood (if disseminated) Pseudomonas aeruginosa Adhesins: -Protein pilus adhesin (bind asialoGM1) -Non-pilus adhesin (binds mucus) CYSTIC FIBROSIS! Nosocomial infections: water borne Acute pneumonia Empyema Abscesses Staining: Acid Fast Stain Growth: very slow; Lownstein Jensen or Middlebrook agar Rapid ID: -rRNA/DNA probes -PCR to detect common insertion sequence Sample: sputum Shape: G(-) rods Biochemical: oxidase (+), aerobic Alginate: polysaccharide capsule for biofilm formation; regulated in response to environmental signals Infections in CF: -CF patients have defect in CFTR leading to decreased sialylation of surface glycolipid (asialoGM1) -Alginate gel + excess mucus leads to barrier to phagocytosis AND antimicrobials -Anti-pseudomonal Abs may be defective -Lung tissue damage due to persistent colonization and elastase release -Rarely spreads beyond lungs! Elastase: protease that degrades lung elastin Exotoxin A: ADP ribosylation EF2 Aspergillus spp. (Fungus) Multiple Drug Resistance: -Mutations leading to loss or porins -Alteration of LPS No dimorphic growth phase Infectious conidia: germinate to mold form Hyphae: bind fibrinogen and complement components Histoplama capsulatum (Fungus) Dimorphic growth phase: -Mold in the environment (produces infectious conidia) -Pathogenic yeast in tissue Common environmental mold: emerging cause of nosocomial infections Conditions caused: -Acute pneumonia -Lung abscesses Predisposing Factors -Asthma -Chronic bronchitis -TB -Immunosuppression Structure: -Septate hyphae with conidia -Mold form grows rapidly, easily identified Transmission: inhalation of infectious conidia Radiology: fungus ball in pulmonary cavity Farmer’s Lung or Allergic Aspergillosis Environmental source: bird and bat droppings (Central and Southeastern US) Transmission: inhalation of conidia (no person to person) Exposure is common but disease is rare: -Primary infection site is lungs -Grows inside MØ and produces granuloma similar to TB (can disseminate to organs of reticuloendothelial system) Normal Immune Response: -T cell activation of MØ prevents intracellular growth -Long-term immunity to re-infection Blastomyces dermatitidis (Fungus) Dimorphic growth phase: similar to Histoplasma Difference: yeast cells exist extracellularly, NOT in MØ Samples: -Lung aspiration -Bronchial lavage -Biopsy Distribution: middle and SE US Transmission: inhalation of conidia More common in males Chronic Pneumonia: PMN infiltration and granuloma formation (mimics pulmonary tumor or TB) Radiology: granuloma similar to TB Sputum: NOT USEFUL Blood or biopsy required Growth (Slow): BAP or Sabouraud agar Structure: dimorphic; mold forms tuberculate maccroconidia (finger like projects with spores) Detection: widespread exposure and cross reactivity to other pathogens -DTH skin reaction to mycelial Ag -Complement fixing Ab test -Immunodiffusion -DNA probes Large yeast cells with broad buds Slow growth: ~4 weeks Serodiagnosis: hard because of cross-reactivity with other fungi Dissemination possible: -Chronic infection of skin and bone most common -Possible even in subclinical infections Coccidiodes immitis (Fungus) Dimorphic Growth Phase: -Mold (produces arthroconidia) -Spherule (invasive tissue form that produces reproductive endospores) Valley Fever: common in SW US Transmission: inhalation of arthroconidia Immune Response: -T cell mediated -Cytokine-activated macrophages -Large yeast cells can resist oxidative and non-oxidative killing mechanisms Usually mild disease: acute pulmonary infection with cough, chest pain and myalgia Chronic Pneumonia: if decreased T cell response -Dissemination possible (skin, bones, joints, meninges), although rare Disease Process: -Arthroconidia inhaled and are phagocytosed (PMNs, MØs) -Spherule grows too large for phagocytosis and bursts, releasing endospores, which are endocytosed and prevent phagolysosome fusion (inflammatory rxn) -Inflammation results in granuloma formation Pneumocytsis carinii/jirovecii (Fungus) Protozoan: based on morphology and drug susceptibility Fungus: based on rRNA and sequence homology with other fungi Very common infection of generally low virulence: causes PCP in immunocompromise -Premature infants -Chemo patients -Organ transplants patients -AIDS (presenting manifestation) -Use of corticosteroids -Leukemia Immune Response: -Cell-mediated immunity to arthroconidia and endospores -T cell anergy can result in chronic infection (due to heavy pathogen load after spherule burst) -Progressive diffuse pneumonia -Other concurrent infections are common -Alveoli filled with desquamated cells, organisms, monocytes and fluid (foamy appearance) Symptoms: typical pneumonia signs absent -Mild/low grade fever -Non-productive cough -Progressive dyspnea, cyanosis, hypoxia -Death by asphyxiation Detection of spherules in histological sections Complement Fixing Ab titers predict outcome: -Low: good CMI response -High: disseminated and T cell anergy Skin test of limited value: due to common exposure Other ID Methods: -Immunodiffusion -DNA probe Sample: sputum (induced with hypertonic saline) -Only useful in AIDs b/c of ↑ number of organisms -Extracellular cysts and trophs -Scattered cysts in contact with alveolar cells (characteristic of latent infection) DNA VIRUSES CAUSING RESPIRATORY INFECTIONS: Virus Characteristics Epstein Barr Virus Genome: linear dsDNA (Gammaherpesvirus) Enveloped Replication: nucleus Pathogenesis Transmission: saliva Site of Primary Infection: URT Spread to B Lymphocytes:: up to 10% may become infected (heterophile Ab secretion and lymphocytosis) Diseases Young Children: infection usually asymptomatic -Fever and sore throat most common -May also cause diarrhea, otitis media, infectious mono (less common) Adolescents/Adults: asymptomatic disease less common -Infectious Mono: fever, sore throate, anorexia, lymphadenopathy, hepatosplenomegaly, lymphocytosis, heterophile Abs Cancer: -Burkitt’s Lymphoma (malaria may be a cofactor) -Nasopharyngeal carcinoma (Southern China; genetic, dietary and environmental cofoactors) -Hodgkin’s Lymphoma (EBV detected ~50% of cases) Cancer in Immnocompromise: -Post-transplant lymphoproliferative disorders and lymphomas -X-linked lymphoproliferative -AIDS associated lymphomas (tend to occur in CNS) Cytolomegalovirus (Betaherpesvirus) Genome: linear dsDNA Enveloped Replication: nucleus Transmission: virus shed in urine, saliva and other body fluids Hairy Oral Leukoplakia: in mouth of AIDs patients -White, wart like lesions on the side of the tongue (NOT TUMORS) Usually asymptomatic: may cause infectious mono-like disease (heterophile Ab negative) Immunocompromise: CMV pneumonia and retinitis possible Adenovirus Genome: linea dsDNA Non-enveloped: icosahedral -Fibers at vertices (characteristic) Replication: nucleus Transmission: -Respiratory spread (most common); will still spread to GI tract -Fecal/oral spread -Iatrogenic spread (ie. to conjunctiva) Bind: CAR receptor and integrin co-receptor on host cell Infect: mucosal epithelial cells of the respiratory tract, GI tract and eye Viral Entry: endocytosis Viral Release: cell lysis (inefficient, but a lot of viral particles made) Neonatal/Fetal CMV: major problem -Risk of death, mental retardation and deafness Acute Respiratory Infections: highly infectious -Fever, sore throat, cough, nasal congestion, tonsillitis Acute Respiratory Disease: military recruits (mild URI pneumonia) -Vaccine available for military use only Pneumonia: possible complication of any Adenovirus RTI -Common cause of childhood pneumonia or pneumonia in immunocompromise Pharygoconjunctival Fever: conjunctivitis + URTI (often from pools) Epidemic Keratoconjunctivitis: minor corneal abrasions required GI Disease: only Type 40 /41 (infant gastroenteritis) Urethritis/Cystitis: uncommon (Type 27) Parvovirus B19 (Parvoviridae) Genome: linear ssDNA Non-enveloped: icosahedral Replication: nucleus (AUTONOMOUS) Many infections are asymptomatic: -Infection in school age children more common -Abs increase with age Transmission: respiratory route, transplacental (if primary B19 infection in pregnant woman) Erythema Infectiosum (Fifth Disease): First Phase: non-specific flu-like symptoms -Viremia -Formation of IgM-parvovirus immune complexes Second Phase: deposition of immune complexes -Erythematous rash -Arthritis Transient Aplastic Crisis: in people with hemolytic anemia -Replicates in bone marrow (erythroid precursors) -Transient reduction in RBC production that is not a major problem in normal indiciduals Immunocompromise: chronic infection of BM persistent anemia Congenital B19: can cause hydrops fetalis (fatal anemia of fetus) -No abnormalities in survivors