Exam 4 Flashcards
Respiratory illness can be caused by avian influenza. True / False
- True, does not have human-human transmission
What is nontypeable H. influenzae?
- Means it contains no capsule
Diseases cause by chlamydophila pneumoniae
- Pneumonia: more severe infections involve only one lung lobe, difficult to differentiate from atypical pneumonias (mycoplasma pneumoniae, legionella pneumphila and resp viruses). Possibly involved with atherosclerosis - Bronchitis and sinusitis
Complications of pneumonia
1.) Pleural effusion: excess fluid in pleural cavity, limits expansion of lung 2.) Hematologic: anemia, DIC, thrombocytopenia 3.) Low po2, weight loss, muscle atrophy, bronchiectasis (dilation of bronchi/oles d/t muscle/elastic tissue damage)
Streptococcal pharyngitis. Symptoms, causative agent, lab tests, pathogenesis, treatment, vaccination?
- Symptoms: Redness of throat, patches of adhering pus, scattered tiny hemorrhages, fever - Agent = S. pyogenes (Lancefield = group A) - Lab tests = beta-hemolytic, catalase negative - Pathogenesis = a.) M-protein: antiphagocytic and essential for virulence b.) Capsule: in some strains that inhibits phagocytosis (explains severity of some presentations) c.) SPE (streptococcal pyrogenic exotoxins): these are super antigens (9 of them) that cause fever, rash, TC proliferation and B-cell suppression - Treatment: most cases will recover in 7 days, but treatment with penicillin or macrolide (erythromycin or azithromycin) - Vaccine: not available
SARS Coronavirus. Diseases caused, symptoms, transmission
- Diseases: SARS (severe acute respiratory distress) – no cases since 2004, pneumonia - Symptoms: fever, malaise, myalgia, dry cough, SOB, diarrhea, abnormal liver function, lymphopenia - Transmission: fecal-oral, close contact and aerosolized
What slows down the mucociliary escalator and predisposes individuals to RT infections?
- Viral infections - Smoke - Alcohol - Narcotics
Candida (C. albicans primarily). Morphology of fungi, source, disease(s) caused and presentation, risk factors for disease, diagnosis, treatment?
- Morphology: dimorphic, existing in both yeast and hyphal forms. Yeast in normal flora, hyphal forms in tissue when in disease-state - Source: normal flora, in food and on fomites - Diseases caused/presentation: 1.) Oral candidiasis (thrush): diffuse erythema and white patches in mouth, sometimes into esophagus (in immunosuppressed individuals) 2.) Other brain, blood and urogenital infections (discussed later) - Risk factors: infants, adults on steroids, antineoplastics and abx, also AIDS and other immunosuppressed individuals - Diagnosis: observation of budding yeast and hyphal structures in tissue - Tx: mouth washes or lozenges containing nystatin and azole compounds
India ink is used for diagnosis of what microorganism?
- Crytococcus neoformans
Zygomycetes (rhizopus, absidia, mucor). Morphology of fungi, source, disease(s) caused and presentation, risk factors for disease, diagnosis, treatment?
- Morphology: non-septated hyphae, sporangia with sporangiospores - Source: soil, vegetation, food, ubiquitous - Diseases caused: 1.) Rhinocerebral zygomycosis: infection originates in sinus via inhalation of spores and extends into nose, hard palate, eye and brain in some cases. Symptoms initially include nasal congestion, blood-tinged rhinorrhea, tender sinuses, headache and fever. Progresses to facial and periorbital edema and visual disturbances. Can further progress to brain resulting in AMS, coma and death 2.) Lungs , skin and GI infections in immunosuppressed or burn victims where traumatic inoculation has occurred. GI infections in neonates and premature infants seen too - Risk factors: immunosuppressed, diabetics, burn-victims (rare in healthy individuals) - Diagnosis: broad aseptate hyphae, branching at 90 degree angles in material - Tx: amphotericin B
Definition of pneumonia
- Inflammation of lung parenchyma with fluid accumulation in the alveoli which blocks effective gas exchange
Klebsiella pneumoniae pneumonia. Lab tests, clinical presentation, pathogenesis/virulence factors, treatment/resistance, vaccine
- Lab tests: gram neg rod, capsule mucoid colonies, oxidase negative - Presentation: lobar pneumonia, bloody currant jelly sputum (foul-smelling as facultative anaerobe) - Pathogenesis: necrosis and abscess formation from LPS and capsule - Treatment: Aminoglycoside + beta-lactam (gentamycin/cephalexin + tobramycine/ampicillin). ESBL (extended-spectrum beta-lactamase) resistance strains are problematic to treat - No vaccine
Mycobacterium tuberculosis. Transmission, TB symptoms with active TB, diagnosis/lab tests, treatment, vaccine, risk factors,
- Transmission: respiratory aerosol droplets - Symptoms: gradual onset, fatigue, weight loss, weakness, fever, night sweats, chest pain, dyspnea, cough is absent or mild with scant sputum can become sever with yellow/green/blood-streaked sputum - Pathogenesis: Mtb inhaled as droplet into lungs, enters alveoli, taken up with alveolar macrophages, lymphocytes recruited to site, Mtb evasion of killing leads to granuloma formation and infection is walled off by macrophages from surrounding tissue. T and NK cells surround caseous necrotic granuloma mass and prevent spread in latent infections. In active/reactivation, Mtbs are actively dividing and increase inflammation and tissue damage. In disseminated cases, alveolar macrophages migrate to hilar LNs. Pathology of TB is consequence of CMIs response – when adequately controlled granulomas form and disease process halted, when inadequate, TB is active or becomes reactivated - Diagnostics: 1.) Latent TB: Ghon focus, which is lung lesion containing live Mtb seen on CXR as it calcifies or Ghon complex, which is calcified lesion in affected hilar lymph 2.) Active/reactivation TB: CXR shows focal infiltration with cavitation (d/t granuloma breaking apart) often in apical posterior segment of upper lobes of either lungs. 3.) Mantoux/Tuberculin skin test: intradermal injection of proteins derived from cell envelope – positive in infected individuals and always in BCG-vaccinated individuals 4.) IFN-gamma release assay: measure IFN-gamma in whole blood when stimulated with Mtb antigens, means T cells were previously sensitized. Use for pts vaccinated with BCG 5.) Lab: acid-fast staining, PCR, Culture (slow) - Treatment: 4 drug cocktail (isoniazid, ethambutol, pyrazinamide and rifampin) give for 2 months followed by 26 months of isoniazid and rifampin. D/t side effects of isoniazid, concern for compliance - Vaccine: BCG-vaccine using bovis species, not protective - Risk factors: primary TB infections greater in HIV population, also 200-300 times more likely for reactivation TB if latently infected
Causative agents of fungal oral cavity infections?
- Candida, primarily candida albicans
8 yo male involved in accident at home while playing in basement near natural gas furnace and incurs partial thickness burns to 20% of body. In hospital, he requires intubation and mechanical ventilation because of inhalation injury. Pt develops symtoms c/w typical pneumonia. CXR shows lobal pattern of consolidation. Sputum reveals G- rod, which is oxidase positive and negative for lactose fermentation. Which of the following is best choice for treatment? A. Ticarcillin and aminoglycoside B. Aminoglycoside C. Rifampin and aminoglycoside D. Isoniazid, ethambutol, pyrazinamide, rifampin E. No treatment, infection will spontaneously resolve
- Causative agent is Pseudomonas aeruginosa, which is G-neg rod, oxidase positive and obligate aerobe. Causes infections in burn victims among others. Pt has been on vent where this bacterium can be seen preferentially. Option A is best treatment
Most frequent cause of death in CF patients
- Pseudomona aeruginosa respiratory disease
Describe treatment options for influenza. Which virus subtypes are these effective against?
1.) Ion channel blockers: amantadine and rimantadine - Block M2 ion channels in influenza A viruses, currently resistant to these drugs, so not recommended for use by CDC 2.) Neuraminidase inhibitors: zanamivir (relenza) PO inhalation, oseltamivir (tamiflu) PO, peramivir (Rapivab) - inhibits virion release and spread and effective against influenza A and B - must be given in first 48 hours to reduce disease and symptoms
How to distinguish between Chlamydophila pneumoniae and Mycoplasma pneumoniae clinically?
- Symptomatology similar mycoplasma pneumoniae, however small gram-negative, obligate intracellular pathogen via lab results. Treatment is same
URT tissues that are sterile?
- Mastoid air cells - Middle ear - Sinuses - Trachea - Bronchi and bronchioles - Alveoli - Conjunctiva (typically, but d/t location it is common to find microorganisms, which land and don’t stay)
Most common cause of common cold? Other causes?
- Rhinovirus - Non-SARS coronavirus, adenovirus and coxsackieviruses - Also, influenza (B and C), RSV and parainfluenza
How is antigenic drift made possible?
- Reassortment in another species
Normal flora of nose/nares
- Staph epidermidis - Staph aureus - Corynebacterium
How is the influenza virus vaccine produced?
1.) Classic method: in embryonated chicken eggs 2.) Initial production in eggs, then production in mammalian cells (rapid, less egg protein carried over, but ini) 3.) Baculovirus expression vector: baculovirus engineered to express hemagluttinin protein (rapid, egg-free)
Staph aureus pneumonia. Lab tests, pathogenesis/virulence factors, treatment including resistance, vaccine?
- Lab tests: G+ cocci in clusters, catalase pos, coagulase positive - Pathogenesis: a.) Exotoxins including TSST-1 b.) Coagulase: clots blood c.) Protein-A binds Fc portion of ab d.) Panton-Valentine leukocidin (PVL) implicated in cases of necrotizing pneumonia, it is a pore-forming toxin - Treatment: beta-lactams (penicillins, cephalosporins) if sensitive. MRSA is resistant to all beta-lactams. Requires treatment with linezolid (50S inhibitor) or vancomycin - No vaccine yet
What comprises the LRT tract where infections can arise?
- Trachea, bronchi, bronchioles, lungs and alveoli
If a patient presents with scarlet fever, what are symptoms to have preceded this and what is the causative agent?
- Strep throat symptoms: fever, redness throat, pus in post pharynx, hemorrhages to pharynx - Agent = S. Pyogenes
Causative bacterial agents of otitis media and sinusitis
- H. influenzae and Strep pneumoniae (same as conjunctivitis) and Moraxella catarrhalis - Chlamydophila pneumoniae can cause sinusitis too
Most common cause of bronchiolitis and pneumonia in children less than 1 years old?
- RSV
Other mycobacterial infections similar to mycobacterium tuberculosis
- Non-tuberculous mycobacteria: 1.) Mycobacterium avium-intracellulare: complex of severe mycobacteria, immunocompromised pts or those with lung disease present with infection resembling TB 2.) Mycobacterium kansasii: commonly in elderly and COPD pts, this is a chronic granulomatous pulmonary disease • work-up and treatment is similar to Mtb
Causative agents of fungal lung infections?
- Histoplasma capsulatum* - Blastomyces dermatitidis* - Paracoccidioides brasiliensis* - Coccidioides immitis* - Cryptococcus neoformans (encapsulated) - Pneumocystis jiroveci (previously carinii) - Aspergillus (fumigatus and flavus) * dimorphic
Since most cases of strep throat resolve on their own, why is it necessary to treat? How can this occur?
- Strep pyogenes can lead to: 1.) Scarlet fever: result of SPE release 2.) Acute rheumatic fever: cross rxn by immune system to our own tissues including heart leading to arrhythmias 3.) Necrotizing fasciitis: result of SPE release 4.) Acute glomerulonephritis: 1-4 weeks after strep pharyngitis or 3-6 weeks after strep. Pyogenes skin infection – d/t antigen-ab complexes destroying glomeruli
Non-SARS coronavirus. Disease caused, transmission, pathogenesis, treatment, vaccine?
- Disease: common cold - Transmission: large droplets, outbreaks common in spring and winter, infections common in infants and children - Pathogenesis: replicate in epithelial cells of respiratory tract (upper) in cooler temps, enveloped virus - Treatment: meds to alleviate symptoms - No vaccine, reinfections occur despite previous infection
20 yo male with fever, cough, swollen LNs 10 days after exploring cave with numerous bat-roosting sites. CXR pattern similar to primary TB, tuberculin test negative. Sputum yielded mycelial growth when incubated at room temp. Isolates show abundant tuberculate macroconidia. What is the most likely causative agent and diagnosis?
- Histoplasmosa capsulatum causing histoplasmosis
Most common causative agents of hospital acquired pneumonia
- Gram negatives (more commonly): Pseudomonas aeruginosa, E. coli, Klebsiella pneumoniae, acinetobacter spp., H. influenzae - Gram pos: S. aureus, S. pneumoniae
Replication cycle of Chlamydophila pneumoniae
1.) Elementary body (EB) attaches to and enters cell 2.) EB reorganizes to a reticulate body (RB) 3.) RB undergoes several rounds of binary fission 4.) RBs reorganize into EBs 5.) EBs emerge and begin cycle with newly susceptible cells
Pseudomonas aeruginosa pneumonia. Lab tests, source, pathogenesis/virulence factors, treatment, vaccine, risks?
- Lab tests: G- rods, obligate aerobe oxidase positive, blue/yellow-green pigments in culture that is grape smelling - Source: water with minimal nutrients, hand soaps, dilute antiseptics, humidifiers, resp sink traps and contaminated aerosols - Pathogenesis: a.) Toxin A: halts protein synthesis via ADP ribosylation of EF-2 b.) Leukocidin: pore forming toxin targeting leukocytes c.) PLC: membrane disruption d.) Capsule: anti-phagocytic e.) Pyocyanin: blue compound toxic to host f.) Pyoverdin: fluorescent green iron uptake protein - Treatment: Antipseudomonal penicillins (Ticarcillin / piperacillin) + aminoglycoside (amikacin, gentamycin or tobramycin) - No vaccine - Risks: noteworthy for causing infections associated with extensive burns, CF patients and pts on cytotoxic drugs. Humidifiers, respirators and sink traps have been problem resulting in infected aerosols
Which influenza virus is/are much more severe?
- Types A and B, A is often severe d/t antigenic changes occurring from drift and shift.
Diseases causes by chlamydia trachomatis. Pathogenesis
- Trachoma: conjunctival infection that progressively causes conjunctiva to become scarred and eyelids to turn inward, abrading the cornea leading to vision loss - Adult inclusion conjunctivitis: cause by serovars associated with genital infections, similar to other bacterial conjunctivitis, corneal scarring as seen in trachoma is less common - Neonatal conjunctivitis: neonates exposed to bacterium at birth, symptoms 5-12 days after, untreated have risk for pneumonia from bacteria - Infant pneumonia: rhinitis initially, then bronchitis with dry cough, afebrile - Urogenital infections (discussed later) - Pathogenesis: gain access to cells by minute abrasions or laceractions, direct destruction of host cells during replication and host inflammatory response leads to tissue destruction. Worse immune response with subsequent infection
Aspiration pneumonia is commonly associated with what patient groups?
- Alcoholics, coma patients and stroke patients
Causative agents of laryngitis, tracheitis and epiglottitis
- Most likely viral, but could be bacterial: group A strep (strep. Pyogenes), H. influenzae and staph aureus
Bacterium associated with parrots/parakeets
- Chlamydophila psittaci causes pneumonia
When should influenza anti-viral medication be used prophylactically?
1.) Those at risk for complications who have been vaccinated after flu season has begun 2.) Non-immune health care workers and families who care for high risk pts 3.) When there is poor match between vaccine strain and circulating strains
Compare: community acquired pneumonia vs hospital acquired pneumonia
- CAP: any pneumonia not acquired in a healthcare setting - HAP: any pneumonia acquired in a healthcare setting, associated highly with immunocompromised, those using ventilator, frequently gram-negative MDR bacteria
Diseases caused by pseudomonas aeruginosa
- Pneumonia, septicemia, UTIs, wound infections, meningitis in pts with extensive burns, folliculitis, ocular infections, endocarditis and osteomyelitis in IV drug users, ecthyma gangrenosum lesions in sepsis patients
How are influenza viruses named?
- A/Texas/1/77(H3N2) - A=serotype - Texas=location of isolation - 1=isolate number - 77=year it was isolated - H=hemagluttinin subtype - N=neuraminidase subtype
Alpha-hemolysis typically indicates what pathogen?
- Streptococcus pneumoniae is the first thing one should think - Could also be viridians group (S. mutans/mitis/milleri and salivarius)
Legionella pneumophila. Disease caused, presentation, lab tests, pathogenesis/virulence factors, source, treatment, vaccine?
- Disease: Legionnaire’s disease – severe toxic pneumonia and Pontiac fever (acute non-fatal respiratory disease similar to acute influenza) - Presentation of Legionnaire’s: myalgias, headache, rapid rising fever, dry cough that may become productive, chills, pleurisy, vomiting, diarrhea, confusion and delirium – ill over 3-6 days and results in shock, respiratory failure or both, elevated WBCs seen - Lab tests: G neg facultative intracellular parasite – coccobaccili intracellularly, pleomorphic extracellularly, culture and detect via antibody fluorescence or PCR - Pathogenesis: 1.) Pili/flagella: targets and attaches to alveolar macrophage, enters in endocytic vacuole 2.) Hijacks cell: injects bacterial proteins into cytosol, prevents fusion with lysosome, recruits ribosome, mitochondria and ER to vacuole now called LCV (Legionella-containing vacuole) and replicates in high numbers and starts process again after lysis of host. This leads to inflammation, lung necrosis and systemic toxicity in host - Source: high humidity – therefore freshwater lakes, streams, ground water, potting soil – mainly parasite of amoeba – in human outbreaks: cooling towers/AC units in hotels, factories, hospitals, respiratory devices - Treatment: NOT beta-lactams as many produce beta-lactamases, treat with macrolide or fluoroquinolone - No vaccine
Strep pneumoniae. Lab tests, pathogenesis/virulence factors, presentation of pneumonia/sputum, treatment, vaccine?
- Lab tests: alpha-hemolytic, catalase negative, gram poss diplococci, bile solubility pos (no growth), optochin sensitive, urine test positive for polysaccharide capsule - Pathogenesis: a.) Surface adhesins: colonize pharynx b.) IgA protease: cleaves IgA and prevents clearance c.) Pneumolysin: pore forming toxin, colonization, invasion, complement and inflammation activator d.) Teichoic acid and peptidoglycan: inflammation e.) Polysaccharide capsule: antiphagocytic - Presentation: cough, dyspnea, severe pleuritic chest pain, crackles, rust-colored sputum, rhinorrhea, spiking fevers with chills, poor oxygenation - Treatment: penicillins, macrolides, more serious cases require azithromycin and cephalosporin - Vaccine: 23-valent pneumococcal polysaccharide OR 13-valent pneumococcal-diphtheria conjugated toxoid vaccine
Diptheria. Symptoms, causative agent, lab tests, pathogenesis, treatment, vaccination?
- Symptoms: mild sore throat, slight fever, high fatigue/malaise, neck swelling, whitish gray membrane over throat, tonsils and nasal cavity - Agent: Corynebacterium diphtheria - Lab tests: Chinese letter growth in culture - Pathogenesis: membrane (represents clotted blood, epithelial cells of mucous membrane and leukocyte infiltrate), diphtheria exotoxin (lysogenized by bacteriophage) absorbed by blood stream in inactive forms – B binds receptor, A (true enzyme) inactivates EF-2 via ADP ribosylation stopping protein synthesis and inducing cell death – damage to heart, kidneys and nerve cells, which have B subunit receptor - Treatment: antiserum against toxin, erythromycin and penicillin - Vaccination: TDaP or DPT (toxoid vaccine)
Rhinovirus. Disease caused, transmission, pathogenesis, treatment, vaccine?
- Disease: common cold - Transmission: respiratory secretions, direct contact with these and fomites, low inoculum needed - Pathogenesis: attaches and infects nasal epithelium, cell damage and clear fluid outpours from lamina propria, damaged cells spreads infection - Treatment: meds to alleviate symptoms (antihistamines, decongestants) - No vaccine, previous infection only creates immunity to that serotype – 100+ serotypes around
