Micro - Respiratory Flashcards
(43 cards)
Virus persistence on dry inanimate surfaces
Adenovirus - 7 days – 3 months
Rhinovirus - 2 hours – 7 days
Coronavirus - 3 hours
RSV - Up to 6 hours
Upper RT sx’s
- Sinusitis
- Rhinitis
- Otolaryngitis
- Laryngitis
- Pharyngitis
Lower RT sx’s
- Bronchitis
- Bronchiolitis
- Pneuomnias - CAPs (acute or subacute/chronic), nosocomial
Viruses w/main pathology elsewhere besides RT
Measles, chickenpox, smallpox, coxsackievirus, norwalk virus
Adenovirus
Family: Adenoviridae Genus: Mastadenovirus
Replication = Class I (nucleus)
Clinical syndromes: pharyngitis, conjunctivitis
• Fiber protein: attachment to host cell rec
• Rec varies w/ viral serotype:
– Serotypes 2 & 5: rec = CAR (Coxsackie Adenovirus Receptor)
• Cell surface glycoprotein belonging to IgG superfamily.
• Penton base has toxic activity
– Inhibition of cellular mRNA synthesis
– Cell rounding
– Tissue damage
Rhinoviruses
Virus family: Picornaviridiae
Icosahedral, non-enveloped
Clinical syndrome: Common cold. Humans are sole reservoir. Young children: more severe. Single community: often contains simultaneously circulating serotypes
– Single individual may be co-infected.
Relatively stable in environment, optimum temperature for growth is 33-35C (URT ideal for infxn), Ag drift.
Cell receptor = ICAM-1, Viral shedding
via surface cleft/canyon
Coronaviruses
Family: Coronaviridiae
• HCoV-229E, HCoV-OC43, SARS-CoV
Clinical syndromes: Common cold, SARS
Enveloped, helical nucleocapsid, characteristic fringe = surface/spike glycoproteins. S protein. Peplomers - define tropism, attach to prots or carbs, site of main Ag epitopes: Abs are neutralizing.
Re-infection by the same serotype possible: neutralizing Abs are short-lived. Transmission via droplets: fecal-oral route also possible.
Replication optimal at 33-34C in ciliated nasal epithelium. Difficult to isolate & grow
Human parainfluenza viruses (HPIV)
Virus Family: Paramyxoviridae
Subfamily: Paramyxovirinae
Genera: Respirovirus: HPIV 1 & 3
Rubulavirus: HPIV 2 & 4. Also includes mumps
Clinical syndrome: laryngotracheobronchitis; bronchitis
Enveloped. Glycoprotein with HN activity
• Fusion Factor (F) – viral entry. Abs against F protein = neutralizing
• V proteins (fusion proteins): evasion of immune response.
• Functions: – Prevent apoptosis, alter cell cycle, inhib dsRNA signalling – Prevent IF biosynthesis
Pneumovirus
Family: Paramyxoviridae, Subfamily: Pneumovirinae, Genus: Pneumovirus
• Enveloped, helical nucleocapsid
• Virally-encoded surface proteins:
– Fusion factor (peplomer): main viral Ag
– G glycoprotein : involved in attachment – Two subgroups: A & B
• Lacks glycoprotein with HN activity
Croup aka laryngotracheobronchitis
- HPIV, Pneumovirus, RSV
- Mostly young children and infants
- Swelling and narrowing of the airway
- Cough sounds like barking of a seal
RSV
• Entry is via epithelia of nose and eye.
– Large droplets on contaminated hands or surfaces (self-
inoculation).
• F & G proteins mediate attachment; F mediates membrane fusion.
• Primary site of replication = nasopharyngeal epithelium.
– Direct cytopathic effect loss of function.
• Can spread into lower RT after 2-5 days via various suggested mechanisms
• CD8+ T cells: subsequent dz enhanced when children vaccinated using heat-killed vaccine
Influenza
Virus survives drying for ± 24 hours, depending on ambient humidity
• Epidemics rarely continue in a community for more than 4 to 6 weeks
– Most people recover spont and gain long- lasting (but weak) immunity to that strain.
– Patient is contagious from before sxs
appear (end of day 1) for next 7 days
– Risk of secondary infxnn highest in time
from 6 to 12 days after infxnn
Children: same as those in adults, plus
– Higher fever
– G.I symptoms: (Vomiting, Abdominal pain)
– Earache (Otitis Media)
– Muscle pain and sometimes swelling
– Croup often but not always
– Febrile Convulsions (Children under 3: Rare)
Complications:
• Rare Neurological syndromes: Guillain Barre, Encephalitis, Reye’s Syndrome in Children – aspirin and aspirin containing drugs.
Influenza A
Only influenza A further classified by subtype on the basis of HA and NA. Influenza A subtypes and B viruses are further classified by strains.
Influenza A: All 15 “H” and 9 “N” found in Birds, domestic Ducks most commonly. Chickens -> sweeping epidemics. Pig is mixing bowl. Man can get from pig or duck
Hemagglutinin: • Major Ag against which neutralizing antibodies are directed.
– Highly variable -> evolution of new strains.
• 4 HA subtypes described in humans: HA1-3, HA5
Requires cleavage to be active:
– Carried out by cellular proteases found only in RT.
– Proteases probably define tissue tropism
Neuraminidase = Sialidase enzyme:
• removes term sialic acid residues from glycoproteins and
glycolipids.
Two subtypes described in humans: N1 and N2.
NO stimulation of neutralizing antibodies
Influenza B
Influenza B viruses are usually found only in humans.
•Two lineages of influenza B: •Victoria-like •Yamagata-like
•Only 1 is covered by the trivalent seasonal flu vaccine.
SHORTER TIME TO DEATH THAN INFLUENZA A
Amantadine & Rimantadine
– Inhibit uncoating of Influenza A only Target is M2 Protein
– No effect on Influenza B or C
• Excessive use of antimicrobials virtually guarantees the development of drug- resistant infectious agents
– Amantidine Resistant Influenza A
Zanamivir & Oseltamvir (Tamiflu®)
– Inhibit Neuraminidase: Without this, virus binds to its own sialic acid and forms useless clumps – blocking release.
– Work on Influenza A and B, not on C
• Excessive use of antimicrobials virtually guarantees the development of drug- resistant infectious agents
– Tamiflu Resistance
STREPTOCOCCI General Characteristics
Metabolism - fermentative with lactic acid production
Oxygen requirements - facultative anaerobes, • growth enhanced by CO2
• Nutritionally fastidious
– Normal culture medium = Blood agar (BA) • Yeastextract+peptone+5%blood
Lancefield classification NOT useful for some streptococci, e.g., S. pneumoniae. Used with serology & hemolysis patterns for preliminary ID (before 16S rRNA sequencing avail).
Streptococcus pyogenes
Group A Streptococcus = sens to Bacitracin. Beta hemolytic. Pharyngitis. LEUKOCIDIN, Hyaluronic acid capsule, M protein, Streptolysin, Streptokinase, Hyaluronidase, Pyrogenic exotoxins
Streptococcus pneumoniae
Clinical syndrome: pneumonia, sinusitis, otitis media. Alpha Hemolysis = sens to optochin
Part of nasopharyngeal flora – 5-40% of healthy individuals. No animal/env reservoir.
Transmission: exogenous: person to person: droplets. • Endogenous. Winter & early spring incidence.
Pathogenesis: • Capsule, IgA protease, Pneumolysin, Autolysin, Transformation. Bloodstream in 15-30% of cases. Pneumolysin - Inhibits ciliated epithelial cell activity
Cytotoxic for alveolar and endothelial cells
Causes inflammation
Decreases PMN effectiveness
“polyvalent”capsularpolysaccharidevaccine, e.g., Pneumovax, Pnu-immune.
• Immunizesagainst23ofthemostcommon serotypes. young and elderly and those with:
– Chronic disease – HIV
– Alcoholism
• Also:7-valentconjugatedvaccine:T-cell dependent response.
Corynebacterium diphtheriae
• 4 biotypes:gravis, mitis, belfanti and Gram+ve intermedium. Other non-pathogenic Corynebacteria spp. are normal flora in pharynx, nasopharynx and on skin.
– C. jeikeium: associated with bacteraemia, IV catheter colonization.
– C. minutissimum: RTI’s, wound infections.
Endemic in some subtropical and tropical countries. outbreaks in countries with breakdown in health infrastructure
Hemophilus influenzae
Clinical syndromes: Otitis media, pneumonia, epiglottitis most common cause of epiglottitis.
Also associated: S. pneumoniae, C. diphtheriae, N. meningitis.
Gram –ve; pleomorphic. Facultative anaerobe. Normal component of Upper RT flora
Serotyped according to capsule (a to f)
• Coagulase negative, catalase positive
Culture: requires chocolate agar with X and V growth factors.
– X factor = acts as hemin
– V factor = nicotinamide adenine dinucleotide (NAD). (both released from blood following gentle heating). Is the ONLY Haemophilus species that requires both.
Bordetella pertussis
Clinical syndrome: whooping cough (chronic bronchitis). Gram –ve coccobacillus. Unvaccinated children. Adults important as reservoir. Highly communicable.
Sample: Nasopharyngeal swab or secretions.
**Not cotton swab ** Not throat swab
very susceptible to drying.
• Culture (100% specific) – nutritionally fastidious: charcoal blood agar + cephalosporin (E.g., Bordet-Gengou)
Types of vaccines: a) Whole cell (formalin-inactivated) b) Acellular components, e.g., Fha, PT • Lower rate of side effects • aP = acellular Pertussis
Klebsiella pneumoniae
Clinical syndrome: bronchopneumonia, lung abscesses
Enterobacteriaeceae. Gram -ve bacillus. Large capsule (mucoid appearance).
• Part of microbial flora: ~5% of healthy individuals.
• Two high affinity iron uptake systems: aerobactin & enterochelin.
• Necrotization of lung tissue – due in part to response to endotoxin (LPS).
• Range of microorganisms in addition to K.
pneumoniae can include:
– S. aureus, Anaerobes and microaerophiles from normal mouth flora. Microaerophils on outside use up O2; anaerobes grow on inside.
Legionella pneumophila
Clinical Syndromes: 1.Legionnaire’s disease (pneumonia) 2.Pontiac fever (self-limiting)
• Gram–verod.Motile.Non-sporeforming. Can be associated with epidemics
• Exposure=inhalationofcontaminatedaerosols.
– Person-person transmission = rare.
• Can survive~50C for >30 minutes
• Facultatively intracellular (alveolar macrophages).
• Uptake via phagocytosis; prevent fusion of phagosome-lysosome.
• Much dmg = host inflammatory response.
• Virulence factors
– Intracellular growth
– Role of endotoxin?
– Role of extracellular protease?