Micro - Respiratory Flashcards

(43 cards)

1
Q

Virus persistence on dry inanimate surfaces

A

Adenovirus - 7 days – 3 months
Rhinovirus - 2 hours – 7 days
Coronavirus - 3 hours
RSV - Up to 6 hours

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2
Q

Upper RT sx’s

A
  • Sinusitis
  • Rhinitis
  • Otolaryngitis
  • Laryngitis
  • Pharyngitis
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3
Q

Lower RT sx’s

A
  • Bronchitis
  • Bronchiolitis
  • Pneuomnias - CAPs (acute or subacute/chronic), nosocomial
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4
Q

Viruses w/main pathology elsewhere besides RT

A

Measles, chickenpox, smallpox, coxsackievirus, norwalk virus

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5
Q

Adenovirus

A

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

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6
Q

Rhinoviruses

A

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

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7
Q

Coronaviruses

A

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

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8
Q

Human parainfluenza viruses (HPIV)

A

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

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9
Q

Pneumovirus

A

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

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10
Q

Croup aka laryngotracheobronchitis

A
  • HPIV, Pneumovirus, RSV
  • Mostly young children and infants
  • Swelling and narrowing of the airway
  • Cough sounds like barking of a seal
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11
Q

RSV

A

• 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

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12
Q

Influenza

A

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.

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13
Q

Influenza A

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

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14
Q

Influenza B

A

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

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15
Q

Amantadine & Rimantadine

A

– 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

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16
Q

Zanamivir & Oseltamvir (Tamiflu®)

A

– 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

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17
Q

STREPTOCOCCI General Characteristics

A

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).

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18
Q

Streptococcus pyogenes

A

Group A Streptococcus = sens to Bacitracin. Beta hemolytic. Pharyngitis. LEUKOCIDIN, Hyaluronic acid capsule, M protein, Streptolysin, Streptokinase, Hyaluronidase, Pyrogenic exotoxins

19
Q

Streptococcus pneumoniae

A

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.

20
Q

Corynebacterium diphtheriae

A

• 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

21
Q

Hemophilus influenzae

A

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.

22
Q

Bordetella pertussis

A

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
23
Q

Klebsiella pneumoniae

A

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.

24
Q

Legionella pneumophila

A

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?

25
Pseudomonas spp
• Weakly pathogenic to persons w/nml innate and acquired immunity – Most common infxn is Otitis Externa: Swimmer’s ear • Dangerous for persons w/struc defects in body defenses – Burn victims – Cystic Fibrosis * Gram Negative Rods, Strictly aerobic. Highly motile with multiple flagella. Versatile Metabolism. * Non-hemolytic. Produces very mucoid colonies on conventional agar * Some strains produce the two pigments: Pyocyanin and Fluorescein, giving a green color to colorless media
26
Pseudomonas and Cystic Fibrosis
Clinical syndrome: Necrotizing Bronchial Pneumonia * Pseudomonas aeruginosa and Burkholderia cepacia considered bona fide CF Pathogens * Abnml CF mucus constitutes ready-made biofilm for these organisms * Chronic inflam causes accum of WBCs, which only makes things worse. * Permanent, highly drug-resistant infxns are the rule for both. * Often fatal.
27
Mycobacterium sp.
``` • Grow in long parallel chains “cords”. Aerobic. Non-spore forming. Resist drying but still sensitive to heat. Grows slowly in lab: 2-8 weeks. Important species: • M. tuberculosis • M. bovis • M. avis ```
28
Tuberculosis pathogenesis
• Intracellular survival in alveolar macrophages • Mechs: 1) Prevent oxidative burst & inhibit phagosome-lysosome fusion -> sulfolipids 2) Resist lysosomal enzs, ROS -> Cell wall lipids, LAM, secretion of SOD 3) Escape phagosome -> cytoplasm LAM & Mycolic acids Secrete siderophores: Exochelins Very high affinity for ferric ions Culture: require enriched or special medium • Löwenstein-Jensen agar • Oleic acid - albumin broth • Antimicrobial susceptibility testing = increasingly important (MDR strains)
29
Tuberculosis treatment
* First-line: Isoniazid, Rifampin, Streptomycin, Ethambutol * Second-line: Para-aminosalicyclic acid, Cycloserine, Fluoroquinolones Prevention: Prophylactic antimycotics, BCG (Bacillus Calmette-Guérin) vaccine, Attenuated M. bovis strain * MDR-TB: Resistant to both isoniazid (INH) and rifampin * XDR-TB: MDR + resistant to any fluoroquinolone + 1 of the three following injectable drugs: Amikacin, Capreomycin, kanamycin * TDR-TB: XDR-TB that is completely resistant to all tested drugs (preliminary definition)
30
Subacute LRT Infections aka “Walking” Pneumonias or “Atypical” pneumonias
``` • Prokaryotes – Mycoplasma sp. – Chlamydia sp. – Legionella sp. – Miscellaneous viruses ``` • Eukaryotes – Usually fungi: – Histoplasma sp. – Blastomyces sp. – Coccididioides sp. – Candida sp.
31
Mycoplasma sp. “Walking Pneumonia” | Chlamydophilia sp. “Walking Pneumonia”
• Most common in Children > 5 Years old through young adults • Outbreaks lasting months occur in crowded institutional settings (Military, Colleges, etc.) • No quick, simple or cheap etiologic lab diagnosis – Organism can be cultured, slowly and on special media – Quick PCR based tests are emerging, but they are not really “cheap” nor “simple” * CDC does not separate out Chlamydophilia sp. Pneumonias from the Mycoplasma sp. Ones * Common in “middle age” Children, but 50% of cases occur in adults. Reinfection seems to be common. * No special risk groups.
32
Respiratory Fungal Infections
Clinical Symptoms Mostly mild (fever and cough) or asx. More severe: chills, malaise, fever, chest pain. Sputum production, weight loss. Granulomatous lesions on skin or mucous mems (**may mimic TB**) Pathogenesis Key stages 1. Reach alveoli 2. Convert to form capable of replication at 37C – Mycelial->yeast form.May enhance survival of the fungi since yeasts aren’t killed as easily by phagocytes. 3. Colonize respiratory mucosa. Samples for identification of the dimorphic fungi: • Sputum, Bronchoalveolar lavage (BAL) Transtracheal aspirate, Lung biopsy Techniques used will include: 1. Direct microscopy 2. Fixed specimens: Giemsa stain, indirect FA stain 3. Culture 4. Nucleic acid probes: Ab detection: limited d/t false positives and cross-rxn. • DTH skin tests useful for dx of Coccidiodiomycosis: Mycelial phase antigen: coccidioidin • Spherule phase antigen: spherulin Exoantigen test • Basis:immunodiffusion – Look for presence of specific cell free antigens produced by mycelial phase of the fungi.
33
Histoplasma capsulatum
``` 2 clinically significant varieties i. H. capsulatum var capsulatum – Pulmonary & disseminated infections – Eastern US and Latin America – Thinner cell walls; smaller size (2-4 ``` ii. H.capsulatum var duboisii – Skin and bone lesions – Tropical Africa (“African histoplasmosis”) – Thicker walled; larger yeasts (8-15
34
Blastomyces dermatitidis
• Found in decaying organic matter. • Outbreaks assoc w/contact w/ soil • Most infxnns: mid and eastern N. America. 2 presentations 1) pulmonary and 2) extrapulmonary disseminated.
35
Coccidioides sp.
MOST VIRULENT OF ALL THE HUMAN MYCOTIC PATHOGENS. | • Inhalation of a few conidia
36
Cryptococcus neoformans
* Worldwide distribution * Grows well in soil enriched by pigeon droppings (NB: birds are not vectors). * Most common fungal infection seen in AIDS patients. * Inhalation triggers production of capsule – Composed of glucuronoxylomannan (GXM). * Cryptococci have strong affinity for CNS (neurotropic). * Capsule detectable in blood and fluids: seems to down regulate the immune response. * Can oxidize exogenous catecholamines -> melanin: prevents fungi from phagocytic oxidative damage.
37
Pneumocystis jirovecii
``` Unusual fungus • Lacks ergosterol in cell walls • Difficult to grow in culture Epidemiology: • Worldwide Geographic distribution • Mayormaynotbetransmissible. ```
38
Aspergillus sp.
Clinical syndromes: varied • Various Aspergillus: fumigatus, flavus, Niger Epidemiology: Worldwide. Decaying matter,air, and soil. Outcome of infxn is strongly dependent on host factors 2 forms of aspergillosis: 1. Allergic 2. Invasive:hyphae invade tissue. Can also cause acute pneumonia in severely immunocompromised individuals. e.g, Neutropenia. Sxs: – Deadly, invasive pneumonia – Hemoptysis – High mortality
39
Chemotherapy
Aspergillus sp., Pneumocystis
40
Assisted ventilation
Aspergillus sp.
41
Malnutrition
C. neoformans, Pneumocystis
42
HIV infxn, AIDS
C. neoformans, Pneumocystis
43
Neutropenia (WBC <500/mm3)
Aspergillus, other moulds and yeast-like fungi