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83 Cards in this Set
- Front
- Back
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What type of organism is Bordetella pertusis. Are they nutritionally fastidious?
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Small, nonmotile, aerobic Gram- rod.
These are nutritionally fastidious |
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Transmission of B. pertussis
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Occurs via respiratory droplets...airborne
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Attachment of B. pertussis to the respiratory cilia. Are they invasive?
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Pili protein called hemagglutinin. Once bound they secrete a tracheal cytotoxin that kills the cilia.
They are not invasive, instead, they produce a toxin that increases cAMP levels, and thus protein kinase A, by irreversibly anactivating the Gi-protein complex(via ADP-ribosylation). This inhibits normal cell signaling |
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Bacterium that releases a tracheal cytotoxin that stops cilia from beating. What does this lead to?
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B. pertussis:
This occurs once the hemmuglutinin protein binds the cilia. Causes a mucopurulosanginous exudate to build up in the lungs, compromising the small airways, and predisposing to individual to paroxysmal coughing episodes. |
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Paroxysmal coughing episodes are associated with? Why?
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B. pertussis:
Pertussis toxin that inhibits normal cells signaling. Hemagluttinin protein that facilitates adhesion to cilia. Tracheal cytoxin that kills cilia Hemolysin that destroys epithelial cells |
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A mother brings in her 2 y/o child on a cold day in December for runny nose, hoarseness, barking cough and low-grade fever. This had all developed within 24-48 hrs. Breathing was forced, and noisy, especially upon inspiration. His immunization were up to date. CXR revealed visible upper airway narrowing. Diagnosis? Txmt?
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PIV or RSV
Txmt included nebulized glucocorticoids and epinephrine. Also, humidification of the air may be helpful. |
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What type of virus is Parainfluenze virus?
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SS RNA
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Transmission of PIV
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inhalation of respiratory droplets
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Parainfluenza virus initiates infection by? What mediates virion entry? Target for pathology? Inflammation extends into what mucosal layer?
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H (hemmaglutinin) protein attaches to sialic acid on host cells.
The F (fusion) protein, causes fusion of the envelope with the host cell membrane. It is also responsible for cell-to-cell spread, manifested by development of syncytia. The larynx and trachea are the main targets, and inflammation extends into superficial mucosal membrane |
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PIV envelope contains what antigens? Infected cells produce, and can be detected by?
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H and F proteins
Infected cells produce syncytia and can be detected by Heme absorption |
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In PIV, what area is most susceptible to airway compromise? Worsens on inspiration or expiration?
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cricoid cartilage:
Narrowest pt and cannot expand Inspiratory stridor |
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What causes the bark-like cough of croup in PIV or RSV
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Edema of the vocal cords and subglottic larynx leads to hoarseness, and to the chracteristic bark-like cough.
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Laryngeal and tracheal inflammatory changes in the superficial mucous membrane, resulting in loss of cilia, cell damage, and edema, leading to airway compromisation, especially at the cricoid cartilage level.
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PIV croup
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Atypical pneumonia with absent clinical findings
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M. pneumoniae
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A 20 y/o woman presents with fever, headache, and progressive dry cough that became productive with clear sputum. There was minimal cervical adenopathy, with a normal chest exam. WBC count was normal, as was all other clinical findings. However, CXR showed bilateral, patchy inflitrates. Most likely cause? Txmt?
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Atypical pneumonia:
M. pneumonia DOC is erythromycin or doxycycline |
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Why are cell-wall inhibitors such as B-lactams and cephalosporins, not the correct txmt for M. pneumonia
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The bacteria are wall-less
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Smallest free-living, self-replicating organism. How do they stain? Unique feature?
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Mycoplasmas:
They do not contain a cell wall, and thus do not stain. |
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4 most important features of atypical pneumonia
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1. nonproductive cough
2. variable CXR (patchy,diffuse infiltrates). 3. No bacteria on smear 4. no response to B-lactams |
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Useful for identification of M. pneumoniae
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Fourfold rise in IgG titers between acute and convalescent phases. Obtained 2-3 weeks apart. This is a retrospective diagnosis.
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Major mode of transmission of M. pneumonia
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person-person transmission:
Either inhalation or contact with respiratory secretions |
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Commonly cause outbreaks of pneumonia among military and institutional settings
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M. pneumoniae
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What leads to prolonged cough in M. pneumoniae. What cytotoxic product does it produce?
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Bacterial adherence leads to inhibition of ciliary movement.
Produces H2O2, which leads to cell disruption in the respiratory mucosa, and uncommonly to damage of RBC's (hemolytic anemia) |
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Stimulates T and B lymphocytes, leading to the formation of IgM, which reacts with a variety of host tissues and antigen I on rbc's
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M. pneumoniae
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In some young males, this organism may develop an extensive rash, involving the mucus membranes and large areas of the body. This is called erythema muliforme or Steven Johnson Syndrome
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M. pneumoniae
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Peak activity of RSV? Occur as? Most common age group?
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January or February
Cause community outbreaks Infants 2-6 months old |
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Whate type of virus is RSV? What proteins does its envelope contain?
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SS RNA
Fusion (F) protein and second glycoprotein (G) |
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Unlike influenza virus and PIV, what does RSV not contain?
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H protein
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Replication leads to fusion of neighboring cells into a characteristic, large multinucleated syncytium
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RSV
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Incubation of RSV within the nasopharynx? When does it spread to bronchioles? Most often causes?
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2-8 days...then replication and migration 1-3 days later
Bronchiolitis |
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A 5 month old child was brought into the ER in February, with a 2 day Hx of cough, respiratory difficulty, nasal discharge, and low-grade fever. She attends a day care center. PE showed inspiratory wheezes, and bilateral crackles. WBC was normal. A CXR showed hyperinflation and peribronchiolar infiltrates. Diagnosis? Cause? Txmt?
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Bronchiolitis due to RSV:
Result of inflammation of the terminal bronchioles, necrosis, and sloughing of the epithelial cells, lining the bronchioles. Further, the bronchioles of an infant are very small, and during inflammation, the passage of air to and from the alveoli is restricted leading to wheezing and hyperinflation. No txmt |
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Result of inflammation of the terminal bronchioles, necrosis, and sloughing of the epithelial cells, lining the bronchioles.
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RSV
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Specific area of the respiratory tree most affected by RSV
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terminal bronchioles
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Why does RSV cause more pronounced symptoms in infants?
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Result of inflammation of the terminal bronchioles, necrosis, and sloughing of the epithelial cells, lining the bronchioles.
The bronchioles of an infant are very small, and during inflammation, the passage of air to and from the alveoli is restricted leading to wheezing and hyperinflation. |
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What outer membrane envelope antigens does influenza contain
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H:
hemagluttinin N: neuraminidase |
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Current human types of influenza virus
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A(H1N1)
A(H3N2) |
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Severs the virus as it buds from the plasma membrane or from mucus
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neuraminidase
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Point mutation that results in a change in the configuration of a specific epitope on the surface of the influenza virion
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Antigenic drift:
Usually change of H antigen |
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Occurs due to genetic reassortment that results in a complete change in the configuration of a specific epitope on the surface of influeunza virion
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Antigenic shift
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Transmission of influenza?Incubation?
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Person to person through airborne respiratory droplets.
avg of 48 hrs |
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Clinically effacacious for influenzae A if given within 48 hrs of onset and for 3-5 days.
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Amantadine and rimantidine.
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Useful for both influenza A and B
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Neuraminidase inhibitors:
Zanamivir or oseltamivir |
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Influenza viral pneumonia has what characteristics?
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Interstitial, with diffuse and patchy inflammation localized to interstitial areas at alveolar walls.
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Cause systemic symptoms of influenza
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Cytokines liberated from damaged infiltrating leukocytes
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What types immunity protect against influenza
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Humoral response specific to the strains after resolution of infection or active immunization.
Mucosal immunity via IgA in the respiratory tract. |
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Where does influenza replicate?
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Within mucus-secreting ciliated cells and in other epi cells, resulting in their degenerations.
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Pathogenesis of influenza?
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Virus attaches via H antigen to sialic acid on host ciliated epi cells of the trachea and bronchi. Neuraminidase degrades the protective layer of mucus, allowing viral entry. The virus then fuses with the host membrane, which initiates infection. The virus replicates, causing cell death.
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Motire, flagellated, pleomorphic rods that stain faintly with gram stain
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Legionella pneumophila
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Definitive method for the diagnosis of legionellosis
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culture
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How does legionella grow?
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Nutritionally fastidious, aerobic, grows slowly on selective agar medium
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Organism survives for months in tap water and cooling towers, in association with slimy growth of ameba
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legionella
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natural reservior for legionella
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freshwater ameba
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How is Legionella transmitted?
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Organisms are aerosolized and spread via airborne routes...they are not transmitted person-person
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What subset of pts are particularly at risk for legionella
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Older +50, smokers, alcoholics, immunocompromised individuals...anyone with mucociliary dysfunction.
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Pathogenesis of legionella
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Flagellated organsims penetrate the mucus layer of the lower respiratory tract, and adhere via pili, where the outer membrane binds C3, and is opsonized. The strictly intracellular bacteria, prevent phagosome-lysosome fusion, and replicate within macrophages. Cell mediated immunity that is activated by macrophages, is hte primary host defense. It is the cytokines and reactive mediators from PMN's and T cells that causes tissue injury
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CXR of legionella
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pathcy, diffuse infiltrates
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Main mechanism of tissue damage in legionella
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Cytokines and other reactive mediators from PMN's and T cells that inflict the lung tissue damage.
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Legionairres disease is associated with what laboratory findings?
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hyponatremia and hypophosphatemia...due to systemic disease. Also, has acute, severe, fibropurulent pneumonia with alveolitis and bronchiolitis.
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Acute, flu like, non-pneumonic illness, occurring shortly after exposure to legionella.
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Pontiac fever
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SSRNA togavirus with envelope that contains hemagglutinin
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rubella
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May cause fetal malformations and death, especially in the first trimester, via transplacental infection from a mother with viremia
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rubella
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May cause, mild, febrile disease with diffuse, punctate and maculopapular rash. Often it presents with few constitutional symptoms
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rubella
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How is rubella and measles transmitted
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Respiratory droplet spread or by direct contact with pts.
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Koplik spots of the mouth are pathognomonic for?
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measles
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What causes the rash and febrile exanthems seen in measles and rubella
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Virus specific T-cells attack virus-infected vascular endothelial cells of dermal capillaries.
Antibody-antigen complex mediated vasculitis may also contribute to exanthem illness |
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Pathogenesis of rubella
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Enters and infects the nasopharynx and lungs, attaching to and invading the respiratory epi. It then spreads hematogenously(primary viremia) to the reticuloendothelial system and replicates. This is followed by a febrile illness(secondary viremia), 6-20 days after illness, spreading the virus to other tissues.
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Pathogenesis of measles
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Infects epi of upper respiratory tract. Following primary replication, the virus enters the blood stream and infects the reticuloendothelial cells, where it replicates again. Following secondary replication in the blood stream(viremia) the virus infects many wbc's, particularly monocytes, and spreads to the skin and respiratory tract, leading to coryza, cough, and conjuctivitis(3C's). In cubation period is 7-8 days preceding rash onset. A biologic chracteristic of viral infection in target cells, is the production of multinucleated giant cells with inclusion bodies in the nucleus and cytoplasm.
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Prominent vesicular rash of the face, extremities, palms, and soles
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smallpox
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34 y/o male presents with vesicular chicken-pox rash. 4 days ago he developed a sudden onset of fever, headache, and back pn, however these were resolving before the rash began. He also states that he has had chicken pox before. Pssoible cause?
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Smallpox
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What type of virus is smallpox?
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Large complex ds DNA virus
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Small pox is caused by?
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Variola major
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In a presumptive smallpox case, what is the key function of the lab?
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1. rule out chickenpox
2. Obtain instructions for properly collecting vesicular fluid. |
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When does the smallpox virus become non-contagious
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6 days:
Once the pustular rash goes away. |
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Prodrome stage of smallpox?
What happens next? |
2-4 days:
Fever, headache, fatigue, body aches 4-6 days: Highly contagious Rash begins on tongue and mouth. These spots develop into sores and erupt. The rash then moves to the face, then arms/legs, and then palms/soles. By the 4th day the rash becomes bump filled with pustular fluid and often have a depression. They then become vesicules, burst, and scab. |
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Characteristic rash with bumps filled with thick, opaque fluid and often have a depression.
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smallpox
4th day |
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Smallpox is spread via?
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Exposure to an aerosal release of the virus.
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Incubation period of smallpox. When is the person most contagious?
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7-17 days
Upon development of the rash, 4 days after the start of the prodrome. |
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SARS-CoV is most easily transported via?
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respiratory droplets produced when an infected person coughs or sneezes.
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As opposed to classic coronaviruses (common cold), SARS infection is found where?
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lower respiratory tract
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Causes diffuse alveolar damage and multinucleated giant cells without viral inclusions.
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SARS
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SARS is caused by?
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Coronavirus: large, enveloped RNA virus
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Contain an outer envelope bearing distinctive clud shaped peplomers, providing a crown like appearance.
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SARS
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Human infection is strongly correlated with rodent urine or feces
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hanta virus
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Cellular receptors for Hantavirus
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b3 integrins
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