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331 Cards in this Set
- Front
- Back
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exudates and hemorrhagic spots are indicative of what in pharyngitis?
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bacterial infections
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pseudomembranes in pharyngitis are indicative of (3)
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pharyngeal diptheria
furospirochetal infection infectious mononucleosis |
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vesicles and ulcers on the pharyngeal mucosa are indicative of (2)
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herpes simplex virus
pharyngeal candidiasis |
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how are retropharyngeal abscesses detected? (2)
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gram staining and aerobic culture
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why do you need to drain the pus in an abscess?
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if you do not drain the pus, antibiotics will not work
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what is the single most indicative sign of epiglotittis?
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stridor
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what is the major consideration in bronchitis in children?
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B. pertussis (whooping cough)
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2 pathogens that might cause chronic bronchitis
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Strep pneumonia
haemophilus influenza |
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which type of pneumonia will be seasonal?
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viral influenza
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what is the cause of chronic pneumonia?
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TB
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what type of pneumonia is most common in AIDS patients?
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candida pneumocystis
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what is the most common community acquired pneumonia?
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streptococcus pneumonia
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what 3 pathogens can be aspirated and cause pneumonia?
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coccidioses immitis
M tuberculosis B anthracis |
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what is the disadvantage of using sputum in diagnosing a LRTI?
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often gets contaminated with the specimen of the oropharyngeal flora (saliva) - this will be evident with squamous epithelium
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what is a transtracheal aspiration sample best for testing? (2)
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pneumonia
lung abscess |
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what is a broncho-alveolar lavage best for testing? (1)
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pneumocystis carinii pneumonia
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what is a direct aspiration through the chest wall best for testing (2)
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pneumonia or empyema
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patchy infiltrates on a CXR will indicate
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bronchopneumonia
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uniform consolidation on a CXR will indicate
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lobar pneumonia
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diffuse, interstitial pattern on a CXR will indicate (2)
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viral pneumonia or pneumocystis carinii pneumonia
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Key characteristics of streptococcus pyogenes (4)
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Gram +
non acid-fast non-spore forming non-motile |
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alpha hemolytic groups that have a hazy zone with green discoloration around the colony is indicative of
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strep pyogenes
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2 tests for strep pyogenes
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glucose fermentation (will yield lactic acid)
catalase negative (staph will be catalase positive) |
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key symptoms of a strep pyogenes infection (4)
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fever, malaise
redness of throat sore throat/diffuculty swallowing white patches of pus with hemorrhagic sports or yellow/white exudates |
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what does strep pyogenes have the potential to develop into? (3)
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otitis media
acute rheumatic fever scarlet fever |
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4 virulence factors in strep pyogenes
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hyaluronic acid
M factor Protein G Protein F |
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what does hyaluronic acid do for virulence?
|
method of immune invasion
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what does M factor do for virulence?
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degrades C3b and thus escapes phagocytosis
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what does protein G do for virulence?
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binds to Fc portion of the Ab and inhibits phagocytosis
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what does protein F do for virulence?
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mediates attachment
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what 3 things can the exotoxins of strep pyogenes cause?
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scarlet fever
toxic shock necrotizing fasciitis |
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what will a positive throat swab for strep pyogenes show?
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visible clumps produced by antigen and antibody
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what will a negative throat swab for strep pyogenes show?
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no clumping, smooth milky reaction
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How do you differentiate group A strep from group B?
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only group A is bacitracin sensitive
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Is there a strep pyogenes vaccine?
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No, there are too many strains which also leads to repetitive infections
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First choice treatment for strep pyogenes
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penicillin (beta-lactam)
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how do you treat step pyogenes in penicillin sensitive patients?
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erythromycin and first generation cephalosporins
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what causes scarlet fever?
|
strep pyogenes infected by a virus
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what are the key signs of scarlet fever (6)
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strawberry tongue
sand-paper rash dark red lines in skin folds fever lethargy sore throat |
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what is the drug of choice for scarlet fever?
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penicillin
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what drug is used to treat scarlet fever in penicillin sensitive individuals? (2)
|
tetracycline or clindamycin
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what is quinsy?
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painful abscess around the tonsil
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what is Rheumatic fever? (2)
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antibody generated against streptococcal antigens that cross react with antigenic epitopes on cardiac cells
usually begins 3 weeks post strep infection |
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what are two key features of rheumatic fever?
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joint pain
nodules under the skin |
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what is the jones criteria?
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criteria for diagnosing rheumatic fever; must have 2 of the major or one major and one minor
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major criteria of the jonoes criteria (5)
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carditis
arthritis chorea subcutaneous nodules erythema marginatum |
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treatment for rheumatic fever
|
ten day course of penicillin or a sigle penicillin G injection
maintentence dose of penicillin to prevent relapse |
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what is sub acute bacterial endocarditis?
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results from infection of the damaged valves of the heart by normal flora of the mouth (strep viridans) and skin (strep epidermidis)
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what are the virulence factors of strep pneumonia (2)?
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very thick capsule which prevents phagocytosis
pneumolysin |
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key features of strep pneumonia (4)
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alpha hemolytic
gram + reside in pairs normal flora of URT |
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key symptoms of strep pneumonia (4)
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purulent, rust colored sputum
chest congestion cough fever with shaking chills |
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what is the number one cause of pneumonia in alcoholics?
|
strep pneumonia
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what is the number one cause of meningitis in adults?
|
involvement of the meninnges from strep pneumonia
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how is strep pneumonia differentiated from strep viridans?
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susceptibility to optochin or bile solubility
|
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is there a vaccine for strep pneumonia?
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yes, two:
older people should seek pneulomax (immunity to 23 strains) children may get a cojugate vaccine (immunity to 7 strains) |
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what is the first line treatment for strep pneumonia?
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penicillin
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how do you treat penicillin resistant strains of strep pneumonia?
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macrolides
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can a patient develop immunity to s pneumonia?
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no, it does not occur due to a large amount of serotypes
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what are the key features of diptheria (4)
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corynebacterium
gram + rod chinese letter patterns/side by side palisades catalase is produced and many strains produce acid through carb fermentation |
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what is the tinsdale agar used for?
|
selective and differential for diptheria
potassium tellurite allows the development of dull grey or black colonies indicating tellurite reductase activity |
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what is loefflers medium used for?
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to cultivate C diptheria
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what is the source of a diptheria infection
|
symptomatic and asymptomatic patients
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what are the characteristic symptoms of diptheria
|
starts with respiratory symptoms
characteristic membrane on the tonsils and pharynx = grey-white membrane that is adherent to the underlying tissue and not easily removed (result of clotted blood and leukocytes that are killed by exotoxins) |
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diagnosis of diptheria
|
entirely clinical because direct smear is not a reliable tool
a definitive diagnosis can be made by isolating and identifying the organism |
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is there a vaccine for diptheria?
|
yes, the vaccine is for the diptheria toxoid
booster should be given every 10 years |
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treatment for diptheria
|
anti-serum against toxoid should be administered asap (but patient should be tested for hypersinsitivity first)
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treatment with penicillin or erythromycin in diptheria
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will only inhibit transmission, not protect against the adverse effects of the toxin
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can one develop immunity to diptheria?
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yes, antibodies are made against the toxin
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what does H influenza grow best on?
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chocolate agar
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what will h influenza not grow on?
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blood agar
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why is the type B capsule of h influenza significant?
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it is a polymer of ribose, ribitol, and phophate
highly associated with virulence |
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where can type B h influenza produce infections? (6)
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CNS
epiglottis soft tissue bronchitis sinusitis otitis media |
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what does h influenza require to grow in culture? (2)
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hematin (X-factor)
NAD (nicotine adeamide diphosphate, V factor) |
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children under 2 with h influenza mostly suffer from
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meningitis
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children 2-5 with h influenza mostly suffer from (2)
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epiglottitis
pneumonia |
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which forms of h influenza are invasive?
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only capsulated forms
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how is h influenza diagnosed?
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combination of clinical findings and typical gram stain
must be confirmed by isolation of the organisms from the site of infection or blood |
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is there a vaccine for h influenza?
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yes
a conjugate vaccine against HiB has reduced the incidence of invasive H influenza by 99% |
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what is the treatment for H influenza?
|
third generation cephalosporin
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can you develop immunity to H influenza?
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yes
an antibody to the capsule is produced infants are protected for up to 6 months from maternal antibody |
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key features of bordetella pertussis (3)
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strictly encapsulated
strictly aerobic very sensitive to sunlight and drying so it only survives briefly outside the respiratory tract |
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what does bordatella pertussis grow on?
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special medium (Regan-Lowe of Bordet-gengou) supplemented with nicotinamide and charcoal
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how long does it take a b. pertussis colony to grow?
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3-7 days
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what does a b pertussis colony look like?
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tiny drops of mercury
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what are the 3 stages of b pertussis?
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catarrhal
paroxysmal convalescent |
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what is the catarrhal stage of pertussis? (3)
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profuse, mucoid rhinorrhea for 1-2 weeks
malaise, fever, sneezning, anorexia most communicable at this stage |
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what is the paroxysmal stage of pertussis (3)
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paroxysmal coughing with whoop
lymphocytosis most infectious at this stage |
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what is the convalescent stage of pertussis (1)?
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symptoms gradually subside
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what are the virulence factors of pertussis? (6)
|
pertussis toxin
AB toxin G protein increased cAMP adenylate toxin tracheal cytotoxin |
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why is the increase in cAMP in pertussis bad?
|
it leads to an increase in mucous secretion
this leads to decreased killing ability of phagocytes, a massive release of lymphocytes in the blood, and ineffective NK functions |
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how does the tracheal cytotoxin lead to cough in pertussis?
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it produced NO which causes the death of ciliated cells so pt can't clear airways
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how do you diagnose pertussis?
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confirmed by isolation of the organism via nasopharyngeal secretions or swab
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what is a rapid method to diagnose pertussis?
|
direct fluourescent antibody
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is there a vaccine for pertussis?
|
yes
killed pertussis |
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what is the treatment for pertussis?
|
erythromycin or clarithromycin (in the catarrhal phase)
antibiotics will only eliminated the bacteria, not the toxin |
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can one become immune to pertussis?
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yes,
the body produces IgG against PT, pili, and pertactin immunity is not lifelong but second attacks tend to be mild |
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key characterisitics of m. tuberculosis (3)
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acid fast
strictly aerobic does not form spores |
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composition of the cell wall of TB (4)
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mycolic acid (60%)
mycosides sulfolipids LAM (structurally similar to LPS) |
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how does TB's high lipid content affect its survival?
|
makes it highly resistant to drying, disinfectants, and strong acids/alkali
also means it must be heated before staining in order to melt the lipids |
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what type of test can be used to screen TB sputum?
|
auramine-rhodamine staining; mycobacterium will fluouresce a bright apple green
sensitive but not specific |
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who is PPD positive in when it is 5mm
|
HIV+, anyone with recent TB exposure
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who is PPD positive when it is 10mm
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high risk population, IV drug abusers, poverty, immigrants
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who is PPD positive when it is 15mm?
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low risk population
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what is sulfatides in TB
|
sulfolipids in cell envelope
inhibit phagosome-lysosome fusion, allowing intracellular survival if fusion does occur, the waxy nature of the cell envelope reduces the killing effect |
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what is cord factor in TB
|
causes serpentine growth in vitro
inhibits leukocyte migration disrupts mt respiration and oxidative phosphorylation |
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what components of TB lead to DTH?
|
tuberculin and mycolic acid
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Key symptom of primary TB
|
may remain asymptomatic
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what is a tubercle?
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granulomas consisting of a central core containing TB bacteria in enlarged macrophages and a surrounding area of fibroblasts, lymphocytes, and neutrophils
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what is a ghon's complex?
|
ghon's focus (1st site of infection) + lymphadenopathy
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key symptoms of secondary TB (3)
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hemoptysis
low grade fever night sweats |
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when does disseminated extrapulmonary TB occur?
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when TB baccilus is disseminated to organs or tissues outside the lungs
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what organs are most at risk for extrapulmonary TB? (6)
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regional lymph nodes
kidneys long bones and spine genital tract GI tract brain and meninges |
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ways to diagnose TB (4)
|
PPD
CXR direct smear staining with ziehl neelsen procedure Quantiferon |
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Why is growing a TB colony not a good diagnostic procedure?
|
it takes 4-6 weeks to grow
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is there a TB vaccine?
|
yes, but it is not given in the US
live attenuated strain of M bovis contraindicated in the immunocompromised |
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what is the disadvantage of isoniazid as a TB drug?
|
peripheral neuropathy
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what is the disadvantage of ethambutol as a TB drug?
|
eye complications
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what is the disadvantage of rifampin as a TB drug?
|
orange urine
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what is the disadvantage of pyrazinamide as a TB drug?
|
hepatitis
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what is the disadvantage of streptomycin as a TB drug?
|
ototoxicity
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treatment of active TB
|
6-9 months
INH, rifampin, ethambutol for 2 months INH, rifampin for 4-7 months |
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how long is an extrapulmonary TB treated?
|
12 months
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what test will be positive with a mycobacertia kansaii infection?
|
PPD
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where is mycobacteria kansasii found?
|
urban people in IL, OK, TX
|
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how does mycobacteria avium-intracellulare manifest?
|
as cavitary pulmonary disease
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what is the key symptom differentiated TB from avium intracellulare?
|
diarrhea in avium
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treatment of m. avium intracellulare
|
macrolides
prognosis is grave |
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what is a common cause of granulomatous in children?
|
mycobacteria scrofulaceum
|
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what are the key factors of leionella? (2)
|
gram - rod
difficult to stain with gram staining |
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what does leionella require for growth?
|
charcoal
cysteine ferric ions slightly acidic conditions |
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who is most at risk for legionaires? (2)
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smokers
chronically immunosuppressed |
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key symptoms of legionaires (5)
|
headache
muscle ache fever with chills and rigors dry cough some people have GI problems |
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2 factors that aid in the phagocytosis of legionaires
|
Porin proteins - bind to complement (C3b)
macrophage invasion potentiator - surface protein that aids with entry |
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why is penicillin ineffective against legionaires?
|
leigionella produces beta-lactamase
|
|
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what is the treatment for legionella?
|
erythromycin alone or in combination with rifampin
|
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key characteristics of mycoplasmal pneumonia (3)
|
smallest known self-replicating orgainsm
lack a cell wall do not stain with gram stain |
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what does m. pneumonia grow on?
|
a special medium that will produce a fried-egg appearance
|
|
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why is penicillin ineffective against m. pneumonia?
|
it lacks a cell wall
|
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|
most common presentation of m. pneumonia
|
individual is usually ambulant, "walking pneumonia"
|
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How does m. pneumonia affect the respiratory tract?
|
bacteria interferes with ciliary action leading to desquamation of the mucosa and an inflammatory reaction
|
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why is culture not used in diagnosing m. pneumonia
|
growth is slow and takes a week or longer
|
|
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how do you diagnose m pneumonia?
|
usually serologic
single high complement fixation of IgM specific antibody titer |
|
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is there a vaccine for m pneumona?
|
No
|
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How is m pneumonia treated?
|
erythromycin and tetracyclin
|
|
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can one become immune to m pneumonia?
|
yes but the immunity disappears in 6-12 months
|
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key features of klebsiella pneumonia (2)
|
large polysaccharide capsule that interferes with complement deposition
strikingly mucoid |
|
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who is most at risk for k pneumonia? (3)
|
debilitated patients
alcoholics immunocompromised |
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What makes k. pneumonia resistant to antimicrobials?
|
R factors
|
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what is they key symptom of k. pneumonia?
|
curant jelly sputum
|
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how does k. pneumonia gain entry to the lungs?
|
oral cavity
|
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what is the main concern with k pneumonia?(2)
|
permanent lung damage due to host cell death that forms absecces
shock may also be induced by exotoxin |
|
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what is the primary way to diagnose k pneumonia?
|
culture on mac agar which demonstrates lactose fermentation
|
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is there a vaccine for k pneumonia?
|
no
|
|
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what is the treatment for k pneumonia
|
ciprofloxacin
|
|
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what is k pneumonia resistant to?
|
penicillin
|
|
|
key features of pseudamona aurgenosa (6)
|
only psuedomona that is not an opportunistc pathogen
motile non-spore forming commonly produce a fluourescent yellowish pigment which combines with a blue pigment to produce a strinkingly geen color distint fruity odor oxidase positive |
|
|
what is responsible for p. aureginosas slime?
|
alginate (mannuronic + glucuronic acid)
|
|
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what are the virulence factors of p. aureginosa? (3)
|
exotoxin A (expression is influenced by O2)
exoenzyme S elastase |
|
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what does exotoxin A in p aureginosa do?
|
enters the cell and inactivated elongation factor 2
no systemic effects but is locally cytotoxic |
|
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what does exoenzyme S in p aureginosa do?
|
ADP-ribosylates several intracellular proteins including vimentin
|
|
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diagnosis of p aureginosa (4)
|
beta-hemolytic
oxidase positive produces procanin grows at 42C |
|
|
where can p aureginosa be caught?
|
the hospital via respirators, solutions, sinks, etc
|
|
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who is at greatest risk for p aurgenosa? (2)
|
neonates and IV drug users
|
|
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What is p auregenosa resistant to and why?
|
resistant to antimicrobials via porin proteins which are mutations of genes encoding target molecules and plasmid mediated mutation
|
|
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how should p aurgeinsoa be treated? (3)
|
beta-lactams:
anti-pseufomonals penicillins third generation cephalosporins |
|
|
is there a vaccine for p auregenosa?
|
yes but only for burn patients, CF patients, and immunocompromised
|
|
|
key features of chlamydia(3)
|
obligate intracellular bacteria
lack a rigid cell wall non-seasonal |
|
|
what does chlamydia trachomatis cause? (2)
|
genital infections
conjunctivitis |
|
|
what does chlamydia psittaci cause?
|
respiratory infections
|
|
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what does chlamydia pneumonia cause?
|
respiratory infections
|
|
|
key symptoms of chlamydia
|
usually mild or asymptomatic (walking pneumonia)
more severe infections appear in the form of pharyngitis or LRTI |
|
|
what bacteria is related to atherosclerosis?
|
chlamydia
|
|
|
why is diagnosis of chalmydia difficult?
|
because it is an intracellular organism and must be grown in living cells
|
|
|
what are 2 reliable methods of chlamydia diagnosis?
|
PCR
IFM using antibody directed against EB |
|
|
is there a vaccine for chlamydia?
|
no
|
|
|
that is the key feature of chlamydia psittaci?
|
it is a zoonitic disease that can be transmitted to humans through inhalation of respiratory secretions or durst from infected bird droppings
|
|
|
what are the key signs of c. psittaci? (3)
|
causes focal necrosis in the liver and spleen
alveolar necrosis and occasional hemorrhage are also seen mucus plugs in the airway |
|
|
diagnosis of c psittaci
|
serodiagnosis to confirm clinical and radiological findings
4-fold increase in titer of complement |
|
|
how do you treat c psittaci?
|
macrolides and tetracycline
|
|
|
key features of bacillus anthracis (3)
|
spore forming
gram + rods form very long chains of rods |
|
|
what prevents the phagocytosis of anthrax? (2)
|
D-glutamic acid polypeptide capsule which allows the organisms to survive and produce more exotoxin
form colonies with rough, uneven surface projections with multiple curled extensions resembling medusa head |
|
|
anthrax toxin components (4)
|
temperature sensitive plasmids
Factor I factor II factor III |
|
|
what does factor I in anthrax do?
|
edema factor, necessary for the edema producing activity of the toxin
|
|
|
what does factor II in anthrax do?
|
protective antitoxic antibodies
|
|
|
what does factor III in anthrax do?
|
lethal factor
|
|
|
key features of cutaneous antrhax (3)
|
most common form
usually acquired through injured skin or mucous membranes may be fatal if it enters the blood stream |
|
|
how does pulmonary anthrax manifest itself?
|
begins abruptly with high fever and chest pain
|
|
|
what is the key pathological feature of pulmonary anthrax?
|
mediastinal hemorrhagic lymphadenitis
|
|
|
what type of specimen should be collected for anthrax?
|
sputum
|
|
|
what will exclude anthrax in a culture? (2)
|
hemolysis
motility |
|
|
what prevents the phagocytosis of anthrax? (2)
|
D-glutamic acid polypeptide capsule which allows the organisms to survive and produce more exotoxin
form colonies with rough, uneven surface projections with multiple curled extensions resembling medusa head |
|
|
anthrax toxin components (4)
|
temperature sensitive plasmids
Factor I factor II factor III |
|
|
what does factor I in anthrax do?
|
edema factor, necessary for the edema producing activity of the toxin
|
|
|
what does factor II in anthrax do?
|
protective antitoxic antibodies
|
|
|
what does factor III in anthrax do?
|
lethal factor
|
|
|
key features of cutaneous antrhax (3)
|
most common form
usually acquired through injured skin or mucous membranes may be fatal if it enters the blood stream |
|
|
how does pulmonary anthrax manifest itself?
|
begins abruptly with high fever and chest pain
|
|
|
what is the key pathological feature of pulmonary anthrax?
|
mediastinal hemorrhagic lymphadenitis
|
|
|
what type of specimen should be collected for anthrax?
|
sputum
|
|
|
what will exclude anthrax in a culture? (2)
|
hemolysis
motility |
|
|
is there a vaccine for y pestis?
|
no, because there are so many rodent vessels
|
|
|
how do you treat y pestis?
|
streptomycin
|
|
|
can one become immune to y pestis?
|
yes, CMI response is critical for this
|
|
|
key features of norcardia (3)
|
gram + rods
aerobic may tend to stain gram - with intracellular gram + beads |
|
|
what will norcardia grow on?
|
blood or chocolate agar after 2-3 incubation in air
|
|
|
appearance of norcardia in culture
|
initially have a dry wrinkled appearance but then develop white to orange pigment
branching pattern and acid fastness may be used for a presumptive diagnosis |
|
|
what does norcardia smell like?
|
wet dirt
|
|
|
how is norcardia acquired? (2)
|
pulmonary = inhalation of aeriolized bacteria
cutaneous = injection by a thorn prick |
|
|
what is the pulmonary form of norcardia?
|
asteroids
|
|
|
how does norcardia avoid phagocytosis
|
dissruption of acidification ph phagosomes or by resisting oxidative burst
|
|
|
what does norcardia do to the lungs?
|
acute inflammation with suppuration and destruction of parenchyma (multiple abscesses may occur)
|
|
|
what are the respiratory manifestations of norcardia? (3)
|
acute
chronic relapsing |
|
|
what are the common signs of norcardia? (3)
|
cough
production of cavity and extension to pleura dissemintation to brain with focal neuro signs |
|
|
diagnosis of norcardia
|
clincal features with radiologic and bacteriological findings
|
|
|
what type of specimen should be used for norcardia diagnosis?
|
multiple sputum samples
|
|
|
how do you treat norcardia?
|
sensitive to sulfonamide anibiotics
therapy should continue for 6 weeks |
|
|
key features f ehococcus (3)
|
produces a characterisitc salmon pink colong
varies from cocci to bacilli facultative intracellular pathogen of macrophages |
|
|
where is rhodoccus found?
|
in the soil
|
|
|
who does rhodoccus effect?
|
causes invasive pulmonary disease in immunocompromised patients
|
|
|
what are other manifestations of rhococcus? (2)
|
lymphadenopathy
eye drainage and pain |
|
|
treatment for disseminated rhodoccus
|
combinaion of IV antibiotics
vancomycin + imipenem |
|
|
treatment for localized rhodoccus (3)
|
single antibiotic, either
erythromycin rifampin ciprofloxacin |
|
|
3 viral causes of the common cold
|
rhinovirus
corona virus adeno virus |
|
|
key features of the rhinovirus (4)
|
member of picorna virus
small RNA non enveloped SS+ |
|
|
what does rhinovirus target?
|
respiratory epithelium via virus specific receptors; infected cells then lose their ciliary motion
|
|
|
what is the response to rhinovirus?
|
cell injury causes inflammatory mediators which induce acute symptoms
|
|
|
what is the treatment for rhinovirus
|
pleconaril is an anti-picornavirus that may shorten the course of symptoms
|
|
|
how does pleconaril work?
|
it prevents uncoating of the virus thus inhibiting the relase of the nucleic acid
|
|
|
key features of adenovirus (4)
|
non enveloped
double stranded resistant to low pH, bile, and proteolytic enzymes however, easily inacitvated by heat |
|
|
key transmission route for adenovirus
|
fecal-oral
|
|
|
key respiratory symptoms of adenovirus (3)
|
fever (more frequent than common cold)
sore throat with grey-white pus enlarged cervical lymph nodes |
|
|
key non-respiratory symptoms of adenovirus (2)
|
acute hemorrhagis cystitis with hematuria and dysuria
gastroenteritis |
|
|
is there a vaccine for adenovirus?
|
yes, but only reserved for military
contains live virus |
|
|
key feature of corona virus in culture
|
petal or club shaped spike projecting from the surface giving the appearance of a crown of thorns
|
|
|
how does corona virus cause damage?
|
induces cell mediated immune response and production of neutralizing antibody
|
|
|
type I corona virus
|
common cold
|
|
|
type III corona virus symptoms (6)
|
SARs
sudden high fever features of pneumonia respiratory distress diarrhea 10% fatal rapid transmission through droplets |
|
|
key features of the influenza virus (2)
|
orthomyxovirus family
genome with 8 segments |
|
|
virulence factors in influenza virus (2)
|
hemagluttin (binds to receptors on ciliated cells)
neuraminidase (destroys receptors to which hemagluttin binds) |
|
|
which strain of the influenza virus is most severe and widespread?
|
A
|
|
|
why is influenza virema rarely detected?
|
specifically infect epithelial cells via sialic acid moiety
|
|
|
where does the influenza virus multiply
|
within ciliated respiratory epi
|
|
|
what does influenza virus multiplication cause (3)
|
inhibition of protein and nucleic acid synthesis
release of lysosomal hydrolytic enzymes desquamation of both ciliated cells and mucous producing cells |
|
|
what causes local inflammation in influenza virus?
|
activation of complement
|
|
|
what does influenza virus recovery depend on? (3)
|
efficient production of IFN to limit virus replication
rapid generation of NK cells generation of virus specific CTL |
|
|
what is reyes syndrome?
|
occurs in children 2-12 days after onset of influenza virus
severe fatty liver and cerebral edema risk increases with exposure to salicilates |
|
|
how can specific strains of influenza virus be differentiated?
|
virus culture
|
|
|
is there a vaccine for influenza virus?
|
yes, 2
killed vaccine (2 strains of A + 1 strain of B) live, attenuated given intranasally |
|
|
what is the treatment for influenza virus and how does it work?
|
mantadine and riamtadine are effective by blocking the ion channel of the viral M2 protein thus interfering with viral uncoating
|
|
|
key features of parainfluenza virus (3)
|
non segmented
SS - contains fusion proteins which spike out from the envelop |
|
|
what is the major cause of croup?
|
parainfluenza virus
|
|
|
key features of RSV (3)
|
belongs to paramyxovirus family
SS RNA - non segmented genome |
|
|
2 key glycoproteins of RSV
|
F-fusion protein
G protein - highly glycosylated for attachment to host cells |
|
|
when are RSV outbreaks most common?
|
late fall to late spring, peaking in mid winter
|
|
|
what gives rise to the dyspnea in RSV?
|
sloughed off cells, mucous, and clotted plamsa clog the bronchioles (which are already inflammed)
|
|
|
how should RSV specimens be transported?
|
on ice
|
|
|
who is serology of RSV not useful for?
|
young infants
|
|
|
is there a vaccine for RSV?
|
no
|
|
|
how is RSV treated?
|
antiviral ribavirin may be considerd in patients with underlying conditions, otherwise supportive
|
|
|
key features of hantavirus (2)
|
causative agent = sin nombre
enveloped virus |
|
|
what is a predisposing factor to hantavirus?
|
close contact with rodents
|
|
|
how does hantavirus cause damage?
|
massive amount of antigen is present in the lung capillaries as well as heart; inflammatory response causes a large amount of plamsa to leak into the lungs thus suffocating the patient
loss of intracellular fluid leads to hypotension, shock, and death |
|
|
early symptoms of hantavirus (5)
|
fever
muscle ache nausea vomitting diarrhea |
|
|
what is the characteristic diagnosis of hantavirus?
|
large, atypical lymphocytes combined with bandemia and dropping platelet count
|
|
|
treatment of hantavirus
|
supportive
|
|
|
key features of pneumocystis carinii jiroveci
|
fungal
considered to be protozoa until 80s mode of transmission not established humans become seropositive within the first few years of life |
|
|
cell membrane of pneumocystis
|
lacks ergasterol so not sensitive to traditional anti-fungal agents
|
|
|
who is affected by pneymocystis
|
immunodeficient
|
|
|
key symptoms of pneumocystis (3)
|
gradual onset
dyspnea, tachypnea death usually due to respiratory failure |
|
|
how does pneumocystis cause damage?
|
alveolar walls become thickened and scarred, preventing the passage of oxygen
|
|
|
why is sputum not a good specimen for pneumocystis?
|
yeild is low because it is found in the alveoli
|
|
|
what is the best way to collect a pneumocystis specimen?
|
BAL
|
|
|
treatment for pneumocystis
|
treat with trimethoprim-sulphamethoxasole
recommended as soon ad CD-4 count drops below 200 - AIDS patients must continue until CD4 rises above 200 |
|
|
can one become immune to pneumocystis
|
yes
macrophages and CD4s play most important role |
|
|
key features of coccidiomyosis (3)
|
mold form grows in soil
hyphae devlop barrel shaped arthrospores found in areas where soil is rich in carbon and salt content (semi-arid/semi-hot) |
|
|
what is coccidiomyosis also known as?
|
valley fever
|
|
|
when is coccidiomyosis dormant?
|
winter and spring
|
|
|
what is a less common symptom of coccidiomyosis?
|
tender nodules localized to the shin and pain in the joints (due to hypersensitivity)
|
|
|
what are fungiomas?
|
nodular growths found in chronic progressive pulmonary disease from coccidiomyosis
|
|
|
what causes damage in coccidiomyosis?
|
inflammatory response
|
|
|
what is the major cause of croup?
|
parainfluenza virus
|
|
|
key features of RSV (3)
|
belongs to paramyxovirus family
SS RNA - non segmented genome |
|
|
2 key glycoproteins of RSV
|
F-fusion protein
G protein - highly glycosylated for attachment to host cells |
|
|
when are RSV outbreaks most common?
|
late fall to late spring, peaking in mid winter
|
|
|
what gives rise to the dyspnea in RSV?
|
sloughed off cells, mucous, and clotted plamsa clog the bronchioles (which are already inflammed)
|
|
|
how should RSV specimens be transported?
|
on ice
|
|
|
who is serology of RSV not useful for?
|
young infants
|
|
|
is there a vaccine for RSV?
|
no
|
|
|
how is RSV treated?
|
antiviral ribavirin may be considerd in patients with underlying conditions, otherwise supportive
|
|
|
key features of hantavirus (2)
|
causative agent = sin nombre
enveloped virus |
|
|
what is a predisposing factor to hantavirus?
|
close contact with rodents
|
|
|
how does hantavirus cause damage?
|
inflammatory response causes a large amount of plasma to leak into the lungs, suffocating the patinet
|
|
|
early symptoms of hantavirus (5)
|
fever
muscle ache nausea vomitting diarrhea |
|
|
what is the characterisitic diagnosis of hantavirus?
|
large, atypical lymphoctye combined with bandemia and dropping platelet count
|
|
|
treatment for hantavirus
|
supportive
|
|
|
key features of pneumocystis carinii jiroveci (4)
|
fungus
used to be considered protozoa until late 80s mode of transmission unknown humans are seropositive in first few years of life |
|
|
cell membrane of pneumocystis
|
lacks ergasterol so not sensitive to traditional anti fungals
|
|
|
key symptoms of pneumocysits (3)
|
gradual onset
dyspnea, tachypnea death usually due to respiratory failure |
|
|
how does pneumocystis cause damage?
|
alveolar walls become thickened and scarred, preventing the free passage of oxygen
|
|
|
why is sputum not a good specimen for pneumocystis?
|
because it is found in the alveoli
|
|
|
what is the best way to collect a specimen for pnuemocystis?
|
BAL
|
|
|
what is the treatment for pneumocystis?
|
immediate treatment with trimthoprim sulphamethoxazole
|
|
|
when should pneumocystis treatment being?
|
as soon as CD4 falls below 200
AIDS patients must continue treatment until CD4 goes back to 200 |
|
|
key features of coccidiomycosis (3)
|
mold form grows in soil
hyphae develop barrel shaped arthrospores (very infectious) found in areas where soil is rich in carbon and salt (semi-arid/semi-hot) |
|
|
what is coccidiomycosis also known as
|
valley fever
|
|
|
when is coccidiomycosis dormant?
|
winter and spring
|
|
|
what is a less common symptom of coccidiomycosis?
|
tender nodules localized to the shin and pain in the joints (due to hypersensitivity)
|
|
|
what are fungiomas?
|
nodular growths that cause chronic progressive pulmonary disease due to coccidiomycosis
|
|
|
is coccidiomycosis self limiting?
|
in healthy indivuduals
in a small number of cases the site of inflammation can undergo necrosis and cavitation of the lungs develops |
|
|
how do you treat coccidiomycosis?
|
amphotericin B and flucanozole which have to be given for long periods of time and have considerable side effects
|
|
|
what is histoplasmosis also known as?
|
ohio valley fever
|
|
|
how does histoplasmosis grow below 35 degrees?
|
white or brown hair like mycelium
|
|
|
how does histoplasmosis grow above 37 degrees?
|
on blood agar creates a creamy white textured colony; does not have a capsule
|
|
|
where is histo most found?
|
soils contaminated with bat droppings
|
|
|
what does the mold form of histo look like?
|
large conidia with projecting knobs
|
|
|
what are the key symptoms of histo? (3)
|
most are asymptomatic
widely variable course of disease may manifest pulmonary or systemic skin lesions |
|
|
what are the key systemic symptoms of histo (3)
|
hepato- and splenomegaly in children
anemia, circulatory collapse, and death lesions in brain, intestines, etc |
|
|
what patients will have persistent colonization of histo and what will it look like?
|
emphysema and bronchitis patients
symptoms similar to TB |
|
|
how is histo detected in disseminated disease?
|
detection of circulating polysaccharide antigen in serum or urine via enzyme immunoassay
|
|
|
treatment of histo
|
amphotericin B and itraconazole
|
|
|
can one become immune to histo?
|
yes, cell mediated response is most important
|
|
|
most frequent infections of aspergillosis (3)
|
a fumigatus
a flavus a niger (sometimes) |
|
|
what does aspergillus mold look like?
|
rapidly growing with branching septaie hyphae
characteristic of conidia on conidiophoree |
|
|
how is aspergillus transmitted
|
inhalation from the environment
survive well in the enviornment |
|
|
key features of allegic aspergilliosis of the lung (3)
|
transient pulmonary infiltrates
eosinophilia rise in aspergillus-specific antibodies |
|
|
key features of invasive aspergillus of the lung (4)
|
associated with pre-exisiting condition
lung tissue may involve blood vessel leading to hemoptysis acute pneumonia may occur mortality approaches 100% |
|
|
what is the classic diagnostic sign of aspergilliosis
|
classical air crescent sign of fungal ball or aspergillioma
|
|
|
what is the problem with diagnosis of aspergilliosis
|
distinguishing colonization from invasion so must get a speciment through BAL or aspiration
|
|
|
why is serology not helpful in diagnosing aspergilliosis
|
because anti-aspergiollus antibody is present in healthy individuals
|
|
|
treatment for aspergillus
|
amphoterecin B and intraconazole are recommended but may not be effective
may need surgical excision of localized lesion |
|
|
can one become immune to aspergillus?
|
yes, innate immunity plays the most important role
|
