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101 Cards in this Set
- Front
- Back
Rhinovirus is a _____.
A. picornavirus B. coronavirus C. adenovirus D. orthomyxovirus E. paramyxovirus |
A.
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The capsid adhesin on Rhinovirus bind to what molecule(s) on nasopharynx epithelial cells?
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ICAM1 and LDL-1
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What is a special surface structure on Rhinovirus that aids in binding and viral release?
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structual cleft or "canyon"
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What's the genomic content of Rhinovirus?
What is it code for? |
single strand (+) RNA.
RNA polymerase, protease, and 4 capsid proteins. |
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Is Rhinovirus enveloped?
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No.
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What temperature is Rhinovirus best grown under?
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33 degree C (as in nasal mucosa).
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Viral shedding peaks around days____.
A. 0-2 B. 2-4 C. 5-7 |
B.
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What type(s) of body's defense against Rhinoviral replication?
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This viral replicaiton occurs in cytoplasm. So endogenous IFN(αβγ), IL12 and mobilization of cytotoxic cells.
Humoral response also plays a role: IgA at mucosal surface. |
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Symptoms of common cold caused by Rhinovirus infection result from_____?(3)
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1. edema,seromucinous exudation(protein eg. fibrinogen)
2. chemical mediators (bradykinin, histamine, prostaglandins, interleukins) 3. mininal epithelium destruction by virus |
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What are some key symptons of commom cold?
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1. nasal discharge/obstruction
2. sneezing 3. sore/scrachy throat 4. cough (due to irritation of nasal discharge) 5. fever more common in infants 6. yellow/greenish exudate: organism in paranasal sinus |
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How long do the symptoms usually last?
When do the symptoms peak? |
1-2 weeks.
Day 2-3. |
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What are some complications with common cold?
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1. colonization by new flora due to damaged epithelium
2. sinusitis, otitis: due to inability to remove bacteria 3. asthma:inadequate INF-β response and preferential Th2 response with IgE production. 4. COPD |
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How is common cold diagnosed?
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1. clinical presentation
2. culture |
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What kind of treatment do you give to patients with common cold?
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symptomatic treatment:
1. antihistamine 2. anti-inflammatory drugs 3. warm saline gargles or anesthetic lozenges for sore throat. |
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What is warm saline used to treat?
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sore throat
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What is anesthetic lozenges used to treat?
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sore throat
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Are vaccines available for common cold?
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No.(except influenza)
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What are the two most important organisms that cause Pharyngitis?
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1. rhinovirus
2. streptococcus pyogenes (Group A streptococci) |
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What is herpangina?
And it is caused by what organism? |
Painful mouth infection caused by coxsackieviruses.
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What are some observations of herpengina?
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1. vesicular eruption of soft palate(usually tonsils and uvula)
2. fever 3. sore throat, pain on swallowing |
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Herpangina is most common in people of what age group?
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Children: 3-10 yrs.
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Describe the development steps of vesicular eruption.
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punctate macule
erythematous papules vesicular lesion |
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Streptococcus pyogenes is ____.
A. α hemolytic B. β hemolytic C. γ hemolytic |
B
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What is Streptococcus pyogenes' serological type?
A. A B. B C. C D. D E. G |
A.
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What is Streptococcus agalactiae's serological type?
A. A B. B C. C D. D E. G |
B.
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β hemolytic organisms include___.
A. type A and C B. type A and B C. type C and G D. both choice B and C |
D.
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Give two examples of β hemolytic organisms.
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1. streptococcus pyogenes
2. streptococcus agalactiae |
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What distinguishes β hemolytic organisms from α hemolytic organisms on a plate?
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β hemolytic organisms: complete lysis.
α hemolytic organisms:partial lysis, appear green |
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What serologic group is γ hemolytic?
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Type D.
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Give some examples of type D streptococci.
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streptococcus bovis
streptococcus faecalis streptococcus faecium |
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Is streptococcus pyogenes GP or GN?
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GP
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Which organism is an invasive extracellular pathogen that causes strep throat?
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streptococcus pyogenes
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Which group of coxsackievirus is most common?
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type A
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What strategy does streptococcus pyogenes use to fight our immune system?
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avoid phagocytosis:
1. capsule made of hyluronic acid: block neutrophils 2. M and F protein: avoid complement activation, activate phagocytosis by epithelial cells |
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What does the capsule of streptococcus pyogenes contain and what is its function?
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hyluronic acid: block neutrophils.
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What does the cell wall of streptococcus pyogenes contain?
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group specific carbohydrate: can be used for serological typing and distinguish from other species.
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What are some actions of M protein in streptococcus pyogenes?
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1. bind to factor H to degrade C3b
2. binds fibrinogen: interfere with complement activation 3. stimulate uptake into epithelial cells |
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How does infection with streptococcus pyogenes cause rheumatic fever?
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Body's defense to make antibodies against M protein. Sometimes the antibodies made cross react with cardiac myosin and actin, thus cause the disease.
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What types of tissue does streptococcus pyogenes ahdere to?
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many types (so it can infect many types of tissue).
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What extracellular products do streptococcus pyogenes make?
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1. hemolysins: SLO and SLS.
2. enzymes: hyaluronidase, streptokinase, DNAses, C5 peptidases. 3. pyrogenic exotoxin(SPE): type A,B,C,E,F. |
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What is the purpose of hemolysins?
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1. lyse RBC : provide iron for bacterial growth
2. lyse phagocytes: protect bacteria from phagocytosis |
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What are the two hemolysins in streptococcus pyogenes?
Which one is immunogenic? |
SLO and SLS
SLO |
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Since SLO is immunogenic, why do antibodies fail to form during skin infections?
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SLO is inacivated by cholesterol and skin sterols.
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Which liquidation enzyme produced by streptococcus pyogenes are used in stroke patients to dissolve the clot?
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streptokinase
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What liquidation enzymes fo streptococcus pyogenes produce?
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1. hyaluronidase
2. streptokinase 3. DNAses 4. C5 peptidase |
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Which type of pyrogenic exotoxin(SPE) is used by streptococcus pyogenes to invade tissues?
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Type B: potent protease
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What are some actions of pyrogenic exotoxin(SPE)from streptococcus pyogenes?
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1. superantigens: stimulate T cell response, massive cytokine release which lead to hypotension and shock
2. act on endothelial cells to cause capillary leakage. |
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Will antibody to extrecellular toxins from streptococcus pyogenes help protect the effect of these toxins?
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Yes.
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What are some effects of extrecellular toxins from streptococcus pyogenes?
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1. pharyngitis
2. systemic shock, organ failure |
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What are some features of streptococcus pyogenes in convalescent carriers?
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1. decrease in number
2. lack M protein 3. less infectious |
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How does streptococcus pyogenes spread?
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1. direct person to person
2. food, water borne |
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What diseases do localized streptococcus pyogenes infection cause?
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1. pharyngitis
2. scarlet fever 3. pyoderma(impertigo) |
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What is the usual duration of infectivity of streptococcus pyogenes?
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2-3 weeks
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Streptococcus pyogenes infection may be repetitive even with appropriate antibiotics. Why?
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1. new strain (new M protein).
2. lack of development of protective anibody. 3. production by β-lactamase by other respiratory flora. 4. "resting" phase-less penicillin susceptible. 5. able to internalize into epithelial cells |
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What's the difference of pharyngitis in its symptomatic manifestations between small and older children?
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In small children: little fever or excudate, complications such as spread to ears and sinuses.
Older children: edema and redness of mucous membranes purulent exudate enlarged cervical nodes high fever |
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What are is the symptomology of scarlet fever?
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1. rash with deeper red areas
2. sandpaper like skin, peels after recovery 3. strawberry tongue |
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When does scarlet fever appear after infection with streptococcus pyogenes?
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day 2
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What is pyoderma/impertigo?
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superficial skin infection
multiple vesicular lesions on an erythematous base that eventually crust over. |
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Which of the following age group is most susceptible to pyoderma?
A. 0-2 year old B. 2-5 year old C. 5-7 year old D. 5-15 year old |
B.
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T/F: Strep A strains that cause pharyngitis usually have the same M types as ones that could cause impertigo.
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F.
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Which of the following age group is most susceptible to pharyngitis?
A. 0-2 year old B. 2-5 year old C. 5-7 year old D. 5-15 year old |
D.
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What are some disease manifestations of invasive infections caused by group A streptococci?
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1. bacteremia
2. focal infection: menigitis,pericarditis, pneumonia) 3. severe skin or soft tissue infections: erysipelas, cellulitis, necrotizing fasciitis or myositis. |
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Which age group is the most susceptible host to invasive group A streptococci?
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ages 15-45: underlying disease may exist (ischemia, immunocompressed, IV drug use, neonate)
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What is Erysipelas?
What can cause this? |
Spreading of inflammation of dermis layer with involvemnet of cutaneous lymphatic vessels. Often seen on face, lower limbs.
Caused by invasive group A streptococci. |
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Cellulitis involves inflammation of which layer of skin?
A. dermis B. deep dermis and subcutaneous tissue C. deep subcutaneous |
B.
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What patients are at risk of developing cellulitis?
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1. IV drug abuse
2. patients with impaired lymphatic drainage |
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Necrotizing fasciitis/myositis involves inflammation of which layer of skin?
A. dermis B. deep dermis and subcutaneous tissue C. deep subcutaneous |
C.
It can get into blood and cause toxic shock. |
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Erysipelas, cellulitis, and necrotizing fasciitis/myositis can be cause by which organism?
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Group A streptococci
Clostridium perfringens |
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What are some manifestations of toxic shock?
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1. hypotension
2. renal failure 3. ARD (Adult Respiratory Distress syndrom) 4. DIC (disseminated intravescular coagulation) 5. liver failure 6. skin rash |
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Toxins from which type of organsim are common causes of toxic shock?
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Group A streptococci
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What is ARD?
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Adult Respiratory distress syndrome: oftern cause by toxic shock.
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What is DIC?
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Disseminated Intravscular Coagulation: oftern cause by toxic shock.
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What are some clinical manifestations of ARF(Acute Rheumatic Fever)?
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pharyngitis:
carditis: usually limited polyarthritis chorea subcutaneous nodules. |
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What is the cause of ARF?
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Antibody made is cross-reactive with cardiac muscles.
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What cells/tissue could be damaged during ARF?
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Sarcolemma in cardiac myofibers
skeletal muscle smooth muscle of endothelium heart valve neurons and subthalmic nuclei |
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ARF:
1. number of M-types involved 2. recurrence common? 3. preventible with antecedent strep infection? 4. follows respiratory infection? 5. follows skin infection? |
1. lots
2. yes 3. yes 4. yes 5. no |
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PSGN:
1. number of M-types involved 2. recurrence common? 3. preventible with antecedent strep infection? 4. follows respiratory infection? 5. follows skin infection? |
1. few
2. no 3. no 4. yes 5. yes |
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How do you diagnose ARF?
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1. clinical and laboratory findings
2. culture and serology |
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What are some clinical manifestation of PSGN(acute post-strepcoccal glomerulonephritis?
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1. proteinuria
2. hematuria 3. edema 4. high BP 5. low serum complement levels |
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When after throat infection does PSGN usually develop?after skin infection?
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1. 10 days
2. 21 days |
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What is the pathogenic mechanism of PSGN?
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immuno-complex onto glomeruli
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What is the diagnosis of PSGN?
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culture
detection of antistreptococcal antibodies (not useful for skin infections) |
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What is the DOC for group A streptococci? How long should it be adminstered?
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oral penicillin for 10 days
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Which drug should be used to treat group A streptococci infection if a patient is allergic to penicillin?
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Erythromycin(macrolide)
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Whis drug should be used in combination with penicillin if group A streptococci infection is very severe?
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Clindamycin: shut down toxin synthesis
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When should cephalosporin be used to treat group A streptococci?
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anaphlylaxis type allergy
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Is there vaccine available for group A streptococci?
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No.
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When are pyrogenic exotoxin(SPE) type A and C from streptococcus pyogenes produced?
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After lysogenic convergion of streptococcus
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Why does common cold cause excabertions in asthma?
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1. host inadequate IFN-β respnse to suppress viral repication.
2. host exhibit Th2 response to make IgE instead og Th1 response. |
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What is the etiologic agent in diptheria?
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Corynebacterium diptheriae
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Corynebacterium diptheriae:
1. Gram stain 2. shape |
1. GP
2. rod: club shape, chinese character |
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Where do Corynebacterium sp (other than Corynebacterium diptheriae) usually colonize?
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skin
mucosal surfaces |
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How does diptheriae spread?
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airborne
skin contact |
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Diptheria A/B toxin:
1. What is A's function? 2. What is B's function? |
1. irreversibly catalyze ADP-ribosylation of elongation factor-2
2. bind to HB-EGF on host cells |
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How long is the incubation time for diptheriae?
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2-6 days (intermediate length)
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What tissues are most susceptible to diptheriae toxin?
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cardiac
nerve renal |
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What is key to diptheriae diagnosis?
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clinical suspicion
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What are some preventions toward diptheriae?
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1. active immunization: toxoid-> antibody against B-fragment
2. passive immunization: equine antitoxin (must apply soon) |
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Which antibiotics can be used to treat diptheriae?
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penicillin
erythromycin |
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Why do we still need to immunize people during convalenscent stage?
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natural infection does not always induce protective levels of antitoxins.
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What does the pseudomembrane formed during diptheriae infection contain?
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fibrin
bacteria necrotic cells inflammatory cells |