cap sinusitis pharyngitis im0306.ppt
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Outpatient Management of CAP, Outpatient Management of CAP, Sinusitis, AECB and PharyngitisSinusitis, AECB and Pharyngitis
David A. Pegues, MD
Division of Infectious Diseases
David Geffen School of Medicine at UCLA
2
Etiologic Agents in Community-Etiologic Agents in Community-acquired Respiratory Tract Infectionsacquired Respiratory Tract Infections
* Also Mycoplasma pneumoniae, Chlamydia pneumoniae, Legionella pneumophila, and rarely Staphylococcus aureus.
10% - 15%
8% - 12%
23% - 25%
2% - 8%
20% - 25%
20% - 25%
30% - 35%
15% - 25%
30% - 35%
25% - 30%
7% - 10%
35% - 55%
Acute otitis media
Acute maxillary sinusitis
AECB
CAP*
Moraxella catarrhalis
Haemophilus influenzae
Streptococcus pneumoniaeDisease
Zeckel ML, et al. Clin Ther. 1992;14(2):214-229.Hoberman A, et al. Pediatr Infect Dis J. 1996;15(10)955-962.Bartlett JG, et al. N Engl J Med. 1995;333(24):1618-1624.
3
CAP Statistics--United StatesCAP Statistics--United States
• Influenza and pneumonia--leading infectious cause of death:– 5th leading cause of death in persons aged > 65 y
• 5.6 million cases of CAP per year:– 1.1 million cases hospitalized– average LOS 2 days longer for those aged >65 y vs. <65 y
• Mortality:– overall--1-5%; hospitalized cases--25%
• Cost: – $14 billion/y in healthcare costs and $9 billion/y in lost wages
4
CAP Probabilities in CAP Probabilities in Ambulatory CareAmbulatory Care
Metlay JP, Fine MJ. Ann Intern Med 2003;138:109-18.
• Baseline CAP prevalence 5%• Scenario 1:
– patient with cough only
– 1%-13% probability of CAP
• Scenario 2:– cough, fever, tachycardia,
crackles
– 18%-42% probability of CAP
• Scenario 3:– CAP prevalence 10%
– 32%-60% probability of CAP if all 4 signs present
5
120
100
80
60
40
20
0
18–34 35–49 50–64 65–79 =80Age Group, Years
Cas
es p
er 1
00,0
00 P
op
ula
tio
n
Chlamydia pneumoniae *
Legionella spp *
Mycoplasma pneumoniae *
Streptococcus pneumoniae †
Chlamydia pneumoniae *
Legionella spp *
Mycoplasma pneumoniae *
Streptococcus pneumoniae †
, , Age-Specific Rates of Hospital Age-Specific Rates of Hospital Admission for CAP, by PathogenAdmission for CAP, by Pathogen
Marston BJ, et al. Arch Intern Med 1997:157:1709-18.
6
37 y.o. father with 2 children in daycare, 37 y.o. father with 2 children in daycare, cough, fever, and altered mental statuscough, fever, and altered mental status
7
Modifying Factors that Increase the Risk of Modifying Factors that Increase the Risk of Infection with Specific PathogensInfection with Specific Pathogens
• Drug-resistant pneumococci:
– age > 65 yr
-Lactam therapy w/in 3 mo
– alcoholism
– immune-suppressive illness
– multiple medical comorbidities
– exposure to a child in day care
– Enteric gram-negatives – residence in a nursing home
– cardiopulmonary disease
– multiple medical comorbidities
– recent antibiotic therapy
– Pseudomonas aeruginosa – structural lung disease
– >10 mg of prednisone/day
– broad spectrum abx. for >7 d in the past month
– malnutritionAmer Rev Resp Dis 2001;163:1730-54.
8
ImpactImpact ofof PenicillinPenicillin SusceptibilitySusceptibility onon MedicalMedical
OutcomesOutcomes forfor AdultAdult PatientsPatients withwith BacteremicBacteremic
PneumococcalPneumococcal PneumoniaPneumonia
• Retrospective cohort study conducted in the greater Atlanta
region during 1994
• 192 adult patients with bacteremic pneumococcal pneumonia
Pen-NS Pen-S RR
(n=44) (n=148) (95% CI)
PSI risk class IV or V 20 (46) 46 (31) P=0.05
Death from pneumonia 10 (23) 16 (11) 2.1 (1-4.3)
Suppurative complications 4 (9) 3 (2) 4.5 (1-19.3)Metaly JP, et al. Clin Infect Dis 2000;30:520-28
9
A healthy 30 y.o. female with insidious onset of A healthy 30 y.o. female with insidious onset of fever, malaise, HA and non-productive coughfever, malaise, HA and non-productive cough
10
Group 1:Group 1: Outpatients, No Cardiopulmonary Outpatients, No Cardiopulmonary Disease, No Modifying FactorsDisease, No Modifying Factors
Organism• Streptococcus pneumonia• Mycoplasma pneumoniae • Chlamydia pneumoniae• Hemophilus influenzae • Respiratory viruses • Legionella spp. • Mycobacterium tuberculosis • Endemic fungi
Therapy• azithromycin or
clarithromycin
or• doxycycline
Amer Rev Resp Dis 2001;163:1730-54.
11
Group 2:Group 2: Outpatients, with Cardiopulmonary Outpatients, with Cardiopulmonary Disease, and/or Modifying FactorsDisease, and/or Modifying Factors
Organism• S. pneumoniae (incl. DRSP)• M. pneumonia, C. pneumoniae• Mixed infection • H. influenzae• Enteric gram negatives • Respiratory viruses• M. catarrhalis• Legionella spp.• Aspiration (anaerobes)• M. tuberculosis• Endemic fungi
Therapy -lactam
– cefpodoxime– cefuroxime– high-dose amoxicillin– amoxicillin/clavulanate– ceftriaxone then cefpodoxime
plus• macrolide or doxycycline
or• antipneumococcal FQ alone
Amer Rev Resp Dis 2001;163:1730-54.
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Initial Empiric Therapy for CAP in Initial Empiric Therapy for CAP in Adult Outpatients, IDSA 2003Adult Outpatients, IDSA 2003
Patient variable Preferred treatment optionsPreviously healthy
No recent antibiotic therapy macrolide or doxycyclineRecent antibiotic therapy respiratory fluoroquinolonealone,
advanced macrolide + high-dose amoxicillin, oradvanced macrolide + high-dose amoxicillin-clavulanate
Comorbidities (COPD, diabetes, renal or congestive heart failure, or malignancy)
No recent antibiotic therapy advanced macrolide or a respiratory fluoroquinoloneRecent antibiotic therapy respiratory fluoroquinolone alone, or
advanced macrolide plus a beta-lactamSuspected aspiration Amoxicillin-clavulanate or clindamycinInfluenza with superinfection beta-lactam or a respiratory fluoroquinolone
Mandell LA, et al. Clin Infect Dis 2003;37:1405-33.
Pneumonia Pneumonia Severity IndexSeverity Index
• Risk classes I and II:– low risk of death
– treat as outpatients
• Elderly or risk class III:– consider short
hospitalization (1 day)
• Risk class IV and V– hospitalize
• Inpatient treatment:– O2 saturation <90
– hemodynamic instability
– co-morbid conditions
– inability to take PO meds
Halm EA, Teirstein AS. NEJM 2002:347:2039-45.
14
Score 0 –1: Low risk. Suitable for outpatient treatment.
Score 2: Intermediate risk. Consider hospitalization.
Score =3: High risk. Urgent hospitalization.
Lim WS et al. Thorax. 2003;58:377–382.
• Confusion*
• Urea >7 mmol /L
• Respiration >30/min
• Systolic BP <90 mmHg or diastolic BP <60 mm Hg
• Age >65 years•
Mortality predictors
-
0
5
10
15
20
25
Mortality, %
CURB -65 SCORE
0–1 2 =3
Risk groups
*Mental Test Score of <8 or new disorientation in person, place, or time.
1.5
9.2
22
Risk Assessment: CURB-65Risk Assessment: CURB-65
15
Decreased LOS 6Early mobilization
Decreased LOS 4
No difference in LOS, decreased cost and mortality* ,5
Critical pathway
Decreased LOS/cost 3
Decreased 30 - day mortality 2Appropriate antimicrobials
Decreased 30 - day mortality* ,1Blood cultures within 24 hr
Decreased 30 - day mortality* ,1,2Early antimicrobials
OutcomeFactors
Decreased LOS 6Early mobilization
Decreased LOS 4
No difference in LOS, decreased cost and mortality* ,5
Critical pathway
Decreased LOS/cost 3Early IV to PO switch
Decreased 30 - 2Appropriate antimicrobials
Decreased 30 - day mortality* ,1Blood cultures within 24 hr
Decreased 30 - day mortality* ,1,2
OutcomeFactors
1.Meehan TP et al. JAMA . 1997;278:2080 – 2084.2.Gleason PP et al. Arch Intern Med . 1999;159:2562 – 2572.3. Ramirez JA et al. Arch Intern Med . 1999;159:2449 – 2454.4.Marrie TJ et al. JAMA . 2000;283:749 – 755.5. Dean NC et al. Am J Med. 2001;110:451 – 457.6.Mundy LM et al. Chest . 2003;124:883 – 889.
LOS=length of stay.*Retrospective studies with patients at least aged 65 years.
LOS=length of stay.*Retrospective studies with patients at least aged 65 years.
Factors Improving Outcome in CAPFactors Improving Outcome in CAP
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Timing of Antibiotic Administration and Outcomes Timing of Antibiotic Administration and Outcomes for Medicare Patients Hospitalized With CAPfor Medicare Patients Hospitalized With CAP
• Retrospective study of a national random sample of 18,209 Medicare patients:– >65 years hospitalized with CAP from 7/98-3/99
– 75.6% did not receive outpatient antibiotics
• Antibiotic within 4 hours of arrival at the hospital: in-hospital mortality (6.8% vs 7.4%; AOR, 0.85), 30 d mortality (11.6% vs 12.7%; AOR, 0.85) LOS exceeding 5-day median (42.1% vs 45.1%; AOR, 0.90)
Houck, PM, et al. Arch Intern Med. 2004;164:637-44.
17
Recommendations for the Use of Recommendations for the Use of 23-Valent Pneumococcal Vaccine 23-Valent Pneumococcal Vaccine
Group Strength of evidence
Revaccination
Immunocompetent Age >65 y
A
2nd dose if vaccinated >5 y ago and were <65 y old then
Age 2-64 y and chronic disease
A, B Not recommended
Age 2-64 y and asplenic
A Age >10 y: 2nd dose if vaccinated >5 y ago
Age 2-64 y and living in special environment
C Not recommended
Immunosuppressed C Age >10 y: 2nd dose if vaccinated >5 y ago
MMWR 1997; 46 (RR8).
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Efficacy of Pneumococcal Polysaccharide Vaccine in Efficacy of Pneumococcal Polysaccharide Vaccine in Patients at Moderate to High Risk of Serious DiseasePatients at Moderate to High Risk of Serious Disease
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Effect of Empiric Therapy with Macrolides on Effect of Empiric Therapy with Macrolides on Length of Stay in Patients Hospitalized with CAPLength of Stay in Patients Hospitalized with CAP
Stahl JE, et al. Arch Intern Med. 1999;159:2576-80.
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FailureFailure ofof MacrolideMacrolide AntibioticAntibiotic TreatmentTreatment inin
PatientsPatients withwith BacteremiaBacteremia DueDue toto
Erythromycin-ResistantErythromycin-Resistant S.S. pneumoniaepneumoniae
• Matched case-control study at 4 hospitals:– bacteremic pneumococcal infection– case patients (n = 86)--erythromycin-I or -R S. pneumoniae– controls (n = 141)--erythromycin-susceptible S. pneumoniae
• Taking a macrolide at time blood culture obtained: – 18/76 (24%) cases vs. 0/136 controls (P <<0.001)
• Low-level-R efflux/M phenotype (mef): – 5/21 (24%) cases vs. 0/40 controls (P = .002)
• Breakthrough bacteremia during macrolide Rx: risk among patients infected with an erythromycin-R pneumococcus
– associated with both efflux and methylase mechanism
Lonks, JR, et al. Clin Infect Dis 2002;35:556-64
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In Vitro*In Vitro* MIC MIC9090 Activity Against Activity Against
Lower Respiratory PathogensLower Respiratory Pathogens
20.2516<0.250.120.030.06M. catarrhalis (ß-lac+ )
0.5<0.12<0.12<0.250.120.030.06M. catarrhalis (ß-lac-)
22>16160.030.0150.03H. influenzae (ß-lac+)
21180.030.0150.03H. influenzae (ß-lac-)
82280.510.25S. pneumoniae
Cefurmg/L
Amox/Clavmg/L
Amoxmg/L
Clarimg/L
Gatimg/L
Levomg/L
Moximg/L
Felmingham et al. J Antimicrob Chemother. 2002 Sep;50 Suppl S1:25-37. Hoban & Felmingham. J Antimicrob Chemother. 2002 Sep;50 Suppl S1:49-59. Fung-Tomc JC, et al. J Antimicrob Chemother. 2000 Apr;45(4):437-46
22
Declining Susceptibility of Declining Susceptibility of S. pneumoniaeS. pneumoniae to Levofloxacin to Levofloxacin
•Between 1997 and 2002, 26 US hospitals collected susceptibility data for community-acquired S pneumoniae isolates
•6 FQs tested: ciprofloxacin, gatifloxacin, levofloxacin, moxifloxacin, ofloxacin, and trovafloxacin
•Increase in levofloxacin use associated with decreased susceptibility to S pneumoniae across all geographical regions
•Levofloxacin MIC90 1.0; range <0.5 to >4.0
Bhavnani SM et al. ICAAC 2003, Chicago, Ill. Abstract A 2017.
50%0.4 to >3.0Southwest
0.4 to 1.5-3.0
Levofloxacin use increase (Rx/10
0 persons)
126%West
MIC increase
23
Pathophysiology of Pathophysiology of Acute Maxillary SinusitisAcute Maxillary Sinusitis
• Ostial obstruction is a primary factor pO2 Clearance of debris
• Predisposing conditions– Allergic rhinitis
– Upper respiratory infections
– Malformations
– Polyps
– Septal deviation
– Foreign bodies
– Tumors
– Upper tooth infections
24
Pathophysiology—RhinosinusitisPathophysiology—Rhinosinusitis
Adapted from: Kennedy DW, ed. Sinus Disease: Guide to First-Line Management. Darien CT, Health Communications, 1994.
Secretions thicken;
pH changes.
Ostiumis closed.
Mucosal gas metabolism
changes.
Cilia and epithelium
are damaged.
Change in host milieu creates culture medium for bacterial growth in
closed cavity.
Retained secretions cause
tissueinflammation.
Bacterial infection develops in the
sinus cavity.
Mucosal thickening creates further blockage.
Secretions stagnate.
Mucosal congestion or anatomic
obstruction blocks airflow and drainage.
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*Facial pain or pressure alone does not constitute a suggestive history in the absence of other findingsin the Major category. Osguthorpe JD. Am Fam Physician. 2001;63:69-76.
Major
Facial pain/pressure/fullness*
Nasal obstruction/blockage
Nasal discharge/purulence
Hyposmia/anosmia
Fever (acute phase)
Minor
Headaches
Halitosis
Fatigue
Dental pain
Cough
Ear pain/pressure/fullness
Signs and Symptoms Associated Signs and Symptoms Associated with the Diagnosis of Sinusitiswith the Diagnosis of Sinusitis
26 Piccirillo, J. F. N Engl J Med 2004;351:902-910
Plain Radiograph and CT Scans of Plain Radiograph and CT Scans of the Paranasal Sinusesthe Paranasal Sinuses
27 Piccirillo, J. F. N Engl J Med 2004;351:902-910
Various Signs and Symptoms Used Various Signs and Symptoms Used to Predict the Presence of Sinusitisto Predict the Presence of Sinusitis
28
Principles of Appropriate Antibiotic Use for Principles of Appropriate Antibiotic Use for Acute Sinusitis in AdultsAcute Sinusitis in Adults
Snow V, et al, Ann Intern Med 2001;134:495-7.Snow V, et al, Ann Intern Med 2001;134:495-7.
• Most cases of acute rhinosinusitis in ambulatory care are caused by viral URIs
• Viral and bacterial rhinosinusitis are difficult to differentiate on clinical or radiographic grounds
• Clinical Dx of bacterial rhinosinusitis should be reserved for patients with Sx >7 days
• Sinus radiography is not routinely recommended
• Acute bacterial sinusitis does not require antimicrobial treatment when symptoms are mild to moderate:– Up to 2/3 of patients improve with symptomatic management
• Patients with severe or moderate persistent symptoms should be treated with and antimicrobial
29
AAOHNS Rhinosinusitis AAOHNS Rhinosinusitis GuidelinesGuidelines
Anon JB et al. Otolaryngol Head Neck Surg. 2004;130(suppl 1):1-45.
Moxi/gati/levoRifampin+clindamycin
Moxi/gati/levoAmox/clavCeftriaxoneCombination therapy
Reevaluate patient
Mild disease with no recent antimicrobial use (past 4-6 weeks)
TMP/SMXDoxycyclineAzithro, clarithro, erythro
Amox/clavAmoxCefpodoximeCefuroximeCefdinir
Mild disease with recent antimicrobial use (past 4-6 weeks) or moderate disease
Severity
Reevaluate patient
Moxi/gati/levoAmox/clavCeftriaxone
Moxi/gati/levo Clindamycin and rifampin
β-Lactam Allergic
No
Yes
No
Initial Therapy Switch Therapy Options
Reevaluate patientYes
30
30 y.o. female with HSP and 30 y.o. female with HSP and chronic nasal dischargechronic nasal discharge
• 30 yo F• Henoch Schonlein
purpura, Dx 2001– CellCept 500 bid– prior prednisone
• >12 mths Hx:– anosmia, altered taste,
post nasal drip, sinus pressure
31
Chronic Sinusitis: HistoryChronic Sinusitis: History
• Primary symptom:– nasal congestion or obstruction; duration >6-12 wks
• Secondary symptoms:– pain, pressure, and postnasal discharge.
• Symptoms are poorly localized and mild:– may be extremely difficult to recognize.
• In children:– purulent rhinorrhea with or without postnasal drip.
• Cough and occasional wheezing episodes.
32
Chronic Sinusitis: TherapyChronic Sinusitis: Therapy
• Sinus irrigation:• buffered saline (e.g., Sinus Rinse--NeilMed)• antimicrobial, betadine, acetic acid• at least BID
• Decongestants:• topical, systemic
• Corticosteroids:• topical, systemic
• Surgery
33
A 15-year-old boy with sinusitis causing right A 15-year-old boy with sinusitis causing right proptosis, telecanthus, and malar flatteningproptosis, telecanthus, and malar flattening
34
Allergic Fungal Sinusitis (AFS)Allergic Fungal Sinusitis (AFS)
• ~ 5-10% of patients with chronic rhinosinusitis have AFS. • History of atopy:
– ~2/3 allergic rhinitis and 50% asthma.
– 90% elevated specific IgE to one or more fungal antigens.
• Geography:– temperate regions of relatively high humidity
– US--most commonwithin the Mississippi basin, the Southeast, and the Southwest.
• Demographics:– Adolescents and young adults; mean age at Dx--21.9 years
– M/F ratio ~50/50
35
AFS Lab StudiesAFS Lab Studies• Total IgE:
– > 1000 U/mL (normal, <50 U/mL).– indicator of AFS clinical activity.
• RAST versus skin testing – positive skin tests and in vitro (RAST) responses to fungal and
nonfungal antigens. – broad sensitivity to a number of fungal and nonfungal antigens. – generally, only a single fungus is isolated by culture of allergic
fungal mucin
• Nonspecific allergy testing – Gell and Coombs type I hypersensitivity
36
AFS TreatmentAFS Treatment
• Corticosteroids:– oral, intranasal
• Immunotherapy:– RAST or quantitative skin test:
• typical panel of nonfungal antigens
• all relevant molds (fungi) available.
– Duration of Rx--3-5 years.
• Antifungal therapy:– systemic, topical.
• Surgery
37
Initiating Factors (e.g., Smoking, Childhood Respiratory Disease)
Bacterial Products(LOS)
Alteration of Elastase–Anti-Elastase
Balance
Increased ElastolyticActivity in Lung
Progression of COPD
Impaired MucociliaryClearance
Inflammatory Response
(Cytokines, Enzymes, etc.)
LOS = lipooligosaccharideMurphy et al, 1992.
BacterialColonization
Damage to AirwayEpithelium
Infection and Inflammation of Acute Bacterial Infection and Inflammation of Acute Bacterial Exacerbations of Chronic BronchitisExacerbations of Chronic Bronchitis
38 Sethi, S. et al. N Engl J Med 2002;347:465-471
New Strains of Bacteria and New Strains of Bacteria and Exacerbations of COPDExacerbations of COPD
• The role of bacterial pathogens in AECB is controversial
• Studied 81 outpatients with COPD over 56 months– collected clinical information and sputum samples monthly and during
exacerbations– performed molecular typing of sputum isolates
• 1975 clinic visits, 374 for AECB
• Risk of exacerbation: new (33.0%) vs. no new strains (15.4%); (RR = 2.15)
• New strain of H. influenzae, M. catarrhalis, or S. pneumoniae increased risk of an exacerbation
• Supports the causative role of bacteria in AECB
39
Likely PathogensH influenzae
Haemophilus sppM catarrhalis
S pneumoniaeKlebsiella spp
Other GNBProbability of -lactam resistance
Treatment: 1st Line1. Fluoroquinolone 2. -lactam/-lactamase inhibitor
Alternative Treatment1. May require parenteral Rx2. Consider referral to specialist; hospitalization
Anthonisen Type 1
Increased sputum volumeIncreased sputum purulence
Increased dyspnea
Complicated
FEV1 < 50% > 4 AECB/y
Cardiac diseaseUse of home O2
Chronic oral steroid useAntibiotic use in the past 3 mo
Balter MS et al. Can Respir J. 2003;10:3B-32B.
Role of Antimicrobial Therapy in AECBRole of Antimicrobial Therapy in AECB
40
0
20
40
60
80
100
Moxifloxacin
Comparator
ITT PP(95% CI; 1.40, 14.87) (95% CI; 0.26, 15.95)
71%
63%70%
62%
Wilson R et al. Chest. 2004;125:953-964.
MOSAIC Study: Clinical Cure of MOSAIC Study: Clinical Cure of ABECB at 7-10 Days PosttherapyABECB at 7-10 Days Posttherapy
Moxifloxacin 400 mg QD for 5 days vs. Amox 500 gm tid for 7 days, clarithromycin 500mg bid for 7 days, or cefuroxime 250 mg bid for 7 days
Clin
ica
l Cu
re (
%)
191/274 185/298 P < .02251/354 236/376
41 Bisno. N Engl J Med. 2001;344:205-211.
Bacterial Pharyngitis: GABHSBacterial Pharyngitis: GABHS
• Group A -hemolytic streptococci (GABHS)/S pyogenes –Most common bacterial cause
• Accounts for approximately 15%–30% of all pediatric and adult pharyngitis cases–Affects primarily school-aged children
• Peak incidence: winter to early spring
42
Clinical PredictorsClinical Predictors
• Physicians, are not able to reliably predict which patients will have a positive throat culture for GAS
– Sensitivity (55-74%) and specificity (58-76%)
• Centor criteria: tonsillar exudates, tender anterior cervical adenopathy, fever by history, absence of cough
• 3 of 4 criteria: PPV 40 to 60 %; <1 of criteria: NPV 80%
– Sensitivity and specificity: 75 % vs. throat cultures
• Some consider the clinical criteria to be too liberal:
– overtreatment of 50 %
– restrict Rx to those with positive rapid antigen testing (RAT) or culture
43
GABHS = Group A -hemolytic streptococci.Bisno et al. Clin Infect Dis. 1997;25:574-583.
Throat Culture vs Rapid Throat Culture vs Rapid Antigen Detection TestsAntigen Detection Tests
• Throat culture– Gold standard for
diagnosis of GABHS– Sensitivity: 90%–95%– Throat swab: both tonsils
and posterior pharyngeal wall
– Results: 24 hours
• Rapid antigen detection tests– Rapid results– More expensive than
culture– Specificity: 95%– Sensitivity: 80%–90%– Negative result: confirm
with blood agar-plate culture
44
Diagnostic and Treatment Diagnostic and Treatment Algorithm of Acute PharyngitisAlgorithm of Acute Pharyngitis
GABHS = Group A -hemolytic streptococci.Bisno et al. Clin Infect Dis. 1997;25:574-583.
Clinical and epidemiologic features
Not suggestive of GABHS
Symptomatic therapy
Antimicrobial therapy
Possible GABHS
Throat culture
Rapid antigendetection test
– –
+ +
47
Management strategiesManagement strategies
• Four reasons to treat a GABHS with antibiotics; none are very compelling in adults: To prevent rheumatic fever — treatment works, but this
complication has nearly disappeared in North America
To prevent peritonsillar abscess — again a vanishing complication
To reduce symptoms — there is a modest (~ 1 day) reduction in symptoms with early treatment
To prevent transmission — this is important in pediatrics due to extensive exposures but not in adults
48
RecommendationsRecommendations
Empirically treat patients who have all four clinical criteria
Do not treat with antibiotics or perform diagnostic tests on patients with zero or one criterion.
Perform RAT on those with two or three criteria and use antibiotic treatment only for patients with positive RAT results.
• Another approach is to treat empirically those adults with three or four of the clinical criteria
49
TherapyTherapy
• Penicillin--remains first-line therapy for GAS infections – Pen V 500 tid for 10 days
– benzanthine PCN G 300,000 units + procaine IM
– 5-30% Rx failure rate
• Erythromycin--alternative if PCN-allergic
• Empiric, broad spectrum antibiotic therapy for the treatment of sore throat:– e.g., newer macrolides, cephalosporins, or Augmentin
– increased cost and potential to increase antibiotic resistance among respiratory pathogens