Chapter One

Infectious diseases
Pharmacotherapy:

III. Central Nervous System

(CNS) Infections
Learning Objectives

· By the end of the session you should be able to:

Discuss the pathophysiology of CNS infections
Describe the clinical presentation of CNS
infections
List the most common pathogens causing
CNS infections
State the goals of therapy for CNS infections
Design appropriate empirical antimicrobial
regimens for pts suspected of having CNS
infections

2
Learning Objectives

· By the end of the session you should be……

Modify empirical antimicrobial regimens based
on laboratory data and other diagnostic criteria
Discuss the management of close contacts of
patients diagnosed with CNS infections.
Describe the role of adjunctive agents in the
management of CNS infections.
Formulate a monitoring plan to assess efficacy
and adverse effects of therapy for CNS
infections.

3
 Case study
· JD is a 17-year-old high school senior who visited her
sister at her college dormitory for 1 week prior to her
sister leaving for winter break. JD now presents to the
emergency department with a 2-day history of headache
and fever.
· Physical findings and laboratory values include
temperature of 38.3ºC (101ºF) and WBC count of
14,400/mm3 (14.4 × 109/L), with 90% PMNs. Examination
reveals nuchal rigidity and a petechial truncal rash. JD
reports light sensitivity and nausea with vomiting. She has
tried over-the-counter analgesics and antipyretics with no
relief from her headache or fever.
4
 Case study
· What signs and symptoms consistent with meningitis are
present in JD?
· What clues to causative pathogen are present in JD?
· What is the empirical regimen of choice for JD?
· How are laboratory data (including culture & sensitivity
data) used to refine empirical antibiotic regimen?
· Which drugs are recommended for prophylaxis of close
contacts of patients with meningitis?

5
 Anatomy and Physiology
· Brain and spinal cord are enshrined by a
protective covering known as the meninges and
suspended in CSF
acts as a “shock absorber” to outside trauma
· The meninges consist of three layers of fibrous
tissue:
pia mater, arachnoid, and dura mater
· Subarachnoid space:
Separates the pia mater from the more loosely
enclosed arachnoid membrane
CSF resides here
CNS infections: Terminology and definitions
· Meningitis
inflammation of the membranes of the brain and
spinal cord (meninges) and the CSF in contact with
these membranes
· Encephalitis
inflammation of the brain tissue, usually caused by a
viral infection
· Myelitis
inflammation of the spinal cord
· Meningoencephalitis
inflammation of brain and meninges
· Meningomyelitis, Encephalomyelitis, Meningo-encephalomyelitis,
Brain abscess….
 CNS Infections: Introduction
· Describes a variety of infections involving the brain
and spinal cord and associated tissues, fluids, and
membranes
· Include a wide variety of clinical conditions and
etiologies:
meningitis, meningoencephalitis, encephalitis, brain and
meningeal abscesses, and shunt infections.
· Improperly treated, CNS infections are associated
with high rates of morbidity and mortality
· Antimicrobial therapy and preventive vaccines
have vital role
 CNS Infections: Etiology
· CNS infections may be caused by a variety of
bacteria, fungi, viruses, and parasites.
· Bacterial meningitis is the most common cause
of CNS infections.
· Most common causes of bacterial meningitis:
Streptococcus pneumoniae(pneumococcus)
Neisseria meningitidis(meningococcus)
Group B Streptococcus
Listeria monocytogenes
Haemophilus influenzae
 CNS Infections: Etiology
· Neisseria meningitidis (Meningococcus)
leading cause of bacterial meningitis in children and
young adults in the United States
Deafness unilaterally, or more commonly bilaterally
Purpuric lesions, petechiae, or both.
· Streptococcus pneumoniae (Pneumococcus
or Diplococcus)
leading cause of meningitis in adults
occurs in the very young (less than 2 years of age) and
the very old
Neurologic complications, such as coma and seizures,
are common.
 CNS Infections: Etiology
· Haemophilus influenzae
In the past, H. influenzae was the most common
cause of meningitis in children 6 months to 3 years of
age, but this has declined dramatically since the
introduction of effective vaccines.
Approximately 30% to 40% of H. influenzae are
ampicillin resistant.
For this reason, many clinicians use a third-
generation cephalosporin (cefotaxime or
ceftriaxone) for initial antimicrobial therapy.
 CNS Infections: Etiology
· Listeria monocytogenes
Affects primarily neonates, alcoholics,
immunocompromised patients, and the elderly.
The combination of penicillin G or ampicillin with an
aminoglycoside results in a bactericidal effect.
Patients should be treated for 2 to 3 weeks after
defervescence to prevent the possibility of relapse.
Combination therapy is given for at least 10 days with
the remainder completed with penicillin G or ampicillin
alone.
 CNS Infections: Risk Factors
· Environmental
recent exposures (e.g., close contact with meningitis or
respiratory tract infection, contaminated foods)
· Recent infection in the patient
respiratory infection, otitis media, sinusitis, mastoiditis
· Immunosuppression
· Surgery, trauma
neurosurgery, head trauma
· Noninfectious causes:
malignancy, medications (e.g., sulfonamides, NSAID, IV
immunoglobulin), autoimmune disease (e.g., lupus), and
trauma
 The most common pathogens causing bacterial
meningitis, by age group and other risk factors

Factor Predisposing Bacterial Pathogen

Age
Less than 3 months Group B Streptococcus(Streptococcus agalacticae), Escherichia
coli, Listeria monocytogenes, Klebsiella pneumoniae
3 months to ˂18 years Haemophilus influenzae, S.pneumoniae, N.meningitidis
18 years to ˂ 60 years S.pneumoniae, N.meningitidis
>60 year S.pneumoniae, N.meningitidis, L.monocytogenes, Gram
negative bacilli
Immunodeficiency S.pneumoniae, N.meningitidis, L.monocytogenes, Gram
negative bacilli, Pseudomonas aeruginosa, Mycobacterium
tuberculosis, Cryptococcosis
Basilar skull fracture S.pneumoniae, H.influenzae, Group A streptococci

Post neurosurgery Staphylococcus aureus, coagulase negative staphylococci, Gram

negative bacilli, P.aeruginosa
 CNS Infections: Pathophysiology
· To initiate a CNS infection, pathogens must gain
entry into the CNS by
Contiguous spread
Hematogenous seeding
Direct inoculation
Reactivation of latent infection
· Contiguous spread
occurs when infections in adjacent structures
(e.g.,sinus cavities or the middle ear) invade directly
through the BBB(e.g., Hib)
 CNS Infections: Pathophysiology
· Hematogenous seeding
Occurs when a more remote infection causes
bacteremia that seeds the CSF (e.g., pneumococcal
pneumonia)
· Direct inoculation of bacteria into the CNS
result of trauma, congenital malformations, or
complications of neurosurgery
· Reactivation of latent infection
results from dormant viral, fungal, or mycobacterial
pathogens in the spine, brain, or nerve tracts
· Once through the BBB, pathogens thrive and
replicate due to limited host defenses in the CNS
 CNS Infections: Pathophysiology
· Neurologic tissue damage is the result of the
host’s immune reaction to bacterial cellular
components (e.g., lipopolysaccharide,teichoic
acid, and peptidoglycan), which triggers cytokine
production, particularly TNF-α and IL-1
Bacteriolysis resulting from antibiotic therapy further
contributes to the inflammatory process.
· Cytokines increase permeability of the BBB,
allowing influx of neutrophils and other host
defense cells that contribute to the development of
cerebral edema and increased intracranial
pressure characteristic of meningitis.
 CNS Infections: Pathophysiology
· The increase in intracranial pressure is
responsible for the hallmark clinical signs and
symptoms of meningitis
· Unaltered, these pathophysiologic changes may
result in cerebral ischemia and death.
CNS Infections: Clinical Presentation and Diagnosis

· General
Evaluate patient risk factors and recent exposures
Evaluate other possible causes: space-occupying
lesion (which may or may not be malignant), drug-
induced CNS pathology autoimmune disease, and
trauma
· Signs and Symptoms
95% of patients with bacterial meningitis have two of
the following:
• Headache, fever, neck stiffness, and altered mental
status
Nausea (74%)
Signs and Symptoms….
Focal neurologic defects (including positive
Brudzinski’s sign and Kernig’s sign) (33%)
Seizures, Malaise, restlessness. Photophobia
· In neonates, infants, and young children:
altered feeding and sleep patterns, vomiting,
irritability, lethargy, bulging fontanel, seizures,
respiratory distress, and petechial/purpuric rash
· Predictors of an unfavorable outcome:
seizures, focal neurologic findings, altered mental
status, papilledema, hypotension, septic shock, and
pneumococcal meningitis
Differential Signs and Symptoms
· Purpuric and petechial skin lesions
typically indicate meningococcal involvement,
although the lesions may be present with H.
influenzae meningitis.
Rashes rarely occur with pneumococcal meningitis.
· H. influenza meningitis and meningococcal
meningitis both can cause involvement of the
joints during the illness.
· A history of head trauma with or without skull
fracture or presence of a chronically draining
ear is associated with pneumococcal
involvement.
Symptoms and signs
 Kerning’s sign
Kerning's sign – a
symptom of
meningitis in
which the
hamstring
muscles in the
legs are so stiff
that the patient is
unable to extend
his legs at the
knee when the
thighs are held at
a right angle on
the body.
 Brudzinski’s sign
Brudzinski's
sign – as the
neck is
pulled
forward, the
hips and
knees bend
involuntarily.
Rash of meningococcemia
Laboratory Tests… LP and CSF analysis

· The characteristics of normal CSF:

Opening pressure: 50-180 mmH2O.
Color- Clear
Cells:
• RBC - none
• WBC < 5 cells (Mononuclear
cells-lymphocytes/monocytes)
• If WBC is increased = pleuocytosis
Protein 20-45 mg/dl
CSF sugar/ serum sugar > 50%
Laboratory Tests… LP and CSF analysis

· Abnormal Cerebrospinal Fluid

Elevated opening pressure (may be decreased in
neonates, infants, and children)
Cloudy CSF
Decreased glucose
Elevated protein
Elevated WBC (differential provides clues to
offending pathogen)
Lumbar Puncture
Complications Contraindications
· Major: · Absolute:
 Cerebral herniation
 Skin infection over site of LP.
 Injury to the spinal cord or
 Papilledema,
nerve roots
 Focal neurologic signs,
 Hemorrhage, or
 ↓Mental Status
 Infection
· Relative:
· Minor
 ed ICP without papilledema
 Backache,
 Suspicion of mass lesion
 Post-LP headache, and
 Spinal cord tumor
 Radicular pain or
 Spinal epidural abscess
numbness.
 ↓ Platelate (< 20,000/mm3)
30
 31

CSF gram stain for some of the causes

• Gram-positive diplococcic→ pneumococcal

infection
• Gram-negative diplococcic→ meningococcal
infection
• Small pleomorphic gram-negative coccobacilli
suggest Haemophilus influenzae.
• Gram positive rods and coccobacilli suggest
listerial infection.
 32

Treatment: Goals of Therapy

• The treatment goals for CNS infections include:

• eradication of infection with amelioration of
signs and symptoms
• prevention of neurologic sequelae, such as
seizures, deafness, coma, and death
 33

Treatment: General Principles

• Administration of fluids, electrolytes, antipyretics,

analgesia, and other supportive measures are
particularly important for patients presenting with
acute bacterial meningitis.
• Prompt initiation of IV high-dose bactericidal
antimicrobial therapy directed at the most likely
pathogen(s) is essential
• due to the high morbidity and mortality associated with
CNS infections
• Parenteral (IV) therapy is administered for the full
course of therapy to ensure adequate CSF
penetration throughout the course of treatment
 34

Pharmacologic Treatment

• Empiric antimicrobial therapy should be

instituted as soon as possible to eradicate the
causative organism
· Antimicrobial therapy should last at least 48 to
72 hours or until the diagnosis of bacterial
meningitis can be ruled out.
· Continued therapy should be based on the
assessment of clinical improvement, cultures,
and susceptibility testing results.
· Once a pathogen is identified, antibiotic therapy
should be tailored to the specific pathogen.
 35

Pharmacologic Treatment

· With increased meningeal inflammation, there

will be greater antibiotic penetration.
· Problems of CSF penetration may be overcome
by direct instillation of antibiotics by intrathecal
routes of administration
36
37
38
39
EMPIRIC THERAPY OF BACTERIAL MENINGITIS IN
THE ADULT- cont’d

Antimicrobial Agent Total Daily Dose and Dosing Interval

for Adults
Ampicillin 12 g/d, q4h
Ceftriaxone 4 g/d, q12h
Ceftazidime 6 g/d, q8h
Penicillin G 20–24 million U/d, q4h
Vancomycin 2 g/d, q12hb

Note:
1. All antibiotics are administered intravenously;
2. Doses indicated assume normal renal and hepatic function.
3. The list includes only those antibiotics commonly used for bacterial
meningitis in our country (Ethio.)
 Definitive therapy
Organism Antibiotic of First Alternative Duration of
Choice Antibiotics Therapy
Gram-positive

Streptococcus 10–14 days

pneumoniae
Penicillin Penicillin G or Cefotaxime,
susceptible Ampicillin Ceftriaxone,
Chloramphenicol
Penicillin Cefotaxime or Cefepime,
intermediate Ceftriaxone Meropenem ,
Moxifloxacin ,
Linezolid
Penicillin Vancomycin plus
resistant Cefotaxime or
Ceftriaxone
 Definitive therapy
Organism Antibiotic of First Alternative Recommended
Choice Antibiotics Duration of
Therapy
Gram-negative

Neisseria 7 days
meningitis

Penicillin Penicillin G or Cefotaxime,

susceptible Ampicillin Ceftriaxone,
Chloramphenicol

Penicillin Cefotaxime or Chloramphenicol

resistant Ceftriaxone , Meropenem,
Fluoroquinolone
 Definitive therapy
Organism Antibiotic of First Alternative Recommended
Choice Antibiotics Duration of
Therapy
Gram-negative
Haemophilus 7 days
influenzae
Negative Beta- Ampicillin Cefotaxime,
Lactamse Ceftriaxone,
Chloramphenicol
Posetive Beta Cefotaxime or Cefepime ,
lactamase Ceftriaxone Meropenem,
Fluoroquinolone

L. monocytogenes Penicillin G or Trimethoprim-

Ampicillin ± sulfamethoxazole
Gentamicina , Meropenem
 Corticosteroids In Bacterial Meningitis
• The rationale for steroid therapy in meningitis
stems from the fact that steroids reduce the
synthesis and release of the proinflammatory
cytokines TNF-α and IL-1β from monocytes and
astrocytes
· 10mg(0.15 mg/kg/dose) given IV Q 6 hours for 2
to 4 days 15 to 20 minutes before or with the
first dose of antibiotic .
· Shown to decrease Mortality and morbidity in S.
pneumoniae but NOT N. meningitidis.
45
 Prevention - Chemoprophylaxis
· Neisseria meningitidis (Meningococcus)
Close contacts are at an increased risk
Adults: Rifampin 20mg/kg PO (max 600mg) Qday x 4
doses
Children 1 month to 12 years of age
• Rifampin 10 mg/kg of PO BID for four doses
children younger than 1 month
• Rifampin 5 mg/kg PO BID for four doses.
· H. influenzae type b
children should receive 20 mg/kg (maximum 600 mg) and
adults 600 mg daily in one dose for 4 days
Fully vaccinated individuals should not receive prophylaxis
Prevention - Vaccination
· S. pneumoniae:
A heptavalent conjugate vaccine is available for use in
infants between 2 months and 9 years of age.
All healthy infants < 2 YOA to be immunized with the
heptavalent vaccine at 2, 4, 6, and 12 to 15 months.
· Haemophilus influenzae
Hib conjugate vaccines
• Begun in children at 2 months
• > 5 years with sickle cell disease, asplenia, or
immunocompromising diseases
· N . Meningitidis:
?Asplenia, epidemics, at risk (college, military)
Evaluation of Therapeutic Outcomes
· Signs and Symptoms
High potential for rapid deterioration associated with
meningitis:
• signs and symptoms of fever, headache, meningismus
(e.g., nuchal rigidity, Brudzinski's or Kernig's sign), vital
signs, and signs of cerebral dysfunction should be
evaluated every 4 hours for the initial 3 days and then
daily thereafter
· Microbiologic Findings
· CSF Examination
 Other CNS Infections

· Tuberculous meningitis
Primary cause Mycobacterium tuberculosis
CDC recommends a regimen of four drugs for empiric
treatment with
• Isoniazid, rifampin, pyrazinamide, and ethambutol, 15
to 20 mg/kg/day (maximum 1.6 g/day) for the first 2
months generally followed by isoniazid plus rifampin for
the duration of therapy
Supplemental doses of pyridoxine hydrochloride
(vitamin B6), 50 mg/day, are recommended to prevent
the peripheral neuropathy
 Other CNS Infections

· Tuberculous meningitis
Treatment duration:
• 9 months or longer with multiple-drug therapy, and
• patients with Rifampin-resistant strains should receive
18 to 24 months of therapy.
The use of glucocorticoids remains controversial.
administration of steroids such as oral prednisone, 60
to 80 mg/day (1 to 2 mg/kg/day in children), or 0.2
mg/kg/day of IV dexamethasone, tapered over 4 to 8
weeks
• Improves neurologic sequelae and survival in adults and
• decrease mortality, long-term neurologic complications,
and permanent sequelae in children.
 Other CNS Infections

· Cryptococcal Meningitis
most common form of fungal meningitis
major cause of morbidity and mortality in
immunosuppressed pts
Treatment
• Management of raised ICP
• Antimicrobials:
• Amphotericin B 0.5 to 1 mg/kg/day X 2 weeks and if
improving combined with flucytosine,100 mg/kg/day, is
more effective
• Fluconazole
• 400 mg QD x 6 weeks
• 200 mg QD until CD 4 > 200 for at least 6 months.
 Other CNS Infections

· Treatment….
 Induction
• Amphotericin B 0.7-1 mg/kg/day plus 5-flucytosine
100mg/kg/day x 2 weeks then
 Consolidation
• Fluconazole 400 mg/day x 6-10 weeks then
 Suppression
• Fluconazole 200 mg/day until CD4 >200 for minimum of
6months?
• AIDS-associated cryptococcal meningitis need life long
maintenance or suppression therapy with fluconazole
 Other CNS Infections

· HSV encephalitis: Acyclovir 10mg/kg IV Q8h

· Brain Abscess: Streptococci & Bacteroides
Metronidazole Plus (Ceftriaxone or high dose Penicillin
G)
· Drug-induced Aseptic
NSAID’s especially if patient has lupus
Trimethoprim / Sulfamethoxazole
Ciprofloxacin
Penicillin, Cephalosporins
 Isonazid, Pyrazinamide
 Chapter One
Infectious diseases
Pharmacotherapy:

IV. Infectious diseases of the eye

 Outline
• Eyelid diseases
• Cojunctivitis
– Bacterial
– Viral
– Fungal
– Trachoma
• Keratitis
– Bacterial
– Fungal
– Viral
 Diseases of Lid margin

• Blepharitis
• Chalazion and Hordeolum
• Blepharitis
–inflammation of the eyelid margins that
may be acute or chronic
–Acute (ulcerative or nonulcerative)
–Chronic (meibomian gland dysfunction,
seborrheic blepharitis)
 Blepharitis
• Acute ulcerative blepharitis
–is usually caused by bacterial infection (usually
staphylococcal). It may also be due to a virus (eg,
herpes simplex, varicella zoster).
• Acute nonulcerative blepharitis is usually
caused by an allergic reaction
• Chronic blepharitis is noninfectious
inflammation of unknown cause
• May predispose to chalazia,
blepharoconjunctivitis, loss of lashes
 Blepharitis Types

• Staphylococcal blepharitis
–Chronic irritation worse in mornings
–Scales (collarettes) around base of lashes
–Hyperemia and telangiectasia of anterior lid
margin
• Seborrhoeic blepharitis
–shiny and hyperemic anterior lid margin
–oily secretions and greasy scales
–eye lashes stuck together
 Blepharitis Types

• Meibomianitis (meibomian gland

dysfunction)
–inflamed and blocked meibomian gland
orifices
–thickened posterior lid margin
–toothpaste-like plaques from meibomian
glands
–meibomian cyst formation
Blepharitis: note the crusting in the lashes and the thickened lid margin
 Blepharitis Treatment
• Lid hygiene - with 25% baby shampoo
• Antibiotic ointment at bedtime for 2-3 weeks
(Bacitracin or erythromycin)
• Tear substitutes - for associated tear film
instability
• Systemic tetracyclines - for severe posterior
blepharitis
• Warm compresses - to melt solidified sebum in
posterior blepharitis
• In general, blepharitis is not curable only
controllable and exacerbations are common
 Chalazion and Hordeolum
• Usually begins as diffuse swelling followed by
localization of a nodule to the lid margin
• Chalazion
– is noninfectious obstruction of a meibomian gland
causing extravasation of irritating lipid material in the
eyelid soft tissues with focal secondary
granulomatous inflammation
• Hordeolum(stye)
– is an acute, localized, pyogenic (usually
staphylococcal) infection or abscess of the eyelid that
may be external or internal
 Acute hordeola
Internal hordeolum External hordeolum (stye)
( acute chalazion )

• Staph. abscess of meibomian • Staph. abscess of lash follicle and

glands associated gland of Zeis or Moll
• Tender swelling within tarsal plate • Tender swelling at lid
margin
• May discharge through skin • May discharge63through
or conjunctiva skin
Hordeolum/Chalazion: Treatment

• Hot compresses for 5 to 10 min 2 or 3 times a

day can be used to hasten resolution of
chalazia and external hordeola
• Chalazion:
–Incision and curettage or intrachalazion
corticosteroid therapy (0.05 to 0.2 mL
triamcinolone 25 mg/mL) may be indicated if
chalazia are large, persist for more than
several weeks despite conservative therapy
Hordeolum/Chalazion Treatment

• External hordeolum that does not respond to

hot compresses can be incised
• Systemic antibiotics (eg, dicloxacillin or
erythromycin 250 mg po qid)
– are indicated when cellulitis accompanies a
hordeolum
• Treatment of internal hordeola
– oral antibiotics and incision and drainage if needed
– Topical antibiotics are usually ineffective
 Orbital Disease
• Preseptal cellulitis
• Orbital cellulitis
• Preseptal Cellulitis
– An inflammatory process involving soft tissues
anterior to orbital septum
– Causes
• Skin trauma or insect
• bites of lids or eyebrows
• Spread from local infection: Upper respiratory or ear
infection
 Preseptal Cellulitis

• Signs
–Usually unilateral,Tender and red, Periorbital
oedema
• Treatment
–Systemic antibiotics
–The younger the patient and the more severe the
disease the more likely to initiate inpatient
treatment (IV antibiotics)
Preseptal Cellulitis

Orbital Cellulitis: Note the periorbital edema and erythema

and the chemosis (conjunctival swelling)
Picture from Section 6 of the Basic and Clinical Science Course published by the Foundation of the American Academy of Ophthalmology

68
 Orbital Cellulitis

• A life threatening infection of the soft tissues behind

the orbital septum………Medical Emergency
• Commonest organisms: S. pneumoniae, S. aureus,
S pyrogens & H. Influenzae
• Rapid onset of proptosis, visual impairment Pain,
fever
• Signs: periorbital edema, warm & red, proptosis,
ocular motility defect, optic nerve dysfunction
• Treatment:
– Admission
– I'V antibiotics➡ cloxacillin, ceftazidime, vancomycin,
metronidazole
 Molluscum contagiosum
• A virus which spreads by direct contact
• Molluscum nodule is a painless, waxy, umblicated
nodular lesion
• The virus may spread to conjunctiva => chronic
follicular conjunctivitis
• May be multiple in AIDS pts
• Treatment
– complete excision
– Cryotherapy
– incision of central portion
 Conjunctivitis

• Nonspecific term for inflammation and

erythema of the conjunctiva.
• Several causes:
–Bacterial, Viral, Allergic, Chemical
• Conjunctivitis……Discharge
• Discharge Cause
• Purulent…………..Bacteria
• Clear………………Viral
• White mucous…….Allergies
Conjunctivitis: Bacterial conjunctivitis
1. Acute bacterial conjunctivitis
– More common in children than adults
– Caused by direct eye contact with infected secretions
– Most common etiologic agents
• H. influenzae
• S. pneumoniae
• S. aureus
• Moraxella catarrhalis
– Clinical features:
• Conj injection
• Mucopurulent discharge
• Crusted eyelid margin
• Others: eyelid edema, chemosis etc.
 Acute bacterial conjunctivitis

• Diagnosis:
– Clinical
– Gram stain &Culture
– Neonates or immunocompromised hosts
– Severe purulent discharge
– Cases unresponsive to initial RX
• Treatment
– Drops: CAF, ciprofloxacin or other fluoroquinolones,
gentamicin, tobramycin, polymyxin B…
– Ointments: TTC, erythromycin…
 2. Gonococcal conjunctivitis:
• Caused by N. gonorrhoeae
• STD: transmitted by genital-hand-ocular contact, or
perinatal contact
• Hyperacute conjunctivitis with copious purulent
discharge, severe chemosis, eyelid edema…
• May lead to corneal melting and perforation if untreated
• Management
– systemic antibiotics
» Ceftriaxone IM/IV,
» spectinomycin IM or
» oral fluoroquinolones
– Topical supplement
– Copious irrigation with saline
 3. Ophthalmia Neonatorum
• Conjunctivitis occurring in the 1 month of life by
st

various agents (bacterial, viral, chemical)

• A significant source of ocular morbidity,
blindness
• Infants are infected during passage through the
birth canal
• Causes:
– Neisseria, Chlamydia, Herpes simplex, Chemical
conjunctivitis
• Prophylaxis
– 2% silver nitrate, erythromycin oint, 5% povidone
iodine
Ophthalmia Neonatorum….. Neisseria

• The most serious form is caused by Neisseria

gonorrheae
• Onset: typically in the 1st 3 or 4 days (may be
delayed for up to 3wks)
• Marked chemosis, copious discharge, & possibly
rapid corneal ulceration and perforation
• Treatment
– Systemic Antibiotics
• Ceftriaxone iv or im daily for 1wk
• Penicillins- not preferred b/c of increasing resistance
– Topical irrigation of the eyes
– Rx the parents
Ophthalmia Neonatorum….. Chlamydia

• Onset usu.~1wk of age

• Mild swelling, hyperemia, a papillary reaction
with minimal to moderate discharge
• Follicular conj rxn can occur after ~1mo. of age
• DX: culture from conj scrapings
• Treatment
– usu. self limited
– systemic- oral erythromycin, 50mg/kg/day in four
divided doses for 10-14 days
– Rx the parents
Ophthalmia Neonatorum….. Herpes simplex

• More rare form of o. neonatorum

• later than N gonor or C trachomatis usu. 2 nd

week
• Ophthalmia Neonatorum….. Chemical
conjunctivitis
– the 1 24 hr after silver nitrate
st

– mild, self limited irritation & redness of conj

– self-limited by the 2 day
nd
 Viral Conjunctivitis
Adenoviral keratoconjunctivitis
• Transmitted by direct contact or fomites
• Tearing, light sensitivity and foreign body
sensation
• Photophobia and reduced vision from corneal
infiltrates
• Therapy:
–Primarily supportive:
• Cool compress and
• Artificial tear
• Topical antibiotics if bacterial superinfection
Viral conjunctivitis: note the diffuse redness and watery
discharge
 Trachoma
• A leading cause of preventable eye disease
• Most common in dry, hot, dusty climatic zones
• Always associated with poverty and unhygienic
living conditions
• Caused by Chlamydia trachomatis (both
bacterial and viral characteristics)
– Serotypes A-C
• Transmitted by direct contact with eye and nasal
discharges
 Clinical Features
• Varies from a mild asymptomatic conjunctivitis to
severe and blinding disease
• It is a chronic disease that progresses gradually
revealing specific conjunctival and corneal
changes
• Trachoma is essentially a spectrum of diseases
generally classified in to two:
1. Active trachoma:
• more common in children
2. Cicatricial trachoma:
• the result of multiple episodes of active trachoma
• More common in adults
 Active trachoma
• At first, there is a mild conjunctivitis with
vasodilation of the conjunctival vessels
• Redness, irritation, mild itching and mild to
moderate mucopurulent discharge
• After ~2wks, the specific changes of trachoma
become apparent.
• The changes are usually conjunctival and
corneal
• Conjunctival Changes
– Follicles:- enlarged nodules of lymphoid tissue under
the conj epithelium
 Conjunctival Changes….
• After repeated infections, a network of scars
can be seen, most easily in the upper tarsal
conj
• In mild cases, these scars are simple and
clinically insignificant
• In severe cases, the collagen fibers in the scar
slowly contract and cause marked deformity of
the conjunctiva and tarsal plate
Follicles Conjunctival scars

85
 Corneal changes
• The C. trachomatis also invade the corneal
epith (esp the upper part)
• Superficial punctate keratitis = early sign of
corneal involvement
• Pannus: The growth of blood vessels from the
limbus in to the cornea + inflammatory changes
• Herbert’s pits: small pits at the limbus formed
by scarring and shrinkage of limbal follicles
• ==>diagnostic of previous trachoma
 Eyelid scarring
• As the fibrous tissue contracts, the margin of the
eyelid turns inwards against the eyeball ==>
Entropion
• The eye-lashes are also misdirected and rub
against the cornea ==> trichiasis
• The trichiasis irritates the cornea and stimulates
further squeezing of the orbicularis oculi muscle
==> blepharospasm ==> Worsening of the
entropion
• The tarsal plate may become thickened and
deformed
• The meibomian glands may become obstructed or
destroyed ==> dry eye
 Diagnosis of
Entropion with trichiasis trachoma
Clinical! (using the WHO
grading system)
Most commonly used,
practical, convenient and
cheap method
Lab:
Detection of Chlamydia
antigen by
immunofluorescence
Antibodies by ELSA
PCR =>expensive&time
consuming
 WHO simplified trachoma grading system
Abbr SIGN DEFINITION

TF Trachoma 5 or more follicles in the upper tarsal

follicular conj
TI Trachoma Severe inflammation of the upper tarsal
intense conj that obscures >1/2 of the deep
tarsal vessels
TS Trachomatous The presence of scarring in the tarsal
scarring conj
TT Trachomatous At least one eyelash rubbing on the
trichiasis cornea
CO Corneal opacity Easily visible corneal opacity affecting
the central cornea
 Treatment: Active trachoma:
• Sensitive to: Tetracyclines, Macrolides
• Topical or systemic
• In mild cases, topical TTC 1% ointment BID
for 6 wks
• In severe cases, add systemic TTC or
doxicycline for adults and erythromycin for
children => 2wks
• Azithromycin:
– Recent highly effective drug in a single systemic dose
– Children 20 mg/kg, adults 1g stat
– Called a “magic bullet”
– Easy for community treatment
– Expensive
 Treatment: Cicatricial trachoma
• Trchiasis
– Epilation, Excision, Cryotherapy
• Entropion
– Tarsotomy (various techniques to evert lid margin)
• Corneal scar
– Difficult (corneal graft and prosthetic corneas, not
suitable or affordable for most pts.)
• Prevention
• Addressing the severe form of trachoma that can
easily lead to blindness
• “GET” (Global Elimination of Trachoma) Strategy
Called SAFE strategy:
– Surgery, Antibiotics, Facial clinliness,
Environmental hygiene
• Surgery:
– For trichiasis & entropion
– Eliminates immediate threat to blindness
– Top priority
• Antibiotics
– Treat individuals to reduce active cases spreading the
disease in the community
– In hyperendemic areas, preschool or school age
children should either be treated all or screened to
treat those with the disease
• Facial cleanliness
• Environmental hygiene
– Pipe water supply
– Proper garbage disposal
– Pit latrine
– Teaching school children about personal hygiene
– Community health education
 Bacterial Keratitis
• Very uncommon in a normal eye and usully only
develops when the ocular defenses have been
compromised.
• Bacteria that can penetrate an apparently
normal corneal epithelium are
– N. gonorrhoeae, N. meningitides, C. diphtheriae, H.
influenzae, etc.
• Risk factors for impaired ocular defense
– Contact lens wear
– Trauma
– Ocular surface diseases: dry eye, herpetic keratitis,
trichiasis, allergic disease
– Others: immunosuppressive drugs, diabetes, vit A
deficiency, measles…
 Bacterial Keratitis
• Symptoms:
– Rapid onset of pain (moderate to severe),
– Photophobia,
– Tearing , discharge and
– Visual reduction
• Signs:
– Decreased vision
– Critical signs: Focal white opacity (infiltrate) in the
corneal stromal, An ulcer exists if there is also stromal
loss with an overlying epithelial defect that stains with
fluorescein
– Corneal haziness
– Hypopyon (pus in A/C)
– Corneal ulcer and perforation
– + pusy discharge
 …bact keratitis

Expanding oval, yellow-white, Stromal suppuration and

dense stromal infiltrate hypopyon

95
 Bacterial Keratitis
• Causative organisms
– Gram positive cocci (staph spp. Strept spp.)
– Aerobic gram negative bacilli (pseudomonas
aeruginosa, H. influenzae, moraxella catarrhalis)
– Enteric gram negative bacilli
– Normal skin flora (staph aureus, strept viridans…)
• Work up:
– Corneal scrapings for gram stain and culture
– Antimicrobial susceptibility testing
– Culture of the eyelid and conjunctiva, medication
bottles, contact lenses etc…
 Bacterial Keratitis
• Principles of Treatment:
– Based on clinical grounds
– Usually a combination of broad spectrum antibiotics to
cover possible etiologies e.g. cephalosporins +
fluoroquinolones
– Antibiotics specific to the causative agent based on
gram stain or culture
1. Topical antibiotics:
– Frequent application: range Q hrly to QID
Bacteria group Antibiotic Concentration

G +ve cocci Cefuroxime 0.3%

Vancomycin 5%

G –ve rods Gentamicin 1.4%

Fluoroquinolone 0.3%

Ceftazidime 5%

G –ve cocci Fluoroquinolone 0.3%

Ceftriaxone 5%

Mycobacteria Amikacin 2%

Clarythromycin

Nocardia Amikacin 2%

Trimethoprim + 1.6%

sulphamethoxaz 8%
 Bacterial Keratitis
2. Oral antibiotics
–Ciprofloxacin 500mg po BID for 7-10days
–In: impending corneal perforation; scleral
involvement. Potential for systemic involvment
3. Subconjunctival antibiotics
–In poor compliance with topical drugs
4. Mydriatics/ Cycloplegics:
–To reduce pain from ciliary spasm
–Atropine 1% or cyclopentolate 1%
 Fungal Keratitis
• Occurs mostly in agricultural workers
• Frequently preceded by ocular trauma with organic
matters
• Major causes of vision loss in tropical & developing
Countries
• Etiologies:
– Filamentous fungi (e.g., Fusarium or Aspergillus
species most commonly):
• Usually from trauma with vegetable matter in previously
healthy eyes
• Most common pathogen in tropical climates
– Non-filamentous fungi (e.g., Candida species):
• Usually in previously diseased eyes, e.g., Keratitis, exposure
keratopathy, chronic use of corticosteroid drops
• Responsible for most cases in temperate climates
 Fungal Keratitis: Clinical features:
• Symptoms:
– Foreign body sensation, decreased vision, pain,
photophobia, red eye, watery discharge
• Signs:
– Granular infiltrate within epithelium and stroma
– Gray-white color, dry rough cornea
– Typical irregular feathery-edged infiltrate
– In advanced cases: suppurative stromal keratitis, anterior
chamber inflammation, hypopyon, corneal perforation
• Work up
– Gram & giemsa stains
– Culture
– Corneal biopsy
 Fungal Keratitis with Suppurative Keratitis with
“satellite” lesions, and hypopyon
feathery borders

Fungal Keratitis with

hypopyon
102
 Fungal Keratitis: Treatment:
• Debridement of necrotic tissues
• Topical antifungal agents
– Natamycin 5% suspension
– Miconazole 1% solution (from the IV preparation),
– Fluconazole 1% aqueous solution
– Itraconazole 1% cream, 200-400 mg/day PO
– Amphotericin B 0.15% solution (from the IV preparation)
• Systemic antifungals:
– For severe keratitis or endophthalmitis
– ketoconazole 400mg/day PO
– Itraconazole 100mg/day PO
• Broad spectrum topical antibiotics:
– For bacterial super-infection
 Viral Keratitis
• Causative agents:
– Herpes Simplex Virus,
– Herpes Zoster Virus (Varicella-Zoster Virus),
– Adenoviruses
• Herpes Simplex Keratitis
– HSV infection is a large worldwide public health
problem
– Two types
• HSV-1: common cause of orofacial and ocular infection
• HSV-2: genital infection
– Either primary ocular infection or recurrent infection
 Primary ocular herpes
• Most common on skin and mucosal surface
innervated by CN V
• Retrograde spread to trigeminal ganglion to
establish latent infection
• Reactivation may occur any time along the
branches of trigeminal nerve
• Typically manifests as a unilateral
blepharoconjunctivitis
• Clinical presentations:
– Follicular conjunctival reaction
– Preauricular lymphadenopathy
– Vesicles on the skin or eyelid margin
– Dendritic corneal epithelial ulcers
 Dendritic keratitis

• Dendritic ulcer with terminal bulbs

• Stains with fluorescein

106
 Recurrent ocular HSV infection
• Caused by reactivation of the virus in latently
infected sensory ganglion, and transport through
axon to ocular surface
• Presentations:
– Blepharoconjunctivitis = similar to primary infection
– Epithelial keratitis (dendritic or geographic ulcer)
• Foreign body sensation, photophobia, redness, blurred
vision
– Stromal keratitis
• Associated with significant visual morbidity
• Stromal corneal edema, whitening, or vascularization
• May develop corneal abscess in case of necrotizing
herpetic keratitis (similar to bacterial keratitis)
– Herpetic iridocyclitis:
• May accompany stromal keratitis or occur independently
 Management
• Most cases of HSV epith keratitis resolve
spontaneously.
• However, treatment shortens the clinical course
• Antivirals:
– Topical: acyclovir 3%, trifluridine 1%, vidarabine 3%,
– Oral: acyclovir, valacyclovir
• Topical steroids:
– Contraindicated in the presence of active herpetic epith
keratitis
– Are the main stay of treatment for stromal herpetic
kekratitis where the epithelium is intact
 Herpes Zoster Ophthalmicus
• The Varicella-Zoster virus causes chickenpox
(varicella) and shingles (herpes zoster)
• After the initial attack of chickenpox, the virus
travels in retrograde manner to the dorsal root
and cranial nerve ganglia.
• Reactivation by reduced cellular immunity
causes shingles
– HIV, elderly, chronic use of immunosuppressive
drugs
 Herpes Zoster Ophthalmicus
• Clinical features
– Skin lesions:
– unilateral painful erythema with maculopapular rash
=> grouped vesicles => pustules => crusts with
depigmented scars
• Rx: oral acyclovir 800mg 5X per day for 7-10
days
– other antivirals – valacyclovir
• Acute epithelial keratitis
– Transient, small, fine dendritic lesions with tapered
ends
• Rx: topical antivirals
Respiratory Tract Infections
Pharmacotherapy

V. Upper Respiratory Tract

Infections
 Respiratory Tract Infections
 Anatomy of the Respiratory Tract
 Sinuses
 Ear (otitic)
 Pharynx
 Lungs
▪ Bronchus
▪ Alveolus
 Defense mechanisms:
 Mucocillary
clearance,
 Secretory IgA
 Cough,
Mechanical
Barrier
Infections of the Respiratory Tract
 Upper Respiratory Tract
 Sinusitis
 Otitis Externa & Media
 Pharyngitis
 Lower Respiratory Tract
 Bronchitis
 Pneumonia
▪ Community Acquired
▪ Nosocomial (HAP, VAP, HCAP)
▪ Aspiration…
Case 1 - Sinusitis

 A 43-year-old man has a two-week history of nasal

congestion, postnasal drip, and fatigue. He has
used an over the- counter nasal decongestant and
acetaminophen, without relief
 During the past few days, facial pain and pressure
have developed and have not responded to
decongestants
 In addition, his nasal discharge has turned from
clear to yellow
 How should he be treated?
 Sinusitis
 Is an inflammation and/or infection of the paranasal
sinus mucosa.
 The term rhinosinusitis is used by some specialists,
because sinusitis typically also involves the nasal
mucosa
 The majority of these infections are viral in origin
 It is important to differentiate between viral and
bacterial sinusitis to aid in optimizing treatment
decisions
 Viral: Usually improves in 5-7 days
 Sinusitis
 Bacterial sinusitis: categorized into acute and
chronic sinusitis
 Acute sinusitis
 lasts <30 days with complete resolution of symptoms
 Most often caused by the same bacteria implicated in
acute otitis media: S. pneumoniae and H. influenzae
 These organisms are responsible for about 70% of
bacterial causes of acute sinusitis in both adults and
children.
 Sinusitis
 Chronic sinusitis
 episodes of inflammation lasting more than 3 months
with persistence of respiratory symptoms
 can be polymicrobial, with an increased prevalence of
anaerobes as well as less common pathogens including
gram-negative bacilli and fungi.
 Sinusitis: Treatment
 The goals of treatment of acute sinusitis
 reduction in signs and symptoms,
 achieving and maintaining patency of the ostia
 eradication of bacterial infection with appropriate
antimicrobial therapy
 minimizing the duration of illness
 prevention of complications, and
 prevention of progression from acute disease to chronic
disease
Algorithm…Sinusitis
 Sinusitis: Treatment
 Approximately 65% of patients with acute sinusitis will
recover spontaneously (these are likely patients with viral
sinusitis)
 Nasal decongestant sprays such as phenylephrine and
oxymetazoline that reduce inflammation by
vasoconstriction are often used in sinusitis.
 Oral decongestants may also aid in nasal or sinus patency.
 To reduce mucociliary function, irrigation of the nasal
cavity with saline and steam inhalation may be used to
increase mucosal moisture, and mucolytics (e.g.,
guaifenesin) may be used to decrease the viscosity of nasal
secretions.
 Sinusitis: Treatment
 Antihistamines should not be used for acute bacterial
sinusitis in view of their anticholinergic effects that can dry
mucosa and disturb clearance of mucosal secretions.
 Antimicrobial therapy is superior to placebo in reducing
or eliminating symptoms, although the benefit is small
 Amoxicillin is first-line treatment for acute bacterial
sinusitis.
 The current recommendations are 10 to 14 days, or at
least 7 days, of antimicrobial therapy after signs and
symptoms are under control
 Case 1 - Sinusitis
 Amoxicillin* 500 mg three times daily for 10 days
 Continued use of nasal saline and decongestant
therapy
 * Doxycycline or trimethoprim–sulfamethoxazole also
reasonable
 Ifpatient’s symptoms did not improve after 72
hours
 Switch to azithromycin, levofloxacin, or high-dose
amoxicillin–clavulanate
 Case 2 – Otitis Media
 An otherwise healthy 17-month-old boy had a cold
accompanied by two days of rhinorrhea, cough, and
fever (temperature of up to 38.8°C [102°F]).
 On day 5 he became fussy and woke up crying
multiple times during the night.
 The following day he was afebrile, and a physical
examination was normal except for findings of slight
redness of the left tympanic membrane with no middle-
ear fluid and a bulging right tympanic membrane with
white fluid behind it obscuring the umbo.
 How should this child be treated?
 Otitis Media
 An inflammation of the middle ear
 Three subtypes of otitis media:
 Acute otitis media,
 Otitis media with effusion, and
 Chronic otitis media
 Acute otitis media
 involves the rapid onset of signs and symptoms of
inflammation in the middle ear that manifests clinically
as one or more of the following:
▪ otalgia (denoted by pulling of the ear in some infants), hearing
loss, fever, or irritability.
 Otitis Media
 Otitis media with effusion (accumulation of liquid
in the middle ear cavity)
 differs from acute otitis media in that signs and symptoms
of an acute infection are absent
 Otitismedia is most common in infants and
children
 Risk factors
 winter season, attendance at a daycare center, non–breast-
feeding in infants, early age at first infection and
colonization with middle ear pathogens.
 Otitis Media: Pathophysiology
 Acute bacterial otitis media usually follows a viral upper
respiratory tract infection that causes eustachian tube
dysfunction and mucosal swelling in the middle ear
 See the next slide for causative organisms
 S. pneumoniae isolates are often intermediate resistant
to penicillin (8% to 34%) and some are highly penicillin
resistant (12% to 21%).
 Penicillin-resistant isolates are often resistant to multiple
antibiotics.
 β-Lactam resistance occurs in about 23% to 35% of H.
influenzae and in up to 100% of M. catarrhalis.
Otitis Media
Otitis Media - Clinical Presentation
 Resolution of acute otitis media occurs over 1
week.
 Pain and fever tend to resolve over 2 to 3 days,
with most children becoming asymptomatic at 7
days
 Effusions resolve slowly, 90% have disappeared
by 3 months.
Otitis Media – Treatment
 The goals of treatment include
 Reduction in signs and symptoms, eradication of
infection
 Prevention of complications
 Avoidance of unnecessary antibiotic use is another
goal in view of S. pneumoniae
Otitis Media – Treatment
 Differentiateacute otitis media from otitis media
with effusion or chronic otitis media
 Recognize that amoxicillin is the mainstay of therapy
and that penicillin resistance can be overcome, in
many cases, with high-dose amoxicillin therapy
 Acetaminophen or NSAID, such as ibuprofen, should
be offered early to relieve pain in acute otitis media
 One strategy to reduce antibiotic use in this setting is
"delayed therapy …. 48 to 72 hours
Duration of Treatment and Observation
Option

 Duration of treatment
 10 days standard [ < 2 years of age , Ethiopia]
 5-7 days (short course)
▪ Children > 6 years old with mild to moderate disease
 Observation without antibiotics for 48-72 hours:
 6 months to 2 years, otherwise healthy with non-severe
illness at presentation and an uncertain diagnosis
 2 years of age and older without severe symptoms at
presentation or with an uncertain diagnosis
Antibiotic Prophylaxis of Recurrent Infections

 Recurrent otitis media is defined as at least

three episodes in 6 months or at least four
episodes in 12 months.
 Recurrent infections are of concern because
patients younger than 3 years of age are at
high risk for hearing loss and language and
learning disabilities
 Data from studies generally do not favor
prophylaxis.
Antibiotic Prophylaxis of Recurrent Infections

 Vaccination against influenza and

pneumococcus may decrease risk of acute
otitis media, especially in those with recurrent
episodes.
 Immunization with the influenza vaccine
reduces the incidence of acute otitis media by
36%.
Case 2 – Otitis Media

 Bulging tympanic membrane with visible pus

 Immediate antibiotic therapy with high-dose
amoxicillin
 Acute otitis without bulging eardrums
 likely to clear spontaneously
 Consider delayed antibiotic-prescribing strategy
(waiting 48 to 72 hours to prescribe antibiotics
while giving the patient acetaminophen)
Pharyngitis

Case – Pharyngitis

 A 10-year-old girl presents

with a sore throat and fever that has lasted for 1 day. She appears
flushed and moderately ill
 Physical examination reveals a temperature of 39°C, tender
bilateral anterior cervical lymph nodes that are 1 to 2 cm in the
greatest dimension, and erythema and whitish-yellow exudate over
enlarged tonsils and the posterior pharynx.
 A rapid antigen-detection test from a throat-swab specimen is
positive for group A streptococcus.
Pharyngitis
 An acute infection of the oropharynx or
nasopharynx
 Viral causes are most common
 Group A β-hemolytic Streptococcus, or
Streptococcus pyogenes , is the primary
bacterial cause
 Viruses cause most of the cases of acute
pharyngitis
 A bacterial etiology for acute pharyngitis is far
less likely
Pharyngitis
 Group A Streptococcus is the most, and it is the
only commonly occurring form of acute
pharyngitis for which antimicrobial therapy is
indicated
 Nonsuppurative complications such as acute
rheumatic fever, acute glomerulonephritis, and
reactive arthritis may occur as a result of
pharyngitis with Group A Streptococcus
 Children ages 5 to 15 years are most susceptible
Pharyngitis
 The incubation period is 2 to 5 days, and the
illness often occurs in clusters
 Guidelines suggest that testing for Group A
Streptococcus be done in all patients with
signs and symptoms
 Only those with a positive test for Group A
Streptococcus require antibiotic treatment
 Scoring System: Modified Centor Criteria for Clinical
Prediction of Group a -Hemolytic Streptococcal
Pharyngitis
 Pharyngitis:Treatment
 The goals of treatment of pharyngitis are to
 improve clinical signs and symptoms
 minimize adverse drug reactions
 prevent transmission to close contacts
 prevent acute rheumatic fever and suppurative
complications such as peritonsillar abscess,
cervical lymphadenitis, and mastoiditis
 Pharyngitis:Treatment
 Symptomatic treatment (pain)
 Acetaminophen (better option than NSAID)
 Rest, fluid, lozenges, salt water gargles
 Antibiotics if clinical signs & symptoms
consistent with group A streptococcus and
positive laboratory test (rapid strep screen or
culture)
 Penicillin is the drug of choice in the
treatment of Group A streptococcal
pharyngitis
 Pharyngitis:Treatment
 In patients allergic to penicillin, a macrolide such as
erythromycin or a first-generation cephalosporin such
as cephalexin (if the reaction is non IGE–mediated
hypersensitivity) can be used
 Newer macrolides such as azithromycin and
clarithromycin are as effective as erythromycin and
cause fewer GI adverse effects
 If pts are unable to take oral medications, IM
benzathine penicillin can be given although it is painful
 Duration of therapy for Group A streptococcal
pharyngitis is 10 days to maximize bacterial eradication
Evaluation of Therapeutic Outcomes

 Most cases of pharyngitis are self-limited;

however, antimicrobial therapy will hasten
resolution when given early to proven cases of
group A Streptococcus
 Symptoms generally resolve by 3 to 4 days even
without therapy
 Children should be kept home from daycare or
school until afebrile and for the first 24 hours after
antimicrobial treatment is initiated, after which
time transmission is unlikely
Respiratory Tract Infections
Pharmacotherapy

VI. Lower Respiratory Tract

Infections