Ear and Eye infections; Drugs! Flashcards Preview

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Flashcards in Ear and Eye infections; Drugs! Deck (39):


conjunctiva- thin membrane

discharge, red eye, irritation, and sensitivity to palpitation; caused by dilation and congestion of subepithelial vessels
Could be viral, bacterial, or allergic


Viral conjunctivitis

Neonatal – HSV-1 (acute)
Post-natal – Adenovirus (most common)

recent upper respiratory tract infection, preauricular adenopathy
benign and self limited in immunecompetent
treat with cold compress and topical vasoconstrictors



non-enveloped, double-stranded DNA virus Lytic in epithelial cells and latent in lymphoid highly contagious spread through fomites like swimming pools


Acute bacterial conjunctivitis

Children- Staphylococcus aureus, Streptococcus pneumoniae, Haemophilus influenzae

Adults- Staphylococcus aureus

Self-limited but treating decreases patient morbidity and transmission
Empiric treatment with both Gram positive and negative coverage
Moxifloxacin solution (best coverage, expensive, >3 yr)
trimethoprim-polymyxin B


Neisseria gonorrhoeae

Copious yellow-green discharge (purulent)
Preauricular adenopathy
Gram stain for gram-negative intracellular diplococci and growth on chocolate agar supplemented with vancomycin, colistin, nystatin, and trimethoprim (nonsterile site)
Treat promptly with systemic ceftriaxone otherwise can quickly progress to corneal ulceration and perforation, can augment with topical antibiotics and irrigation


Ophthalmia neonatorum

conjunctivitis or keratoconjunctivitis occurring within first four weeks of birth

Timing of infection can help predict etiology
N. gonorrhoeae, C. trachomatis, Staphylococcus, Streptococcus, E. coli, H. influenzae or H. simplex
Prophylaxis with erythromycin ointment
Treat with appropriate antimicrobial often erythromycin
Cultures and smears for diagnosis



erythromycin, azithromycin

Inhibits translation by binding 23S rRNA of the 50S subunit

Spectrum: Broad coverage of respiratory pathogens, Chlamydia

Resistance: Increased efflux, hydrolysis of drug by esterases, methylation of drug binding site

Adverse effects:
GI discomfort, Hepatic failure, and Prolonged QT interval
Inhibitors of cytochrome P450 enzymes (check with other medications)


Chlamydia trachomatis

Inclusion conjunctivitis (serotypes D-K)
Trachoma (serotypes A-C), leading cause of blindness worldwide due to multiple infections since no long lasting immunity
Diagnosis: direct fluorescent antibody
Coinfections should be considered, most often N. gonorhoaea
Treat with systemic azithromycin and improve hygiene
Treat sexual partner(s) and widespread prophylaxis is being used to try to eliminate Trachoma by 2020.

Elementary body is taken up by mucosal epithelial cells of uterus and eye converts to metabolically active reticulate body which divides by binary fission. Converts back and then is released to infect neighboring cells. Interferon-gamma can create persistent form which is reactivated when the drug is removed.


Herpes simplex virus

Similar presentation to adenovirus although lesions can be painful especially if scarring of the cornea occurs and often only one eye

Avoid corticosteroids since can facilitate corneal penetration

If corneal involvement treat with topical trifluridine and systemic acyclovir and consider prophylactic treatment with erythromycin to prevent bacterial superinfection

often affects neonates



pyrimidine analog effective against acyclovir resistant virus because it can be phosphorylated by host kinases also making it much more toxic and should only be used topically




vision defects, photophobia, pain (cornea has lots of nerve endings), and foreign body sensation
Trauma, drying of the epithelia, and hypoxia increase susceptibility.
Viral keratitis is caused by HSV-1, adenovirus, and VZV.
Bacterial keratitis Staph. aureus and epidermidis, Pseudomonas aerugrinosa, and Bacillus cereus.
Fungal infection in warm, humid climate
Acanthamoeba, a free-living ameba, frequently resides in improperly stored contact lens cleaning fluids and initiates eye infections.
Treatment- for bacteria Moxifloxacin eye drops
for HSV-1 trifluridine + acyclovir


Pseudomonas aeroginsoa

Gram negative, aerobic rod, flagella

Free living found in water and soil with minimal nutrition requirements and can use 75 different organic compounds for growth
Plant and nosocomial pathogen
Contact lens wearers are at greater risk
Opportunistic infection- if decrease in host defense (trauma) can infect most tissues
Naturally resistant to many antibiotics and disinfectants partly due to its ability to form biofilms
Bacterial cell surface adherence factors and secreted cytotoxins like elastase and alkaline protease destroy corneal epithelium.
The host immune response damages the cornea leading to scarring and loss of visual acuity



iris, ciliary body, and choroid

inflammation of uveal tract can leading to blurred vision permanent vision loss

Iritis (anterior uveitis)- often not infectious, photophobia, pain, and decreased visual acuitiy
Treponema pallidum, Herpes simplex, varicella-zoster
Chorioretinitis (poster uveitis)- most common, floaters, no pain



choroid and retinal layers

blurred vision and visual field defects

Blood borne route via retinal arteries, frequently manifestation of systemic disease
Congenital Toxoplasma and CMV (ganciclovir implant) are most common especially in HIV positive individuals and neonates
Two parasitic worm infections (Toxocara canis and Onchocerca volvulus) cause eye infections; the latter causes “river blindness” and is transmitted by sand flies.



vitreous and/or aqueous humors

Pain, redness, and decreased vision
Bacteria/ fungi
Exogenous- Recent intraocular surgery esp. cataract
with agent coming from normal flora: Pseudomonas, Staphylococci or Candida
Endogenous- hematogenous spread
Fluoroquinolone or vancomycin injected into eye


Acute otitis media

bacterial or viral
pain, red ear drum, pus, and fever

Streptococcus pneumoniae: 25-50%
Haemophilus influenzae (mostly non-typable): 15-30%
Moraxella catarrhalis: 3-20%
Viral (especially RSV, rhinovirus): 5-22%


Otitis media with effusion

build up of fluid in Eustachian tube
No infection in ear associated with URI, cigarette smoke, allergies
antibiotics won’t help usually resolves on its own


Streptococcus pneumoniae

Gram positive, diplococcus

Transmitted by contact with secretions
Asymptomatic colonization of naso-oropharynx
can be a carrier for weeks to months especially in winter
If spreads to middle ear or terminal airways leads to rapid inflammation
Chronic diseases, including alcoholism, diabetes mellitus, and chronic renal disease, interfere with normal defense can increase susceptibility
91 serotypes due to unique surface capsules-
Vaccine covers 23 most likely to cause meningitis


Streptococcus pneumoniae virulence factors

Resistance due to changes in the
penicillin binding protein

Capsule- blocks phagocytosis by interfering with the
deposition of complement on surface of organism

Choline-binding proteins- bind carbohydrates present
on surface of epithelial cells

Neuraminidases- cleave sialic acid in host mucins

Autolysin A (LytA)- degrades peptidoglycan and causes
α-hemolysis during growth

Pneumolysin- pore forming toxin is released disrupts cilia

Iron acquisition A (PiaA) and uptake A (PiuA)


Haemophilus influenzae

Small, pleomorphic, gram-negative, coccobacillus, nonmotile, biofilms, facultative anaerobe
Humans are only known host
Fastidious require additional blood factors for growth hematin (X) and NAD (V) both present in chocolate agar
Nontypeable- nonencapsulated (NTHi) colonize nasopharynx in 80% of people and if spreads to the eustachian tubes causes otitis media.
Many express β-lactamases
Other mucosal sites of infection include
genital tract and conjunctivitis


Moraxella catarrhalis

Gram-negative, aerobic, diplococcus, oxidase-positive, nonmotile, fastidious-chocolate agar, pili
Colonization of upper respiratory track in infants
95% of M. catarrhalis produce β-lactamases
Hockey puck test- easily slide across agar and be stacked


Recommended treatment for Acute Otitis Media

6-24 months start empiric treatment: Amoxicillin provides coverage against Streptococcus pneumoniae, Haemophilus influenzae with limited side effects (?).
If no improvement within 48 hours switch to Amoxicillin- Clavulanate
If penicillin allergy, treat with Azithromycin

Pain management- acetaminophen and ibuprofen
If multiple infections prophylaxis may be considered
Respiratory Viral Vaccine may have some benefit


Otitis externa- common etiologies

Acute localized- most often Staphylococcus
pustule or furuncle associated with hair follicles
Acute diffuse- Pseudomonas aeroginosa
itches, red canal, and painful
Malignant- Pseudomonas aeroginosa, invasion of adjacent bone and cartilage which can progress to cranial nerve palsy and death. More common in elderly, poorly controlled diabetes, and immunocompromised.
Fungal- Aspergillus and Candida


Staphylococcus aureus

clustered, Gram positive cocci present in the anterior nares

Virulence factors
Capsule and Protein A binds Fc portion of IgG to interfere with phagocytosis
Coagulase binds prothrombin initiating the polymerization of fibrin and clotting- retard migration of phagocytes to site of infection
Membrane damaging toxins hemolysin and leukotoxin


Otitis externa management

Diagnosis can be complicated with contamination from surface bacteria
Cleansing with topical solutions often of low pH (acetic acid)
to deter bacterial and yeast growth
Avoid flushing unless tympanic membrane is intact
Treat with analgesics (NSAIDs, acetaminophen)
Topical antibiotics are usually sufficient unless cellulitis or fungal
and reach higher concentrations
Neomycin + polymyxin + hydrocortisone



conjunctiva and cornea



α1 adrenergic stimulants

a drug used in eye drops to dilate pupil
2. 2.5% to 10% solution used to produce mydriasis
3. also reverses ptosis in Horner’s Syndrome



treat glaucoma
1. increases aqueous humor outflow & inhibits formation
Primarily increase aqueous humor outflow but also suppress production



Inhibitors of parasympathetic nervous system



Muscarinic agonists
Treatment of Glaucoma:
enhances aqueous humor drainage through trabecular meshwork & canal of Schlemm

i. 1% solution to differentiate IIIrd nerve palsy from “Atropinic” mydriasis
ii. if pilocarpine is active (produces miosis) then the defect must be in the nerve
iii. If pilocarpine is inactive, then the defect must be in the eye



Treatment of Glaucoma
Anticholinesterases: Agents preventing acetylcholine degradation
enhances aqueous humor drainage through trabecular meshwork & canal of Schlemm



Treatment of Glaucoma
Anticholinesterases: Agents preventing acetylcholine degradation
enhances aqueous humor drainage through trabecular meshwork & canal of Schlemm



α1 receptor antagonists
not used to treat eye disease but can have ocular side effects



Norepinephrine depleting agent
have the potential of causing ocular side effects (miosis; ptosis)



activates parasympathetic nerves



ß Blockers
Treatment of Glaucoma
decrease aqueous humor formation



Treatment of Glaucoma
It increases uveo-scleral outflow of aqueous humor (flow through the ciliary muscle)



Treatment of Glaucoma
carbonic anhydrase inhibitors


botulinum toxin

a. Treatment of muscle spasms Strabismus (deviation of the eyes) & Blepharospasm (spasm resulting in closed eyelids)
i. Can treat problems caused by muscle spasms with botulinum toxin (Botox)
1. inhibits acetylcholine release from somatic nerves
2. suppression of acetylcholine release can relieve a muscle spasm causing the strabismus or blepharospasm