Bacterial Conjunctivitis

SIGNS AND SYMPTOMS

Patients with bacterial conjunctival infections present with injection of the bulbar conjunctiva, episcleral vessels and perhaps papillae of the palpebral conjunctiva. The infection often starts in one eye, then soon spreads to the other. There will be thick mucopurulent discharge, and patients usually say that their eyelids and eyelashes are matted shut upon awakening. There may be mild photophobia and discomfort, but usually no pain. Visual function is normal in most cases.

PATHOPHYSIOLOGY
The eye has a battery of defenses to prevent bacterial invasion. These include bacteriostatic lysozymes and immunoglobulins in the tear film, the shearing force of the blink, the immune system in general, and non-pathogenic bacteria that colonize the eye and compete against external organisms that try to enter. When any of these defense mechanisms break down, pathogenic bacterial infection is possible. Invading bacteria, and the exotoxins they produce, are considered foreign antigens. This induces an antigen-antibody immune reaction and subsequently causes inflammation. In a normal, healthy person the eye will fight to return to homeostasis, and the bacteria will eventually be eradicated. However, an extra heavy load of external organisms can be too difficult to fight off, causing a conjunctival infection and setting the eye up for potential corneal infection. The most commonly encountered organisms are Staphylococcus aureus, Haemophilus influenzae, Streptococcus pneumoniae and Pseudomonas aeruginosa. In cases of hyperacute bacterial conjunctivitis, the patient will present with similar signs and symptoms, albeit much more severe. The most common infectious organisms in hyperacute conjunctivitis are Neisseria gonorrhoeae and Corynebacterium diptheroides. There is more danger in hyperacute bacterial conjunctivitis as these organisms can penetrate an intact cornea.

MANAGEMENT
Ordering cultures and sensitivity tests is ideal for diagnosis but usually impractical and expensive. Most clinicians immediately begin treatment with a broad spectrum antibiotic and reserve culturing for hyperacute conditions or those that fail to respond to the initial therapy. There are many antibacterial options. Excellent initial broad spectrum antibiotics include Polytrim (polymixin B sulfate and trimethoprim sulfate), gentamicin 0.3%, and tobramycin 0.3%. These will give good coverage of grampositive and gram-negative organisms, though the aminoglycosides (gentamicin and tobramycin) have weak activity against Staphylococcal species; there are also resistant strains of Pseudomonas. Fluoroquinolones such as Ciloxan, Ocuflox and Chibroxin are also excellent options. Therapy should be aggressive, with administration from QID to Q1H for the first few days. Although antibiotics will eradicate the bacteria, they will do nothing to suppress the concurrent inflammation. If there is no significant corneal disruption, prescribe a steroid such as Pred Forte, Vexol or Flarex along with your antibiotic of choice, or a steroid-antibiotic combination such as Maxitrol (neomycin, polymyxin B, dexamethasone 0.1%), Pred-G (gentamicin 0.3%, prednisolone acetate 0.1%), or Tobradex (tobramycin 0.3%, dexamethasone 0.1%).

CLINICAL PEARLS

Like patients with bacterial conjunctivitis, those suffering from viral and allergic conjunctivitis will often report that their lids are matted shut in the morning with mucopurulent material. However, these patients actually have crusting of the lashes due to drying of tears and serous secretions, not the wet, sticky, mucopurulent matting characteristic of bacterial conjunctivitis. Too often, clinicians will consider the crusting of the lashes to be the same as the mucopurulent matting and misdiagnose the condition. Remember, due to the excellent defense systems of the eye, acute bacterial conjunctivitis is uncommon.

Viral Conjunctivitis
(Pharyngoconjunctival Fever & Epidemic Keratoconjunctivitis)

A Pseudomembrane in EKC

Severe Follicular Reaction

SIGNS AND SYMPTOMS

Most viral infections produce a mild, self-limiting conjunctivitis, but some have the potential to produce severe, disabling visual difficulties. The two most common self-limiting forms of viral conjunctivitis are epidemic keratoconjunctivitis and pharyngoconjunctival fever. Pharyngoconjunc-tival fever (PCF) is characterized by fever, sore throat and follicular conjunctivitis. It may be unilateral or bilateral. It is caused regularly by adenovirus 3 and occasionally 4 or 7. Corneal infiltrates are rare. The disorder varies in severity but usually persists for four days to two weeks. While the virus is shed from the conjunctiva within 14 days, it remains in fecal matter for 30 days. Epidemic Keratoconjunctivitis (EKC) often presents as a bilateral, inferior, palpebral, follicular conjunctivitis, with epithelial and stromal keratitis. Subepithelial corneal infiltrates are much more common in EKC than in PCF and are typically concentrated in the central cornea. EKC is regularly caused by adenovirus types 8 and 19. The key clinical signs of both conditions include: conjunctival injection, tearing, serous discharge, edematous eyelids, pinpoint subconjunctival hemorrhages, pseudomembrane formation and palpable preauricular lymph nodes. In severe cases, conjunctival desiccation causes scarring and symblepharon formation (adherence of the bulbar and palpebral conjunctivas). Both conditions are highly contagious. Patients will usually report recent contact with someone who had either red eyes or an upper respiratory infection. Both forms tend to start in one eye, then spread to the other eye within a few days. In rare cases, the focal subconjunctival hemorrhages can evolve into acute hemorrhagic conjunctivitis.

PATHOPHYSIOLOGY
Viral conjunctival infections are thought to be caused by airborne respiratory droplets or direct transfer from ones fingers to the conjunctival surface of the eyelids. After an incubation period of five to 12 days, the disease enters the acute phase, causing watery discharge, conjunctival hyperemia and follicle formation. Lymphoid follicles are

elevated, with avascular lesions ranging from 0.2 to 2mm in size. They have lymphoid germinal centers that have responded to an infectious agent. Adenovirus type 8 can proliferate in the corneal epithelial tissues, producing the characteristic keratitis and subepithelial infiltrates. This, along with the immune response to viral antigens, causes lymphocytes to collect in the shallow anterior stroma, just beneath the epithelium. Sometimes, a conjunctival membrane will form. These are made up of fibrin and leukocytes, and in prolonged cases, of fibroblast and collagen deposits. Pseudomembranes are much easier to remove than true membranes.

MANAGEMENT
Because EKC and PCF are contagious and self-limiting, the primary treatment once again is patient education. Instruct patients to stay home from work or school until there is absolutely no discharge. Also instruct them not to share utensils, glasses, linens or wash cloths with others. Medical management can range from cold compresses and artificial tears to topical vasoconstrictors (e.g., naphazoline) and steroids (Vexol, Flarex, Pred Forte) two to four times daily. If a membrane is present, peel it off with a wet, cotton-tipped applicator or forceps. After removal, prescribe a topical antibiotic-steroid combination such as Tobradex or Maxitrol q.i.d. Anti-viral drugs such as Viroptic are ineffective against adenovirus. Recently, there has been a breakthrough in the management of adenoviral keratoconjunctivitis. Cidofovir (Vistide), an anti-viral drug used intravenously to treat cytomegalovirus retinitis, appears to be effective in adenoviral keratoconjunctivitis. The topical form creates a faulty viral DNA structure. Twice daily instillation is recommended. This topical anti-viral is also possibly effective against herpes simplex and zoster, and Epstein-Barr virus.

CLINICAL PEARLS
y y y Keep your equipment, instruments and chair area meticulously clean to avoid contaminating your patients and staff. Most practitioners reserve topical steroidal therapy for severe cases (if the infection is on the visual axis and affecting acuity, for example), or recalcitrant cases. EKC infiltrates resolve without scarring the cornea. Tell patients to expect the symptoms to get worse for about seven to 10 days before getting better, and that the infection wont completely go away for three to six weeks. Remember to always taper steroids slowly as the condition recedes.