Phthirus pubis Infestation

The crab louse Phthirus pubis is a tiny insect adapted to living in coarse, widely spaced hair. Infestation most commonly involves pubic, axillary, and body hair. The organism is transmitted by direct person-to-person contact and perhaps by fomites. Infestation of the eyelid often is a marker for sexually transmitted infections, especially in adult patients. For these reasons, infection in children should raise concern for potential sexual abuse. Affected patients typically have unilateral, chronic blepharoconjunctivitis; some patients may be asymptomatic. Although unmagnified ocular examination may rarely reveal signs of the disease, diagnosis is best facilitated by slit-lamp examination, which offers a magnified view of the eyelid margins and eyelashes ( Fig. 61.2 ), revealing adult lice firmly adherent to the eyelashes as well as egg cases (nits) attached to the proximal ends of the hair shafts. Reddish brown flecks of louse excreta may be found at the base of the cilia, and the cilia may be broken. Treatment can be simple mechanical removal of the lice and nits under magnification (slit lamp or other devices).

Slit-lamp photo of Phthirus pubis infestation demonstrating adult lice firmly adherent to the eyelashes and egg cases (i.e., nits) attached to the proximal ends of the hair shafts.

Medical treatment often is preferred for young children because of their inability to tolerate or permit mechanical removal. The organisms also can be smothered by the application of a bland ointment such as petrolatum jelly applied four times each day to the eyelids. Physostigmine ointment administered twice daily can be used. This agent inhibits nerve transmission in the insect and thus is directly toxic to the insect. It should be used with caution in infants and small children. If physostigmine comes into contact with the eye, it has several significant side effects, such as stimulation of accommodation, which can produce blurred distance vision that may last for several hours. Medical treatment should be continued for 2 weeks to ensure eradication of new lice that emerge from nits during the normal life cycle. Lindane shampoo scrubs of the scalp, pubic hair, and body are recommended if infestation is found in these areas. Clothing and bed linen should be laundered, and family members should be examined and treated as necessary. Follow-up 4 to 6 weeks after treatment is recommended to detect reinfestation.

Demodex Infection

Demodex folliculorum and Demodex brevis are mites that frequently infest hair follicles in humans, including the hair follicles of the eyelids ( Fig. 61.3 ). The organisms historically have been considered nonpathogenic parasites, although it is thought they may cause increased hordeola formation as a result of obstruction of eyelid sebaceous glands.

Demodex folliculorum and Demodex brevis are mites that can infect the hair follicles of the eyelids and are found more commonly on eyelashes with cylindrical dandruff.

Demodex is found in patients with rosacea, although a causal relationship is difficult to establish. Rosacea-like eruptions have been attributed to Demodex, and one pathologic report demonstrated a granulomatous dermal inflammation. Treatment with topical pilocarpine gel may alleviate itching caused by Demodex infection. Because of the frequency of Demodex infestation and the paucity of definitive disease caused by the organism, treatment often is unnecessary.

Hordeolum

A hordeolum (i.e., stye) is an infection of the sebaceous glands in the eyelids. When the glands of Zeis are involved, the term external hordeolum is used. The lesion typically points to the skin surface. When the meibomian glands are involved, the term internal hordeolum is used. An internal hordeolum may point toward the skin or toward the palpebral conjunctiva. S. aureus is the most common causal agent of both internal and external hordeola.

Patients with disease of the lid margin, such as those with chronic blepharitis, seborrhea, or rosacea, are prone to recurrent hordeola, especially during the first decade of life. Hordeola are manifested by erythematous, elevated, tender nodules. Nodules typically are 5 to 10 mm in diameter and usually solitary, although they may be multiple or bilateral. Patients with a history of recurrent hordeola may have them in various stages of evolution or resolution.

The lesions usually are self-limited and typically resolve within 5 to 7 days with spontaneous drainage of the abscess. Warm compresses may hasten resolution and improve comfort. Parents should be advised to place a clean washcloth soaked in warm tap water on the involved eyelid for 10 to 15 minutes several times each day. Parents should be advised to ensure that the water is not hot enough to cause a burn. For significant coexisting blepharitis, a topical antibiotic such as erythromycin ointment may prove useful by reducing the normal bacterial skin flora of the eyelid and decreasing the risk for recurrence. Systemic antibiotics rarely are indicated for acute hordeola. Children with frequent recurrences, however, may benefit from a short course of systemic antibiotics such as azithromycin, erythromycin, or tetracycline (only for children older than 12 years). These agents further decrease the bacterial flora on the eyelid and may reduce the risk for recurrence even more. Lid hygiene efforts, as described for the treatment of staphylococcal blepharitis, should be instituted and maintained for children with recurrent hordeola. Surgical drainage of a hordeolum usually is unnecessary.

Chalazion

Cytologically a chalazion may represent either a mixed-cell granulomatous inflammation or a suppurating granuloma. The lesion occurs in a meibomian gland as a result of a foreign body reaction to secretions produced by the gland that have been extruded into surrounding tissue. A chalazion may develop after resolution of an internal hordeolum, in which case it is preceded by an acute stage, or it may develop primarily, without a preceding acute inflammatory phase. A typical chalazion appears as a round, nontender nodule within the substance of the eyelid. Multiple and bilateral chalazia may occur in susceptible patients. Recurrent lesions are not uncommon findings. They are typically 2 to 10 mm in diameter.

Spontaneous resolution of smaller chalazia can be anticipated after a period of observation without treatment, sometimes as long as several months. Larger lesions, particularly those greater than 10 mm in diameter, frequently do not resolve without specific treatment. In patients with an acute or chronic inflammatory component, application of warm compresses may be beneficial. The majority of chalazia resolve in time, but indications for earlier surgical intervention include unacceptable cosmesis, induced visually significant astigmatism, and visually significant ptosis. In rare circumstances, chalazia can result in vision loss from amblyopia. The most common surgical treatment offered is incision and curettage through an internal incision on the palpebral conjunctival surface. Surgery is highly effective. It can be performed in the office, but general anesthesia is required for most young children. Because of the need for general anesthesia, we typically recommend deferring surgical treatment until several months have elapsed without spontaneous resolution. Earlier intervention may be recommended if the chalazion is particularly large, if pigmentary changes have developed in the overlying skin, or if astigmatism or ptosis is present in a young child at risk for the development of amblyopia.

Chalazia can be treated by intralesional steroid injection, surgical incision, or both. Dhaliwal and Bhatia reported that incision plus curettage was the procedure of choice for lesions that have been present for 8.5 months or longer and for lesions 11.4 mm or larger in size, based on the results of a prospective study. The major potential drawback of intralesional steroid injection is the risk for complications developing with an otherwise relatively benign condition. Rarely steroid injection can result in sterile abscess formation or eyelid necrosis. Intralesional injections are done best with a chalazion clamp in place to protect the underlying globe from accidental needle trauma during injection. This device places a metal plate between the chalazion and the eye. If general anesthesia is required, incision and curettage is recommended over intralesional steroid injection.

Posttraumatic Preseptal Cellulitis

Posttraumatic preseptal cellulitis occurs after puncture wounds on the lids, face, or scalp. It also may occur after blunt trauma with no obvious entry wound. The etiologic agents most commonly identified are S. aureus and S. pyogenes, and polymicrobial infections can occur. Other bacterial causes include non–spore-forming anaerobes such as Peptococcus, Peptostreptococcus, and Bacteroides . Infection by aerobic gram-negative bacilli is an uncommon finding _. P. multocida is a common organism that produces posttraumatic preseptal cellulitis after dog and cat bites. Cellulitis secondary to methicillin-resistant S. aureus (MRSA) is increasing in frequency and is a common cause of community-acquired cellulitis in some locations.

Clinical signs and symptoms are determined in large part by the severity of the injury, the interval since injury, and the infecting organisms. The involved lids are edematous, erythematous, and typically quite tender. Fluctuation of subcutaneous tissue may be present if an abscess has developed. Swelling of the uninvolved contralateral eyelids may occur as a result of lymphedema. As with any form of isolated preseptal cellulitis, vision is unaffected, and proptosis and eye movement disturbances are absent. On rare occasions, eyelid edema may be sufficiently severe to preclude adequate evaluation of the eye. Neuroimaging is required in such cases to assess the globe and rule out involvement of structures posterior to the orbital septum. Ophthalmologic consultation is critical in cases of severe posttraumatic preseptal cellulitis because of the potential for concurrent globe injury.

Laboratory analysis includes Gram stain and aerobic and anaerobic culture of any mucopurulent material to aid in therapeutic decisions. Amoxicillin-clavulanate or a related agent is the drug of choice for treating posttraumatic cellulitis caused by a dog bite because of the high prevalence of P. multocida . Tetanus prophylaxis should be guided by standard recommendations. Surgical drainage of large abscesses may be required if a rapid response to antimicrobial therapy does not occur.

Nontraumatic Preseptal Cellulitis

The clinical features of nonsuppurative, nontraumatic preseptal cellulitis depend to a large degree on the causative agent. Erythema and swelling of the involved eyelids are typical and are often accompanied by pain. Signs of orbital infection such as altered vision, proptosis, and eye movement abnormalities are absent.

Before the advent of H. influenzae type b vaccine, this organism frequently was a cause of nonsuppurative preseptal cellulitis in children. It was a particularly dangerous agent because of a high risk for spread to the central nervous system (CNS), which occurred in as many as 2% to 3% of patients. Although rare today, H. influenzae type b infections still may be encountered. Like many infecting organisms, it gains access to subcutaneous tissue through infected nasal passages.

S. pneumoniae is now the most common bacterial cause of preseptal cellulitis in the pediatric age group. It occurs in association with upper respiratory tract infection, although constitutional symptoms usually are less pronounced than those associated with H. influenzae type b infection. A variety of other bacterial agents may cause preseptal cellulitis, but they are seen less commonly. Preseptal cellulitis occasionally has been reported to be due to a variety of other organisms, including Trichophyton (ringworm), tuberculosis, and anthrax.

Adenovirus is another particularly common cause of preseptal cellulitis in children. Adenovirus is an important consideration in the differential diagnosis of childhood preseptal cellulitis because, despite being self-limited, the condition can occasionally mimic bacterial infection and prompt unnecessary treatment with antibiotics. Adenovirus can be recognized by its characteristic copious discharge, which may be serous. Swelling of the lid may be prominent, but erythema usually is minimal. Preauricular lymphadenopathy often occurs in older children, and marked conjunctival hyperemia with or without chemosis and subconjunctival hemorrhage may be present. Photophobia may also be observed in cases of concurrent punctate keratopathy. A history of recent contact with other infected individuals frequently is noted and should be sought. Care should be taken to avoid spreading infection to family members, medical personnel, and others.

Hospital admission should be considered for children younger than 1 year of age with bacterial preseptal cellulitis. Hospitalization also is important for children with signs of systemic toxicity and those with inadequate H. influenzae immunization. A sepsis workup is indicated for children with signs of systemic toxicity and for extremely young children. Ophthalmologic consultation is recommended if orbital involvement is suspected or if clinical examination is inconclusive. Computed tomography (CT) usually is unnecessary for isolated preseptal cellulitis. Cultures of blood obtained from patients with preseptal cellulitis generally are negative but are more likely to be positive in children younger than 2 years. Culture of conjunctival discharge is done often but rarely has significant diagnostic benefit. A severity index for scoring preseptal cellulitis in children has been reported to help guide treatment decisions.

Antibacterial treatment should include intravenous agents for infants and those with signs of serious systemic infection. Intravenous cefuroxime or a combination of nafcillin plus cefotaxime or ceftriaxone frequently is recommended for empiric therapy. When MRSA preseptal cellulitis is suspected because of poor response to treatment or through cultures, clindamycin and trimethoprim-sulfamethoxazole are often the first-line agents. In situations in which MRSA preseptal cellulitis does not respond favorably to these medications, vancomycin or linezolid with rifampin may be effective treatments. Outpatient treatment with intramuscular or oral antibiotics is reasonable for older, less acutely ill children. Systemic antibiotics should be continued for 7 to 10 days. Patients in whom intravenous antibiotics are started initially can switch to an oral antibiotic after they have been afebrile for at least 24 hours and otherwise have improved clinically, unless the possibility of development of sepsis remains a concern. When antibiotic treatment fails, other noninfectious causes should be explored.

Orbital Cellulitis

Orbital cellulitis refers to infection of orbital structures posterior to the orbital septum and is the most frequent cause of acute orbital inflammation. Orbital cellulitis occurs more commonly in children and more frequently during cold weather, when sinusitis is more prevalent.

Initial signs and symptoms can vary from mild inflammation to severe and fulminant orbital disease. Cardinal signs and symptoms of infectious orbital cellulitis include proptosis, limited eye movement (including total ophthalmoplegia), pain with eye movement, and an abnormal pupillary response. Decreased vision or even blindness can occur as the most serious ophthalmic complication. Death can result from intracranial extension of the infection if appropriate treatment is not initiated. Elevated intraocular pressure and chemosis of the conjunctiva are common ancillary signs. Preseptal cellulitis often coexists with orbital cellulitis but is not a prerequisite.

Most cases of orbital cellulitis are caused by spread of infection from an adjacent infected sinus. Ethmoid sinusitis is the most common predisposing factor. Rare cases are due to penetrating orbital trauma or skin infection involving the face, with spread of organisms into the orbit. Orbital cellulitis may occur infrequently after orbital, ocular, or periocular surgery. Orbital cellulitis and cavernous sinus thrombosis have been reported to occur after dental infections and dental surgery.

Comprehensive evaluation of a patient with confirmed or suspected orbital cellulitis includes ophthalmologic and systemic examination. Assessment of visual acuity individually in each eye is important for excluding vision loss and establishing a baseline to aid in monitoring progression of the disease or the effects of therapy. Evaluation of optic nerve dysfunction by examining the pupils for an afferent pupillary defect (APD) is of utmost importance throughout the course of the disease. Careful evaluation of extraocular movement should be performed in all extreme positions of gaze to identify limitation of ocular duction and to evaluate for pain on eye movement. The presence or absence of proptosis can be assessed clinically by viewing the eyes from above (bird’s-eye view) or below (worm’s-eye view) and by comparing their relative positions within the orbits. In severe cases of orbital cellulitis, funduscopic examination may reveal dilation of the retinal venules and signs of compressive optic neuropathy, such as optic disc edema. In severe cases, central retinal artery and vein occlusions have been reported. Systemic evaluation includes determination of temperature, which usually is in the range of 39°C to 40°C (102°F to 104°F). Sinus examination, a screening neurologic examination, and evaluation for signs and symptoms of sepsis and meningitis should be performed.

In any case of clinically definite or suspected orbital cellulitis, CT of the orbit and brain is essential. CT can establish or confirm the diagnosis of orbital cellulitis and provides critical information needed to manage the patient. Imaging of the brain is important because orbital cellulitis can evolve into a brain abscess, meningitis, or cavernous sinus thrombosis. However, when a clinical response to treatment is noted, improvement in CT findings frequently is delayed. Therefore recurrent CT scanning of a child with clinically improving findings is not indicated unless new signs or symptoms of concern develop.

Microbiologic studies often are acutely unhelpful for the routine patient with orbital cellulitis. Nonetheless baseline studies remain important because critical information sometimes is acquired. Blood culture samples should be obtained at a minimum, and a lumbar puncture with culture of cerebrospinal fluid (CSF) should be considered in infants and those with signs of CNS infection. Culture of the ocular, nasal, and nasopharyngeal mucous membranes is of limited value and can be omitted. However, if surgical drainage is performed, samples of any material removed should be obtained for culture.

Optimal management of a child with orbital cellulitis requires a multidisciplinary approach. In addition to evaluation and management by an experienced pediatrician, ophthalmologic and otolaryngologic consultation should be obtained. Neurosurgical consultation is required when involvement of the CNS is diagnosed or suspected. In atypical cases and those not responding to treatment, consultation with an infectious disease specialist is warranted.

The most common offending etiologic bacteria are S. aureus, Streptococcus spp., and Haemophilus spp. (other than H. influenzae ). S. pneumoniae also is implicated frequently, and a variety of less common organisms have been reported. H. influenzae orbital cellulitis rarely has occurred since widespread use of the H. influenzae type b vaccine was implemented. Fungal infection of the orbit occasionally is encountered, typically in immunocompromised individuals.

The differential diagnosis of orbital inflammation in children includes a broad range of noninfectious conditions, including blunt trauma, idiopathic orbital inflammation (orbital pseudotumor), Wegener granulomatosis, sarcoidosis, leukemic infiltration, lymphoma, rhabdomyosarcoma, necrotic retinoblastoma, metastatic carcinoma, and histiocytosis X. Thyroid ophthalmopathy also can be manifested as an acute orbital inflammatory process, although usually its onset is slow and insidious.

Treatment of all patients with orbital cellulitis requires hospitalization and initiation of intravenous antibiotics as soon as possible. Infection with penicillin-resistant organisms is an increasingly common occurrence and must be considered during treatment. Appropriate initial antibiotic therapy may include nafcillin, metronidazole, and cefotaxime as combination therapy. Given the increasing incidence of MRSA, initial treatment with vancomycin or clindamycin should be considered. Other antimicrobial agents may be useful, and local susceptibility patterns should guide the choice of initial antimicrobial therapy. Antibiotic coverage should be modified according to the clinical course and culture results. If the patient fails to respond to antibiotic treatment within 24 to 48 hours, consultation with an infectious disease specialist and repeat CT to look for the development of an orbital abscess should be considered ( Fig. 61.4 ). The mean hospital stay for uncomplicated cases of orbital cellulitis is 10 to 14 days, and oral antibiotics should be prescribed for 7 to 10 days after discharge. When the source of infection is believed to be from sinusitis, a nasal decongestant is commonly prescribed to aid in opening the sinus ostia, promoting drainage of the infected sinus, and speeding resolution. Nasal decongestants should be continued for 7 to 10 days after initiation.

Failure of response of orbital cellulitis to antibiotic treatment may be a sign of development of a subperiosteal orbital abscess (seen here in the right medial orbit).

Although treatment of orbital cellulitis with steroids remains controversial, their use in the treatment of acute and chronic sinusitis has become increasingly common. Studies have shown that steroids can reduce levels of inflammatory cytokines in the sinonasal mucosa of individuals with sinusitis. In a study on the use of steroids in children with orbital cellulitis, Yen and Yen reported no adverse effects of this adjunct treatment with systemic antibiotics. Prospective studies on the use of steroids in orbital cellulitis have been proposed to determine whether they have any clinical benefit.

Children with orbital cellulitis require diligent follow-up while in the hospital. Vision should be assessed at the bedside daily; results may be more accurate if a single examiner routinely assesses vision for a given patient. Pupillary examination for an APD should be performed at each examination. Development of an APD indicates compromise of the optic nerve, warrants escalation of treatment, and usually requires urgent surgical intervention. Worsening of extraocular motility, altered mental status, or onset of CNS signs raises the concern of progression to cavernous sinus thrombosis and should prompt emergency repeat neuroimaging of the brain and orbit, with further intervention as dictated by results of the scan. The close anatomic relationship of the orbit to the brain, with the orbital venous system freely anastomosing with the facial venous plexus and cranial venous sinus system through a series of valveless veins, seriously increases the potential for spread of infection to contiguous structures, including the brain.

Acute surgical intervention to decompress the orbit or drain an orbital or subperiosteal abscess is indicated if vision loss or an APD is identified at any point during treatment. Helpful drainage criteria have been described ( Box 61.1 ). Immediate neurosurgical consideration is indicated if CNS involvement is documented. Most patients without evidence of vision loss, optic nerve dysfunction, or CNS involvement can be managed successfully medically. Provided that clinical improvement continues, no worrisome signs or symptoms of CNS involvement develop, and the patient’s overall clinical status does not worsen, repeat neuroimaging of patients with an orbital abscess is unnecessary. Short-term resolution of an orbital abscess often is not obvious on CT. The radiographic appearance of the abscess typically remains unchanged on early follow-up scans, although it may no longer contain viable organisms.

Sinus drainage by an otolaryngologist frequently is required to hasten resolution. Formation of an abscess is not a prerequisite for surgical intervention, and orbital cellulitis without abscess formation may progress to the point of requiring surgery. Despite prompt and appropriate treatment, serious complications such as permanent vision loss and brain abscess can occur. Most patients, however, can be treated effectively with no permanent sequelae.

Orbital cellulitis caused by fungal infection has a course and prognosis markedly different from those of bacterial orbital cellulitis, particularly cellulitis caused by mucormycosis and aspergillosis. Fungal orbital cellulitis typically occurs in patients who are immunocompromised or patients with metabolic acidosis, such as those with poorly controlled diabetes. It may be manifested as a subacute or chronic process. Orbital apex syndrome is considered to be the most severe form, with loss of function of all cranial nerves traversing the orbital apex into the orbit (i.e., cranial nerves II, III, IV, V, and VI). A black eschar-like lesion may form in the oropharynx or nasopharynx in cases of fungal infection.

Aspergillus orbital infections (most commonly caused by Aspergillus flavus, Aspergillus fumigatus, or Aspergillus oryzae ) are rare findings in children and may take a slow, chronic course over a period of months or years. No clear predisposing factors exist, but it has a predilection for humid climates, and most cases occur in otherwise healthy individuals. Signs and symptoms of orbital infection caused by Aspergillus spp. include loss of vision, constant dull pain, decreased or absent ocular motility, and proptosis with firm resistance to retropulsion. Palate and nasopharyngeal lesions occur but are rare. Biopsy is required for establishing the diagnosis.

Effective treatment of orbital fungal infection requires correction of systemic and metabolic disturbances and administration of intravenous antifungal agents such as amphotericin B. Posaconazole has been shown to be effective as an alternative treatment in those who fail to respond to or cannot tolerate treatment with amphotericin B. Surgical debridement of the orbit or adjacent infected sinuses frequently is required. Treatment often is unsuccessful, and fatalities are not uncommon, particularly with mucormycosis.

The larva of Echinococcus granulosus can produce a hydatid cyst in the orbit. The dog is the definitive host animal, although the organism also may live in the intestines of sheep, goats, cattle, pigs, and other animals. The disease is endemic in the Middle East, Africa, and Asia. Humans become infected by eating contaminated food, typically meat, and infection may occur in any age group. Affected patients have noninflammatory proptosis, decreased ocular motility, and dull orbital pain. Surgical excision is required for treatment. The cyst may be injected with hypertonic saline to kill the parasite, followed by excision.

Mild Bacterial Conjunctivitis

The agents most commonly causing mild bacterial conjunctivitis in children 5 years of age or older are S. pneumoniae and Moraxella spp. H. influenzae was a prominent causative agent before the availability of H. influenzae type b vaccine. S. aureus conjunctivitis is seen most frequently after trauma or surgical manipulation. Conjunctival stains and cultures are usually not necessary, because the disease is almost invariably self-limited or responds rapidly to topical antibiotics.

Many topical antimicrobial agents for bacterial conjunctivitis are readily available and include ciprofloxacin, erythromycin, moxifloxacin, gatifloxacin, ofloxacin, norfloxacin, tobramycin, gentamicin, sulfacetamide, and various combinations. Aminoglycoside-containing compounds such as neomycin can occasionally cause a dramatic allergic blepharoconjunctivitis that is worse than the original disease. The choice of using either drops or ointment is best left to the person who will be instilling the medication, because neither has any proven therapeutic advantage. Newer agents, such as the fourth-generation fluoroquinolones (moxifloxacin and gatifloxacin), should not be used for routine mild bacterial conjunctivitis so as to limit antibiotic resistance. A typical regimen for treatment of mild conjunctivitis is 1 drop or a -inch bead of ointment placed into the inferior conjunctival fornix three to six times daily for 5 to 7 days, depending on the medication. Persistent infection calls for a prompt return to the physician for reconsideration of the diagnosis. Mild bacterial conjunctivitis generally resolves spontaneously in 7 to 14 days even without treatment.

Severe Bacterial Conjunctivitis

Severe bacterial conjunctivitis, characterized by ocular discomfort, pronounced redness, and copious purulent discharge, is usually caused by Neisseria gonorrhoeae, Neisseria meningitidis, S. aureus, S. pneumoniae, and, in children younger than 5 years, H. influenzae . A hyperpurulent state in which the copious purulent discharge reaccumulates in a matter of minutes is characteristic of infection with N. gonorrhoeae . Severe conjunctivitis calls for stains and cultures. Samples from both eyes should be stained and cultured separately, even if only one eye is involved, to allow the uninvolved eye to serve as a control. Gram stains of conjunctival scrapings should be done at the time of culture. A useful culture technique includes the use of a cotton or calcium alginate swab gently rubbed against the palpebral conjunctiva of the lower lid and inoculated onto blood and chocolate agar. If N. gonorrhoeae is suspected, a culture for chlamydia is also indicated, because concurrent infection with both organisms is common.

The treatment of severe bacterial conjunctivitis is based initially on the results of the stains and later modified according to cultures and sensitivities. If Neisseria is strongly suspected, the patient should be treated for Neisseria, even if the laboratory results are not confirmatory. Ocular N. gonorrhoeae infection is a vision-threatening and life-threatening disease. This organism can penetrate the intact cornea and cause microbial keratitis (i.e., infection of the cornea), corneal perforation, and endophthalmitis (i.e., infection inside the eyeball), in addition to the conjunctivitis . N. gonorrhoeae conjunctivitis should be considered in three patient groups: neonates after passage through an infected birth canal, sexually active individuals, and victims of possible sexual abuse. For this reason, a high index of suspicion should be maintained. Pediatric infection with N. gonorrhoeae requires hospital admission and administration of a systemic antibiotic. Because of the prevalence of penicillin-resistant strains, a broad-spectrum (third-generation) cephalosporin, such as ceftriaxone, is the most appropriate choice of antibiotic. Adjunctive treatment of N. gonorrhoeae conjunctivitis with topical moxifloxacin and simple saline irrigation for 5 days can be helpful, but topical agents should never be used as isolated treatment. Moxifloxacin is a particularly good antibiotic choice because it is effective against chlamydia as well.

Conjunctivitis caused by gram-positive cocci can be treated with topical moxifloxacin, gatifloxacin, ciprofloxacin, or erythromycin. Systemic nafcillin, a second- or third-generation cephalosporin, or both can be added as needed for more extensive infections. Gram-negative bacterial conjunctivitis can be treated with topical erythromycin ointment or an aminoglycoside drip such as gentamicin or tobramycin. Systemic antibiotics can be added if needed.

Adenoviral Conjunctivitis

Viruses are another common cause of infectious conjunctivitis in children. Many pediatric cases of viral conjunctivitis are caused by adenovirus. Serotypes 1, 2, 3, 4, 7, and 10 produce an acute form of conjunctivitis with prominent conjunctival follicles. Serotypes 3 and 7 also may cause pharyngoconjunctival fever. This entity is characterized by conjunctivitis, fever, and pharyngitis. Serotypes 8, 19, and 37 can cause epidemic keratoconjunctivitis (EKC). EKC is characterized by a combination of a punctate epithelial keratitis (best viewed by slit-lamp examination) and an immune response that results in subepithelial (i.e., in the corneal stroma) infiltrates. There is commonly a robust inflammatory response causing the formation of membranes on the palpebral conjunctival surface, and there can be extensive subconjunctival hemorrhages and preseptal cellulitis. Photophobia is a prominent feature of this condition, and visual acuity may be markedly decreased. Epidemic keratoconjunctivitis is often associated with pharyngitis and rhinitis, which may precede or be concurrent with the conjunctivitis.

Adenoviral conjunctivitis may be highly contagious. It is transmitted easily from an infected individual to others at home or at school. The incubation period is 5 to 10 days but may be as long as 21 days. The virus is shed from the infected conjunctiva for 7 to 12 days after the onset of infection. Frequently, a prodromal upper respiratory tract infection consisting of fever, pharyngitis, or otitis media occurs. Ocular signs and symptoms include photophobia (with corneal involvement), foreign body sensation, epiphora (tearing), bulbar and palpebral conjunctival injection and chemosis (edema of the conjunctiva), and subconjunctival hemorrhage. Preauricular lymphadenopathy is a common feature in older children and adults.

The diagnosis of adenoviral conjunctivitis is almost always clinical only. Only rarely is laboratory confirmation necessary. Viral cultures are possible when indicated, and a rapid enzyme immunoassay test is available. Treatment of adenoviral conjunctivitis is supportive, aimed at decreasing the symptoms of irritation, photophobia, and blurred vision. Cool compresses and acetaminophen are helpful. For the more aggressive EKC, topical steroids are indicated to quiet the severe immune response. Removal of conjunctival membranes with a moistened cotton swab may relieve the foreign-body sensation. A small amount of bleeding often occurs after removal of the membranes, and they can recur after several days. The use of topical steroid preparations requires careful monitoring, and they should only be prescribed by an ophthalmologist.

The clinician should wear gloves when examining patients with suspected adenovirus infection. Careful hand-washing is essential after direct contact. Instruments or equipment used in examining an infected patient should be cleaned with 10% sodium hypochlorite solution or other solutions known to eradicate the adenovirus.

Mini-epidemics of adenovirus-related conjunctivitis can originate in physicians’ offices. At home, families should exercise caution and separate the towels and bedclothes of the patient from those of others in the household. Children of school age should be kept at home for 7 days or longer to reduce the risk for transmitting the infection to classmates.

Herpes Simplex Virus Conjunctivitis and Complex Forms

HSV conjunctivitis may occur as a primary or secondary infection. Ocular infection usually is caused by HSV-1, except in newborns, in whom HSV-2 predominates. Typical initial signs of HSV conjunctivitis include a serous discharge, scant conjunctival follicle formation on the inferior palpebral conjunctiva, and preauricular lymphadenopathy. Eighty percent of cases are unilateral. Eyelid vesicles often occur in primary infections. Bulbar conjunctival ulceration is an unusual occurrence, but when present, it is virtually pathognomonic of primary HSV-1 infection. Keratitis occurs in as many as 50% of primary cases and is characterized by mild epithelial irregularities. Dendrites (branch-shaped lesions of the corneal epithelium) can occur in primary infections, but reactivated HSV keratitis frequently exhibits the characteristic dendritic pattern. Lid vesicles usually do not develop in cases of reactivated HSV infection.

Primary HSV dermatoblepharitis is seen most commonly in children younger than 6 years, but it may occur at any age. The initial episode may be associated with an upper respiratory tract infection, and recurrences are common. Clinical signs include eyelid vesicular reaction, mild follicular conjunctivitis, preauricular lymphadenopathy, and, occasionally, atypical epithelial keratitis. Secondary bacterial infection can occur. Systemic acyclovir is a safe and effective treatment, although the disease itself typically is self-limited and does not require treatment.

The diagnosis of HSV keratoconjunctivitis usually is made on the basis of the clinical appearance alone. Antigen detection tests or viral cultures can be used when the diagnosis is in question. Viral cultures, when necessary, require special handling. In culturing primary HSV cases, the skin surface is swabbed with an alcohol sponge, and a tuberculin syringe with a 30-gauge needle is used to aspirate fluid from an intact vesicle. If no vesicles are present, a Dacron swab is wiped on the palpebral conjunctiva of the lower lid. The viral transport medium is inoculated and taken to the laboratory for special handling.

Treatment of HSV conjunctivitis alone (in the absence of corneal epithelial disease) is controversial. Oral acyclovir may be used for severe cases of primary HSV infection. Two topical antiviral agents are available: trifluridine solution and ganciclovir ointment.

When epithelial HSV keratitis is reactivated and the typical dendritic (branched) epithelial lesions are seen, the cornea usually is hypoesthetic. Iritis may be associated with HSV keratitis and is characterized by miosis, photophobia, ocular pain, and foreign-body sensation. Vision may be decreased if the epithelial disease involves the visual axis. Epithelial HSV may be atypical, may be more severe, and may be more complicated in patients receiving topical steroids and in immunocompromised patients.

Treatment with topical trifluridine or ganciclovir should be strongly considered in all cases of HSV epithelial keratitis, and due to the risk of visual loss, the argument can be made to use oral acyclovir concomitantly. For HSV stromal keratitis, topical steroids are effective in decreasing corneal scarring but should only be used by an ophthalmologist. When using a topical steroid, coverage with a topical antiviral agent such as trifluridine should always be included to reduce the risk for recurrent active viral proliferation. Ancillary treatments include cycloplegic eye drops to dilate the pupil and pain medications as needed.

Chronic suppression with oral acyclovir is effective in reducing the number of recurrences of HSV epithelial and stromal keratitis, especially in patients with stromal keratitis. Interferon also significantly adds to the efficacy of topical antiviral therapy, but the adverse side effects of interferon must be weighed against its potential benefits.

External Ocular Infections With Varicella-Zoster Virus

Childhood varicella infection (chickenpox) is commonly accompanied by conjunctivitis. Vesicles, ulcers, or both occur occasionally on the bulbar or palpebral conjunctiva. Conjunctivitis associated with varicella infection does not result in permanent visual sequelae. Corneal involvement rarely occurs and typically heals without sequelae. Occasionally it may result in stromal scarring and produce irregular astigmatism and reduced vision.

After primary varicella infection occurs, the virus may persist in latent form in the trigeminal nerve ganglia. Herpes zoster ophthalmicus occurs when the ophthalmic division of the trigeminal nerve is affected by reactivation of the virus. The condition occurs more commonly in immunocompromised patients, and recurrences occur infrequently except in these patients. For this reason, testing for immunocompromise, including HIV, should be considered in individuals with herpes zoster who are otherwise presumed to be immunocompetent.

The diagnosis of herpes zoster ophthalmicus is almost always made on the basis of the characteristic clinical feature of a painful, tender vesicular eruption of one V-1 dermatome. Ocular involvement may include keratitis and uveitis. Corneal epithelial lesions may appear dendritiform, with or without subepithelial infiltrates. Uveitis may occur with or without associated keratitis. Usually the uveitis is mild, but occasionally it may be severe, especially in immunocompromised patients, with the formation of a hypopyon (pus in the anterior chamber) or a hyphema. Immunofluorescence testing of vesicular base scrapings or viral cultures may be helpful if the manifestation is atypical or the diagnosis is in doubt.

Treatment of herpes zoster ophthalmicus involves the administration of oral or intravenous acyclovir. Treatment is most effective when initiated within 72 hours of the appearance of vesicles. The keratitis and uveitis do not respond to topical antiviral therapy. Occasionally topical steroids may be helpful in treating varicella keratitis and uveitis, but such treatment should be administered under the direction of an ophthalmologist.

Chlamydial Conjunctivitis and Trachoma

Chlamydia spp. can cause conjunctivitis and trachoma. Chlamydia psittaci rarely causes ocular disease in humans. Chlamydia trachomatis, however, has numerous serotypes that affect the eye. Serotypes A, B, Ba, and C cause trachoma, and serotypes B, C, D, Da, D–, E, F, G, H, I, Ia, J, and K cause inclusion conjunctivitis, including neonatal inclusion conjunctivitis. Neonatal chlamydial conjunctivitis is addressed in the discussion of neonatal conjunctivitis. Inclusion conjunctivitis in older children and adults is a subacute or chronic inflammation of the conjunctiva. The condition may be unilateral or bilateral. A mucopurulent discharge typically occurs, as do follicles on the bulbar and perilimbal conjunctiva. Preauricular lymphadenopathy is a common feature. Punctate epithelial keratitis with subepithelial infiltrates and a superior micropannus (i.e., vascular growth on the upper edge of the cornea) may develop.

The differential diagnosis of inclusion conjunctivitis includes viral and bacterial conjunctivitis, molluscum contagiosum, and toxic keratoconjunctivitis from chronic administration of topical agents. Laboratory testing may be necessary to confirm the diagnosis. Giemsa staining of conjunctival scrapings may demonstrate the classic intracytoplasmic inclusions. A fluorescent antibody detection test or an enzyme immunoassay can be used for a rapid diagnosis. Chlamydial cultures may be needed when the diagnosis remains in doubt.

Treatment consists of oral erythromycin or doxycycline if systemic infection is suspected. Topical erythromycin or tetracycline alone four times each day for 7 days is effective treatment of infection limited to the conjunctiva. Moxifloxacin has been shown to be effective against chlamydia but is not yet the recommended treatment of choice.

Trachoma, a chronic blinding conjunctivitis, remains a prominent etiology of blindness worldwide, ranking sixth overall, causing 4% of all blindness. It is a disease of impoverished populations that is exacerbated by inadequate supplies of water and poor hygiene and sanitation. Trachoma seldom is seen in fully developed countries. In the United States, it is encountered on Native American reservations in the Southwest and in individuals from endemic foreign areas. Eye-seeking flies play an important role in transmission of Chlamydia from one person to another.

Trachoma causes blindness by producing chronic inflammation of the palpebral conjunctiva of the upper eyelid with secondary scar formation. Contracture of the scars causes entropion of the eyelid and trichiasis (cilia rubbing on the cornea). After many years of infection and reinfection this leads to corneal neovascularization, opacification, and vision loss. Less commonly, the cornea may be infected directly. The complete course of the disease from initial infection to blindness generally takes decades. Children do not become blind from trachoma, but they are the most significant constant chronic reservoir of the disease.

The diagnosis of trachoma usually is made on the basis of clinical findings alone. The disease passes through characteristic stages, from simple inflammation to scarring, entropion, and trichiasis. Multiple stages may coexist in various parts of the eyelids. The World Health Organization classifies the stages of trachoma as follows: TF, trachomatous follicular response; TI, diffuse trachomatous conjunctival inflammation; TS, trachomatous scarring of the palpebral conjunctiva; TT, trachomatous trichiasis; and CO, trachomatous corneal opacification. In the pediatric population, physicians usually encounter only stages TI and TF. The scars on the palpebral conjunctiva, referred to as Arlt lines, are linear and multidirectional. Slit-lamp examination may reveal a superior limbal corneal micropannus and Herbert pits (i.e., hollowed-out areas at the superior limbus), which represent sites of resolved follicles.

Treatment of trachoma now consists of periodic dosing of susceptible populations with azithromycin or, if azithromycin is not available, topical tetracycline or erythromycin ointment instilled twice daily for 2 months, as well as improved sanitation and hygiene to prevent recurrence. Trachoma can be self-limited if hygiene alone is improved. In children older than 8 years of age, doxycycline should be administered orally daily for 40 days. Erythromycin can be substituted in younger children or in patients intolerant of doxycycline.