for the first 2 to 7 days and then tapered over the course of several weeks.

●Topical steroids have been associated with the progression of keratomycosis.

●Intravitreal amphotericin B (5 to 10 μg) has been used for the treatment of Aspergillus endophthalmitis. A repeat injection may be necessary if persistence of organisms is suspected 2 to 7 days after initial injection.

●The use of intravitreal steroids is controversial. Intravitreal dexamethasone (400 μg) as an adjunct to intravitreal amphotericin B has been described.

Surgical

●Mechanical debridement of the fungal growth allows better penetration of antifungal medications.

most common cause of posttraumatic endophthalmitis occurring in the rural setting. It usually enters the eye as a result of penetrating trauma with a contaminated foreign body, although it can also occur following intraocular surgery or as a metastatic infection related to intravenous drug use. Most cases of Bacillus endophthalmitis result in extremely poor visual outcomes. Many patients require enucleation or evisceration. Bacillus species are usually resistant to penicillins and cephalosporins but are sensitive to vancomycin, clindamycin, and fourth-generation fluoroquinolones (e.g. levofloxacin and gatifloxacin).

Infection with B. cereus typically causes a rapid and fulminant endophthalmitis, which may progress to panophthalmitis, often accompanied by fever and leukocytosis. Characteristically, a ring abscess of the cornea develops in 24 to 48 hours

Foster CS: Fungal keratitis. Infect Dis Clin North Am 6:851–857, 1992.

Gassry GG, Hornblass A, Harrison W: Itraconazole in the treatment of orbital aspergillosis. Ophthalmology 103:1467–1470, 1996.

Hunt KE, Glasgow BJ: Aspergillus endophthalmitis: an unrecognized endemic disease in orthotopic liver transplantation. Ophthalmology 103:757–767, 1996.

Levin LA, Avery R, Shore JW, et al: The spectrum of orbital aspergillosis: a clinicopathological review. Surv Ophthalmol 41:142–154, 1996.

Rao NA, Hidayat AA: Endogenous mycotic endophthalmitis: variations in clinical and histopathologic changes in candidiasis compared with aspergillosis. Am J Ophthalmol 132:244–251, 2001.

Weishaar PD, Flynn HW, Murray TG, et al: Endogenous aspergillus endophthalmitis: clinical features and treatment outcomes. Ophthalmology 105:57–65, 1998.

COURSE/PROGNOSIS

●Fulminant panophthalmitis.

●Acute onset in 12 to 48 hours.

●Postoperative retinal detachments.

●Phthisis, no light perception vision, and enucleation are extremely common.

DIAGNOSIS

Clinical signs and symptoms

●Corneal ring infiltrate, diffuse sub-epithelial infiltrates.

●Hypopyon.

●Vitritis.

●Systemic infection (fever, leukocytosis).

6 BACILLUS SPECIES INFECTIONS

041.8

Franco M. Recchia, MD

Nashville, Tennessee

Sean P. Donahue, MD, PhD

Nashville, Tennessee

Denis M. O’Day, MD

Nashville, Tennessee

Bacillus is a genus of nearly ubiquitous, aerobic, gram-positive, spore-forming rods increasingly recognized as a cause of ocular infection. The species B. cereus, B. anthracis, B. subtilis, B. lichenformis, B. thurigiensis and B. circulans have all been reported to cause ocular infection, most importantly a rapidly progressive and devastating endophthalmitis. Bacillus is the

Laboratory findings

●Gram-positive rod on Gram stain.

Differential diagnosis

●Endophthalmitis caused by other organisms. Other leading causes of postoperative and traumatic endophthalmitis include coagulase-negative staphylococcal and streptococcal species. Chronic, low-grade post-surgical endophthalmitis is commonly caused by Propionobacterium acnes.

●Ring abscess secondary to Pseudomonas aeruginosa or Proteus species.

PROPHYLAXIS

●The only prophylaxis is prevention of the injury; thus, the use of protective eyewear cannot be overemphasized.

TREATMENT

A high index of suspicion and prompt institution of appropriate treatment are crucial to any chance of salvaging vision in cases of Bacillus endophthalmitis. Treatment consists of antibiotics (intravitreal, topical, possibly systemic) and vitrectomy surgery. Due to the accelerated and aggressive course of B. cereus endophthalmitis, vitreous tap with antibiotic injection alone is not recommended.

●Local therapy: fortified topical antibiotics (vancomycin HCl 50 mg/mL alternating hourly with fortified gentamicin 13 mg/mL); consider topical or subconjunctival corticosteroids.

●Intravitreal: vancomycin (1.0 mg in 0.1 cc injection).

Chen JC, Roy M: Epidemic Bacillus endophthalmitis after cataract surgery II: chronic and recurrent presentation and outcome. Ophthalmology 107(6):1038–1041, 2000.

Donzis PB, Mondino BJ, Weissman BA: Bacillus keratitis associated with contaminated contact lens care systems. Am J Ophthlmol 105(2):195– 197, 1988.

Drobniewski FA: Bacillus cereus and related species. Clin Microbiol Rev 6:324–338, 1993.

Essex RW, Yi Q, Charles PG, Allen PJ: Post-traumatic endophthalmitis. Ophthalmology 111(11):2015–2022, 2004.

Foster RE, Martinez JA, Murray TG, et al: Useful visual outcomes after treatment of Bacillus cereus endophthalmitis. Ophthalmol 103:390– 397, 1996.

Shamsuddin D, Tuazon CU, Levy C, Curtin J: Bacillus cereus panophthalmitis: source of the organism. Rev Infect Dis 4:97–103, 1982.

mycin 40 mg/kg/day IV in divided doses; gentamicin 3– 5 mg/kg/day IV in divided doses. (The fourth-generation fluoroquinolones levofloxacin and gatifloxacin achieve vitreous concentrations above the minimum inhibitory concentration (MIC90) for Bacillus cereus. However, their use as monotherapy for intraocular infection is not recommended.)

●Surgical: pars plana vitrectomy with intravitreal injection of vancomycin.

COMPLICATIONS

Ocular complications consist of the typical devastating visual outcome. Of 83 eyes reported on before 1996 with posttraumatic Bacillus endophthalmitis, 62 (75%) became phthisical, were enucleated, or had no light perception vision. The vast majority of the remaining cases had light perception vision. Foster and colleagues recently reported on five patients with Bacillus endophthalmitis who maintained acuities ranging from 20/25 to 20/200. All presented within 32 hours of injury and had vitrectomy within 48 hours of injury; all except one received intravitreal vancomycin. Retinal detachment, caused either by the acute injury or by associated intraocular inflammation, is common.

COMMENTS

The best hope of salvaging eyes infected with Bacillus lies with early diagnosis and prompt treatment; thus, penetrating trauma with a metallic foreign body or that occurring in a rural setting should always suggest the possibility of infection by this organism. Intravenous drug abuse is also an important risk factor for metastatic endophthalmitis caused by this organism. Fever and leukocytosis occurring with a fulminant endophthalmitis are especially suggestive of Bacillus spp. because most other organisms causing endophthalmitis do not typically produce systemic signs. When Bacillus spp. are suspected, an immediate diagnostic and therapeutic vitrectomy is indicated, with antibiotic therapy being initiated before surgery if an undue delay is anticipated. Intravitreal, intravenous, and topical antibiotics are important if vision is to be salvaged. Although the prognosis is extremely poor, retention of useful vision is possible.

REFERENCES

Boldt HC, Pulido JS, Blodi CF, et al: Rural endophthalmitis. Ophthalmology 96:1722–1726, 1989.

mitis. Ophthalmic Surgery 22(11):681–686, 1991.

7 BLASTOMYCOSIS 116.0

Jeffrey D. Horn, MD

Nashville, Tennessee

Blastomycosis is an acute or a chronic systemic, potentially life-threatening fungal disease characterized by granulomatous lesions that may involve any part of the body, with a predilection for the lungs, skin and bones. With the exception of eyelid involvement, ocular disease is exceedingly rare. There are reported cases, however, of keratitis, endophthalmitis, choroiditis and orbital disease.

ETIOLOGY/INCIDENCE

●The causative organism is Blastomyces dermatitidis, a thermally dimorphic fungus that exists in the mycelial phase at 25ºC and in the yeast phase at 37ºC.

●Most cases are endemic and occur in the Ohio and Mississippi River Valleys, where the organism has been found in soil.

●Annual incidence is about 4 per 100,000 population in endemic areas with a male predominance.

●Initial infection is usually from inhalation of spores resulting in pulmonary disease, although percutaneous inoculation has rarely been reported.

COURSE/PROGNOSIS

●Pulmonary disease ranges from asymptomatic (up to 50%) to severe pneumonia and may resolve spontaneously. Acute disease resembles influenza or pneumonia symptomatically. Most diagnosed with blastomycosis have chronic pneumonia.

●Extrapulmonary disease results from hematogenous dissemination. It may occur during or after the pulmonary phase.

●The skin is the most common extrapulmonary site affected (80%), followed by bone (25% to 50%), genitourinary system (about 10% in men), and central nervous system (5% to 10%).

●The eyelid has been reported to be affected in 25% of cases, although the recent literature suggests a much lower incidence.

●Ophthalmic manifestations:

●Eyelid: granulomas, cicatricial ectropion;

●Conjunctiva: rare granulomas either contiguous or noncontiguous with corneal involvement;

●Cornea: ulcer, perforation;

●Choroiditis;

●Orbit: cellulites;

●Endophthalmitis/panophthalmitis.

●Topical amphotericin B can be prepared by diluting an intravenous solution to a concentration of 0.15%. Optimal dosing frequency is not known.

●Miconazole is tolerated by subconjunctival injection at a daily dose of 5 mg of the undiluted intravenous preparation. It may be administered topically as a 1% solution and given every hour.

Surgical

●Surgical drainage of lid or orbit abscesses may be needed in addition to antifungal treatment.

●Penetrating or lamellar keratoplasty is indicated in cases of corneal perforation or scarring.

DIAGNOSIS

●Skin lesion is usually papular with a verrucous border and an atrophic center.

●Extravasation of erythrocytes between the dermis and epidermis gives rise to multiple black dots that are characteristic of the disease.

●Culture is the definitive method of diagnosis, but can take up to 30 days.

●Broad-based budding yeast forms (8 to 15 μm) with doublecontoured walls are seen best with periodic acid-Schiff and Gomori methenamine silver stains. Chemiluminescent DNA probes are available.

COMPLICATIONS

●Systemic amphotericin B toxicity can cause fever, chills, hypokalemia, renal failure, and anemia.

●Itraconazole toxicity is relatively uncommon but can cause nausea, vomiting, impotence and elevated plasma aminotransferase levels. Itraconazole requires an acid pH for absorption; therefore, patients on antacids or H2 receptor blockers may have reduced plasma levels.

●Ketoconazole toxicity can cause nausea, vomiting, and testicular and adrenal dysfunction; fatal hepatocellular damage is rare.

Differential diagnosis

●Tuberculosis.

●Staphylococcal infection.

●Squamous cell carcinoma.

●Leprosy.

●Cryptococcosis, and other deep mycoses.

TREATMENT

Systemic

●Amphotericin B is the treatment of choice for life-threaten- ing disease. The initial intravenous dose is 5 mg, increasing

slowly to 50 mg three times per week until a total dose of 2 to 2.5 g is reached.

●Itraconazole, an oral triazole antifungal agent, has been shown to be as effective as amphotericin B for non-life- threatening disease, excluding CNS involvement, without the severe toxic reactions associated with amphotericin B. The dose is 200 to 400 mg/day for 6 months.

SUMMARY

Blastomycosis requires systemic therapy, but for less severe or non-life-threatening disease, newer, safer, more convenient, and equally effective treatment modalities are available. Ocular infection is so rare that the most appropriate therapy remains an unanswered question. Experience with infection in other tissues indicates that treatment should be given for a prolonged period. When there is corneal involvement, consideration should be given to the topical administration of miconazole in combination with systemic therapy.

REFERENCES

Barr CC, Gamel JW: Blastomycosis of the eyelid. Arch Ophthalmol 104:96– 97, 1986.

Bartley GB: Blastomycosis of the eyelid. Ophthalmology 102:2020–2023, 1995.

Dismukes WE, Bradsher RW, Cloud GC, et al: Itraconazole therapy for blastomycosis and histoplasmosis. Am J Med 93:489–497, 1992.

is slightly less efficacious and less well tolerated than itraconazole. It also is much less expensive. The dose is 200 to 800 mg/day for 6 months.

●Fluconazole, another oral triazole antifungal agent, appears to be as efficacious at 400 to 800 mg/day for 6 months as ketoconazole and may be an alternative for patients who are intolerant of itraconazole. More studies are necessary.

Topical

●Topical therapy may be indicated in conjunction with systemic therapy for corneal involvement.

Ophthalmol 33:178–188, 1988.

Pappas PG, Bradsher RW, Kauffman CA, et al: Treatment of blastomycosis with higher doses of fluconazole. Clin Infect Dis 25:200–205, 1997.

Powers TP, Carlson AN, O’Day DM: Deep mycoses. In: Mannis MJ, Macsai MS, Huntley AC, eds: Eye and skin disease. Philadelphia, LippincottRaven, 1996:583–590.

Safneck JR, Hogg GR, Napier LB: Endophthalmitis due to Blastomyces dermatitidis: case report and review of the literature. Ophthalmology 97:212–216, 1990.

TREATMENT

Systemic

The treatment of brucellosis requires four to eight weeks of therapy. More than one therapeutic agent is generally required to prevent relapses. Effective medications are listed:

●Doxycycline 100 mg twice daily for six weeks;

●Cefixime 400 mg daily in one to two doses;

●Rifampin 600–1200 mg/day for six weeks;

●Trimethoprim-sulfamethoxazole 960 mg twice daily for six weeks;

●Streptomycin 15 mg/kg/day IM for 2–3 weeks;

●Netilmicin 150 mg twice daily IM or (1.5–2 mg/kg/dose);

●Ofloxacin 400 mg b.i.d. for six weeks;

●Ciprofloxacin 500 mg twice daily for six weeks;

●Retinal detachment;

●Phthisis bulbi;

●Optic neuropathy.

REFERENCES

Al-Kaff AS: Brucellosis. In: Fraunfelder FT, Roy FH, eds: Current ocular therapy. 5th edn. Philadelphia, WB Saunders, 2000:15–16.

Al-Kaff AS: Ocular brucellosis. Int Ophthalmol Clin 35:139–145, 1995.

Elrazak MA: Brucella optic neuritis. Arch Intern Med 151:776–778, 1991.

Gungor K, Bekir NA, Namiduru M: Ocular complications associated with brucellosis in an endemic area. Eur J Ophthalmol 12(3):232–237, 2002.

Lyall M: Ocular brucellosis. Trans Ophthalmol Soc UK 93:689–697, 1973.

days.

Various combinations of these medications have been used. The World Heath Organization issued guidelines in 1986 recommending doxycycline for six weeks in combination with either streptomycin for 2–3 weeks or rifampin for 6 weeks. Doxycycline/streptomycin has been associated with lower recurrence rates and may be preferable in areas where tuberculosis is also endemic given concern for community resistance to rifampin. Protracted administration of triple regimens may be necessary for neurobrucellosis.

Treatment should continue for one or two months if infection is localized in the heart bone or eye. Doxycycline should be avoided in children and pregnant women.

Ocular

Topical medications used during attacks of uveitis associated with brucellosis infection:

●Atropine;

●Corticosteroids.

Topical and systemic steroids have been used to minimize damage to the eye during the ocular phase of the disease. Relapses are common after tapering corticosteroid therapy. Steroids should be used cautiously and for brief periods if possible for ocular inflammation.

COMPLICATIONS

Systemic

Complications associated with brucellosis infection:

●Pneumonia;

●Hepatitis;

●Splenic abscess;

●Epididymitis/orchitis;

●Prostatitis;

●Endocarditis;

●Arthritis;

●Osteomyelitis;

●Meningoencephalitis.

Ocular

Ocular complications:

●Glaucoma;

●Cataract;

●Ocular hypotony;

●Cystoid macular edema;

losis. N Engl J Med 352(22):2325–2336, 2005.

Rabinowitz et al: Bilateral mutifocal choroiditis with serous retinal detachment in a patient with Brucella infection: case report and review of literature. Arch Ophthalmol 123:116–118, 2005.

Walker J, Sharma OP, Rao NA: Brucellosis and uveitis. Am J Ophthalmol 114(3):374–375, 1992.

Woods AC: Nummular keratitis and ocular brucellosis. Arch Ophthalmol 35:490, 1946.

Young E: Human brucellosis. Rev Infect Dis 5(5):821–842, 1984.

9CAT-SCRATCH DISEASE 078.3

(Bartonella henselae Infection)

Terry D. Wood, MD

Portland, Oregon

Eric B. Suhler, MD

Portland, Oregon

Cat-scratch disease (CSD) is usually a benign, self-limited illness characterized by regional lymphadenopathy lasting weeks to months after local inoculation with the gram-negative bacillus Bartonella henselae. The majority of cases (60–80%) occur in persons under 21 years old. A ‘typical’ CSD infection is manifest by the appearance of a localized skin papule at the inoculation site 3–10 days after exposure. This progresses to a pustule, which may or may not be recalled by the patient. Regional lymphadenopathy follows 1 to 7 weeks later and may be the only sign or symptom detected. The lymph node is tender 80% of the time and suppurates in 15%. ‘Typical’ CSD encompasses 89% of all cases. Of the remaining 11% ‘atypical’ CSD cases, approximately half involve the ocular structures. The most common of these is Parinaud’s oculoglandular syndrome, which encompasses 6% of all cases and presents as a unilateral granulomatous conjunctivitis. One to two percent develop neurologic findings; encephalopathy is the most common manifestation in this sub-category, and focal findings may involve the cerebral cortex, thalamus, or the basal ganglia. Neuroretinitis, a clinical syndrome comprised of papillopathy and an exudative maculopathy typically manifesting as a ‘macular star,’ is a relatively common neurologic sequelae, although it is often initially misdiagnosed as optic neuritis. It is however, important to note that neuroretinitis is not associated with multiple sclerosis, making the appearance of a macular star a welcome finding in a young patient presenting

with optic nerve edema. Less commonly reported intraocular manifestations of B. henselae infection include central retinal artery occlusion, central retinal vein occlusion, peripapillary angiomatosis and neovascular glaucoma.

ETIOLOGY/INCIDENCE

●Causative agent, Bartonella (formerly Rochalimea) henselae.

●Removed from Rochalimea sp./order Rickettsiales when it was discovered not to be an obligate intracellular parasite.

●Fastidious, pleiomorphic, gram-negative bacillus.

●Most infections are caused by a scratch from a young, fleainfested bacteremic kitten, although transmission may also occur from a cat bite or lick (role of fleas in the transmission of human disease is unclear, although B. henselae DNA has been isolated from the fleas of bacteremic cats).

●Fleas appear to serve as the vector of transmission between cats.

●Bacteremic cats are usually less than 1 year old, are asymptomatic, and do not require treatment.

●Inoculation has also been reported from other animals (monkey, rabbit, squirrel).

●Skin test (Hanger–Rose):

●Former hallmark of diagnosis, now largely abandoned due to concerns regarding transmission of viral/prion infections.

●Serum immunofluorescent assay (IFA):

●Routinely available;

●Sensitivity of 84%, specificity of 96%; positive predictive value of 91%;

●Significant positive titers found in 3% of healthy controls;

●PCR gaining increasing use in diagnosis when serology is equivocal or inconclusive:

●Culture: difficult;

●Slow growing organism; requires 1–4 weeks.

Differential diagnosis

●Tularemia.

●Sporotrichosis.

●Tuberculosis.

●Lymphoma.

●Syphilis.

Less common: sarcoid, coccidiomycosis, actinomycosis, blastomycosis, infectious mononucleosis, mumps, pasteurellosis, yer-

winter months (60%).

●Mean age of onset is 12 years; predominance of patients are 7–30 years of age.

●Incidence of disease 1/10,000.

●May occur in intrafamilial epidemics in families with kittens.

●No evidence to support person-to-person transmission.

rickettsiosis, listerelliosis, ophthalmia nodosa.

●Work up:

●History and physical exam directed toward likely differential diagnoses, CBC, CXR, PPD with controls, RPR, FTA-ABS, B. henselae IFA;

●If clinically indicated conjunctival or lymph node biopsies, blood cultures.

PARINAUD’S OCULOGLANDULAR SYNDROME (POGS)

●Most common form of ‘atypical’ CSD: accounts for 6% all cases of CSD.

●Theorized alternative route of inoculum is from wiping eye after touching cat fur harboring cat saliva with organism (residual from cat self-cleaning).

Clinical presentation characterized by:

●Unilateral granulomatous conjunctivitis;

●Single or multiple soft granulomas, 0.5–2.0 mm (may enlarge and ulcerate);

●Redness, irritation, chemosis and watery discharge;

●No serious corneal complications reported;

●Ipsilateral preauricular/submandibular lymphadenopathy, occasionally cervical.

May be accompanied by fever, malaise, anorexia, weight loss.

DIAGNOSIS/LABORATORY FINDINGS

●Histopathologic (best diagnostic indicator):

●Warthin–Starry silver impregnation stain of biopsied lymph node or other involved tissue reveals clumps of tiny pleiomorphic bacilli;

●Lymph nodes usually show evidence of granulomatous inflammation and stellate microabscesses which may coalesce.

TREATMENT

●Symptomatic: warm compresses, analgesics, antipyretics.

●Aspiration of the lymph node only if distention causes pain:

●Needle drainage from site 1–2 cm away in unaffected skin.

Direct incision and drainage may lead to persistent sinus formation and is contraindicated.

●Consider antibiotics in moderate to severe cases or if the patient is systemically ill. Treatment, if effective, will usually improve clinical course within 48 hours:

●Rifampin, 10–20 mg/kg/d, PO q 12 or 24 hourly: dosing (87% effective).

Often used as adjuvant to other antibiotics as listed below.

●Ciprofloxacin, 20–30 mg/kg/d given PO q 12 hourly: dosing (84% effective);

●Gentamicin sulfate, 5–7 mg/kg/d IV given q 8 hourly for 7 days: dosing (73% effective);

●Trimethoprim/sulfamethoxazole (Bactrim/Septra); 6– 12 mg/kg/day TMP and 30–60 mg/kg/day SMX given PO, q 12 hourly: dosing (58% effective);

●Macrolide and tetracycline antibiotics also deemed effective in many case reports — course of treatment: 4–6 weeks. Should be afebrile by 1 week, decreasing lymphadenopathy, no constitutional symptoms by 5–10 days.

BACILLARY ANGIOMATOSIS (EPITHELIAL ANGIOMATOSIS)

Clinical features

●Single or multiple cutaneous, subcutaneous, mucosal, visceral, or retinal lesions.

●Reddish vascular papules, nodules, or tumors, rarely plaque-like.

●Often similar in appearance to Kaposi’s sarcoma; range in size from small papules to large, ulcerating, exophytic growths which may erode underlying bone.

●Ophthalmic structures reported involved have included the conjunctiva and optic nerve head/peripapillary retina.

●Systemic manifestations may include fever, chills, malaise, anorexia, headache.

●Occurs more commonly and is more severe in AIDS/immunocompromised patients.

DIAGNOSIS

Based on histopathologic finding on Warthin–Starry and H & E staining.

Differential diagnosis

Kaposi’s sarcoma (must be ruled out histologically in HIV patients), pyogenic granuloma, angiosarcoma, hemangioma.

●Primary site of pathology appears to be the optic nerve;

●Fluoroscein angiography shows leakage and/or staining of the disc but no leakage from the perifoveal capillaries;

●More often unilateral, however both sides may be involved clinically and/or angiographically;

●May present with sudden loss of visual acuity and/or field, transient visual obscurations, floaters, dyschromatopsia, or be completely asymptomatic;

●Visual acuity at presentation may vary from 20/20 to light perception; usually between 20/40 and 20/200.

DIAGNOSIS

Primarily clinical

●Serologic: acute and convalescent titers useful.

●PCR useful in cases where serology is equivocal.

Differential diagnosis

●Syphilis, Lyme, TB should be ruled out if clinically indicated.

●Also tularemia, toxoplasmosis, HSV, HZV, EBV, psittacosis, parasitic disease/DUSN, salmonella, leptospira, histoplasmosis, toxocara.

●Influenza, mumps, coxsackie viruses, sarcoid.

●Hypertensive retinopathy/increased intracranial pressure especially with bilateral disease.

TREATMENT

Resolves rapidly with antibiotic regimens listed above. Standard course of 3–4 weeks.

NEURORETINITIS (LEBER’S IDIOPATHIC STELLATE NEURORETINITIS)

●First hypothesized association with CSD in 1984.

●Generally reported to occur in 1–2% cases of CSD.

●Twenty-six percent of confirmed cases B. henselae infection in one series.

●CSD is implicated 2/3 of patients with the clinical presentation of neuroretinitis.

Clinical features

●Optic disk edema, usually diffuse, varies in severity, may see disk hemorrhage. Resolves over 2 weeks to 2 months.

●Optic atrophy may follow uncommonly. ‘Macular star’ lipid exudates. Protein/lipid rich exudation from the nerve spreads to Henle’s layer in parafoveal region. Resolves over 6–12 months.

●May see residual RPE deficits.

May also see:

●Peripapillary or macular serous retinal detachments;

●Focal or multifocal retinal infiltrates/retinitis;

●Vitritis and/or anterior uveitis;

TREATMENT

Atypical CSD with neurologic manifestations (i.e. neuroretinitis, others as below) are usually treated with antibiotic regimens as listed above.

There is no consensus on the duration of treatment; most reports 4–8 weeks, and there is no documented proof of efficacy of treatment versus nontreatment; anecdotal reports describe hastened visual recovery. Systemic steroids are controversial; they have been used in some series, but have not been shown to be beneficial or harmful.

PROGNOSIS

Most patients (>90%) have very good recovery of Snellen acuity (20/40 or better); a small subset will have profound, persistent visual loss.

In patients with excellent Snellen acuity, subtle subjective disturbance often remain (i.e. metamorphopsia, dyschromatopsia).

Other posterior pole manifestations of CSD (uncommon)

●Optic neuritis.

●Branch retinal arterial occlusions.

●Serous retinal detachments.

●Peripapillary angiomatosis.

●Inflammatory mass of the optic nerve head.

●Panuveitis (has been reported to mimic VKH).

be observed adherent to the iris surface. Other anterior chamber findings may include mutton-fat precipitates, flare, cells, and hypopyon, along with anterior or posterior synechiae, or both.

●Posterior uvea (choroid), retinitis, choroiditis and chorioretinitis. Acute lesions vary from a large three disk diameter perimacular chorioretinal exudates to whitish-yellow, metallic, small (0.1–0.25 disc diameter) oval, depigmented slightly elevated, edematous appearing choroidal or chroioretinal patches scattered randomly throughout the fundus. Vascular sheathing and striate retinal hemorrhages occur. Retinal edema with detachment is associated with active choroiditis. The vitreous reaction can vary from a mild cyclitis to a dense turbid inflammatory exudate containing spherules.

With resolution of the acute inflammation chorioretinal lesions shrink and appear as sharply demarcated, punched-out, scars evolving with varying degrees of hyperpigmentation and depigmentation.

Diagnosis

A high index of suspicion on the part of physicians is important in establishing this diagnosis. A history of living in endemic areas, travel to or temporary residence in such areas should alert the physician to the possibility of coccidioidomycosis.

Laboratory findings

Direct examination of tissue from biopsy or cytologic specimens, and anterior chamber fluid, may demonstrate endosporulating spherules and/or granulomas.

●Coccidioides species grow in most routine culture media as early as 3 to 4 days.

●Laboratory personnel need to be notified about the possibility of isolation of this fungus due to potential for infection.

Serologic testing

Serologic testing can detect IgM antibody demonstrating acute infection and IgG antibody, demonstrating present or past infection.

Differential diagnosis

Includes other fungal infections, and granulomatous lesions.

TREATMENT

Serious ocular infections need to be treated with systemic antifungal medications. The value and safety of intraocular injection is unproven, but amphotericin B has been administered topically and by intraocular injection. For systemic treatment, consultation with an infectious disease specialist is strongly recommended. Oral azoles are the mainstay of current therapy with fluconazole having the greatest documented efficacy.

●Topical steroids should be used judiciously and sparingly to control inflammation once diagnosis of intraocular infection is confirmed and appropriate antifungal therapy is initiated.

Systemic

●Fluconazole 400 to 800 mg/day has been used with success in patients with systemic infection even with meningeal involvement and is the most commonly used medication. The drug achieves good ocular levels.

●Amphotericin B, (AmB) IV indicated in severe systemic disease (0.3 mg/kg to 1.0 mg/kg/day in life-threatening illness).

●Amphotericin B lipid complex and liposomal amphotericin B are available for patients who do not tolerate AmB due to nephrotoxicity; efficacy in treatment of ocular coccidioidomycosis is unknown (5 mg/kg/day).

●Itraconazole has been used for non-meningeal involvement.

The newer azoles (voriconazole and posaconazole) and echinocandin (caspofungin) have in vitro activity but their efficacy in treatment of ocular disease is unknown.

COMPLICATIONS

Local destruction, extraocular muscle palsies, corneal scarring and/or perforation, scleral necrosis and staphyloma, anterior and posterior synechiae, panophthalmitis, optic atrophy, and blindness.

An excellent source of information for physicians and patients alike is the Valley Fever Center for Excellence: http://www.vfce. arizona.edu/.

REFERENCES

Deresinski SC, Mirels LF, Kemper CA: Coccidioides immitis. In: Gorbach SL, Bartlett JG, Blacklow NR, eds: Infectious diseases. 3rd edn. Philadelphia, Lippincott Williams & Wilkins, 2004:2227–2245.

Luttrull JK, Wan WL, Kubak BM, et al: Treatment of ocular fungal infections with oral fluconazole. Am J Ophthalmol 119(4):477–481, 1995.

Moorthy RS, Rao NA, Sidikaro Y, Foos RY: Coccidioiomycosis iridocyclitis. Ophthalomol 101(12):1923–1928, 1994.

Rodenbiker HT, Ganley JP, Galgiani JN, Axline SG: Prevalence of chorioretinal scars associated with coccidioidomycosis. Arch Ophthalmol 99(1):71–75, 1981.

Rodenbiker HT, Ganley JP: Ocular coccidioidomycosis. Surv Ophthalmol 24(5):263–290, 1980. Review.

11 DERMATOPHYTOSIS 110.9

Although antibiotics are thought to have little effect on the clinical course of the respiratory diphtheria infection, they may be of benefit in terminating toxin production. Antibiotic therapy is also of value because diphtheria infection typically is mixed with other bacteria, including staphylococci and pneumococci and many other organisms; in severe cases, streptococci are often present and there is evidence that tissue damage is due to the mixed infection rather than to the diphtheria toxin alone. Additional benefits of antibiotics are hastened clearance of the carrier state and prevention of spread of the organism to others:

Frequent instillations of penicillin G sodium ointment 1000 units/g or erythromycin (0.5%) ointment are administered in addition to systemic antibiotics.

If the infection involves the eyelid skin, cutaneous diphtheria responds well to local application of compresses soaked in penicillin solution 250 to 500 units/mL and diphtheria antitoxin 20,000 units IM.

A canthotomy should not be done in an effort to separate the lids because the incision invariably becomes infected and actually increases the area of toxin absorption.

Diphtheria membranes usually slough away spontaneously

600,000 units IM twice daily for 7 to 16 days);

●Penicillin V PO may be substituted after the third day in patients with uncomplicated infections;

●Penicillin G (4 to 6 million units IV daily divided in four equal doses) may be used with IV solutions.

In patients allergic to penicillin:

●Erythromycin (25 to 50 mg/kg/day IV for 10 to 14 days) may be substituted. However, erythromycin resistance has occurred in some recent diphtheria outbreaks; C. diphtheriae also is frequently resistant to cephalexin, colistin, lincomycin and oxacillin. The organism is usually sensitive to ampicillin, clindamycin, tetracycline and rifampin. Regardless of the antibiotic, therapy should be continued for at least 7 days.

Steroids have been used to prevent or ameliorate myocarditis associated with diphtheria, but recent opinion holds that corticosteroids or corticotrophins are not of value in the treatment of diphtheria or any of its complications.

Ocular

Treatment of external ocular diphtheria has two goals: neutralization of toxin and eradication of live organisms. There are several regimens for the topical and systemic administration of antitoxin and the amount given is often based on empiric decision. In general, the more severe the disease or the more extensive the membrane formation, the greater the amount of antitoxin required.

After giving a test dose to rule out anaphylaxis:

●Diphtheria antitoxin 10,000 to 100,000 units is applied topically to the affected eye every 4 to 6 hours for 24 to 48 hours;

●A subconjunctival injection of diphtheria antitoxin also may be considered as an alternative to topical application.

Commercially available immune and hyperimmune globulin preparations have low diphtheria antitoxin titers and thus are not particularly useful; however:

●A high-titer γ-globulin preparation made from the blood of persons with high titers of antitoxin is available as an investigational preparation that may be useful in special circumstances, such as for a patient who is highly allergic to the horse serum used to prepare commercial antitoxin. Intended for use in prophylaxis, it is obtainable from the Communicable Disease Division, State Department of Public Health, Lansing, Michigan. The treatment dose has not been established; this preparation should never be given intravenously.

Antibiotics are not effective against diphtheria toxin but are indicated for the eradication of the bacilli and superinfections.

because this leaves a raw, suppurating surface and facilitates absorption of toxin. With this caveat, however, a glass rod or cotton-tipped applicator moistened with sterile saline may be used at intervals to break early symblepharon formation in the fornices.

Supportive

Patients with diphtheria should be isolated and hospitalized; bedrest is important for 3 weeks because of the frequency of myocardial involvement. Aspirin and codeine may be indicated for relief of pain.

Precautions

Before antitoxin administration, tests for hypersensitivity to horse serum are mandatory. If the patient is allergic to horse serum, antitoxin may be administered after desensitization, or, if available, human diphtheria immune globulin may be substituted. Rarely, a patient may exhibit such marked hypersensitivity that antiserum cannot be administered without the risk of death. The heart rate of all patients should be monitored carefully during the administration of diphtheria antitoxin because anaphylaxis may occur. In addition, all patients with diphtheria should receive careful cardiac monitoring for developing myocarditis. Drugs with depressant effects on the heart must be used with extreme caution in patients with diphtheria.

Patients with diphtheria should be quarantined until two successive cultures of the eye, skin, or other infected areas, taken at 24-hour intervals, are negative. If antibiotics have been given, cultures should not be taken until at least 24 hours after cessation of therapy.

REFERENCES

Burkhard C, Choi M, Wilhelm H: Optic neuritis as a complication in preventive tetanus-diphtheria-poliomyelitis vaccination: a case report. Klin Monatsbl Augenheilkd 218(1):51–54, 2001.

Chandler JW, Milam DF: Diphtheria corneal ulcers. Arch Ophthalmol 96:53–56, 1978.

Dittmann S, Wharton M, Vitek C, et al: Successful control of epidemic diphtheria in the states of the Former Union of Soviet Socialist Republics: lessons learned. J Infect Dis 181(Suppl 1):S10–S22, 2000.

Duke-Elder S, ed: System of ophthalmology. St Louis, CV Mosby, 1976: 46.

Eller JJ: Diphtheria. In: Conn HF, ed: Current therapy. 6th edn. Philadelphia, WB Saunders, 1982:15–19.

Harnisch JP: Diphtheria. In: Isselbacher KJ, et al, eds: Harrison’s principles of internal medicine. 9th edn. New York, McGraw-Hill, 1980:671–675.

Rogell G: Infectious and inflammatory diseases. In: Duane TD, ed: Clinical ophthalmology. Hagerstown, MD, Harper & Row, 1982:33:9–10.

Top FH, Wehrle PF: Diphtheria. In: Wehrle PF, Top FH, Sr, eds: Communicable and infectious diseases. 9th edn. St Louis, CV Mosby, 1981: 197–210.

13EPIDEMIC KERATOCONJUNCTIVITIS 077.1

Paul Jorge Botelho, MD

Baltimore, Maryland

John D. Gottsch, MD

Baltimore, Maryland

Epidemic keratoconjunctivitis (EKC) is an acute, highly contagious, follicular or papillary viral conjunctivitis associated with preauricular adenopathy, conjunctival pseudomembranes and diffuse superficial keratitis. Adenovirus, the causative agent in EKC, is a double-stranded DNA viruses classified according to serotype (1 to 49) and subgenus (A to F). Certain members of adenovirus subgroup D have been reported to cause significant outbreaks of EKC (primarily serotypes 8, 19 and 37). Others adenoviral serotypes associated with keratoconjunctivitis include 2–5,7–11,14,16,21–23 and 29. Adenoviruses have also been identified in cases of pharyngoconjunctival fever and hemorrhagic conjunctivitis.

FIGURE 13.1 Epidemic keratoconjunctivitis with conjunctival hemorrhages.

DIAGNOSIS

Clinical signs and symptoms

Following a 5- to 14-day incubation period, EKC presents as acute unilateral and then bilateral (75% of cases bilateral) papillary, follicular or mixed conjunctivitis. Other signs include hyperemia, chemosis, serous discharge, subconjunctival hemorrhages and fibrin conjunctival pseudomembranes. Often patients present with foreign body sensation associated with diffuse, punctuate superficial keratitis during the first week. The lesions become raised and stain with fluorescein during the second week. After 14 days, subepithelial opacities may develop in up to 50% of patients. These opacities may be associated with pain, photophobia and decreased vision. The lesions usually spontaneously resolve over several months to years and are not associated with scarring or vascularization.

The conjunctivitis and viral shedding can persist for up to two weeks. The patient and the clinician must take precautions to avoid transmitting the pathogen.

Ocular and periocular manifestations

●Preauricular adenopathy, eyelid edema and serous discharge with lid matting.

●Diffuse papillary or follicular conjunctivitis with hyperemia, chemosis, subconjunctival hemorrhages and membrane or pseudomembrane formation (33% of cases) (Figure 13.1).

●Cornea diffuse superficial punctuate keratitis within the first week, followed by focal elevated punctuate epithelial lesions that stain with fluorescein during week two and in up to 50% of patients subepithelial opacities develop after 2 weeks associated with photophobia and blurred vision.

Laboratory findings

Laboratory testing for the presence of adenovirus serotypes linked to eye infections in suspected cases of EKC may assist the clinician in confirming the diagnosis and implementing measures to control nosocomial outbreaks. Cases of follicular conjunctivitis with superficial keratitis, especially when unilateral, may pose a diagnostic challenge. In the differential diag-

nosis are herpes simplex virus and adult inclusion conjunctivitis from Chlamydia trachomatis serotypes D–K.

●The gold standard for confirmatory diagnosis is viral isolation on cell culture from conjunctival scrapings. Viral isolation can take 1–2 weeks for completion. Recently, a shell-vial technique employing accelerated virus isolation and identification can reduce viral isolation time to three days. Because viable viral sample from conjunctival scrapings is needed, the sensitivity of this method is reduced compared to other techniques. It remains the definitive test of serotype identification in cases associated with epidemic outbreaks.

●Direct fluorescent anibody assay (DFA) is a rapid screening technique for adenoviral detection. Vigorous swabbing of the conjunctiva is performed to obtain an adequate sample size to avoid false negatives. Expertise is required to interpret the immunofluorescent results. Other methods of adenovirus antigen include enzyme immunoassay and immunochromatography.

●Polymerase chain reaction (PCR) assay for adenoviral detection is more sensitive than antigen detection and viral isolation methods. A comparison of PCR to a commercial immunoassay (adenoclone) found the PCR assay was positive in 46 of 58 adenoclone negative cases and positive in 11 of 11 adenoclone positive, culture positive swabs. It also maintains high specificity to common adenoviral pathogens. Newly designed primers in PCR assays have improved the sensitivity for adenoviral DNA recognition allowing for detection of most adenoviral subgroups associated with eye infections. Currently, PCR assays can be performed in several hours.

●Multiplex PCR assay can simultaneous screen for the presence of known viral and chlamydial pathogens associated with follicular keratoconjunctivitis. Using a series of primers in one reaction, the sensitivity of detecting adenovirus, herpes simplex virus and Chlamydia trachomatis using the multiplex PCR assay was equal to or greater than with conventional means for each pathogen individually. The test, which can be performed in seven hours, may reduce diagnostic confusion and allow the clinician to initiate the proper treatment plan and isolation precautions promptly.

TREATMENT

●Currently there are no effective topical or systemic antivirals agents in the management of EKC. No clinical trials have documented efficacy of antivirals with regards to duration of symptoms, severity of disease, reduction of viral shedding or decreased incidence of persistent subepithelial infiltrates.

●Supportive treatment including topical artificial tears four times daily, topical decongestants, topical antihistamines and cold packs can be offered.

patient screening and isolation, handwashing, instrument disinfectants, furlough of infected employees, wearing disposable gloves for every patient, cleaning all therapeutic or diagnostic contact lenses for 30 minutes in chloramine-T, use of disposable occluders and soaking tonometers for 30 minutes in chloramine-T solution following each use.

COMMENTS

Outbreaks of EKC can present a significant health risk with

ciated with epithelial keratitis or subepithelial infiltrates may benefit from topical corticosteroids. In chronic cases of subepithelial infiltrates, judicious use of a mild topical corticosteroid such as fluorometholone 0.1% can improve comfort and vision.

●Phototherapeutic keratectomy (PTK) has been described as an alternative to topical corticosteroid use in the management of persistent nummular superficial subepithelial infiltrates following EKC. A reduced rate of recurrent nummuli following PTK was reported in several studies.

●Cidofovir [(S)-1-(3-hydroxy-2-phosphonylmethoxypropyl)ade nosine] or S-HPMPA, a broadspectrum, long-acting nucleoside analogue which inhibits viral DNA polymerase, was evaluated in vivo by Gordon et al. The authors found that pretreatment with topical 0.1% cidofovir reduced the peak viral titer when given 1 day before inoculation into New Zealand white rabbits infected with adenovirus type 5. The topical cidofovir was administered six times a day for five days. However, a rebound increase in viral titers were noted in 25% of cases. A subsequent in vivo study (same pathogen and animal model) using cidofovir 0.2% topically 6 times a day for 10 days demonstrated a decrease in viral titers and reduction in the number of days of viral shedding. Delayed onset nasolacrimal blockage was reported in this study. Clinical trials comparing topical cidofovir to placebo in cases of EKC have not been reported to date.

PREVENTION OF TRANSMISSION INCLUDING NOSOCOMIAL INFECTIONS

●Modes, duration and ease of transmission of adenovirus in acute cases of EKC are discussed with the patient in detail. Patients with acute EKC are excused from work or school for up to two weeks while convalescing.

●Of paramount importance when managing a suspected case of EKC is the implementation of a procedure policy to prevent transmission to other patients. Numerous reports of nosocomial EKC epidemics have been described, including transmission of EKC via an ophthalmologist’s hands or instruments after managing an in-office case to a neonatal intensive care unit. Patients suspected to have acute conjunctivitis should be relatively isolated from other patients. Sources of transmission during an office visit include magazines, chair rests, slit lamp patient handles and multidose bottles of topical fluorescein. Following examination of any patient with communicable conjunctivitis, thorough cleaning of all examination equipment with chloramine-T should be performed immediately.

●Published guidelines regarding prevention and control of EKC at teaching eye institutes concluded that the following steps may decrease cases of rate of nosocomial infections;

new PCR based adenoviral detection assays, prompt diagnosis and management of cases of EKC may limit the transmission of this highly contagious viral pathogen.

REFERENCES

Chaberny IE, Schnitzler P, Geiss HK, Wendt C: An outbreak of epidemic keratoconjunctivitis in a pediatric unit due to adenovirus type 8. Infect Control Hosp Epidemiol 24(7):514–519, 2003.

Cheung D, Bremner J, Chan JTK: Epidemic keratoconjunctivitis-do outbreaks have to be an epidemic? Eye 17:356–363, 2003.

Cooper RJ, Yeo AC, Bailey AS, Tullo AB: Adenovirus polymerase chain reaction assay for rapid diagnosis of conjunctivitis 40(1):90–95, 1999.

Elnifro EM, Cooper RJ, Klapper PE, et al: Diagnosis of viral and chlamydial keratoconjunctivitis: which laboratory test? Br J Ophthalmol 83:622– 627, 1999.

Elnifro EM, Cooper RJ, Klapper PE, et al: Multiplex polymerase chain reaction for diagnosis of viral and chlamydial keratoconjunctivitis. Invest Ophthalmol Vis Sci 41(7):1818–1822, 2000.

Gordon YJ, Romanowski EG, Araullo-Cruz T: Topical HPMPC inhibits adenovirus type 5 in the New Zealand rabbit ocular replication model. Invest Ophthalmol Vis Sci 35(12):4135–4143, 1994.

Gottsch JD, Froggatt JW, III, Smith DM, et al: Prevention and control of epidemic keratoconjunctivitis in a teaching hospital. Ophthalmic Epidemiol 6(1):29–39, 1999.

Kaufman HE: Treatment of viral diseases of the cornea and external eye. Progress in Retinal and Eye Research 19(1):69–85, 2000.

Percivalle E, Sarasini A, Torsellini M, et al: A comparison of methods for detecting adenovirus type 8 keratoconjuctivitis during a nosocomial outbreak in a neonatal intensive care unit. J Clin Virol 28:257–264, 2003.

Quentin CD, Tondrow M, Vogel M: Phototherapeutic keratectomy (PTK) after epidemic keratoconjunctivitis 96(2):92–96, 1999.

14 ERYSIPELAS 035

(St. Anthony’s Fire)

Richard L. Abbott, MD

San Francisco, California

Erysipelas is an acute, localized inflammation of the skin and subcutaneous tissue that is characterized by redness, edema and induration.

ETIOLOGY/INCIDENCE

The pathogenic organisms are usually group A β-hemolytic streptococcus, although occasional group B, C and G strains

COURSE/PROGNOSIS

The site of infection is the extremities or face. The primary facial infection often is a nasopharyngitis, from which the organism is transferred to the skin through an abrasion or a minute wound.

Erysipelas may begin with an abrupt onset of fever, chills, malaise and nausea. A definite zone of redness soon appears, with edema, tenderness and a well-defined, advancing border. In more severe cases, vesicles may form on the surface. Typically, the infection involves the lymphatic spaces and is spread through these channels to neighboring areas. Constitutional symptoms include high temperature, headache, vomiting and localized pain. Without treatment, the disease is usually selflimited and runs its course within 4 days to several weeks. As the facial lesions spread, ocular involvement often occurs, consisting of marked edema and erythema of the lids. The edema is frequently extensive enough to prevent opening of the eyes. The disease may also progress to gangrene of the eyelids. Although less common, inflammation spreads from the lids to the conjunctiva, producing chemosis and external ophthalmoplegia. Other complications include dacryoadenitis, orbital thrombophlebitis, cellulitis, abscess and cavernous sinus thrombosis. A late result in chronic infections may be a solid edema or elephantiasis of the eyelids.

DIAGNOSIS

Clinical signs and symptoms

Ocular or periocular manifestations

●Conjunctiva: chemosis, exudative or membranous conjunctivitis.

●Cornea: superficial punctate keratitis secondary to bacterial toxins or exposure with lid ectropion (late), ulcerative keratitis.

●Eyelids: abscess, blepharitis, ectropion, elephantiasis, erythema, gangrene, madarosis, marked edema necrosis, trichiasis.

●Iris: iridocyclitis.

●Lacrimal system: dacryoadenitis, dacryocystitis.

●Orbit: abscess, cellulitis, thrombophlebitis.

●Vitreous or retina: chorioretinitis, metastatic vitreous abscess.

Laboratory findings

●Most often, it is difficult to definitively identify the inciting organism.

●The use of blood cultures, needle aspirates, or biopsy specimens has yielded fewer than 10% positive cultures.

●Detection of Streptococcus spp. in skin specimens with direct immunofluorescence is helpful.

Differential diagnosis

●Ophthalmic herpes zoster.

●Allergic contact dermatitis.

●Myosis of collagen disease.

TREATMENT

Systemic

●Penicillin G is the drug of choice in treating erysipelas.

●Treatment should be instituted promptly and continued for 10 to 14 days to prevent the possibility of systemic spread.

●Intravenous penicillin G should be given in a minimum divided daily dosage of 6 million units.

●Once there is evidence of clinical improvement, the route of administration can be changed to oral medication.

●Penicillin V potassium should be given daily in four divided doses of 250 mg for the duration of the 10to 14-day therapy period.

●In patients sensitive to penicillin, erythromycin may be substituted.

●Erythromycin may be given orally at an initial dosage of 500 mg four times daily for several days and then reduced to 250 mg four times daily for 10 days.

●In severely ill patients, erythromycin 500 mg IV should be given twice a day for the first 2 or 3 days before oral therapy is begun.

Ocular

●In severe cases resulting in tissue destruction and lid necrosis, meticulous cleaning and debridement of the wounds on a daily basis should be the mainstay of local therapy.

●The wounds are surgically debrided and cleansed with a 1:1 solution of hydrogen peroxide and sterile saline and repacked daily with iodoform gauze.

●The use of warm saline compresses and topical broadspectrum antibiotic ointments helps accelerate the healing process and may prevent secondary bacterial contamination.

●The application of topical erythromycin ointment within the cul-de-sac helps prevent the occurrence of a secondary bacterial conjunctivitis.

●If there is a significant degree of lid contracture in the healing process, exposure keratitis may develop.

●This condition is best treated initially with tear substitute and lubricating ointments.

●Surgical repair of a cicatricial ectropion or other lid deformities may be required.

●It is prudent, however, to wait a minimum of 3 to 6 months before considering surgical intervention to allow the healing process to stabilize and reduce the likelihood of an undercorrection or overcorrection.

Supportive

●Attention should be given to the patient’s physical, nutritional, emotional and recreational activity needs.

●Hospitalization is usually indicated, with the patient on bedrest.

●The patient should be isolated until the fever subsides and strict hygienic measures should be used by all hospital personnel who have contact with an infected patient.

●Alcohol and tepid sponge baths may be used to reduce high temperature.

●Vital signs should be monitored regularly.