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11 Oct 2013

Bacterial Keratitis Clinical Presentation


History

Patients with microorganism inflammation sometimes complain of fast onset of pain, photophobia, and minimized vision. it's necessary to document an entire general and ocular history in these patients to spot any potential risk factors that might have created them at risk of develop this infection, together with the following:

  •  contact wear (Note the sort of lens, sporting time, and sort of medical care system.)
  •     Trauma (including previous tissue layer surgery)
  •     Use of contaminated ocular medications
  •  minimized medical specialty defenses
  •  liquid tear deficiencies
  •     Recent tissue layer illness (herpetic inflammation, neurotrophic keratopathy)
  •     Structural alteration or position of the eyelids
Physical

External and biomicroscopic examination of those patients reveals some or all of the subsequent features:

  •     Ulceration of the epithelium; membrane infiltrate with no vital tissue loss; dense, activity stromal inflammation with vague edges; stromal tissue loss; and encompassing stromal oedema
  •  magnified anterior chamber reaction with or while not hypopyon
  •     Folds within the Descemet membrane
  •  higher lid oedema
  •     Posterior synechiae
  •  encompassing membrane inflammation that's either focal or diffuse
  •  mucous membrane congestion
  •     Adherent humour exudate
  •  epithelium inflammatory plaque
Causes
Any issue or agent that makes a breakdown of the membrane epithelial tissue may be a potential cause or risk issue for microorganism rubor. what is more, exposure to some virulent microorganism which will penetrate intact epithelial tissue (eg, Neisseria gonorrhoeae) additionally might end in microorganism rubor.

  •  far and away the foremost common reason behind trauma to the membrane epithelial tissue and therefore the main risk issue for microorganism rubor is that the use of contact lenses, notably extended-wear contact lenses. Of patients with microorganism rubor, 19-42% area unit lens system wearers. Incidence of microorganism rubor secondary to use of extended-wear contact lenses is regarding 8,000 cases per annum. The annual incidence of microorganism rubor with daily-wear lenses is three cases per 10,000.
  •     Contaminated ocular medications, lens system solutions, or lens system cases[1]
  •  diminished medicine defenses secondary to deficiency disease, alcoholism, and polygenic disorder (Moraxella)
  •  liquid tear deficiencies
  •     Recent membrane malady (including herpetic rubor and secondary neurotrophic keratopathy)
  •     Structural alteration or misplacement of the eyelids (including entropion with trichiasis and lagophthalmos)
  •     Chronic inflammation
  •     Use of topical corticosteroids
Differential Diagnoses

  •     Blepharitis, Adult
  •     Conjunctivitis, Viral
  •     Endophthalmitis, Bacterial
  •     Entropion
  •     Gonococcus
  •     Herpes Simplex
  •     Herpes Zoster
  •     Keratitis, Fungal
  •     Keratitis, Herpes Simplex
  •     Keratitis, Interstitial
  •     Keratoconjunctivitis, Atopic
  •     Keratoconjunctivitis, Epidemic
  •     Keratopathy, Band
  •     Keratopathy, Neurotrophic
  •     Keratopathy, Pseudophakic Bullous
  •     Nasolacrimal Duct, Obstruction
  •     Ocular Rosacea
  •     Scleritis
  •     Ulcer, Corneal
Laboratory Studies

    Scrapings of the tissue layer ulceration, together with the sides, ought to be obtained employing a sterile spatula or blade, and that they ought to be plated in chocolate, blood, and Sabouraud agar plates.
 magnifier slides area unit used for stained smears with Gram, Giemsa, and imperviable stain or acridine orange/calcofluor white (if fungi or Acanthamoeba area unit suspected).
    Samples of the eyelids/conjunctiva, topical ocular medications, lens system cases, and solutions conjointly is also civilised.
    If the patient has been treated partly and therefore the rubor is delicate or moderately severe, antibiotic medical care is suspended for twelve hours before getting corneal/conjunctival samples for culture and sensitivity, to extend the yield of a positive culture.
    Cotton swabs contain fatty acids, that have AN repressing impact on microorganism growth. On the opposite hand, metallic element alginate moistened with trypticase soy broth is wont to acquire culture material to inoculate directly onto the culture media.
 local anaesthetic (proparacaine complex zero.5%) ought to be wont to put out the patient before culture scraping as a result of it's the smallest amount repressing impact. In distinction, topical anesthetic and hard drug have organic process effects.
    Repeat cultures is obtained if the initial cultures were negative and therefore the ulceration isn't rising clinically.
 tissue layer diagnostic assay employing a tiny trephine or a tissue layer blade ought to be thought-about in cases of deep stromal infiltrates, significantly if cultures area unit negative and therefore the eye isn't rising clinically.

Imaging Studies

    Slit lamp photography are often helpful to document the progression of the rubor, and, in cases wherever the particular etiology is doubtful, it's wont to get further opinions, notably in indolent and chronic cases not responding to antimicrobial medical aid.
    A B-scan ultrasound are often obtained in eyes with severe tissue layer ulcers with no read of the posterior section wherever endophthalmitis is being thought-about.

Procedures

 tissue layer biopsy: A deep lamellar excision are often created employing a disposable skin punch or atiny low Elliott tissue layer trephine. The superficial tissue layer is incised and concentrated with a surgical blade to close to two hundred microns. Then, a lamellar dissection is performed, and also the material is plated directly onto culture media. some can also be sent for histopathologic analysis.

Histologic Findings

During the initial stages, the epithelial tissue and also the stroma within the space of injury and infection swell and bear mortification. Acute inflammatory cells (mainly neutrophils) surround the start ulceration and cause mortification of the stromal lamellae. In cases of severe inflammation, a deep ulceration and a deep stromal symptom could coalesce, leading to cutting of the tissue layer and biological process of the infected stroma.

As the natural host defense mechanisms overcome the infection, body substance and cellular immune defenses mix with medication medical aid to retard microorganism replication. Following this method, activity of the organism and cellular trash happen, while not more destruction of stromal albuminoid. throughout this stage, a definite bounds could seem because the animal tissue ulceration and stromal infiltration consolidate and also the edges become rounded.

Vascularization of the tissue layer could follow if the rubor becomes chronic. within the healing stage, the epithelial tissue resurfaces the central space of ulceration and also the death stroma is replaced by connective tissue made by fibroblasts. The reparative fibroblasts square measure derived from histiocytes and keratocytes that have undergone transformation. Areas of stromal cutting could also be replaced part by animal tissue. New vas growth directed toward the world of ulceration happens with delivery of body substance and cellular elements to market more healing. The expert layer doesn't regenerate however is replaced with animal tissue.

New epithelial tissue slowly resurfaces the irregular base, and organic process step by step disappears. With severe microorganism rubor, the progressive stage advances on the far side the purpose within which the regressive stage will cause the healing stage. In such severe ulcerations, stromal keratolysis could reach tissue layer perforation. body structure blood vessels could participate in waterproofing the perforation, leading to associate adherent vascularized eye disease.

Medical Care

If no organisms are identified on the slide smear, initiate broad-spectrum antibiotics with the following: tobramycin (14 mg/mL) 1 drop every hour alternating with fortified cefazolin (50 mg/mL) 1 drop every hour.

If the corneal ulcer is small, peripheral and no impending perforation is present, intensive monotherapy with fluoroquinolones is an alternative treatment. Other antimicrobials can be used, depending on the clinical progress and laboratory findings.

The fourth-generation ophthalmic fluoroquinolones include moxifloxacin (VIGAMOX, Alcon Laboratories, Inc, Fort Worth, TX) and gatifloxacin (Zymar, Allergan, Irvine, CA), and they are now being used for the treatment of bacterial conjunctivitis. Both antibiotics have better in vitro activity against gram-positive bacteria than ciprofloxacin or ofloxacin. Moxifloxacin penetrates better into ocular tissues than gatifloxacin and older fluoroquinolones; in vitro activity of moxifloxacin and gatifloxacin against gram-negative bacteria is similar to that of older fluoroquinolones. Moxifloxacin also has better mutant prevention characteristics than other fluoroquinolones. These findings support the use of the newer fluoroquinolones for the prevention and treatment of serious ophthalmic infections (eg, keratitis, endophthalmitis) caused by susceptible bacteria.

In view of these findings, moxifloxacin or gatifloxacin may be a preferred alternative to ciprofloxacin as the first-line monotherapy in bacterial keratitis.

Additionally, 0.5% moxifloxacin and, to a lesser extent, levofloxacin and ciprofloxacin have demonstrated significant effectiveness for reducing the number of Mycobacterium abscessus in vivo, suggesting the potential use of these agents in prevention of M abscessus keratitis.

Three patients with Acanthamoeba keratitis were successfully treated with a topical application of 0.1% riboflavin solution and 30 minutes of UV irradiation focused on the corneal ulcer.[2]

The frequency of antibiotic administration should be tapered off according to the clinical course using some of the following parameters:

  •     Blunting of the perimeter of the stromal infiltrate
  •     Decreased density of the stromal infiltrate
  •     Decreased stromal edema and endothelial inflammatory plaque
  •     Decreased anterior chamber inflammation
  •     Reepithelialization of the corneal epithelial defect
  •     Improvement in painful symptoms
Surgical Care

The most common explanation for tissue layer perforation is infection by bacterium, virus, or fungus, accounting for 24-55% of all perforations, with microorganism infections being the foremost common. PK, sclerocorneal patch, or application of cyanoacrylate tissue adhesive could also be necessary in cases of tissue layer perforation or close perforation, following the rules provided below.

 general endovenous associatetibiotics (alternatively Cipro five hundred mg PO bid) ought to be started once an infected tissue layer ulceration has perforated and for three days following the PK.
 a transparent plastic defend ought to be placed over the attention.
 the utilization of general anaesthesia typically is most well-liked for plastic surgery surgery. anaesthesia will be used for application of tissue adhesive.
 the scale of the transplant ought to be the tiniest trephine capable of incorporating the perforation website and any infected or ulcerous border. Donor typically is outsized by zero.5 mm.
    Cataract removal is left for a sequent procedure as a result of the chance of expulsive hemorrhage and endophthalmitis.
    Posterior and anterior synechiae ought to be lysed gently.
    The anterior chamber ought to be irrigated to get rid of any death or inflammatory detritus.
    The donor membrane ought to be secured with sixteen interrupted 10-0 nylon sutures.
    Subconjunctival injections of antibiotics will be given while not depot steroid injection.
 surgical  use of frequent topical fortified antibiotics. Corticosteroids four times on a daily basis will be used straight off when surgery if it's believed that the infection was excised fully. as an alternative, steroids will be withheld for many days to watch for infection. Once the acute surgical  amount is over, long care is analogous as that for uncomplicated PK.

Consultations

Consultation with vitreoretinal colleagues could also be useful if the diagnosing of endophthalmitis is taken into account.

References

    Hall BJ, Jones L. Contact Lens Cases: The Missing Link in Contact Lens Safety?. Eye Contact Lens. Jan 19 2010;

    Khan YA, Kashiwabuchi RT, Martins SA, Castro-Combs JM, Kalyani S, Stanley P. Riboflavin and ultraviolet light a therapy as an adjuvant treatment for medically refractive acanthamoeba keratitis report of 3 cases. Ophthalmology. Feb 2011;118(2):324-31.

    Haas W, Pillar CM, Torres M, Morris TW, Sahm DF. Monitoring Antibiotic Resistance in Ocular Microorganisms: Results From the Antibiotic Resistance Monitoring in Ocular MicRorganisms (ARMOR) 2009 Surveillance Study. Am J Ophthalmol. Oct 2011;152(4):567-574.e3. .

    Lalitha P, Srinivasan M, Manikandan P, Bharathi MJ, Rajaraman R, Ravindran M, et al. Relationship of In Vitro Susceptibility to Moxifloxacin and In Vivo Clinical Outcome in Bacterial Keratitis. Clin Infect Dis. Mar 23 2012;[Medline].

    Bower KS, Kowalski RP, Gordon YJ. Fluoroquinolones in the treatment of bacterial keratitis. Am J Ophthalmol. Jun 1996;121(6):712-5.

    Caballero AR, Marquart ME, O'Callaghan RJ, Thibodeaux BA, Johnston KH, Dajcs JJ. Effectiveness of fluoroquinolones against Mycobacterium abscessus in vivo. Curr Eye Res. Jan 2006;31(1):23-9.

    Genvert GI, Cohen EJ, Donnenfeld ED. Erythema multiforme after use of topical sulfacetamide. Am J Ophthalmol. Apr 15 1985;99(4):465-8.

    Goldstein MH, Kowalski RP, Gordon YJ. Emerging fluoroquinolone resistance in bacterial keratitis: a 5-year review. Ophthalmology. Jul 1999;106(7):1313-8.

    Hirst LW, Harrison GK, Merz WG. Nocardia asteroides keratitis. Br J Ophthalmol. Jun 1979;63(6):449-54. [Medline].

    Hirst LW, Smiddy WE, Stark WJ. Corneal perforations. Changing methods of treatment, 1960--1980. Ophthalmology. Jun 1982;89(6):630-5.

    Hyndiuk RA, Eiferman RA, Caldwell DR. Comparison of ciprofloxacin ophthalmic solution 0.3% to fortified tobramycin-cefazolin in treating bacterial corneal ulcers. Ciprofloxacin Bacterial Keratitis Study Group. Ophthalmology. Nov 1996;103(11):1854-62; discussion 1862-3.

    Knapp A, Stern GA, Hood CI. Mycobacterium avium-intracellulare corneal ulcer. Cornea. 1987;6(3):175-80.

    Leibowitz HM. Clinical evaluation of ciprofloxacin 0.3% ophthalmic solution for treatment of bacterial keratitis. Am J Ophthalmol. Oct 1991;112(4 Suppl):34S-47S.

    Moore MB, Newton C, Kaufman HE. Chronic keratitis caused by Mycobacterium gordonae. Am J Ophthalmol. Oct 15 1986;102(4):516-21.

    Newman PE, Goodman RA, Waring GO 3d. A cluster of cases of Mycobacterium chelonei keratitis associated with outpatient office procedures. Am J Ophthalmol. Mar 1984;97(3):344-8. .

    Parmar P, Salman A, Kalavathy CM. Comparison of topical gatifloxacin 0.3% and ciprofloxacin 0.3% for the treatment of bacterial keratitis. Am J Ophthalmol. Feb 2006;141(2):282-286.
    Pate JC, Jones DB, Wilhelmus KR. Prevalence and spectrum of bacterial co-infection during fungal keratitis. Br J Ophthalmol. Mar 2006;90(3):289-92.

    Poggio EC, Glynn RJ, Schein OD. The incidence of ulcerative keratitis among users of daily-wear and extended-wear soft contact lenses. N Engl J Med. Sep 21 1989;321(12):779-83.

    Schein OD, Glynn RJ, Poggio EC. The relative risk of ulcerative keratitis among users of daily-wear and extended-wear soft contact lenses. A case-control study. Microbial Keratitis Study Group. N Engl J Med. Sep 21 1989;321(12):773-8.

    Schlech BA, Alfonso E. Overview of the potency of moxifloxacin ophthalmic solution 0.5% (VIGAMOX). Surv Ophthalmol. Nov 2005;50 Suppl 1:S7-15.

    Stern GA, Buttross M. Use of corticosteroids in combination with antimicrobial drugs in the treatment of infectious corneal disease. Ophthalmology. Jun 1991;98(6):847-53.

    Stern GA, Schemmer GB, Farber RD. Effect of topical antibiotic solutions on corneal epithelial wound healing. Arch Ophthalmol. Apr 1983;101(4):644-7.
    Varma R, eds. Cornea/external diseases. Essentials of Eye Care: The Johns Hopkins Wilmer Handbook. Lippincott Williams & Wilkins;1997:152-203.

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